Cardiology

CARDIOLOGY ANATOMY of the HEARTYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY

R ATRIUM (Tricuspid valve) – R VENTRICLE L ATRIUM (Mitral Valve) – L VENTRICLE The MITRAL and TRICUSPID (atrioventricular valves). Valves prevented being everted during systole (into atria) by

chordae tendinae and papillary muscles that contract in systole.

Pulmonary semilunar valve- Pulmonary artery. Aortic semilunar valve – Aorta (passively close at the end of

systole- ventricular pressure now less than in arteries).

Atria and ventricles separated by ANNULUS FIBROSUS A band of fibrous connective tissue- provides skeleton for

attachment of muscle and insertion of the valves. Prevents conduction between atria and ventricles except at AV

NODE. AV node near the inetratrial septum and mouth of the

coronary sinus.

During diastole, ventricles fill. At initiation of systole, atria contract and complete ventricular

filling. As ventricles contract, pressure rises sharply, and AV valves

close. When ventricular pressure exceeds pulmonary/aortic pressure,

semilunar valves open, and ejection occurs. Semilunar valves closed by backflow from aretries.

Force of contraction generated by MYOCARDIUM. Ventricles have thicker myocardium than atria. Inside of heart lined with ENDOCARDIUM (thin cell layer)-

Thin, slick sheet of connective tissue located on the inner surface of the myocardium. It is continuous with the blood vessels.

Outer surface of myocardium lined with EPICARDIUM (Visceral layer of serous pericardium)

Heart enclosed in PERICARDIUM (sac) o Fibrous Pericardiumo Serous pericardium (visceral and parietal layer, in-

between is the pericardial cavity) PERICARDIAL CAVITY, enclosed in the serous pericardium,

contains interstitial fluid as lubricant.

Myocardium made of cardiac myocytes (muscle cells) Connected together by network of intercalated disks The disks provide a structural attachment (glue together at

dermosomes) and electrical connection through GAP JUNCTIONS.

Myocardium acts as a FUNCTIONAL SYNCYTIUM- a single functional unit, even through individual cells separate.

Muscles are arranged in spiral and circular bundles.

Muscle contracts the chambers constrict and blood is expelled out of the chamber.

SA NODE initiates the contraction To AV NODE BUNDLE OF HIS To PURKINJE FIBRES

CIRCULATIONYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY

SUPERIOR and INFERIOR VENA CAVA. PULMONARY TRUNK R. and L. PULMONARY ARTERIES L. and R. PULMONARY VEINS AORTA

o BRACHIOCEPHALIC ARTERYo COMMON CAROTID ARTERYo LEFT SUBCLAVIAN ARTERYo DESCENDING AORTA

Blood supply from LEFT and RIGHT CORONARY ARTERIES BOTH have descending and marginal… just the left also has a circumflex. Arise from the aortic sinus, at the base of the aorta. Remain patent throughout cardiac cycle, and not blocked by cusps of aortic semilunar valve. RIGHT CORONARY- runs between pulmonary trunk and R. Atrium, to AV sulcus. Then descends to lower heart, dividing into posterior descending and right marginal LEFT CORONARY, runs behind pulmonary trunk and forward between it and L. Atrium, divides into the 3 further trunks. Anastamosis between L and R Marginal branches. Anastamosis between anterior and posterior descending branches.

Blood returns via coronary sinus and anterior coronary veins LEFT CORONARY ARTERY

o Left Atriumo Left ventricleo Interventricular septumo Anterior wall of right ventricle

RIGHT coronary artery o Right Atriumo Right Ventricleo (in most people) supplies AV and SA NODEo Arterial disease here can cause AV block or slow HR.

Coronary perfusion pressure: difference between the diastolic pressure in aorta and diastolic pressure in RA, which creates the perfusion pressure (coronary arteries fill in diastole)

In tachycardia, less time spent in diastole- inc risk of ischemia

CIRCULATIONYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY

LEFT CORONARY ARTERY

The left main coronary artery (LMCA) arises from the left aortic sinus, It quickly divides into the anterior interventricular branch also known as the left anterior descending (LAD) artery and the

circumflex artery. The LAD runs along the anterior interventricular sulcus, (groove in the anterior surface of the heart that separates the left and

right ventricle) down towards the apex. LAD runs around to the posterior surface of the heart in another groove called the posterior interventicular sulcus. The LAD artery supplies blood to the walls of both the left and right ventricles. The circumflex, follows a different course to the LAD. It runs along the atrioventricular groove, which seperates the atria from the

ventricles, giving rise to the left marginal branch in the process. The circumflex then continues around the heart, terminating on its posteroinferior aspect, to supply blood to both the left and

right atrium.

RIGHT CORONARY ARTERY

The right coronary artery (RCA) arises from the right aortic sinus, and along the right atrioventricular groove. From here, it curls around towards the inferior surface of the heart, forming the posterior interventricular branch, more

commonly known as the posterior descending artery (PDA). The PDA runs along the posterior interventiculas sulcus, to supply blood to the walls of both the left and right ventricle. However, before turning towards the diaphragmatic surface of the heart the RCA gives rise to the right marginal branch, that

runs along the right margin, to supply the wall of the right ventricle. Important branches from the RCA include, the conus branch and the sino-atrial node artery. As an aside, compared to the left ventricle the right ventricle has a greater ratio of muscle fibres to capillaries: it is more likely to

suffer toxic damage but less likely to suffer ischaemic damage.

CORONARY BLOOD FLOW

Small arteries and arterioles are key players in altering vascular resistance and thus regulating myocardial blood flow.

Myocardial blood flow is closely linked with oxygen demand, with an increase in cardiac activity resulting in an increase in demand for oxygen.

This is achieved by an increase in myocardial blood flow, involving autoregulation. Whenever there is a change in coronary perfusion pressure, through changes in aortic pressure, the

process of autoregulation ensures that myocardial blood flow is always maintained. Adenosine and nitric oxide (NO) are important mediators in the regulation of coronary blood flow as

well as the involvement of the sympathetic and parasympathetic nervous system.

QUICK RELATION TO EGC

ISCHEMIA: ST depression and T-wave inversion INJURY: ST elevation INFARCTION: ST elevation PREV INFARCTION: Q waves

SEPTAL: V!, V2

ANTERIOR: V3, V4

LATERAL: V5, V6, V1, aVL

INFERIOR: II, III, aVF

V1 V4I

ARTERIAL OCCLUSIONYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY

LAD: the LEFT ANTERIOR DESCENDING, from left coronaryo V1 (septal)o V2 (septal)o V3 (anterior)o V4 (anterior)o V5 (lateral)o V6 (lateral)

L. Circumflex o 1 (all lateral)o aVLo V5 and V6 (maybe)

R. Coronary Arteryo II (inferior)o III (inferior)o aVF (inferior)

THE CARDIAC CYCLE- VENTRICLE AP YYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY

What is an action potential? It is when a cell transiently depolarizes, due to ion channels. CARDAC ACTION POTENTIAL is a lot longer than those in nerves or skeletal muscle. Because of a PLATEAU PHASE in cardiac muscle, lasting 200-300ms.

VENTRICULAR MUSCLE ACTION POTENTIAL

o (4) -90 RESTING POTENTIAL The membrane at rest is most permeable to K+ ions, so the RESTING POTENTIAL is most dependent on the K+

gradient. (K+ out) There is transmission from an adjacent cell through intercalated disks. An action potential is initiated when the membrane is depolarized to a THRESHOLD POTENTIAL.

o (0) RAPID DEPOLERISATION: Rapid Na+ channels are stimulated to open, flooding the cell with positive Na+ ions. Transmembrane potential is the is the difference in voltage inside, compared to outside the cell. Positive

change. The Na+ going in is large enough to overcome the outward current through K+ channels.

THE CARDIAC CYCLE- VENTRICLE AP YYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY

What is an action potential? It is when a cell transiently depolarizes, due to ion channels. CARDAC ACTION POTENTIAL is a lot longer than those in nerves or skeletal muscle. Because of a PLATEAU PHASE in cardiac muscle, lasting 200-300ms.

VENTRICULAR MUSCLE ACTION POTENTIAL

o (4) -90 RESTING POTENTIAL The membrane at rest is most permeable to K+ ions, so the RESTING POTENTIAL is most dependent on the K+

gradient. (K+ out) There is transmission from an adjacent cell through intercalated disks. An action potential is initiated when the membrane is depolarized to a THRESHOLD POTENTIAL.

o (0) RAPID DEPOLERISATION: Rapid Na+ channels are stimulated to open, flooding the cell with positive Na+ ions. Transmembrane potential is the is the difference in voltage inside, compared to outside the cell. Positive

change. The Na+ going in is large enough to overcome the outward current through K+ channels.

THE CARDIAC CYCLE – SA NODE Action PotentialYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY

SA NODE INITIATING THE HEART BEATo SA node is primary heart pacemaker.o Innervated by

Parasympathetic VAGUS CNX (dec Heart rate, not contraction) Sympathetic T1- T4 Spinal nerves (innervate atria and ventricles too so can

increase contraction force as well as HR)o The SA node cells have no ‘resting potential’- regular spontaneous Action Potentials are

generated.o SA node cells are special, as slow Ca2+ channels carry the current, rather than the fast

Na+ channels.o Relies on CALCIUM influx, rather than SODIUM.o In terms of how fast they depolarize, the action potentials are much slower than in eg.

Skeletal muscle or cardiac muscle.o Can be referred to as ‘slow-response action potentials’- the curve doesn’t go up sharp.o Conduction velocity is slow- slower conduction cell to cell.o An action potential in the SA node is generated at -40- (rather than -60 in cardiac

myocytes)- ie… the cell has to get even more positive before an action potential is created- its harder.

o The Ca2+ channels activate in a more positive environment than the Na+ ones.o The rate of decay of the resting potential, (to make an action potential) determines the

heart rate.

THE CARDIAC CYCLE – SA NODE Action PotentialYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY

SA NODE INITIATING THE HEART BEATo SA node is primary heart pacemaker.o Innervated by

Parasympathetic VAGUS CNX (dec Heart rate, not contraction) Sympathetic T1- T4 Spinal nerves (innervate atria and ventricles too so can

increase contraction force as well as HR)o The SA node cells have no ‘resting potential’- regular spontaneous Action Potentials are

generated.o SA node cells are special, as slow Ca2+ channels carry the current, rather than the fast

Na+ channels.o Relies on CALCIUM influx, rather than SODIUM.o In terms of how fast they depolarize, the action potentials are much slower than in eg.

Skeletal muscle or cardiac muscle.o Can be referred to as ‘slow-response action potentials’- the curve doesn’t go up sharp.o Conduction velocity is slow- slower conduction cell to cell.o An action potential in the SA node is generated at -40- (rather than -60 in cardiac

myocytes)- ie… the cell has to get even more positive before an action potential is created- its harder.

o The Ca2+ channels activate in a more positive environment than the Na+ ones.o The rate of decay of the resting potential, (to make an action potential) determines the

heart rate.

THE CARDIAC CYCLE – CARDIAC MUSCLE CONTRACTIONYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY

Between the ends of adjacent cardiac muscle cells are specialised intercellular junctions called INTERCALATED DISCS. These are irregular transverse thickenings of the sarcolemma that contain structures called DESMOSOMES. Desmosomes are like spot-rivets, that hold adjacent cardiac muscle fibres together. The intercalated discs act as points of anchorage for the contractile proteins, and they contain channels called GAP JUNCTIONS. These connect the cytoplasm of adjacent cardiac muscle fibres and permit the extremely rapid low-resistance spread of action

potentials from one cell to another. Adjacent fibres are caused to contract almost simultaneously Three types of cardiocytes are found in the myocardium.

o 1. AUTORHYTHMIC CELLS: Cells found at the junction of the great veins and the right atrium have the fastest intrinsic rhythm (this is the sinoatrial (SA) node or 'pacemaker' of the heart).

o Spontaneously discharge about 100 times per minute. o Nervous and hormonal input can alter the rate of this automatic discharge so that the normal heart rate is about 70

beats per minute.o 2. PURKINJE FIBRES (conduction fibres) allow fast conduction of action potentials around the heart. o 3. MYOCYTES (contractile cells)

CONTRACTION- depends on CALCIUM!o Remember: calcium induced calcium release. In the absence of external Ca2+, there can be no contraction.o Cardiac muscle contraction occurs by utilising the sliding filament model already described for skeletal muscle. o The action potential spreads from the cell membrane into the T tubules.o Calcium enters the cell from the ECF (this doesn't happen in skeletal muscle).

THE CARDIAC CYCLE – CARDIAC MUSCLE CONTRACTIONYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY

Between the ends of adjacent cardiac muscle cells are specialised intercellular junctions called INTERCALATED DISCS. These are irregular transverse thickenings of the sarcolemma that contain structures called DESMOSOMES. Desmosomes are like spot-rivets, that hold adjacent cardiac muscle fibres together. The intercalated discs act as points of anchorage for the contractile proteins, and they contain channels called GAP JUNCTIONS. These connect the cytoplasm of adjacent cardiac muscle fibres and permit the extremely rapid low-resistance spread of action

potentials from one cell to another. Adjacent fibres are caused to contract almost simultaneously Three types of cardiocytes are found in the myocardium.

o 1. AUTORHYTHMIC CELLS: Cells found at the junction of the great veins and the right atrium have the fastest intrinsic rhythm (this is the sinoatrial (SA) node or 'pacemaker' of the heart).

o Spontaneously discharge about 100 times per minute. o Nervous and hormonal input can alter the rate of this automatic discharge so that the normal heart rate is about 70

beats per minute.o 2. PURKINJE FIBRES (conduction fibres) allow fast conduction of action potentials around the heart. o 3. MYOCYTES (contractile cells)

CONTRACTION- depends on CALCIUM!o Remember: calcium induced calcium release. In the absence of external Ca2+, there can be no contraction.o Cardiac muscle contraction occurs by utilising the sliding filament model already described for skeletal muscle. o The action potential spreads from the cell membrane into the T tubules.o Calcium enters the cell from the ECF (this doesn't happen in skeletal muscle).

THE CARDIAC CYCLE – THE ACTUAL CYCLEYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY

The sequence of mechanical events that occur during a heart beat Ie. Diastole, Systole, and the Pause. Cycle begins when SA node initiates a heart beat

o It’s the end of diastoleo Atrium and ventricles are relaxedo Mitral and Tricuspid (atrioventricular valves) are openo Pulmonary and Aortic (semilunar valves) are closed- as the arterial pressure- both pulmonary and aortic pressure is

greater than the relaxed ventricular. 1. ATRIAL SYSTOLE (ATRIAL contraction)

o Blood from Atrium - Ventricleso Fills the ventricles and completes ventricular fillingo AV valves openo Semilunar valves closed o Ventricles are already partially filled from when the whole heart was relaxed.o Ventricles receive the last 30% blood- final vol of approx. 130ml.

2. ISOVOLUMETRIC CONTRACTION (VENTRICLES CONTRACT)o Ventricles filled with blood contracto Tricuspid and Mitral valves close as pressure now high in ventricleso Ventricular volume unchanged, but the pressure rockets.o Semilunar valves still closed.

THE CARDIAC CYCLE – THE ACTUAL CYCLEYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY

The sequence of mechanical events that occur during a heart beat Ie. Diastole, Systole, and the Pause. Cycle begins when SA node initiates a heart beat

o It’s the end of diastoleo Atrium and ventricles are relaxedo Mitral and Tricuspid (atrioventricular valves) are openo Pulmonary and Aortic (semilunar valves) are closed- as the arterial pressure- both pulmonary and aortic pressure is

greater than the relaxed ventricular. 1. ATRIAL SYSTOLE (ATRIAL contraction)

o Blood from Atrium - Ventricleso Fills the ventricles and completes ventricular fillingo AV valves openo Semilunar valves closed o Ventricles are already partially filled from when the whole heart was relaxed.o Ventricles receive the last 30% blood- final vol of approx. 130ml.

2. ISOVOLUMETRIC CONTRACTION (VENTRICLES CONTRACT)o Ventricles filled with blood contracto Tricuspid and Mitral valves close as pressure now high in ventricleso Ventricular volume unchanged, but the pressure rockets.o Semilunar valves still closed.

THE CARDIAC CYCLE – SOUNDS and CONDUCTIONYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY

Heart Sounds HS I-II+0

o S1: Closure of AV Valveso Lubo Normally close together, if split- might indicate delayed conductiono In L or R bundle of HIS.o AV valves close during ventricular contraction, so ie. A ventricle is contracting a bit late

o S2: Pulmonary/aortic valve closureo Splits in young people due to inspiration of exercise- longer ejection period in right ventricle.o Lungs are lower pressure, want to keep blood, less returns to Left ventricleo Increase in blood into Right ventricle from vena cava, as sucked into Right Atrium, and wants to go into the

lungs.o Takes longer to empty Right ventricle as more blood, pulmonary valve stays open a bit longer than aortic.o Aortic closes slightly earlier, as less blood.

o S3: Rapid refilling, S4: atrial systole (S3 and S4 togther produce a gallop rhythem)- HF.

Electrical conduction pathways

CARDIAC MUSCLEo Muscle cells connected by intercalated discso On the intercalated disc connections are GAP JUNCTIONS, where membranes of cells are very close, consist of low

resistance proteins: CONNEXONSo Allow transfer of small ions, therefore ELECTRICAL CURRENT.o Cardiac muscle is a FUNCTIONAL SYNCTIUM: as its electrically connected.

THE CARDIAC CYCLE – SOUNDS and CONDUCTIONYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY

Heart Sounds HS I-II+0

o S1: Closure of AV Valveso Lubo Normally close together, if split- might indicate delayed conductiono In L or R bundle of HIS.o AV valves close during ventricular contraction, so ie. A ventricle is contracting a bit late

o S2: Pulmonary/aortic valve closureo Splits in young people due to inspiration of exercise- longer ejection period in right ventricle.o Lungs are lower pressure, want to keep blood, less returns to Left ventricleo Increase in blood into Right ventricle from vena cava, as sucked into Right Atrium, and wants to go into the

lungs.o Takes longer to empty Right ventricle as more blood, pulmonary valve stays open a bit longer than aortic.o Aortic closes slightly earlier, as less blood.

o S3: Rapid refilling, S4: atrial systole (S3 and S4 togther produce a gallop rhythem)- HF.

Electrical conduction pathways

CARDIAC MUSCLEo Muscle cells connected by intercalated discso On the intercalated disc connections are GAP JUNCTIONS, where membranes of cells are very close, consist of low

resistance proteins: CONNEXONSo Allow transfer of small ions, therefore ELECTRICAL CURRENT.o Cardiac muscle is a FUNCTIONAL SYNCTIUM: as its electrically connected.

THE CARDIAC CYCLE – THE BASIC LAWSYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY

HEART BLOCKo Complete heart block (third degree) occurs when conduction between atria and ventricles abolished.o Ischemic damage to nodal tissue/ Bundle His.o AVN and Bundle of His then generate HR of around 40bpmo Abnormally slow conduction through AV Node- causes incomplete (1st degree) Heart Block- delay is greater than normal-

extended P-R interval on ECG.o 2nd degree heart block when only a fraction of impulses from atria are conducted- eg. Ventricular contraction only

initiated every 2nd or 3rd atrial contraction (2:1 or 3:1 block)o Wencheback (Mobitz2) is another type of 2nd degree block- P-R interval progressively lengthens, until no transmission

from atria to ventricles, and a QRS is missed. BUNDLE BRANCH BLOCK

o When one branch of bundle of His doesn’t conduct.o The part of the ventricle it serves will still be stimulated by conduction through the myocardium from unaffected areas.o Conduction is slower, activation is delayed and QRS broadened (ventricular systole takes longer)

ARRYTHMIASo Caused, promoted, potentiated by defects in conduction system/ ischemia/ damage

WOLF-PARKINSON WHITE SYNDROMEo AV NODE normal, but a separate extra congenital conduction pathway (bundle of Kent) between atrium and ventricle.o Atrial impulses conducted to ventricles by AV NODE and Bundle of Kent.o Bundle of Kent faster, so part of ventricle stimulated before the rest- wide QRS COMPLEX. (pre-excitation).o A premature impulse can set up a re-entry circuit and bad and fast arrhythmia.

HAEMODYNAMICS

DARCYS LAW:


HEART BLOCKo Complete heart block (third degree) occurs when conduction between atria and ventricles abolished.o Ischemic damage to nodal tissue/ Bundle His.o AVN and Bundle of His then generate HR of around 40bpmo Abnormally slow conduction through AV Node- causes incomplete (1st degree) Heart Block- delay is greater than normal-

extended P-R interval on ECG.o 2nd degree heart block when only a fraction of impulses from atria are conducted- eg. Ventricular contraction only

initiated every 2nd or 3rd atrial contraction (2:1 or 3:1 block)o Wencheback (Mobitz2) is another type of 2nd degree block- P-R interval progressively lengthens, until no transmission

from atria to ventricles, and a QRS is missed. BUNDLE BRANCH BLOCK

o When one branch of bundle of His doesn’t conduct.o The part of the ventricle it serves will still be stimulated by conduction through the myocardium from unaffected areas.o Conduction is slower, activation is delayed and QRS broadened (ventricular systole takes longer)

ARRYTHMIASo Caused, promoted, potentiated by defects in conduction system/ ischemia/ damage

WOLF-PARKINSON WHITE SYNDROMEo AV NODE normal, but a separate extra congenital conduction pathway (bundle of Kent) between atrium and ventricle.o Atrial impulses conducted to ventricles by AV NODE and Bundle of Kent.o Bundle of Kent faster, so part of ventricle stimulated before the rest- wide QRS COMPLEX. (pre-excitation).o A premature impulse can set up a re-entry circuit and bad and fast arrhythmia.

HAEMODYNAMICS

DARCYS LAW:


BLOOD VISCOSITYo Viscosity is caused by frictional forces in a fluid that resist flow.o Blood is 4x as viscous as water because of erythrocytes.o ANAEMIA: haematocrit (cell concentration) is low, viscosity and vascular resistance decrease, Cardiac Output rises.o POLYCYTHEMIA: vascular resistance and blood pressure are increased.

LAMINAR FLOWo As liquid flows through a tube, frictional forces are exerted by the tube wall.o These, and viscous forces in the tube, set up a velocity gradient across the tube.o Flow velocity is greatest at tube centre. (LAMINAR FLOW)o Occurs in the microcirculation.o Erythrocytes move away from vessel wall, and sit in the middle flow, aligned. o Reduces the viscisoty of the blood in the microcirculation, reducing the resistance (Fahraeus-Lindqvist effect)

WALL TENSION (TRANSMURAL PRESSURE)o The wall has a pressure exerted on it: Pressure inside the vessel, minus the interstitial pressure.o This distends the blood vessel wall (ie, the pressure of the blood pushes it out)o This is the FRANK/LAPLACE LAW

Wall Tension = Transmural Pressure vessel rad iuswall Thickness

o In the aorta, where the transmural pressure (blood pushing wall out) is high, atherosclerosis may cause thinning of the blood vessel wall, and the development of a bulge/anyeurysm.

o This increases the vassel radius, and decreases wall thickness, which sets up a viscious cycle of increasing wall tension,


BLOOD VISCOSITYo Viscosity is caused by frictional forces in a fluid that resist flow.o Blood is 4x as viscous as water because of erythrocytes.o ANAEMIA: haematocrit (cell concentration) is low, viscosity and vascular resistance decrease, Cardiac Output rises.o POLYCYTHEMIA: vascular resistance and blood pressure are increased.

LAMINAR FLOWo As liquid flows through a tube, frictional forces are exerted by the tube wall.o These, and viscous forces in the tube, set up a velocity gradient across the tube.o Flow velocity is greatest at tube centre. (LAMINAR FLOW)o Occurs in the microcirculation.o Erythrocytes move away from vessel wall, and sit in the middle flow, aligned. o Reduces the viscisoty of the blood in the microcirculation, reducing the resistance (Fahraeus-Lindqvist effect)

WALL TENSION (TRANSMURAL PRESSURE)o The wall has a pressure exerted on it: Pressure inside the vessel, minus the interstitial pressure.o This distends the blood vessel wall (ie, the pressure of the blood pushes it out)o This is the FRANK/LAPLACE LAW

Wall Tension = Transmural Pressure vessel rad iuswall Thickness

o In the aorta, where the transmural pressure (blood pushing wall out) is high, atherosclerosis may cause thinning of the blood vessel wall, and the development of a bulge/anyeurysm.

o This increases the vassel radius, and decreases wall thickness, which sets up a viscious cycle of increasing wall tension,


WHAT IF THE AFTERLOAD (BP) IS HIGH? WILL SV DECREASE?o Starlings law means that even if the afterload (blood pressure) increases, the stroke volume can be maintained.o The resistance to outflow increases, the left ventricle has to pump against a higher resistance, and the amount of blood

ejected is reduced.o This means the EJECTION FRACTION has decreased, and the proportion of the END DIASTOLIC VOLUME pumped out falls.o The end systolic volume is larger than the beat before. o So when the ventricle is being filled again in diastole, there is already more blood than usual in the ventricle.o The end diastolic volume is now larger! Ventricle wall is stretched more, so STROKE VOLUME INCREASES.o When BP increases, the ENP and EDV increase too, so CO can remain the same, despite pushing against greater force.

AUTONOMIC NSo Externally regulates COo So very important in controlling BP.o Sympathetic stimulation (adrenaline) causes an increase in HR and contractile force.

Positive IONOTROPE, and CHRONOTROPEo The ventricular function curve is shifted upwardso Nor-adrenaline inc this too.o Negative ionotropes decrease force

o Acidity

CVP and Autonomic NS are prime determinants of CO.


WHAT IF THE AFTERLOAD (BP) IS HIGH? WILL SV DECREASE?o Starlings law means that even if the afterload (blood pressure) increases, the stroke volume can be maintained.o The resistance to outflow increases, the left ventricle has to pump against a higher resistance, and the amount of blood

ejected is reduced.o This means the EJECTION FRACTION has decreased, and the proportion of the END DIASTOLIC VOLUME pumped out falls.o The end systolic volume is larger than the beat before. o So when the ventricle is being filled again in diastole, there is already more blood than usual in the ventricle.o The end diastolic volume is now larger! Ventricle wall is stretched more, so STROKE VOLUME INCREASES.o When BP increases, the ENP and EDV increase too, so CO can remain the same, despite pushing against greater force.

AUTONOMIC NSo Externally regulates COo So very important in controlling BP.o Sympathetic stimulation (adrenaline) causes an increase in HR and contractile force.

Positive IONOTROPE, and CHRONOTROPEo The ventricular function curve is shifted upwardso Nor-adrenaline inc this too.o Negative ionotropes decrease force

o Acidity

CVP and Autonomic NS are prime determinants of CO.

CARDIAC REFLEXESYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY

REFLEXESo Fluctuations in MABP (Mean arterial BP) and volume need to be minimized, to maintain adequate cerebral and cardiac

perfusion.o There are autonomic reflexes and local mechanisms.o Intrinsic reflexes (respond to stimuli in CV system)

Baroreceptor Cardiopulmonary Chemoreceptor

o Extrinsic reflexes- Cardiac responding to stimuli elsewhere.o Eg. Pain/temp changes

o Cardiovascular reflexes involveo RECEPTORS: Afferent nerves- sense change, communicate to braino BRAIN: Processes and responds to info, so later activity of efferent nerveso EFFERENT NERVES: control cardiac, vascular and renal function- homeostasis- reverse change.

THE BARORECEPTOR REFLEXo Minimizes fluctuations in moment-moment MEAN ARTERIAL BLOOD PRESSURE (MABP)o Afferent (sensory) nerve endings in CAROTID SINUS (dilations at the origin of the carotid arteries and aortic arch).o They are MECHANORECEPTORSo Sense alterations in wall stretch caused by pressure changes.o Change the frequency they send action potentials- more pressure, more frequent.o MABP decreases…Baroreceptors fire less,

Brain reduces vagal supply to SA node… TACHYCARDIA. Brain inc sympathetic supply to heart and blood vessels.. CONSTRICTION VEINS+ARTERIES, INC

CONTRACTILITY.

Heart Rate

Positive Chronotropes, eg. SYMPATHETIC NS

Negative Chronotropes, e.g. PARASYMPATHETIC NS

Stroke VolEND DIASTOLIC VOLUME

- Compliance- CVP (pessure pushing it) and so EDP (how much fills with blood

before contracts)

END SYSTOLIC VOLUME- Arterial pressure

- Contractility(both of which affected by symp stimulation and tissue health - o2,

pH etc


REFLEXESo Fluctuations in MABP (Mean arterial BP) and volume need to be minimized, to maintain adequate cerebral and cardiac

perfusion.o There are autonomic reflexes and local mechanisms.o Intrinsic reflexes (respond to stimuli in CV system)

Baroreceptor Cardiopulmonary Chemoreceptor

o Extrinsic reflexes- Cardiac responding to stimuli elsewhere.o Eg. Pain/temp changes

o Cardiovascular reflexes involveo RECEPTORS: Afferent nerves- sense change, communicate to braino BRAIN: Processes and responds to info, so later activity of efferent nerveso EFFERENT NERVES: control cardiac, vascular and renal function- homeostasis- reverse change.

THE BARORECEPTOR REFLEXo Minimizes fluctuations in moment-moment MEAN ARTERIAL BLOOD PRESSURE (MABP)o Afferent (sensory) nerve endings in CAROTID SINUS (dilations at the origin of the carotid arteries and aortic arch).o They are MECHANORECEPTORSo Sense alterations in wall stretch caused by pressure changes.o Change the frequency they send action potentials- more pressure, more frequent.o MABP decreases…Baroreceptors fire less,

Brain reduces vagal supply to SA node… TACHYCARDIA. Brain inc sympathetic supply to heart and blood vessels.. CONSTRICTION VEINS+ARTERIES, INC

CONTRACTILITY.


CNS ISCHAEMIC RESPONSE o Generalized peripheral vasoconstrictiono Stimulated by brainstem hypoxia.o During severe hypotensiono Helps maintain bloodflow to brain in shocko Also causes the CUSHING REFLEX: Brainstem hypoxia due to a tumor which is causing increased CSF pressure:

vasoconstriction and hypertension develop. EXTRINSIC REFLEXES

o Moderate pain causes increased MABP and tachycardia.o Severe pain has opposite effect.o Cold causes cutaneous and coronary vasoconstriction- can precipitate angina.

HOW IS THIS ALL CENTRALLY REGULATED!?o Cardiovascular autonomic control arises when areas of the brainstem, hypothalamus, cortex and cerebellum interact.o Afferent nerves carrying the stimulus from the receptors terminate in the NTS (NUCLEUS TRACTUS SOLITARIUS) of the

medulla.o Neurones from here (NTS) project to areas of the brainstem which control parasympathetic and sympathetic outflow.o The nucleus ambiguous and dorsal motor nucleus contain the cell bodies of the pre-ganglionic vagal parasympathetic

neurons- slow the heart when NTS says theres an increased BP.o Neurons from NTS project to areas of ventro-lateral medulla.. blah blah its complicated.o Higher centres eg. Limbic system in cortex modify the action of the brainstem centres, integrated and appropriate

responses are generated.

AUTONOMIC CONTROL OF THE CV SYSTEMo Help maintain appropriate MABP in response to the reflexes and receptors.o Homeostatic adjustment to postural changes.


CNS ISCHAEMIC RESPONSE o Generalized peripheral vasoconstrictiono Stimulated by brainstem hypoxia.o During severe hypotensiono Helps maintain bloodflow to brain in shocko Also causes the CUSHING REFLEX: Brainstem hypoxia due to a tumor which is causing increased CSF pressure:

vasoconstriction and hypertension develop. EXTRINSIC REFLEXES

o Moderate pain causes increased MABP and tachycardia.o Severe pain has opposite effect.o Cold causes cutaneous and coronary vasoconstriction- can precipitate angina.

HOW IS THIS ALL CENTRALLY REGULATED!?o Cardiovascular autonomic control arises when areas of the brainstem, hypothalamus, cortex and cerebellum interact.o Afferent nerves carrying the stimulus from the receptors terminate in the NTS (NUCLEUS TRACTUS SOLITARIUS) of the

medulla.o Neurones from here (NTS) project to areas of the brainstem which control parasympathetic and sympathetic outflow.o The nucleus ambiguous and dorsal motor nucleus contain the cell bodies of the pre-ganglionic vagal parasympathetic

neurons- slow the heart when NTS says theres an increased BP.o Neurons from NTS project to areas of ventro-lateral medulla.. blah blah its complicated.o Higher centres eg. Limbic system in cortex modify the action of the brainstem centres, integrated and appropriate

responses are generated.

AUTONOMIC CONTROL OF THE CV SYSTEMo Help maintain appropriate MABP in response to the reflexes and receptors.o Homeostatic adjustment to postural changes.

CONTROL OF BLOOD VOLUMEYYxxxxxxxxxxxxxxYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYYY

BLOOD VOL CONTROL o Baroreceptors measure short term fluctuations in BP.o Long term, body needs constant blood volume, to sustain constant BP.o Alterations in blood vol affect venous return, and CO.o Changes in CO lead to adaptive effects of the vasculature that : Increase peripheral resistance and therefore BP.o Volume of blood affected by changes in total body contents of

o Watero Na

o These are both controlled by kidneys.o Maintain a stable BP relies on adjusting renal excretion of Na and Water.

PLASMA VOLUME: Na and Osmoregulationo Water content in body altered by sweating/ fluid intakeo Changes the plasma osmolarityo Any deviation from normal sensed by HYPOTHALAMIC OSMORECEPTORS

o Activate thisto Release ADH from pituitary

o ADH is a peptide that suppresses renal water excretiono ADH acts on DISTAL NEPHRON- to increase its reabsorption of water: reducing loss water in urine.o Opposite happens if less osmolarity- more water excreted and less ADH.o THEREFORE PLASMA VOLUME mainly controlled by Na+ content of EXTRAVELLULAR FLUID (in blood).o 95% of the osmotic solute in the ECF is Na+… with Cl- and HCO-o After eg. Eating a salty meal, the plasma osmolarity is changed and the body will adjust the water content (plasma vol)


BLOOD VOL CONTROL o Baroreceptors measure short term fluctuations in BP.o Long term, body needs constant blood volume, to sustain constant BP.o Alterations in blood vol affect venous return, and CO.o Changes in CO lead to adaptive effects of the vasculature that : Increase peripheral resistance and therefore BP.o Volume of blood affected by changes in total body contents of

o Watero Na

o These are both controlled by kidneys.o Maintain a stable BP relies on adjusting renal excretion of Na and Water.

PLASMA VOLUME: Na and Osmoregulationo Water content in body altered by sweating/ fluid intakeo Changes the plasma osmolarityo Any deviation from normal sensed by HYPOTHALAMIC OSMORECEPTORS

o Activate thisto Release ADH from pituitary

o ADH is a peptide that suppresses renal water excretiono ADH acts on DISTAL NEPHRON- to increase its reabsorption of water: reducing loss water in urine.o Opposite happens if less osmolarity- more water excreted and less ADH.o THEREFORE PLASMA VOLUME mainly controlled by Na+ content of EXTRAVELLULAR FLUID (in blood).o 95% of the osmotic solute in the ECF is Na+… with Cl- and HCO-o After eg. Eating a salty meal, the plasma osmolarity is changed and the body will adjust the water content (plasma vol)


ANP: ATRIAL NATRIURETIC PEPTIDEo Released from atrial myocytes when stretched by INCREASED ATRIAL VOL.o Response to Volume Overload.o Causes DISURESIS and NATIURESIS by

INCREASING GFR Decreasing Renin and Aldostreone Secretion Reducing Na+ reabsorption throughout nephron- loose Na+ and therefore water. Dilates arterioles Increases capillary permeability

CARDIAC MONITORING

- Trends more important than single readings- Non invasive techniques better (less risks eg. Pneumothorax/ line infection)

- BLOOD PRESSUREo Measured intermittently using automated sphygmomanometero BP doesn’t reflect CO.. BP can be high, but CO low if peripheral vasoconstriction raises peripheral vascular resistance

(SVR)o Vasodilated septic patients, with low SVR may have a high CO, but still be hypotensive.

- CENTRAL VENOUS PRESSURE (CVP)o Reflects RIGHT ATRIAL PRESSUREo Measured with internal jugular/ subclavian vein catheterso Useful means of assessing circulating blood volume- determine rate to administer fluid.


ANP: ATRIAL NATRIURETIC PEPTIDEo Released from atrial myocytes when stretched by INCREASED ATRIAL VOL.o Response to Volume Overload.o Causes DISURESIS and NATIURESIS by

INCREASING GFR Decreasing Renin and Aldostreone Secretion Reducing Na+ reabsorption throughout nephron- loose Na+ and therefore water. Dilates arterioles Increases capillary permeability

CARDIAC MONITORING

- Trends more important than single readings- Non invasive techniques better (less risks eg. Pneumothorax/ line infection)

- BLOOD PRESSUREo Measured intermittently using automated sphygmomanometero BP doesn’t reflect CO.. BP can be high, but CO low if peripheral vasoconstriction raises peripheral vascular resistance

(SVR)o Vasodilated septic patients, with low SVR may have a high CO, but still be hypotensive.

- CENTRAL VENOUS PRESSURE (CVP)o Reflects RIGHT ATRIAL PRESSUREo Measured with internal jugular/ subclavian vein catheterso Useful means of assessing circulating blood volume- determine rate to administer fluid.

BASIC CHEST PAIN DIFFERENTIALSiix

PLEURITICo Sharp paino Worse on deep inspiration, coughing, movemento Pneumothoraxo Pneumoniao PEo Pericarditis: Retrosternal

CENTRALo Angina (crushing, tightness)o MI (severe angina, longer lasting, symptoms)o Dissecting AA (tearing interscapular pain)o Oesphagitis (burning)o Oesophgeal spasm

CHEST WALL TENDERNESSo Rib fractureo Shingles (pain precedes rash- Herpes Zoster)o Costochondritis (Tietze’s syndrome- inflammation

joints between cartilages) ATYPICAL

o Anxietyo Referred pain from vertebral collapse- nerve root

irritationo Abdominal: Pancreatitis, peptic ulcer, biliarty tree

disorders.

BASIC CHEST PAIN HISTORYiix

ONSET and PROGRESSION

Cardiac ischemia builds up over few mins Brought on exercise, exertion, cold weather, emotion Angina- resolves with rest/GTN- reproducible. Unstable angina- pain at rest/ inc severity/ inc

frequency MI- severe, nausea, vomiting, sweating, lasts at least

30mins, not fully relieved by GTN Spontaneous pneumothorax or PE cause sudden onset

pleuritic pain and dyspnoea (patient usually remembers exactly what doing at time)

SITE & RADIATION

Cardia ischemia, and pericarditis- retrosternal pain. Ischemia- pain tight and crushing- radiates to neck,

back, jaw, arms Pericarditis is pleuritic, relieved sitting forwards, worse

laying flat. Dissecting AA: tearing pain radiating through the back Pulmonary disease- unilateral pain that the patient can

locate specifically Oesophageal disease- retrosternal pain- may mimic

BASIC CHEST PAIN HISTORYiix

ONSET and PROGRESSION

Cardiac ischemia builds up over few mins Brought on exercise, exertion, cold weather, emotion Angina- resolves with rest/GTN- reproducible. Unstable angina- pain at rest/ inc severity/ inc

frequency MI- severe, nausea, vomiting, sweating, lasts at least

30mins, not fully relieved by GTN Spontaneous pneumothorax or PE cause sudden onset

pleuritic pain and dyspnoea (patient usually remembers exactly what doing at time)

SITE & RADIATION

Cardia ischemia, and pericarditis- retrosternal pain. Ischemia- pain tight and crushing- radiates to neck,

back, jaw, arms Pericarditis is pleuritic, relieved sitting forwards, worse

laying flat. Dissecting AA: tearing pain radiating through the back Pulmonary disease- unilateral pain that the patient can

locate specifically Oesophageal disease- retrosternal pain- may mimic

RISK FACTORSiix

IHDo smoking, family, hypercholesterol,

hypertension, diabetes.o (SF C HD Sausage Fest Causes HD!)

PEo travel history, immobility, surgery, fam hist,

pregnancy, malignancyo wells score (Pist FM )

Pneumothoraxo spontaneous- (young, thin men), trauma,

emphysema, asthma, malignancy

LOOK FOR?

abnormal lipids: o xantholasmao tendon xanthoma

Tar stained fingers (IHD) Hot, oedematous calf: DVT Hypertension (IHD) Marfans syndrome Diabetes (IHD)

CHEST PAIN INVESTIGATIONSix

GP, (non-acute chest pain)

FBC (to exclude anaemia). Renal function tests and electrolytes. TFTs. (arrhythmia from hyper T) CRP. Fasting lipids and glucose. Resting ECG. Note: a resting ECG is normal in over 90%

patients with recent symptoms of angina. If an urgent ECG is considered necessary on clinical grounds, admission to hospital is usually required.

Additional tests if a non-cardiac cause is suspected - eg, o CXR, o LFTs and amylase, o abdominal ultrasound.

Referral to a rapid access chest pain clinic is now usual for further assessment and review.

ACUTE PAIN IN HOSPITAL

Blood tests:o FBC,


ECG (ACS)o New onset LBBBo T wave changeso ST depression/elevation

ECG (PE)o Sinus Tachycardiao AFo R. heart straino R. Axis deviationo RBBBo S1Q3T3 (deep S wave in 1, Q wave in 3,

T-wave inversion in 3) ECG (pericarditis)

o Saddle shaped ST change across all leads

X-RAY o Pneumothoraxo Consolidation (pneumonia)o Wide mediastinum (A dissection)o Pulmonary oedema (MI)o Rib fractures

ABGo How severe PE?o Severe pneumonia?o Severe pulmonary oedema?


GP, (non-acute chest pain)

FBC (to exclude anaemia). Renal function tests and electrolytes. TFTs. (arrhythmia from hyper T) CRP. Fasting lipids and glucose. Resting ECG. Note: a resting ECG is normal in over 90%

patients with recent symptoms of angina. If an urgent ECG is considered necessary on clinical grounds, admission to hospital is usually required.

Additional tests if a non-cardiac cause is suspected - eg, o CXR, o LFTs and amylase, o abdominal ultrasound.

Referral to a rapid access chest pain clinic is now usual for further assessment and review.

ACUTE PAIN IN HOSPITAL

Blood tests:o FBC,


ECG (ACS)o New onset LBBBo T wave changeso ST depression/elevation

ECG (PE)o Sinus Tachycardiao AFo R. heart straino R. Axis deviationo RBBBo S1Q3T3 (deep S wave in 1, Q wave in 3,

T-wave inversion in 3) ECG (pericarditis)

o Saddle shaped ST change across all leads

X-RAY o Pneumothoraxo Consolidation (pneumonia)o Wide mediastinum (A dissection)o Pulmonary oedema (MI)o Rib fractures

ABGo How severe PE?o Severe pneumonia?o Severe pulmonary oedema?

PRESENTING WITH PALPITATATIONSx

PALPITATIONS HISTORY kkkkkmmmmm

• What the patient means by palpitations. • It should mean an awareness of the heart beating. • It may really be a pulsatile tinnitus or a carotid bruit.• Ask the patient

o how often it happens, o how long it lasts and o any precipitating or relieving factors.

Sometimes people are only aware of it whilst lying down at night. Determine whether the rate is regular or irregular. Ask the patient to tap out the beat. This may be regular or irregular. It may be a normal rate or fast. Try to estimate the rate. Establish whether there are any symptoms that accompany the

palpitations, such as sweating or breathlessness. These may be organic or psychosomatic in origin. Associated chest pain?.sinister significance! Enquire about consumption of caffeine. Palpitations may be related in

time to consumption but assess daily intake too Ask about alcohol consumption. Ask about smoking. The level of nicotine in cigars tends to be rather

higher than in cigarettes. In young people ask about use of illicit substances, especially cocaine,

'ecstasy' - methylenedioxymethamfetamine (MDMA) - and amfetamines.

CAUSES ooo

Non- Cardiac causes TACYCARDIA:

FAST PACE!!!!

Fever Anaemia Sympathomimetic drugs Thyrotoxicosis Pregnancy Anxiety (pain) Arteriovenous fistulae Cigrettes, alcohol, caffeine Exercise

Causes of Bradycardia

Athletes Hypothyroidism Obstructive jaundice Raised ICP Hypopituitarism Hypothermia

Palpitations

IRREGULAR

PERSISTANT

AF

ECTOPICS

OCCASIONAL

ECTOPIC

AF (paroxysmal)

ATRIAL FLUTTER (with

block)

REGULAR

FAST

VT

SVT

TACHYCARDIA

AF

SLOW

SINUS BRADY

COMPLETE HEART BLOCK

AF- degree of block

PALPITATIONS HISTORY kkkkkmmmmm

• What the patient means by palpitations. • It should mean an awareness of the heart beating. • It may really be a pulsatile tinnitus or a carotid bruit.• Ask the patient

o how often it happens, o how long it lasts and o any precipitating or relieving factors.

Sometimes people are only aware of it whilst lying down at night. Determine whether the rate is regular or irregular. Ask the patient to tap out the beat. This may be regular or irregular. It may be a normal rate or fast. Try to estimate the rate. Establish whether there are any symptoms that accompany the

palpitations, such as sweating or breathlessness. These may be organic or psychosomatic in origin. Associated chest pain?.sinister significance! Enquire about consumption of caffeine. Palpitations may be related in

time to consumption but assess daily intake too Ask about alcohol consumption. Ask about smoking. The level of nicotine in cigars tends to be rather

higher than in cigarettes. In young people ask about use of illicit substances, especially cocaine,

'ecstasy' - methylenedioxymethamfetamine (MDMA) - and amfetamines.

CAUSES ooo

Non- Cardiac causes TACYCARDIA:

FAST PACE!!!!

Fever Anaemia Sympathomimetic drugs Thyrotoxicosis Pregnancy Anxiety (pain) Arteriovenous fistulae Cigrettes, alcohol, caffeine Exercise

Causes of Bradycardia

Athletes Hypothyroidism Obstructive jaundice Raised ICP Hypopituitarism Hypothermia

PALPITATIONS- EXAMINATIONx

If the patient currently has the palpitations then it is easy to assess the rate and regularity of the pulse and to get an ECG to confirm the diagnosis.

Consider the following:o Does the patient look well?o Does the patient look anxious?o Is there exophthalmos to suggest thyrotoxicosis?o Are the fingers stained with nicotine?o Do the hands feel warm or cold?

A fine tremor may suggest thyrotoxicosis or anxiety. Examination of the pulse can give a great deal of information.

o Quality of the pulse: whether it is full and bounding, rather weak or normal. o Quality of the artery. Note whether it is soft and elastic or rather rigid. The brachial artery may be a better place to

assess this. o Rate is regular. If not… AF or ectopic?

Count the rate over an adequate interval. Check the blood pressure Examine the heart, noting the position and character of the apex beat, any parasternal heave or thrills, the normality of the

heart sounds and if there are any additional sounds

PALPITATIONS- WORKING OUT DIFFERENTIALSx

Anxiety: diagnosis of exclusion: It may be part of a panic attack. There may be an occasional 'missed beat'. This is really a misnomer, as what happens is a premature beat, usually from an

ectopic source and this leads to a weak beat followed by a prolonged refractory period during which the ventricles fill more than usual and, when ejection occurs, it is more forceful than usual and so is noticed. Occasional ectopics are fairly common and usually of no sinister significance. They are more likely with a slow pulse.

AF or atrial flutter is often paroxysmal before AF becomes established. It is often quite fast but can be slow. T he crucial feature is the random irregularity but this is more difficult to discern with a faster rate. AF is often associated with shortness of breath on exertion, as it tends to reduce cardiac output by about 20%. As a general rule,

o ventricular tachycardia (VT) has a rate of 120 to 160 BPMo supraventricular tachycardia (SVT) a rate of 160 to 200 BPM.

Paroxysmal tachycardia can result from a junctional re-entry phenomenon. This tends to produce a very fast rate, often in a young person: Wolff-Parkinson-White (WPW) syndrome is well documented. A hyperdynamic pulse may occur with anaemia and thyrotoxicosis. Thyrotoxicosis may produce AF, especially in the elderly where that may be the only feature. Drugs that reduce the resistance in the circulation may also be responsible. These can include nitrates and calcium-channel

blockers. Excessive use of a beta agonist inhaler will cause palpitations. Irregularities of rhythm may occur with cardiomyopathy. Bradycardia may produce palpitations, as a high stroke volume is required to meet the necessary cardiac output. Phaeochromocytoma is a rare cause of paroxysmal palpitations. It tends to occur with multiple endocrine neoplasia

syndromes - usually MEN2 - and usually runs in families.

PALPITATIONS- INVESTIGATIONSx

The gold standard is a full 12-lead ECG taken at the time of palpitations. It should, however, be performed even if the palpitations have resolved. Shows

o irregular rate and it is easy to deduce the type. o abnormalities suggestive of ischaemia, hypertrophy or cardiomyopathy. o occasional ectopics that are not currently causing symptoms. o incomplete heart block. o short PR interval in WPW syndrome.

Basic blood tests o FBC, o U&Es o TFTs.

A 24-hour ECG should be arranged (many GPs now have direct access to this). o The patient is given a device to wear for 24 hours (a Holter monitor) which is returned to the hospital for analysis

the following day. o The time that palpitations start and finish should be noted so this can be correlated with the ECG recording. o As a refinement, an event recorder can be used for patients whose palpitation frequency is less than daily.o For added convenience, leadless monitors have been developed.

If the problem is related to exercise then a treadmill ECG is required. Sometimes there is an irregularity at rest that is suppressed on exercise. These tend to be of rather less sinister significance than an irregularity that arises on exercise.

Echocardiogram: If cardiomyopathy is suspected or if there are abnormal heart sounds.

HEART MURMURS x

Murmurs are vibrations due t turbulent blood flow in heart. Non valvular causes

o Innocent flow murmurs in childreno High CO: fever, thyrotoxicosis, pregnancy.o Congenital heart diseases: ASD, VSD, PDA, Coarctation of aorta.

CLASSIFICATION

EJECTION SYSTOLIC PANSYSTOLIC DIASTOLIC CONTINUOUS

HEART MURMURS x

EJECTION SYSTOLIC (A and P area)

- Originate in either ventricle outflow tract- so either around the pulmonary arteries or the aorta

- They’re either before the valves (in the heart), in the valves, or in the arteries.

- Reach a crescendo mid-systole, die down before second heart sound (semilunar shutting)

- Causes in AORTIC AREA.. either valvular / supravalvular / subvalvular

o Coactation of aortao Supra-aortic stenosiso Aortic sclerosiso Hypertrophic obstructive cardiomyopathy

(subvalvular)o Hyperkinetic Cardiac Output states

- Causes in PULMONARY AREAo Pulmonary arterial stenosiso Pulmonary valve stenosiso Flow murmurs, hyperkinetic states, left-Right

shunts (ASD)- left side bigger- remember

PANSYSTOLIC MURMURS (T and M area)

- Same intensity

HEART MURMURS Hx x

No real symptoms- so need to find out cause/ consequences.

Rheumatic fever (mitral valve) IHD (mitral regurg) Congenital heart disease Hypertension (flow murmus) IVDU Family Hx hypertrophic cardiomyopathy- autosomal

dominant. AORTIC REGURG (associated with)

o Rheumatoid arthritiso Seronegative arthropathies (ankloysing

spondylitis, reiters syndrome, psoriatitic arthritis

o Coarctation of aorta MiTRAL REGURG

o Lupuso Rheumatoid arthritiso Ankylosing spondylitiso Marfanso Ehlers-Danloso Osteogenesis imperfect.

Consequenceso Aortic valve disease and mitral regurg may

be asymptomatic.o LOW CO- fatigue and weakness

HEART MURMURS x

EJECTION SYSTOLIC (A and P area)

- Originate in either ventricle outflow tract- so either around the pulmonary arteries or the aorta

- They’re either before the valves (in the heart), in the valves, or in the arteries.

- Reach a crescendo mid-systole, die down before second heart sound (semilunar shutting)

- Causes in AORTIC AREA.. either valvular / supravalvular / subvalvular

o Coactation of aortao Supra-aortic stenosiso Aortic sclerosiso Hypertrophic obstructive cardiomyopathy

(subvalvular)o Hyperkinetic Cardiac Output states

- Causes in PULMONARY AREAo Pulmonary arterial stenosiso Pulmonary valve stenosiso Flow murmurs, hyperkinetic states, left-Right

shunts (ASD)- left side bigger- remember

PANSYSTOLIC MURMURS (T and M area)

- Same intensity

HEART MURMURS Hx x

No real symptoms- so need to find out cause/ consequences.

Rheumatic fever (mitral valve) IHD (mitral regurg) Congenital heart disease Hypertension (flow murmus) IVDU Family Hx hypertrophic cardiomyopathy- autosomal

dominant. AORTIC REGURG (associated with)

o Rheumatoid arthritiso Seronegative arthropathies (ankloysing

spondylitis, reiters syndrome, psoriatitic arthritis

o Coarctation of aorta MiTRAL REGURG

o Lupuso Rheumatoid arthritiso Ankylosing spondylitiso Marfanso Ehlers-Danloso Osteogenesis imperfect.

Consequenceso Aortic valve disease and mitral regurg may

be asymptomatic.o LOW CO- fatigue and weakness

EXAMINATION OF A MURMUR x

Inspection, palpation, auscultation Time a murmur, note when maximum

intensity and radiation SYSTOLIC

o Pansystolic?o Ejection systolic?

DIASTOLICo Early diastolic? (start from 2nd

sound)o Mid diastolic?

MITRAL STENOSIS x

-

Narrowing of the mitral valve (when LA- LV) Backpressure builds up behind the narrowed valve Reduced amount of blood ejected from LV. Backpressure into lungs. Most caused by past Rheumatic fever- follows a

bacterial infection with streptococcus- body makes autoantibodies to clear infection, but also attack mitral valve- inflammation, damage and thickening.

Can also be calcification, congenital, endocarditis. More effort form LA to pump into LV- get a

hypertrophy of the LA. SYMPTOMS

MITRAL REGURGITATION x

-

Mitral valve doesn’t close properly

MITRAL STENOSIS x

-

Narrowing of the mitral valve (when LA- LV) Backpressure builds up behind the narrowed valve Reduced amount of blood ejected from LV. Backpressure into lungs. Most caused by past Rheumatic fever- follows a

bacterial infection with streptococcus- body makes autoantibodies to clear infection, but also attack mitral valve- inflammation, damage and thickening.

Can also be calcification, congenital, endocarditis. More effort form LA to pump into LV- get a

hypertrophy of the LA. SYMPTOMS

MITRAL REGURGITATION x

-

Mitral valve doesn’t close properly

AORTIC STENOSIS x

-

Aortic Sclerosis is the precursor of calcified, degenerative aortic stenosis

Congenital or calcified from aging. Blood harder to pump into body at ventricular

systole. SYMPTOMS

o Usually none until lateo Anginao Exertional dyspnnoeao Syncopeo . Triad- chest pain, HF, syncope

COMPICATIONSo Sudden death- ventricular dysrrythmia.

AORTIC REGURG x

-

Usually asymptomatic, until ventricle fails! Ventricles make up and make up to pump the body,

loosing a bit every time, then can enlarge and keep up no more.

After rheumatic fever, infective endocarditis, collogen vascular diseases, SLE, lupus, marfans, ehlers-danlos, ankylosing spondylitis, reiters, bechets.

SYMPTOMSo Heart failure when ventricle fails

SIGNSo Low diastolic BPo Wide pulse pressure- large difference

AORTIC STENOSIS x

-

Aortic Sclerosis is the precursor of calcified, degenerative aortic stenosis

Congenital or calcified from aging. Blood harder to pump into body at ventricular

systole. SYMPTOMS

o Usually none until lateo Anginao Exertional dyspnnoeao Syncopeo . Triad- chest pain, HF, syncope

COMPICATIONSo Sudden death- ventricular dysrrythmia.

AORTIC REGURG x

-

Usually asymptomatic, until ventricle fails! Ventricles make up and make up to pump the body,

loosing a bit every time, then can enlarge and keep up no more.

After rheumatic fever, infective endocarditis, collogen vascular diseases, SLE, lupus, marfans, ehlers-danlos, ankylosing spondylitis, reiters, bechets.

SYMPTOMSo Heart failure when ventricle fails

SIGNSo Low diastolic BPo Wide pulse pressure- large difference

TRICUSPID REGURG x

- Mitral Stenosis, can cause pulmonary hypertension, which can cause Tricuspid regurgitation- Trauma or infective endocarditis- Rheumatic fever- Blood goes from RA to RV, but in systole, RV is meant to squeeze it into the lungs and it goes back into RA, pressure on

venous system of body- portal hypertension.- IVDU? Infective endocarditis? SYMPTOMS

o Fatigueo Oedema and ascites (peripheral)o Hepatic pain- liver capsule stretched.

MURMURo PANSYSTOLIC MURMURo Loudest at L sternal edge in inspiration (T)o No radiation

ISCHAEMIC HEART DISEASE- Basics x

Result of an imbalance between Myocardial oxygen supply and demand Term covers

o Anginao ACSo Anything that reduces blood supply to heart!

Due too Atherosclerosis of coronary arteries (COMMON)o Coronary artery spasmo Embolio Aortic stenosis (supplies coronary arteries)o Hypertrophic obstructive cardiomyopathyo Arrythmias- cause dec coronary perfusion.o Anaemiao Syndrome X- normal coronary arteries- but abnormal small vessels.

Risk Factorso Age- Raised cholesterol, hypertension, cigarettes over time.o Male / post-menopausal womeno Family Hx- below 50 / hypercholesterolemia.o Cigarettes (x3)- after 10 years same as non-smokero Blood lipids- HDL protective, LDL and Triglycerides inc risko Hypertension- (also a risk of stroke and renal failure)- drugs decrease risk heart disease by 16%o DM – (2x risk major ISH event)o Race- Asian- more DM.o Weight: overweight 2x risk IHD. (increased BP, total cholesterol, insulin resistance, decreased HDL, dec exercise)

IHD Investigations

ISCHAEMIC HEART DISEASE- Basics x

Result of an imbalance between Myocardial oxygen supply and demand Term covers

o Anginao ACSo Anything that reduces blood supply to heart!

Due too Atherosclerosis of coronary arteries (COMMON)o Coronary artery spasmo Embolio Aortic stenosis (supplies coronary arteries)o Hypertrophic obstructive cardiomyopathyo Arrythmias- cause dec coronary perfusion.o Anaemiao Syndrome X- normal coronary arteries- but abnormal small vessels.

Risk Factorso Age- Raised cholesterol, hypertension, cigarettes over time.o Male / post-menopausal womeno Family Hx- below 50 / hypercholesterolemia.o Cigarettes (x3)- after 10 years same as non-smokero Blood lipids- HDL protective, LDL and Triglycerides inc risko Hypertension- (also a risk of stroke and renal failure)- drugs decrease risk heart disease by 16%o DM – (2x risk major ISH event)o Race- Asian- more DM.o Weight: overweight 2x risk IHD. (increased BP, total cholesterol, insulin resistance, decreased HDL, dec exercise)

IHD Investigations

PATHOLOGY OF ATHEROSCLEROSIS- Basic x

Slowly progressive, focal proliferation of connective tissue in arterial intima. Begins in early life. High lipid levels. LDL – main athrogenic lipid Plaques- mostly made of COLLOGEN synthesized by smooth muscle cells.

o 1. ENDOTHELIAL DYSFUNCTION- associated with high cholesteriol, inflammation, and shear forces.o 2. MACROPHAGES – enter arterial wall, between endothelial cells, take up lipids and become FOAM CELLS.o 3. FOAM CELLS ACCUMULATE in subendothelial zone- forms FATTY STREAKSo 4. FOAM CELLS/MACROPHAGES release toxic products- lead to PLATELET ADHESION, MUSCLE CELL PROLIFERATION,

THROMBUS FORMATIONo 5. Becomes organized- ATHEROSCLEROTIC CAP with FIBROUS CAP.o 6. Progressive enlargement, and narrowing of lumen- exertional angina.o 7. RUPTURE- cause sudden thrombus

Atherosclerosis is initiated by inflammatory processes in the endothelial cells of the vessel wall in response to retained (LDL) Lipoproteins in the blood vary in size. Some data suggests that small dense LDL particles are more prone to pass between the endothelial

cells, going behind the cellular monolayer of endothelium. LDL particles and their content are susceptible to oxidation by free radicals- risk is higher while in the wall than while in the bloodstream. However, LDL particles have a half-life of only a couple of days, and their content (LDL particles typically carry 3,000 to 6,000 fat molecules,

including: cholesterol, phospholipids, cholesteryl esters, tryglycerides & all other fats in the water outside cells, to the tissues of the

body) changes with time. Once inside the vessel wall, LDL particles can become more prone to oxidation. Endothelial cells respond by attracting monocyte white blood cells, causing them to leave the blood stream, penetrate into the arterial walls

and transform into macrophages. The macrophages' ingestion of oxidized LDL particles triggers a cascade of immune responses which over time can produce an atheroma if

HDL removal of fats from the macrophages does not keep up. The immune system's (macrophages and T-lymphocytes) absorb the oxidized LDL, forming specialized foam cells. If these foam cells are not able to process the oxidized LDL and recruit HDL particles to remove the fats, they grow and eventually rupture,

leaving behind cellular membrane remnants, oxidized materials, and fats (including cholesterol) in the artery wall.This attracts more white blood cells, resulting in a snowballing progression that continues the cycle, inflaming the artery. The presence of the plaque induces the muscle cells of the blood vessel to stretch, compensating for the additional bulk, and the endothelial

lining thickens, increasing the separation between the plaque and lumen. This somewhat offsets the narrowing caused by the growth of the plaque, but it causes the wall to stiffen and become less compliant to stretching with each heart beat. TREATING IHD (Basic) x

- GENERAL o Inc exercise, (better collaterial circulation heart, and for VD) smoking stop, diet, weightloss

- DRUGS - ANTIPLATELET

o All patients ASPIRIN 75mg Daily- lowers risk subsequent MI and deatho Risk of GI bleed- melena, take with food, PPIo CLOPIDOGREL if aspirin contraindicated (inhibits platelet aggregation)- mostly used post NSTMI/angioplasty.

- BETA-BLOCKERSo Reduce Sympathetic tone.o Negative ionotropes (reduce contractility)- reduce oxygen demando Neg Chronotripoc (HR)- reduce oxygen demando Increase perfusion of ischaemic area- decreasing HR, increases diastole- time for coronary blood flow.o Contraindications? Asthma, PVD with skin ulceration, 2nd and 3rd degree heart block.o Improve survival post-MIo Good in chronic heart failure- shouldn’t be given in acute.

- NITRATESo Cause peripheral vasodilation- especially in veinso Reduces venous return, and ventricular pre-load.o Reduction in heart wall distension- decreases o2 demand of heart wall- angina relief.o Nitrates are converted to NO- which results in an increased intracellular cyclic guanosine monophosphate

cGMP in smooth muscle. This stimulates calcium binding processes and free calcium vaaliable to trigger muscle contraction is reduced.

o Nitrates and rest relieve angina in minutes.

TREATING IHD (Basic) x

- GENERAL o Inc exercise, (better collaterial circulation heart, and for VD) smoking stop, diet, weightloss

- DRUGS - ANTIPLATELET

o All patients ASPIRIN 75mg Daily- lowers risk subsequent MI and deatho Risk of GI bleed- melena, take with food, PPIo CLOPIDOGREL if aspirin contraindicated (inhibits platelet aggregation)- mostly used post NSTMI/angioplasty.

- BETA-BLOCKERSo Reduce Sympathetic tone.o Negative ionotropes (reduce contractility)- reduce oxygen demando Neg Chronotripoc (HR)- reduce oxygen demando Increase perfusion of ischaemic area- decreasing HR, increases diastole- time for coronary blood flow.o Contraindications? Asthma, PVD with skin ulceration, 2nd and 3rd degree heart block.o Improve survival post-MIo Good in chronic heart failure- shouldn’t be given in acute.

- NITRATESo Cause peripheral vasodilation- especially in veinso Reduces venous return, and ventricular pre-load.o Reduction in heart wall distension- decreases o2 demand of heart wall- angina relief.o Nitrates are converted to NO- which results in an increased intracellular cyclic guanosine monophosphate

cGMP in smooth muscle. This stimulates calcium binding processes and free calcium vaaliable to trigger muscle contraction is reduced.

o Nitrates and rest relieve angina in minutes.

DIAGNOSING ACSx

- After acute MI o Up to 18hrs: No macroscopic or microscopic changeso 24-48hrs (2 days): Pale oedematus muscle (macro), (micro) oedema, acute inflammatory cell infiltration,

necrosis of myocytes.o 3-4 days: yellow rubbery centre with haemorrhagic border (macro), (micro) Obvious necrosis and inflammation,

early granulation tissue.o 3-6 weeks: Silvery scar becoming rough and white, (micro) dense fibrosis.

- Cardiac Enzymeso Intracellular enzymes that leak out of infarcted myocardium into bloodstreamo CREATININE KINASE (peak 1 day)

Peaks in 24hrs Cardiac enzyme, also produced by skeletal muscle and brain. CK-MB can be requested if in doubt- a myocardium-bound isoenzyme, specific heart muscle damage. Site of infarct related to serum level of enzyme. Used to assess reinfarction in patients who have elevated troponin from a previous MI

o ASPARTATE AMINOTRANSFERASE (peak day 1-2)o LACTATE DEHYDROGENASE (peak day 1-2)o TROPONIN I or T (8-12hrs)

Good markers of cardiac damage Proteins involved in myocyte contraction 8-12hrs post MI most reliable Remain elevated for several weeks

MANAGEMENT HYPERTENSION- Basic

THIAZIDE DIURETICSo Lower body sodium stores- BP falls as dec in blood vol, venous return and CO.o Gradually the CO returns to normal, but the hypotensive effect remains as peripheral resistance decreaseso Side effects: GOUT, impaired glucose tolerance.o Low doses (2.5mg bendrofluthiazide) cause little biochemical disturbance without loss of anti-hypertensive

effect. High doses not usually needed. POTASSIUM-SPARING DIURETICS

o Diuretic induced hypokalaemia. BETA-BLOCKERS

o Decrease CO, so initially cause fall in BPo CO returns to normal, but peripheral resistance is ‘set’ to a new lower level so BP remains low.o Renin levels are reduced.o Side-effects: Provokes asthma, and heart block. Neg ionotrope. Cold hands and fatigue.

CALCIUM CHANNEL BLOCKERSo Calcium antagonists.o Dihydropyridines (Nifedipine)- good vasodilating drugs that can cause reflex tachycardia.o Diltiazem- neg ionotrope, and chronotrope- contraindicated in HFo Amlodipine- safe in HFo Flusing, headache, oedema, constipationo Don’t use verapamil with beta-blocker.

ACE INHIBITORSo Inhibit renin-angiotensin-aldosterone axiso Increase in vasodilating bradykiino More effective in yonger patients with higher renin levels- best in young whiteo Good in HF, proteinurig nephropathy, diabeteso Dry cough (secondary to bradykinin), Hyperkalaemia, Transient worsening in serum creatinine (GFR)- as

intraglomerular pressure falls, Acute renal failure (if sepsis, hypovolumeia, renal artery stenosis)o Monitor electrolytes until dose titrated.

ANGIOTENSIN II RECEPTOR BLOCKERSo Block rein angiotensin system- similar to ACEo Good if chronic cough on ACE- don’t effect bradykinin productiono CV protective effect

MINOXIDIILo Potent vasodilator, dec PVR- can cause reflex tachycardia- use beta-blockero Fluid retention (use diuretic)o Hirsutism

ALPHA BLOCKERSo Maintain High CO- reduce aterial and venous resistance

ACUTE CORONARY SYNDROMES: Pathophysiology

Affects 7% population Increases with age, males, post-menopause RF: smoking, hypertension, diabetes, cholesterol,

family. About 20% of all deaths in UK After MI- 30-60% death before hospital, 10% in

hospital, 20% within 2 years (HF or MI) Variant Angina? Vasospasm Stable angina? Fixed Plaque ACS: thrombosis over ruptured complex plaque

CONSEQUENCES OF CORONARY ARTERY OCCLUSION

o LEFT CORONARY ARTERY Supplies LAD and Circumflex: Major contribution

to LV and RV perfusiono RIGHT CORONARY ARTERY

Occlusion causes inferior MI. Main Supply to RV and AV node

o LAD ARTERY Occlusion causes Anterior MI Supplies LV, Septum and RV

o CIRCUMFLEX ARTERY Causes lateral MI

FACTORS LIMITING OXYGEN SUPPLY

Artery NARROWING: Vasospasm and complex plaque


Affects 7% population Increases with age, males, post-menopause RF: smoking, hypertension, diabetes, cholesterol, family. About 20% of all deaths in UK After MI- 30-60% death before hospital, 10% in hospital,

20% within 2 years (HF or MI) Variant Angina? Vasospasm Stable angina? Fixed Plaque ACS: thrombosis over ruptured complex plaque


o LEFT CORONARY ARTERY Supplies LAD and Circumflex: Major contribution to

LV and RV perfusiono RIGHT CORONARY ARTERY







Affects 7% population Increases with age, males, post-menopause RF: smoking, hypertension, diabetes, cholesterol,

family. About 20% of all deaths in UK After MI- 30-60% death before hospital, 10% in

hospital, 20% within 2 years (HF or MI) Variant Angina? Vasospasm Stable angina? Fixed Plaque ACS: thrombosis over ruptured complex plaque


o LEFT CORONARY ARTERY Supplies LAD and Circumflex: Major contribution

to LV and RV perfusiono RIGHT CORONARY ARTERY







Affects 7% population Increases with age, males, post-menopause RF: smoking, hypertension, diabetes, cholesterol, family. About 20% of all deaths in UK After MI- 30-60% death before hospital, 10% in hospital,

20% within 2 years (HF or MI) Variant Angina? Vasospasm Stable angina? Fixed Plaque ACS: thrombosis over ruptured complex plaque


o LEFT CORONARY ARTERY Supplies LAD and Circumflex: Major contribution to

LV and RV perfusiono RIGHT CORONARY ARTERY






CHRONIC STABLE (exertional) ANGINA

Fixed stable coronary artery occlusions limit blood flow causing predictable, reversible cardiac ischemia during exercise.

Stenosis are caused by smooth circumferential atherosclerotic plaques with thick fibrous caps: unlikely to rupture.

Thick fibrous cap, small lipid core. Ischemia often sub-endocardial, as

systolic compression greater than endocardial than epicardial aretries.

VARIANT- PRINZMETALS ANGINA: uncommon, caused by transient coronary artery vasospasm due to over-reactivity (to noradrenaline)/ impaised flow-mediated vasodilation. Often near plaques, but not necessarily related.

ECG VARIABLE: ST segment depression/ T-wave inversion.

No cardiac enzymes, no thrombolysis If high risk: ANGIOGRPAHY.

ACUTE CORONARY SYNDROME (ACS)

Spectrum of increasingly life-threatening conditions in which ischemia (and myonecrosis) follows sudden artery occlusion due to thrombosis (and vasoconstriction).

Initiated by STRESS – INDUCED RUPTURE (hypertension) of small eccentric (non-circumferential), non-occluded (under 50%) COMPLEX plaques, with lipid-rich cores and thin fibrous plaques.

Plaque rupture stimulates o Thrombus formationo Vasospasmo Arterial Occlusion

Length of time and extent of the occlusion determine severity of ischemia: defines the syndrome, ECG changes, symptoms, degree of myocardial necrosis (cardiac enzyme release).

UNSTABLE ANGINAo Coronary artery occlusion of limited extent/duration.o Ischemia, not necrosis

NSTEMI (send for PCI!)o Occlusion may be temporary/ incomplete/ alleviated by collateral vesselso Ischemia and necrosis limited to SUBENDOCARDIUMo Myocardial damage: cardiac enzymes.

STEMI (send for PCI!)o Occlusion causes transmural ischemiao Q-wavesCLINICAL FEATURES OF MI

Crushing/ heavy retrosternal pain Radiates to

o Necko Medial L armo Right chest or shoulder blades

Atypical: Burning, localized eg. Only jaw, absent. STABLE ANGINA

o Precipitated by exercise/anxietyo Relieved in 5 mins by rest/sublingual nitrates.

UNSTABLE ANGINA and NSTEMIo Frequent, unpredictable, over 15minso Respond less to nitrateso New pain? Pain with less exertion? Autonomic

manifestations eg. Nausea and sweating? Radiation to new sites eg. Jaw? Indicate increasing coronary artery occlusion and NSTEMI

o Typically: Crescendo angina: inc freq periods of prolonged, freq angina. Angina at rest/minimal exertion

o Both have ST depression and T wave inversion on ECG.

o NSTEMI- high risk of coronary artery occlusion and death (in 4-6 weeks)

o 8% hospitalized die in 30 days, 8% re-infarction. INCREASED RISK OF FUTURE EVENTS

ACS INVESTIGATION

1st you need to differentiate ACS form other life threatening conditions e.g. Aortic dissection and benign things e.g. Reflux, musculoskeletal.

INVESTIGATIONS

ECGo Site and Size infarct.o ST Elevation (immediate revascularization)o ST Depression and T inversion: NSTEMI doesn’t

benefit from thrombolysis.o Survival at 6 months is similar for a NSTEMI, and

STEMI- even though early mortality higher in STEMI.o Serial ECGS to diagnose.o INFERIOR: RCA, II, III, aVFo ANTERIOR: LAD, l, aVL, V2, V3, V4, V5o INTEROSEPTAL: LAD, V2, V3, V4o ANTEROLATERAL: LAD, V3, V4, V5o APICAL: LAD, II, III, aVF, V5, V6o LATERAL: Circumflex/diagonal, I, aVL, V6o POSTERIOR: Right/Circumflex, R wave in V1,-2 with

ST depression. ENZYMES

o A twofold increase in plasma enzymes in myocardial

CLINICAL FEATURES OF MI

Crushing/ heavy retrosternal pain Radiates to

o Necko Medial L armo Right chest or shoulder blades

Atypical: Burning, localized eg. Only jaw, absent. STABLE ANGINA

o Precipitated by exercise/anxietyo Relieved in 5 mins by rest/sublingual nitrates.

UNSTABLE ANGINA and NSTEMIo Frequent, unpredictable, over 15minso Respond less to nitrateso New pain? Pain with less exertion? Autonomic

manifestations eg. Nausea and sweating? Radiation to new sites eg. Jaw? Indicate increasing coronary artery occlusion and NSTEMI

o Typically: Crescendo angina: inc freq periods of prolonged, freq angina. Angina at rest/minimal exertion

o Both have ST depression and T wave inversion on ECG.

o NSTEMI- high risk of coronary artery occlusion and death (in 4-6 weeks)

o 8% hospitalized die in 30 days, 8% re-infarction. INCREASED RISK OF FUTURE EVENTS

ACS INVESTIGATION

1st you need to differentiate ACS form other life threatening conditions e.g. Aortic dissection and benign things e.g. Reflux, musculoskeletal.

INVESTIGATIONS

ECGo Site and Size infarct.o ST Elevation (immediate revascularization)o ST Depression and T inversion: NSTEMI doesn’t

benefit from thrombolysis.o Survival at 6 months is similar for a NSTEMI, and

STEMI- even though early mortality higher in STEMI.o Serial ECGS to diagnose.o INFERIOR: RCA, II, III, aVFo ANTERIOR: LAD, l, aVL, V2, V3, V4, V5o INTEROSEPTAL: LAD, V2, V3, V4o ANTEROLATERAL: LAD, V3, V4, V5o APICAL: LAD, II, III, aVF, V5, V6o LATERAL: Circumflex/diagonal, I, aVL, V6o POSTERIOR: Right/Circumflex, R wave in V1,-2 with

ST depression. ENZYMES

o A twofold increase in plasma enzymes in myocardial

ACS GENERAL MANAGEMENT

Treatment aims to reduce MYOCARDIAL OXYGEN CONSUPMPTION, whilst increasing supply.

By DECREASING o HR (beta-blockers)o AFTERLOAD: (antihypertensives)

Risk Factor Reductiono Smoking, diet, weightloss, treating

hypertension and DM. Antiplatelet (aspirin) and lipid lowering drugs (Statins) ACE inhibitors- reduce atherosclerosis- better

prognosis.MANAGEMENT OF STABLE ANGINA

NITROVASODILATORSo Efective, but tolerance develops

BETA-BLOCKERSo First line therapyo Improve prognosiso Increase myocardial perfusion in diastole- slow HR and reduce

pre-load and afterload so reduce LV tension. CALCIUM CHANNEL ANTAGONISTS

o Useful when beta-blockers contraindicated.o Relive coronary vasospasm.o Nifedipine, can cause reflex tachycardia, and exercerbate HD

(neg ionotrope) REVASCULARISATION

o Needed if symptoms deteriorate.o Needed if positive exercise stress testo Needed if angiography revelas over 70% stenosis in all 3 main,

left main or proximal LAD arteries.

MANAGEMENT UNSTABLE ANGINA/ NSTEMI

Thrombolytic therapy not beneficial. Nitrates, Beta blocker, CCA and…… ANTIPLATELET THERAPY

o All patients 300mg Aspirin immediatelyo 75mg a dayo Irreversible cyclo-oxygenase inhibition

prevents platelet aggregation within 15mins chewing aspirin- preventing MI/sudden death by 50%

o Clopidogrel inhibits its ADP-Stimulated platelet aggregation, reduces mortality when combined with aspirin after 30days.

GLYCOPROTEIN IIb/IIIa ANTAGONISTSo Most effective platelet inhibitors- Used

after PCI to prevent stent thrombosis. ANTICOAGULANT THERAPY

o IV unfractunated heparin.o Subcut LMWHo Prevent thromboembolic complications in

immobile patients. PCI

o Consider after 48hrs if medical therapy fails.

MANAGEMENT OF INFARCTION/STEMI

Early reperfusion after MI limits infact size and mortality. IMMEDIATELY

o Pain reliefo Monitoringo Oxygen Therapy

MANAGEMENT OF INFARCTION/STEMI

Early reperfusion after MI limits infact size and mortality. IMMEDIATELY

o Pain reliefo Monitoringo Oxygen Therapy

CONTRAINDICATION TO THROMBOLYTIC THERAPY

Absolute

Active Bleeding (GI heamorrhage) Aortic Dissection Neurosurgery/ head injury Recent CNS disease (tumor) under 6months CVA in last 2 months Recent operation (under 4 weeks) Recent Trauma (under 4 weeks) Diastolic Hypertension Coagulopathy (less platelets)

Relative

Previous CVA/TIA Recent CPR Systemic Hypertension Recent Central lines Intracardiac thrombus AAA

TACHYARRYTHMIAS

Tachy is over 100bpm Either Supra-ventricular or ventricular Detrimental if cause symptoms:- terminate immediately with

cardioversion/ drugs!o Hypotension

SINUS TACHYCARDIA

Physiological (exercise) Pathological (thyrotoxicosis/ HF) Stimuli which inc sympathetic tone, accelerates

SA node paceing. TREAT? Remove case.

ARRYTHMIAS

Abnormalities of the Heart Rate/Rhythem Due to Aberrant impulse generation / conduction (eg. Re-entry circuits) AF affects 10% of over 75s Arrythmias (VF/VT) cause 40% deaths in IHD Asymptomatic/stable rhythems can be just observed, while cause corrected eg. Hypokalaemia. Prevention

o Early correction hypoxaemiao Electrolyte disturbances (hypokalaemia)o Acid-base imbalanceo Cardiac ischemiao Vagal stimulation (pain)o Drugs (theophylline)o Cardiac irritants (intra-cardiac catheters)

Antiarrythmic drugso Selected due to rhythem and underlaying pathophysiologyo Therapy often doesn’t work and can cause new arrhythmias.

Other Therapy? DC Cardioversion, Implantable defibrillators, radiofrequency catheter ablation (destroys accessory pathways)/ ectopic pacemakers.

TACHYARRYTHMIAS

Tachy is over 100bpm Either Supra-ventricular or ventricular Detrimental if cause symptoms:- terminate immediately with

cardioversion/ drugs!o Hypotension

BRADYARRYTHMIAS

Under 60bpm Due to Delayed conduction. If symptomatic treat with

o ATROPINEo BETA – AGONISTSo PACING

BP and CO fall if stroke volume cant increase due to reduced compliance / contractility.

SINUS BRADYCARDIA HEART BLOCK

o FIRSTo SECOND: MOBITZ 1+2o COMPLETE

SINUS BRADYCARDIA

Normal ECG p waves, and Av node conduction Treated by addressing causes eg. Vagal reflexes (pain), Drug

Toxicity (beta-blockers), Atropine.

HEART BLOCK

Due to AV node or Conducting tissue ischemia. Common after inferior MI (RCA supplies the AV node) Heart Block after an anterior MI suggests a large infarct… requires

early pacemaker insertion.

ATRIAL FLUTTER

An anticlockwise atrial re-entry circuit. Causes rapid, co-ordinated depolarization. 300bpm Ventricular rate depends on AV Node

refractoriness, with conduction of every 2nd, 3rd or 4th depolarization. (2:1, 3:1, 4:1 block)

Tachycardia with rate of exactly 150bpm suggests Atrial Flutter.

Treat?o Class 1a, 2, 3, 4 drugs / digoxin.o Class 1a may cause VT, so give beta-

blocker or digoxin before, as I think it causes every beat to conduct.

AF

Spontaneous, chaotic, atrial depolarization. Over 300bpm Refractory AVN conductions limits ventricles to

under 200bpm. Ineffective atrial contraction predisposes to

atrial thrombus and thromboembolism. Treat?!

o Anticoagulation (stroke)o Digoxin (controls resting HR)o Beta-blockers (control exercise HR)o DC Cardioversion- normal heart, AF

under a year.

VENTRICULAR FIBRILLATION

Chaotic ventricular rhythm Follows Acute MI Treat?! Immediate DC cardioversion!

o Class 2/3 drugs/ implant defib (recurs)

VENTRICULAR TACHYCARDIA

Due to re-enry circuits eg. Scar tissue from MI, with uniform QRS

Or focal ectopic automaticity (drugs or metabolic) with irregular or phasic TORSADE DE POINTES QRS (polymorphic VT)- unstable and may progress to VF.

Ventricular rate 150 – 250 Treat!? Terminate with cardioversion Or class 1a/1b drugs Use class 2 or 3 to prevent initial reoccurance Implantable defib for ongoing.

AV RE-ENTRANT TACHYCARDIAS

PAROXYSMAL SVT! Re-enrant circuits between atria and ventricles. Or between atria and AV Node- ie in the AV NODE Treat!? Vagal Stimulation Drugs slowing Av node conduction (Adenosine), class

2, class 4 Radio-frequency catheter ablation

BRADYARRYTHMIAS

Under 60bpm Due to Delayed conduction. If symptomatic treat with

o ATROPINEo BETA – AGONISTSo PACING

BP and CO fall if stroke volume cant increase due to reduced compliance / contractility.

SINUS BRADYCARDIA HEART BLOCK

o FIRSTo SECOND: MOBITZ 1+2o COMPLETE

SINUS BRADYCARDIA

Normal ECG p waves, and Av node conduction Treated by addressing causes eg. Vagal reflexes (pain), Drug

Toxicity (beta-blockers), Atropine.

HEART BLOCK

Due to AV node or Conducting tissue ischemia. Common after inferior MI (RCA supplies the AV node) Heart Block after an anterior MI suggests a large infarct… requires

early pacemaker insertion.

PRE-EXCITATION SYNDROMES

An Accessory AV Pathway: BUNDLE OF KENT in Wolf Parkinson White Syndrome.

Bypasses the AV node, depolarizing an area of the ventricle early, shortening the P-R interval (time for atria then ventricles to contract)

Slow transmission from the pre-excited area- no conducting tissue, creates a delta wave on ECG.

Treat!? Class 1a, 1c, III IV drugs And ADENOSINE Radiofrequency catheter ablation

ATRIAL TACHYCARDIA

Automaticity in ectopic atrial pacemakers Treat!?

o ADENOSINE to terminateo Class 1c or 3 drugso Correct underlying metabolic defecto Radiofrequency catheter ablation.

HEART FAILURE AND PULMONARY OEDEMA

When CO insufficient to meet the metabolic needs of the body.

Or can only do so with ELEVATED FILLING PRESSURES. (pre-load)

Initially compensatory mechanisms maintain CO at rest But as HF and CO deteriorates, exercise tolerance falls,

and ‘downstream’ hydrostatic pressures increase Common causes: IHD and Hypertension. Volume overload can cause pulmonary oedema, despite

cgood heart function. 5 year survival under 50%.

LV FAILURE

Most common Downstream pulmonary capillary ‘wedge pressure’

(PCWP) rises to 25 ish. Fluid filters into the alveoli and interstitial spaces, causing

pulmonary oedema, and breathlessness. Low plasma oncotic pressure (hypoalbuminaemia) or

increased membrane permeability (inflammation) can cause pulmonary oedema at lower PCWP.

RV FAILURE

Causes SYSTEMIC CONGESTION (e.g. ankle swelling,

PATHOPHYSIOLOGY OF HEART FAILURE

SYSTOLIC FAILURE

Reduced Myocardial contractility and Ejection Fraction (under 50%) accounts for most of HF.o Due too IHDo Cardiomyopathyo Metabolic toxicityo Valve defectso Arrhythmias

Initially CO maintained by compensatory mechanismso Inc. sympathetic driveo Raised circulating volume (renin)o Raised Filling pressures

These mechanisms have detrimental effects Failing heart responds poorly to preload Subsequent pulmonary and peripheral congestion Large ventricular volumes increase cardiac work and

impair function In pressure overload (aortic stenosis), compensatory

hypertrophy initially improves ventricular Ejection Fraction.

Reduced compliance and capillary density eventually decreases blood supply and contractility.

DIASTOLIC DYSFUNCTION

HEART FAILURE AND PULMONARY OEDEMA

When CO insufficient to meet the metabolic needs of the body.

Or can only do so with ELEVATED FILLING PRESSURES. (pre-load)

Initially compensatory mechanisms maintain CO at rest But as HF and CO deteriorates, exercise tolerance falls,

and ‘downstream’ hydrostatic pressures increase Common causes: IHD and Hypertension. Volume overload can cause pulmonary oedema, despite

cgood heart function. 5 year survival under 50%.

LV FAILURE

Most common Downstream pulmonary capillary ‘wedge pressure’

(PCWP) rises to 25 ish. Fluid filters into the alveoli and interstitial spaces, causing

pulmonary oedema, and breathlessness. Low plasma oncotic pressure (hypoalbuminaemia) or

increased membrane permeability (inflammation) can cause pulmonary oedema at lower PCWP.

RV FAILURE

Causes SYSTEMIC CONGESTION (e.g. ankle swelling,

PATHOPHYSIOLOGY OF HEART FAILURE

SYSTOLIC FAILURE

Reduced Myocardial contractility and Ejection Fraction (under 50%) accounts for most of HF.o Due too IHDo Cardiomyopathyo Metabolic toxicityo Valve defectso Arrhythmias

Initially CO maintained by compensatory mechanismso Inc. sympathetic driveo Raised circulating volume (renin)o Raised Filling pressures

These mechanisms have detrimental effects Failing heart responds poorly to preload Subsequent pulmonary and peripheral congestion Large ventricular volumes increase cardiac work and

impair function In pressure overload (aortic stenosis), compensatory

hypertrophy initially improves ventricular Ejection Fraction.

Reduced compliance and capillary density eventually decreases blood supply and contractility.

DIASTOLIC DYSFUNCTION

CLINICAL FEATURES

Presentation depends ono Onset speedo Underlayingo Ventricular involvement

HF precipitated/ aggravated byo Stresso Acute illnesseso Drugso Pregnancy

Reduced CO causes fatigue, anorexia, exercise limitation. LVF

o Breathlessnesso Hypoxaemiao Orthopnoeao PNDo Cough- frothy pink sputumo GALLOP RHYTHEM (S3, S4 added sounds)o COURSE CREPS LUNG BASES

RVFo Systemic congestion, raised JVPo Hepatomegalyo Ankle oedemao Asciteso Onset may be acute (MI) with cardiogenic

shock/ acute pulmonary oedema.o Chronic: fatigue and gradual fluid retention.

DIAGNOSTIC INVESTIGATIONS

Cardiac Enzymes ECG CXR Serum BNP (b-type natrieuritic peptide) increased by

myocardial wall stress: sensitive and specific for HF. ECHO: wall hypokinesia, ventricular enlargement. Ejection fraction: reduced in HF CO and BP may be normal Cardiac catherisation often needed.

NEW YORK HEART ASSOCIATION CLASSIFICCATION HF

CLASS 1: (mild): no activity limitation, no symptoms from ordinary activity. E.g. Fatigue, dyspnoea, palpitations

CLASS 2: (mild): Slight limitation physical activity. Comfortable at rest, symptoms with ordinary activity.

CLASS 3: (moderate): Marked limitation physical activity, only comfortable at rest- minimal activity causes symptoms.

CLASS 4: (severe): unable to carry out any physical activity without discomfort. Symptoms at rest.CAUSES HF AND PULMONARY OEDEMA

MYOCARDIAL DYSFUNCTIONo IHDo CARDIOMYOPATHIESo PREGNANCYo MYOCARDIAL DISEASE

(amyloidosis)o If you have an inferior MI, you can

have RV failure isolated, as blood supply from RCA.

PRESSURE OVERLOADo LEFT: hypertension, aortic stenosis

(mitral stenosis doesn’t cause LV failure)

o RIGHT: Pulmonary hypertension due to chronic lung disease (cor pulmonale), pulmonary stenosis.

VOLUME OVERLOADo Excessive fluid administrationo Retention (renal failure)o Aortic/ mitral valve regurg causes

LVFo Tricuspid regurg causes RVF.

IMPAIRED FILLINGo Constrictive pericarditis (TB,

rheumatic heart disease, pericardial effusion, cardiac

MANAGE HF

Treat theo CAUSE (IHD/valve)o Pathophysiology (DD)o Precipitating events (arrhythmias)

AFTERLOAD REDUCTION rapidly improves LV function and CO in the failing heart.

But may cause Hypotension. PRELOAD REDUCTION: relieves symptoms (eg. Pulmonary oedema),

but CO is not increased. Non-invasive monitoring and less frequently pulmonary artery

catheterization- may be required to measure filling pressures, CO, vascular resistance.to optimize HF treatment.

ACUTE LEFT VENTRICULAR FAILURE

Priority: Immediate relief of breathlessness of pulmonary oedema.

Sitting position most comfortable. Supplemental OXYGEN (60%) corrects hypoxaemia. Loop DIURETICS (furosemide IV) initially reduce LV preload, and

relieve dyspneoa by pulmonary venous dilation. Subsequent diuresis lowers fluid load and cardiac filling pressures. NITRATES (IV/sublingual) inc venous capacitance, and dilate

coronary arteries in IHD. DIAMORPHONE decreases preload- potent venodilator effects,

and V02, by relieving anxiety.

CAUSES HF AND PULMONARY OEDEMA

MYOCARDIAL DYSFUNCTIONo IHDo CARDIOMYOPATHIESo PREGNANCYo MYOCARDIAL DISEASE

(amyloidosis)o If you have an inferior MI, you can

have RV failure isolated, as blood supply from RCA.

PRESSURE OVERLOADo LEFT: hypertension, aortic stenosis

(mitral stenosis doesn’t cause LV failure)

o RIGHT: Pulmonary hypertension due to chronic lung disease (cor pulmonale), pulmonary stenosis.

VOLUME OVERLOADo Excessive fluid administrationo Retention (renal failure)o Aortic/ mitral valve regurg causes

LVFo Tricuspid regurg causes RVF.

IMPAIRED FILLINGo Constrictive pericarditis (TB,

rheumatic heart disease, pericardial effusion, cardiac

MANAGE HF

Treat theo CAUSE (IHD/valve)o Pathophysiology (DD)o Precipitating events (arrhythmias)

AFTERLOAD REDUCTION rapidly improves LV function and CO in the failing heart.

But may cause Hypotension. PRELOAD REDUCTION: relieves symptoms (eg. Pulmonary oedema),

but CO is not increased. Non-invasive monitoring and less frequently pulmonary artery

catheterization- may be required to measure filling pressures, CO, vascular resistance.to optimize HF treatment.

ACUTE LEFT VENTRICULAR FAILURE

Priority: Immediate relief of breathlessness of pulmonary oedema.

Sitting position most comfortable. Supplemental OXYGEN (60%) corrects hypoxaemia. Loop DIURETICS (furosemide IV) initially reduce LV preload, and

relieve dyspneoa by pulmonary venous dilation. Subsequent diuresis lowers fluid load and cardiac filling pressures. NITRATES (IV/sublingual) inc venous capacitance, and dilate

coronary arteries in IHD. DIAMORPHONE decreases preload- potent venodilator effects,

and V02, by relieving anxiety.

Cardiovascular compensatory mechanisms and the detrimental positive feedback effects they exert in HF.

Reduced CO (digoxin)

BETA SYMPATHETIC ACTIVATION

(Betablockers)

INCREASES CONTRACTILITY

and HR

heart- More Work and oxygen consumption

INC Myocardial DamageINC Ca2+ OverloadINC energy deficit

Cardiac Remodelling

Reduced CO

Reduced CO

ALPHA SYMPATHETIC ACTIVATION

ARTERIAL VASOCONSTRICTION

(arterial vasodilators)

INC AFTERLOAD



Cardiac Remodelling

Reduced CO

Reduced CO

RENIN-ANGIOTENSIN ACTIVATION

ALDOSTERONE: (spironolactone) Fluid retention (diurteics).......

PRELOAD INCREASED!(venodilators)

ANGIOTENSIN II: (angiotensinII receptor blockers)

ARTERIAL VASOCONSTRICTION......

AFTERLOAD INCREASED!Renal artery... FLUID RETENTION

PRELOAD INCRESED



Cardiac Remodelling

Reduced CO

CARDIAC EMERGENCIES: HYPERTENSIVE EMERGENCY

Severe hypertension is o Systolic 220-240o Diastolic 120-140

Used to be called accelerated/malignant hypertension, now based on presence/absence LIFE-THREATENING END ORGAN DAMAGE. (LTOD)- e.g. aortic dissection

This determines treatment urgency. If organ damage, needs to be reduced to safe levels

(diastolic 100) within 2 hrs. Caution: rapid fall in BP can cause strokes, accelerated

renal failure, cardiac ischemia. If NO end organ damage…. Gradual reduction over 6-

72hrs preferred. Most common cause

o Inadequate/discontinued therapy for benign essential HT.

In under 30s or blacks, over 50% have a secondary cause

o Renovascular diseaseo Phaeochromocytomao Endocrineo Drug induced catachlomine release (cocaine)o Pregnancy related

Most end organ damage due to ARTERIOLAR NECROTIZING VASCULITIS

And LOSS OF VASCULAR AUTOREGULATION If untreated, with organ damage, mortality is over 90%

in a year.

HYPERTENSIVE EMERGENCY

Clinical features of end organ damage (HTN) ENCEPHELOPATHY

o Decreased vascular auroregulation- cerebral oedemao Headache, nausea, vomiting, blurred vision, confusion.o Later: Focal neurological deficits, seizures, papilloedema, coma

PULMONARY OEDEMAo Due to Increased LV afterload (not fluid overload): treat by

reducing afterload. PROGRESSIVE RENAL IMPAIRMENT

o Increased urea and creatinine, dec GFR.o Haematuria, proteinuria o HTN can be secondary to glomerulonephritis and renal artery

stenosis- bruit? STROKE SYNDROMES

o Cerebral infarctionso Cerebral Heamorrhageo SAH

RETINOPATHYo Grade3: exudates and hemorrhageo Grade4: Papilloedema.

AORTIC DISSECTIONo Tearing chest/back paino Arm/leg BP differenceo Absent peripheral pulses

ANGINA + MIo Due to inc LV afterload, inc wall stress, dec myocardial

perfusion PREGNANCY RELATED

o Pre-eclampsia, eclampsia.

HYPERTENSIVE EMERGENCY: MANAGEMENT

Severe HTN with end organ failure: REQUIRES ADMISSION! Rarely, immediate BP reduction needed (eg. Dissecting AA) Potent, titratable, vasodilator infusions. Arterial BP monitoring Mandarory! IV Therapies:

o SODIUM NITROPRUSSIDE (rapidly reversible arterio-venous dilator)- administered by infusion pump to avoid hypotensive episodes.

o GTN (arteriovenous dilator)- effective when Myocardial ischemia and pulmonary oedema there.

o LABETALOL: alpha and beta blocker- good for hypertensive encephalopathy. May exacerbate asthma, HF, heart block.

Severe hypertension with no end organ damageo Use oral regimes when possibleo Lower over 24-72 hrso NIFEDIPINE (sublingual) – rapid onset, short half-

life, titratable.o Introduce (as you usually do with hypertension)

Beta blockers ACE inhibitors Calcium antagonists

INFECTIVE ENDOCARDITIS

Usually subacute Infection of heart valves / endocardium Causes a chronic illness when organism is non-virulant

(streptococcus viridans) Can be ACUTE with virulent: STAPHYLOCOCCUS Common in

o Elderly with degenerative aortic and mitral valveo Prosthetic valveso Rheumatic fevero Congenital heart disease

Abnormal valves more susceptible to infection after dental procedures.

Normal valves occasionally infected by virulent organisms. (staphylococcal valve infection after IV drug use)

CNS FEATURESo Embolic infarctiono Abscesseso Meningitis

GENERAL INFECTIONo Low grade fevero Lethargy, malaiseo Anaemia, weightloss

CARDIACo Murmurso HFo Mycotic aneurysms

LATE SIGNSo Clubbingo Splenomegaly

JOINTSo Arthralgiao Septic Arthritis

SKINo Vasculitis rash

SOLES OF FEETo Janeway lesion

IMMUNE COMPLEX DEPOSITIONo RETINAL HEAMORRHAGES (Roth spots)o SUBCONJUNCTIVAL HEAMORRHAGEo SPINTER HEAMORAGES, NAILBED INFARCTSo JANEWAY LESIONS (small, red macular)o OSLERS NODES (subcut swellings in finger/toe pulps,

pain.o MICROSCOPIC HAEMATURIAo GLOMERULONEPHRITISo LUNG: R. SIDED EMBOLIC INFARCTo LOSS PERIPHERAL PULSESo RENAL/CEREBRAL EMBOLIC INFARCTS

Diagnosis initially clinical Suspected in fever, anaemia, high ESR or CRP, microscopic

haematuria, new heart murmurs, flu-like symptoms, weightloss.

Confirmed by repeatedly positive blood cultures, and ECHO confirm diagnosis.

Transthoracic ECHO detects under 50% vegetations- transoesophageal studies better.

Manage

- Look for and treat underlaying infection (dental abscess?)- BENZYLPENICILLIN (empirical antibiotic therapy)- Adjusted when know cultures.- Treat 3-6 weeks- Infected prosthetic valves/ damage valves need

replacement.- Prophylactic antibiotics given to patients with dodgey

ACUTE PERICARDITIS

o Infection (most viral), MI, Uremia, Connective tissue disease, Trauma, TB, Neoplasia. Dresslers syndrome.

DRESSLER’S SYNDROMEo 2 weeks after an MIo Immulogically-mediated febrile pleuropericarditis

Clinical featureso Severe positional (relieved by sitting forward)o Retrosternal chest paino Pericardial rub on Ascultation

Investigationso ECG: CONCAVE ST-SEGMENT ELEVATION IN ALL

LEADSo Cardiac enzymes may be elevated

Manageo Antiinflammatory drugs (ASPIRIN) relieve

discomfort.o Steroids in Dresslers syndrome.

PERICARDIAL EFFUSION

Infection, (TB), Uremia, MI, Aortic dissection, myxedema, neoplasia, radiotherapy.

Clinical featureso Due to cardiac tamponade- when pericardial effusion

impairs ventricular filling, reducing CO.o Breathlessnesso Pericarditic paino Acute cardiovascular collapse

Examinationo Raised JVP- increases on inspiration.o Distant heart sounds

ECGo Reduced voltageo CXR (globular cardiomegaly)o ECHO- (pericardial fluid and cardiac tamponade

induced RV diastolic collapse)- diagnostic. Manage

o Echo-directed pericardial drainage required for tamponade. In constrictive pericarditis- remove it.

WHAT TO DO IN CHEST PAIN EMERGENCY

AIRWAY (patent, manouvres, adjuncts) BREATHING (no resp effort.. ARREST TEAM) CIRCULATION (no pulse.. ARREST TEAM)

CALL FOR SENIOR HELP: (unewell/ deteriorating) SIT UP 15L/min OXYGEN (sats under 94% / sob) MONITOR (pulse oximiter, BP, ECG, Defib) OBS: (BP both arms, ECG) BRIEF Hx, /NOTES/ STAFF EXAMINE: (chest, Rx, Abdo) ESTABLISH LIKELY CAUSES RULE OUT SERIOUS CAUSES CONSIDER

o PCI / THROMBOLYSISo ASPIRIN 300mg PO STATo NEEDLE DECOMPRESSION

INITIATE FURTHER TREATMENT (analegesia) VENOUS ACCESS

o FBC, U&E, LFT, CRP, gluc, cardiac marker, D-dimero CXR

Call senior help- worsening/ no improvement No improvement? REPEAT ECG after 20MINS REASSESS… A, B, C

LIFE THREATENING CAUSES

MYOCARDIAL INFARCTION TENSION PNEUMOTHORAX ACS PERICARDIAL EFFUSION/TAMPONADE AORTIC DISSECTION PE SICKLE CELL CRISIS

NOTES ON EMERGENCY CHEST PAIN

WORRYING FEATURESo Inc/dec HRo Dec BPo Inc RRo Dec GCSo Sudden onseto Sweatingo Nausea & vomitingo Pain to jaw/ L. Arm / Backo ECG Changes

THINK ABOUT COMMONo MI / ACS / ANGINAo PEo MUSCULOSKELETALo PNEUMONIAo PNEUMOTHORAX (simple / tension)o PERICARDITISo REFLUX, PEPTIC ULCER

UNCOMMONo AORTIC DISSECTIONo CARDIAC TAMPONADEo SICKLE CELL CRISIS.

ASK ABOUT: Site, onset, radiation, quality (heavy/ aching/ sharp), intensity (1-10), time onset, duration, associated symptoms (sweating, nausea, palpitations, breathless), exacerbating or relieving factors (breathing, position, exertion, eating), recent trauma/exertion, previous episodes

PMHx: cardiac/ Resp problems / DM / GORD DRUGS: Cardiac / respiratory meds, antacids FHx: IHD / premature cardiac death SH: Smoking / Exercise tolerance INVESTIGATIONS

o ECGo FBC, U&E, LFT, D-dimer, Cardiac markers, ABGo CXR- portable? Standard?o ECHO/ CT if large proximal PE/ aortic root dissection.

TREAT: o 15L OXYGENo IV OPIOIDo ANTI-EMETIC

Diagnosis to excludeo CARDIAC ISCHEMIA (ECG, Hx, Cardiac markers)o PE (dec sats, ECG, risk, D-Dimer, CT-PA)o PNEUMOTHORAX (Mediastinal shift, dec breath sounds)o AORTIC DISSECTION (shock, L+R systolic BP differ by over

15mmHg, mediastinal widening on CXR, abnormal CT/Echo

Stable Angina- Exertion pain- Radiates to L arm/ Jaw- Under 20mins- Breathlessness- Dec when rest/GTN

- Dyspnoea- Tachycardia- Non-tender- Normal after pain goes

- Transient ECG changes- Troponin not elevated- Positive stress ECG- CORONARY ANGIOGRAPHY

Pericarditis- Hx viral-like illness- Pleuritic pain- Increased on lying- Decreased sitting forwards

- Pericardial Rub- Otherwise normal CVS and RS

exams

- Saddle-shaped ST segments on most ECG leads

- Inc CRP & ESR

AORTIC DISSECTION- Sudden onset- Severe inetrscapular pain- Tearing in nature- Breathlessness- Limb weakness / numbness.

- Tachycardia- Decreased BP- Difference in brachial pulses and

pressures- Increased RR- Limb weakness / paraesthesia

- CXR WIDENED MEDIASTINUM- ECHO/ CT: Aortic dilation- ANGIOGRAM: aortic leakPulmonary Embolism

- Breathlessness- PE risk factors- Pleuritic chest pain Pneumothorax

Pneumonia- Productive cough, sputum

Pulmonary Embolism- Breathlessness- PE risk factors- Pleuritic chest pain Pneumothorax

Pneumonia- Productive cough, sputum

ACUTE CORONARY SYNDROME

- General term- presentations of varying levels of myocardial ischemia.- Management and outcome better if you know whats going on exactly.- Typical sounding chest pain lasting over 20 mins?

o New LBBB / ST elevation on ECG? 12hr Troponin will be raised, but not needed for diagnosis: STEMI

o Ischemia other than ST elevation on ECG? NSTEMI:

(TropT: over 0.1) or (TropI over 1)

UNSTABLE ANGINA: under 0.1 or 1.

ACS SERUM CARDIAC MARKERS

o TROPONINS (I or T) A protein: If they’re in the blood-

very likely myocardial injury Can be raised in PE, renal failure,

septicemia, after tachyarrythmias But CK not usually raised as well in

these conditions. Detection can be 6hrs after injury Levels elevated for 14days Troponins used as prognostic

indicator in UNSTABLE ANGINA / NSTEMI

o CK CREATININE KINASE Enzyme found in all muscle and

released in muscle cell lysis. Not specific for cardiac muscle Peaks 24HRS post MI Returns to normal, 48-72 hrs post-

MI Useful in detecting further infarction

in patients with pain 3-14 days post MI.

o CK-MB Cardiac isomer of CREATININE

KINASE enzyme More specific than total CK.

o AST LDH Once used to retrospectively aid in

diagnosis of acute MI- but now better things.

ST ELEVATION MI

WORRYING SIGNS: LV failure and cardiac dysrrythmia. Central crushing heavy chest pain, (over 20mins) Radiating to L arm/jaw SOB, nausea, sweating, vomiting, palpitations, anxiety RISK

o Smoking, obesity, DM, Hypertension, cholesterol, family, previous IHD.

SIGNS o ST Elevation (over 1mm in 2 leads, or 2mm in 1 lead)o New LBBB: subsequent Q waves, and T wave inversiono CXR: Cardiomegaly, LV failureo Cardiac markers raised.

ACUTE TREATMENT (MONAC) o Rapid re-perfusion by percutaneous coronary intervention (PCI) in

those UNDER 12HRS SYMPTOMS.o IE: seek senior help M: DIAMORPHINE 2.5-5mg IV O: OXYGEN 15l/min N: NITRATES: GTN: 2 puffs every 5 mins until no pain- if still pain,

give IV unless hypotensive. A: ASPIRIN 300mg C: CLOPIDOGREL 300mg (ANTIEMETIC)

o WHEN PCI NOT AVAILABLE WITHIN 3 HRS? o Fibrinolysiso Beta blocker: Bisoprolol 10mg/PO- limits mortality and decreases

infarct size- avoid in COPD, hypotension, failure. SECONDARY PROHHYLAXIS (BAN SCAR)

o B: BETA BLOCKERSo A: ACEio N: Nitrates (symptoms)o S: STATINo C: Clopidogrel 1yro A: aspirin lifetimeo R: Risk factors (smoking, DM, obesity, BP, cholesterol)

COMPLICATIONS o Dysrhythmias

AV Block, Bradycardia, VF/VT LVF Valve prolapse Ventricular septal rupture Ventricular aneurysm formation Pericarditis, Dresslers syndrome (pericarditis- fever, pleuritic

pain after heart injury) Recurrent Pain

o CARE AFTER MI o Bed rest 48hrs with continuous ECGo Daily 12lead ECG, and clinical examinationo Thromboembolism prophylaxiso Beta blocker (unless contraindicated), ACEi, Statino Discussion over modifiable risk factors, arrange cardiac rehabo PRIMARY PCI: patients at lower risk of complications, shorter stayso THROMBOLYSIS PATIENTS: consider in-patient angiographyo Review outpatients: 5w and 3m for symptoms, check lipids, BP

RISK STRATIFICATION IN ACS

o Estimation of death allows individualused assessment of risks and benefits interventions

o Careful targeting of resources to those patients who stand to benefit the most.

o Validated scoring algorithmso TIMI: THROMBOLYSIS IN MI RISK

SCORE GRACE: ACS RISK MODEL Data from GLOBAL REGISTRY OF ACUTE

CORONARY EVENTS- huge amount of info from many countries.o Risk scores calculated on admission o Predict in hospital and 6month

mortality.o On discharge: to predict 6month

mortality. High risk?

o Patients need a coronary care unit bed.

o Consider for glycoprotein llb/llla inhibitors and urgent catheterization

Low/intermediate risk?o Observation to ensure pain freeo Futher stratification using exercise

ECG, coronary calcium scoring/ stress imaging (echo/perfusion imaging)- to determine need for catheterization.

NSTEMI

WORRYING SIGNS: LV failure and cardiac dysrrythmia. Central crushing heavy chest pain, (over 20mins) Radiating to L arm/jaw SOB, nausea, sweating, vomiting, palpitations, anxiety RISK


SIGNS o Same as STEMIo Patients tend to be older with more co-morbidities than STEMIo ST DEPRESSION, INVERTED T WAVESo CARDIOMEGALY , FAILURE (CXR)o ELEVATEED TROPONIN (12hrs after worst pain)

ACUTE TREATMENT (MONAC) M: DIAMORPHINE 2.5-5mg IV O: OXYGEN 15l/min N: NITRATES: GTN: 2 puffs every 5 mins until no pain- if still

pain, give IV unless hypotensive. A: ASPIRIN 300mg C: CLOPIDOGREL 300mg

FONDAPARINUX (anticoagulate) Beta-blocker- Bisoprolol 10mg STAT- beware in COPD,

hypotension, failure RISK STRATIFY: for ones needing bed in CCU, catheterization or

glycoprotein inhibotors. SECONDARY PROHHYLAXIS (BAN SCAR)- same as STEMI

o B: BETA BLOCKERSo A: ACEio N: Nitrates (symptoms)o S: STATINo C: Clopidogrel 1yro A: aspirin lifetimeo R: Risk factors (smoking, DM, obesity, BP, cholesterol)

COMPLICATIONS- same as STEMI, but less commono Dysrhythmias

AV Block, Bradycardia, VF/VT LVF Valve prolapse Ventricular septal rupture Ventricular aneurysm formation Pericarditis, Dresslers syndrome (pericarditis- fever, pleuritic

pain after heart injury) Recurrent Pain

UNSTABLE ANGINA

WORRYING SIGNS: LV failure and cardiac dysrrythmia.

Central crushing heavy chest pain, (over 20mins) Radiating to L arm/jaw SOB, nausea, sweating, vomiting, palpitations,

anxiety Typically, episodes of angina, occurring at rest or

minimal provocation, with poor response to GTN. More frequent and painful than usual. RISK


SIGNS o ST DEPRESSION, INVERTED T WAVESo Dynamic ECG changes over timeo Signs of previous MI?o Troponin not elevated.

ACUTE TREATMENT (MONAC) M: DIAMORPHINE 2.5-5mg IV O: OXYGEN 15l/min N: NITRATES: GTN: 2 puffs every 5 mins

until no pain- if still pain, give IV unless hypotensive.

A: ASPIRIN 300mg C: CLOPIDOGREL 300mg

- PLUS! BETA-BLOCKERS to limit ischemia- FONDAPARINUX (disrupt thrombus)

o Same further management as NSTEMI

SECONDARY PROHHYLAXIS (BAN SCAR)- same as STEMI

o B: BETA BLOCKERSo A: ACEio N: Nitrates (symptoms)o S: STATINo C: Clopidogrel 1yro A: aspirin lifetime

STABLE ANGINA

Retrosternal chest discomfort occurring predictably upon exertion Relieved by rest and nitrates. SYMPTOMS

o Central, heavy chest paino Lasting under 20mins- radiating to L.arm and jawo Precipitated by exertion, relieved by rest, or GTN in under 5 minso SOB, nausea, sweating, palpitations. o Tachycardia, cool, sweaty, clammy, pallor- normal after episode.

ECGo Transient ST-depression during paino Flat or inverted T-waveso Signs of previous MI

Cardiac markers not elevated! PRIMARY PROPHYLAXIS- kind of the same.

o B: BETA BLOCKERSo A: ACEio N: Nitrates (symptoms)o S: STATINo A: aspirin lifetime o R: Risk factors (smoking, DM, obesity, BP, cholesterol)o PLUS: Calcium channel agonist, NICORANDIL

PERICARDITIS

Pleuritic chest pain Worse on laying flat and deep inspiration Relieved by sitting forward, recent viral illness SIGNS?

o May be noneo Pericardial rub

ECGo Saddle shaped ST segments in most leads

BLOODSo

High WCCInflammatory markers

ECHOo Pericardial Effusion

TREATo Acutely- reassurance and anaelgesiao Paracetamol, NSAIDSo Should settle 2-4 weeks

AORTIC DISSECTION

Aortic dissection occurs when a tear in the inner wall of the aorta causes blood to flow between the layers of the wall of the aorta, forcing the layers apart.

Severe characteristic chest or abdominal pain- "tearing" with other symptoms from decreased blood supply to organs. Aortic dissection is a medical emergency and can quickly lead to death, even with optimal treatment, as a result of decreased

blood supply to other organs, cardiac failure, and sometimes rupture of the aorta. More common: high blood pressure, known thoracic aortic aneurysm, Marfan syndrome, Ehlers–Danlos syndrome. The treatment of aortic dissection depends on the part of the aorta involved. Surgery in dissections that involve the aortic arch, while dissections further away from the heart treated with blood lowering BP

(systolic under 100) SYMPTOMS

o Sudden onset, severe chest paino Anterior or interscapularo Tearing in natureo Dizziness, breathlessness, sweating, neurological deficits

RISK FACTORSo Smokingo Obesityo DMo High BPo Increased Cholesterolo Family historyo IHD

SIGNSo Unequal radial pulseso Tachycardiao Hypertension/ Hypotensiono Difference in brachial pressures of over 15mmHgo Aortic regurgo Pleural Effusion (left more than right)o Neurological defects from carotid artery dissection

INVESTIGATIONSo ECG normal/ show LV strain or ischemia.o CXR widened mediastinum over 8cm (rare)o Blood can track down and cause irregularity of aortic knuckle and small left pleural effusiono ECHO: shows aortic root leak, aortic valve regurg, pericardial effusiono Consider MRI/CT

ACUTE TREATMENT (HYPOTENSIVE? Treat as shock)o Senior help!!!o OXYGEN (15/min)o CANNULA (2 large bore)o BLOOD: X-MATCH 6unitso OPIDOIDs (anaelgesia)

TREATMENTo Surgery: for type A (Ascending aorta)o Type B (descending aorta)- conservative.

TACHYARRYTHMIAS… EMERGENCY!!!

AIRWAY: (patent, manouvres, adjuncts) BREATHING (no resp effort- crash team) CIRCULATION (no pulse, crash team) SENIOR HELP! If patient unstable

o Reduced GCSo Systolic under 90o Chest paino HF

SIT UP (if hypotensive, lay flat, legs up) OXYGEN (15l/min- non rebreather) MONITOR

o Pulse oximitero Defib paddleso BPo ECG leads

Request full set obs and ECG Hx- BRIEF, CHECK NOTES, MEDS, ASK STAFF EXAMINE- CV, resp, Abdo LIKELY CAUSES and SERIOUS CAUSES- establish INITIATE FURTHER TREATMENT VENOUS ACCESS

o Bloodso FBCo U+Eo D-Dimero Cardiac Markerso TFT

Consider requesting urgent CXR- portable Reassess ABC

LIFE THREATENING CAUSES

VT VF Torsades de Pointes SVT (haemodynamically unstable) Fast AF/ Flutter (Haemodynamic compromise) Sinus Tachycardia- secondary to shock (PE),

iatrogenic.

ADULT TACHYCATRDIA WITH PULSE ALGORHYTHM

UNI! unstable? narrow? Irregular?

1. FIRST- Assess ABCDE- Oxygen and IV access- Monitor: EGC, BP, Sp02, 12-lead ECG- Identify and treat reversible causes.. electrolytes?

2. ADVERSE FEAUURES?- Myocardial Ischemia, HF, Shock, Syncope.- (My heart’s So Speedy)

3. YES … UNSTABLE!!! (adverse features)o SYNCHRONISED DC SHOCKo Up to 3 attemptso AMIODARONE 300mg IV (10-20mins)o Repeat shock followed byo AMIODARONE 900mg over 24hrs.

4. NO… STABLE…o IS QRS NARROW OR BROAD??

BROAD QRS

5. REGULAR / IRREGULAR?

Regular

VT (AMIODARONE)o 300mg Over 20minso 900mg over 24hrs

SVT with BBB (ADENOSINE)

Irregular

AF with BBB Pre-Excited AF (AMIODARONE) POLYMORPHIC VT eg. Torsade de

pointes (MAGNESIUM) 2g/10min

NARROW QRS

5. REGULAR / IRREGULAR?

Regular

Use vagal manouvres ADENOSINE (6mg rapid IV

bolus, then give 12 if needed , then 12)

SINUS RHYTHEM BACK?? If now sinus rhythem, was

probably RE-ENTRY PAROXSMAL SVT

NO SINUS RHYTHEM? ATRIAL FLUTTER: beta blocker.

Irregular

IRREGULAR, NARROW COMPLEX TACHCARDIA

Probably AFo Beta blockero Diltazemo AMIODARONE/DIGOXIN

(in Heart failure)

TACHYARRYTHMIAS

Worrying Features

Decreased GCS Dec BP (systolic under 90) Chest Pain HF

Causes

Common

TACHYARRYTHMIAS

Worrying Features

Decreased GCS Dec BP (systolic under 90) Chest Pain HF

Causes

Common

WOLF-PARKINSON WHITE SYNDROME

A re-entrant tachycardia Due to accessory conduction pathway (bundle of kent) between atria and ventricles. SHORT P-R INTERVAL and DELTA WAVE Avoid Digoxin and verapamil Refer to cardiologist for ablation

ATRIAL FIBRILLATION

WARNING SIGNS o HFo Hypotensiono Decreased GCSo Chest pain

SYMPTOMS o SOBo Palpitationso Dizzinesso Chest Pains

RISK FACTORS o Previous AF

ATRIAL FIBRILLATION- treat

TREAT:

- Haemodynamically compromised?- Help, shock?, oxygen, iv access, cardioversion

(AMIODARONE)

CONSERVATIVE

Treat the precipitant (sepsis?) if new onset and this is obvious

RATE CONTROL

ATRIAL FIBRILLATION



RISK FACTORS o Previous AF

ATRIAL FIBRILLATION- treat

TREAT:

- Haemodynamically compromised?- Help, shock?, oxygen, iv access, cardioversion

(AMIODARONE)

CONSERVATIVE

Treat the precipitant (sepsis?) if new onset and this is obvious

RATE CONTROL

SVT



RISK FACTORS o Previous SVTo Structural cardiac anomalyo Alcoholo Increased T4 (thyroid)

COMPLICATIONS o Hypotension, o Ischemia, o HF, o Deterioration into more sinister arrhythmia.

SVT

SIGNS o Tachycardiao Anxietyo Hypotension (compromise)

Investigate o Narrow complex tachycardia (unless have

BBB too)o P waves merge into the QRS- can be hard

to seeo Regular QRSo Rate over 140

Acute Treatment o Oxygeno 2 large bore cannulao Monitor rhythem on defib

o Vagal manouvreso cardioversion

o If recurrent, cardio might need to test conduction pathways.


WORRYING SIGNS o HFo Hypotensiono Decreased GCSo Chest paino PULSELESS!!!!!!!!

SYMPTOMS o SOBo Palpitationso Dizziness


WORRYING SIGNS o HFo Hypotensiono Decreased GCSo Chest paino PULSELESS!!!!!!!!

SYMPTOMS o SOBo Palpitationso Dizziness

BRADYARRYTHMIAS… EMERGENCY!!!









THINK ABOUTo SINUS BRADYCARDIA

After an inferior MI (gets the SA node) Drugs (digoxin toxicity) Vasovagal Low thyroxine Hypothermia Cushings reflex (bradycardia and

hypertension secondary to increased ICP)

Sleep Anorexia nervosa Physical fitness

ASK ABOUTo Dizzinesso Postural dizzinesso Fits/faintso Weight changeo Visual disturbanceo Nausea and vomiting

PMHx: Cardiac Disease (IHD/AF), Thyroid surgery, DM, Intercranial pathology/ head injury, glaucoma, eating disorder.

Drug Hx: Cardiac meds, (Beta blockers, Ca2+ antagonists, amiodarone, digoxin)

Social Hx: Exercise tolerance, IHD risk factors

o OBS HR, BP, Postural BP RR Sats

o LOOK FOR Pulse rate/rhythem Volume Pallor SOB Dec GCS Drowsy Inc JVP (cannon waves in 3rd degree AV block) Signs of cardiac failure (increased JVP, pulmonary

oedema, swollen ankles) Features of ICP (papilloedema, focal neurology)

Investigate Bradyarrythmiao ECG:

Sinus bradycardia/ complete heart block Evidence ischemia/infarction Evidence digoxin toxicity

o Bloods FBC U&E Glucose Ca2+ Mg2+ TFT Cardiac markers Digoxin level

BRADYARRYTHMIAS ON AN ECG

SINUS BRADYCARDIAo P before every QRS

1st DEGREE AV BLOCKo P-R interval over 0.2 secs (5 small squares)

Investigate Bradyarrythmiao ECG:

Sinus bradycardia/ complete heart block Evidence ischemia/infarction Evidence digoxin toxicity

o Bloods FBC U&E Glucose Ca2+ Mg2+ TFT Cardiac markers Digoxin level

BRADYARRYTHMIAS ON AN ECG

SINUS BRADYCARDIAo P before every QRS

1st DEGREE AV BLOCKo P-R interval over 0.2 secs (5 small squares)

SINUS BRADYCARDIA

Worrying: HF, Hypotension, decreased GCS Symptoms:

o None?o Dizziness, especially on standingo Recurrent fallso Palpitationso SOBo Symptoms of raised ICPo Hypothermia/ decreased T4

ECG

VASOVAGAL ATTACKS

Sudden reflex bradycardia from unopposed parasympathetic nervous inhibition is common.

Light-headedness, visual disturbance, nausea and sweating, then brief LOC,

Prompt recovery of consciousness Precipitants:

o FEARo PAINo POST-MICTURITIONo NAUSEA AND VOMITINGo DILATION ANAL SPHINCTER AND CERVIXo PULLING OF EXTRA-OCULAR MUSCLESo RAISED ICP (straining etc)

DRUGS PRECEEDING BRADYCARDIA

BETA BLOCKERS (even in eye drops) DIGOXIN (if patients in AF revert to sinus) Ca2+ ANTAGONISTS that slow HR

o VERAPAMILo DILTIAZEM

AMIODARONE can cause bradycardia A-AGONISTS: PNENYLEPHERINE used by anaethatists-

increased PVR so causes reflex brady.

SICK SINUS SYNDROME

Dysfunction of the SA Node Precipitated by ischemia/fibrosis Results in bradycardia/ arrest SA block/ SVT with alternating bradycardia/asystole Tachy-brady syndrome Needs pacing if symptomatic.

OTHER TYPES OF BLOCK

1st Degree and MOBITZ1o no treatment unless symptomatic or reversible

cause.

MOBITZ2 and HIGH GRADE AV BLOCKo Can deteriorate into complete heart blocko May need temp/permanent pacingo Espesh when associated with ACS/ anaesthetic.

COMPLETE 3rd DEGREE HEART BLOCK

Worrying?o HF, Hypotension, Decreased GCS

Symptomso None? Dizzy? Palpitations? SOB? Chest pain?

Causeso Underlying ischemic damage (inferior MI)o Post cardiac surgeryo Drug induced (beta blockers, Ca2+ blockers)o Amyloid, Sarcoid, Myeloma, Infective (Lyme)

Signs

SINUS BRADYCARDIA

Worrying: HF, Hypotension, decreased GCS Symptoms:

o None?o Dizziness, especially on standingo Recurrent fallso Palpitationso SOBo Symptoms of raised ICPo Hypothermia/ decreased T4

ECG

COMPLETE 3rd DEGREE HEART BLOCK

Worrying?o HF, Hypotension, Decreased GCS

Symptomso None? Dizzy? Palpitations? SOB? Chest pain?

Causeso Underlying ischemic damage (inferior MI)o Post cardiac surgeryo Drug induced (beta blockers, Ca2+ blockers)o Amyloid, Sarcoid, Myeloma, Infective (Lyme)

Signs

HYPERTENSION EMERGECNY

AIRWAY: Patent? Manouvres? Adjuncts? BREATHING: No resp effort? ARREST CIRCULATION: No pulse? ARREST DISABILITY: GCS under 8? Anesthetist

o IF SYSTOLIC OVER 200, DIASTOLIC 120o Sit upo OXYGEN (15l)- if SOB/ sats under 94%o MONITOR

Pulse oximiter BP




Pulse oximiter BP




Pulse oximiter BP




Pulse oximiter BP

HYPERTENSION: 140/90

SYSTIOLIC over 140 DIASTOLIC over 90 Worrying: Altered mental state, seizures, retinal hemorrhages, acute renal failure, chest pain CRISIS!??!?? Over 200 or over 120! Think about

o Is it a hypertensive crisis? 200/120, or pre-eclampsia?o Other: anxiety, pain, primary (essential) or secondary (thyroid storm, pheochromocytoma).

PHMx of, and signs of diseaseo Previous hypertensiono Phaeochromocytomao Coarctation aorta, (Radiofemoral delay)o renal artery stenosis (renal bruits)o Thyroid disease, (Tremor, exopthalmus)o DM, o Conns syndrome, o Cushings, (Straie, central obesity)o Acromegaly (large hands, feet, face)o Pregnancy (gravid uterus)

Drugso Cardiac meds and Antihypertensiveso Steroids, Contraceptive pill, Levothyroxine/carbimazole, MAOI, antipsychoticso Coke and amphetamines

Familyo Hypertension, endocrine disease, polycystic kidney disease

Social: exercise tolerance and smoking. END ORGAN DAMAGE?

o Fundoscopy (papilloedema, hypertensive retinopathy)o LV hypertrophy: displaced apex beat of S4o HaematuriaHYPERTENSION: 140/90

KEY SECONDARY CAUSES o RENAL ARTERY DISEASE/STENOSIS Renal failure Abnormal urine dipstick Renal bruit Family history may be relevant

Urine Microscopy Renal Doppler USS Autoantibodies Renal biopsy

o PHAEOCHROMOCYTOMA

INVESTIGATIONS

BP: o Confirm with ambulatory measuring

ECG: o LV hypertrophy?

Bloods: o FBC, U&E, Glucose, cholesterol, TFT

Urineo Blood, Protein, b-HCG

HYPERTENSION: 140/90

KEY SECONDARY CAUSES o RENAL ARTERY DISEASE/STENOSIS Renal failure Abnormal urine dipstick Renal bruit Family history may be relevant

Urine Microscopy Renal Doppler USS Autoantibodies Renal biopsy

o PHAEOCHROMOCYTOMA

TREATMENT

Smoking cessation Regular exercise Reduce alcohol and caffeine intake Balanced low-salt diet Modifiable risk factors: DM, lipids PHARMACOLOGICAL THERAPY

Complications are end organ damage and malignant hypertension

PHARMACOLOGICAL TREATMENT

Everyone o HYPERTENSIVE 160/100 (aim for 140/90) or (150/90 if

over 80)o TYPE2 DIABETES: if end organ damage aim for under

130/80- microalbuminuria, or eGFR under 60, retinopathy, Hx TIA/stroke

o TYPE1 DIABETES:o HYPERTENSIVE PATIENTS: with existing cardiovascular

disease/end-organ damage, or predicted 10year risk CV disease over 20%

A: ACEi / Angiotensin receptor blockers (RAMIPRIL) C: Calcium Channel Blockers (AMLODIPINE, VERAPAMIL/ Diltiazem)

HYPERTENSIVE CRISIS

Elevation of BP iver 200 is a hypertensive emergency

When accompanied by end-organ damage Hypertensive urgency when no end organ damage

END ORGAN DAMAGE

CNSo Decreased GCS, confusiono Headacheo Vomitingo New motor weaknesso Seizures, comao CT may show a SAH, ICH,

hypertensive encephalopathy occurs with cerebral oedema following loss of vascular auto-regulation.

EYESo Headacheo Visual Disturbanceo Fundoscopy shows retinal

hemorrhage, and papilloedema. HEART

o Chest paino Orthopneao ECG changes, o Elevated cardiac markerso Pulmonary oedema on CXR

AORTAo Sudden, tearing chest pain radiating

to backo Collapseo Echo/CT may reveal oertic dissection

KIDNEYSo Haematuriao Lethargyo Anorexiao Rapidly worsening renal function

HYPERTENSIVE CRISIS- Treat ACUTELY

NO end organ damage

Calcium Channel Blocker or ACEi (A or C)

END ORGAN DAMAGE

Admit to HDU or ICU Close monitoring of BP, ECG, neurological state, Fluid balance (arterial line, central line, catheterization) Rapid reduction in BP can be dangerous due to cerebral hypoperfusion Only necessary in ACUTE MI / AORTIC DISSECTION

Under 55

A

A&C

A, C, D

Over 55/Black

C

A&C

A, C, D

HYPERTENSIVE CRISIS- Treat ACUTELY

NO end organ damage

Calcium Channel Blocker or ACEi (A or C)

END ORGAN DAMAGE

Admit to HDU or ICU Close monitoring of BP, ECG, neurological state, Fluid balance (arterial line, central line, catheterization) Rapid reduction in BP can be dangerous due to cerebral hypoperfusion Only necessary in ACUTE MI / AORTIC DISSECTION

CARDIAC HISTORY AND EXAMINATION

INSPECTION

OVERALL:o ECG monitor suggestive? Pain? Cannula? Malar flush? (mitral stenosis), tachypnea (HF), Cyanosis (HF), Forceful neck

pulsations eg. Carotid (aortic regurg), ankle oedema (HF) HANDS:

o Splinter haemorrhages (IE) o Clubbing (IE or congenital cyanotic heart disease- caused by supperative disease ie that can lead to pus filled cavities-

Chrohns, UC, empyema, bronchiectasis, CF, fibrosis). o Pallor, o Peripheral cyanosis, o nicotine stainingo cap refill (Over 2 secs dehydration or PVD)o Asterixis- flap sign of CO2 retention (don’t confuse with tremor from b2 agonist salbutamol, or parkinsonian)

NECK:o JVP

FACE:o Malar flusho Anaemia conjunctivao Central Cyanosiso Hypercholersterolemia: Xantholasma o Breathing difficulty

CHEST:o Hands on hips to expose lateral chest walls. Look at back too.o Scars: Midline sternotomy- valve replacement or bypass? If bypass, scar on leg from where artery taken. Thoracotomy

scar: Scar left axilla diagonally down back- previous mitral stenosis (or line from L breast to axilla) o Deformities: sternal depression, scoliosis, kyphosis- can displace apex beat and cause ejection systolic murmur.o Apex- look for cardiac pulsation

PALPATION

ARMS:o Radial pulse: rate, rhythm, character

Brady (under 60), Beta-blockers, heart block, hypothyroidism, young Tachy (over 100), anxiety, exercise, pyrexia, hyperthyroidism, beta2 agonists (salbutamol), hypovolemic shock,

arrhythmia. Rhythem: sinus arrhythmia normal, AF (irreg irreg), Ventricular ectopic beats (rhythem returns to normal on

exercise), regularly irregular? Pulse Deficit (you get this with AF as the filling time at the ventricles and so stroke volume varies with each beat,

so on some, some beats produce no pulse, take HR at apex and wrist, difference in HR is pulse deficit.o Radio-radial delay Aortic dissection Proximal arterial disease (atherosclerosis of axillary artery)

o Radio-femoral delay Co-arctation of the aorta (stricture of the aortic arch, distal to the L. Subclavian artery) Delayed and weak femoral pulse Other things pointing to co-arctation? Raised BP, continuous murmur over scapula, systolic murmur L sternal

edge (P/T)o Collapsing pulse

Aortic regurgitation Ask if pain in shoulder

o BP Sitting and standing Hypertrophic obstructive cardiomyopathy.

NECK: o Carotid pulse (edge of adam’s apple and move back)

Pulse character- valvular lesions cause it to be abnormal

o Radio-radial delay Aortic dissection Proximal arterial disease (atherosclerosis of axillary artery)

o Radio-femoral delay Co-arctation of the aorta (stricture of the aortic arch, distal to the L. Subclavian artery) Delayed and weak femoral pulse Other things pointing to co-arctation? Raised BP, continuous murmur over scapula, systolic murmur L sternal

edge (P/T)o Collapsing pulse

Aortic regurgitation Ask if pain in shoulder

o BP Sitting and standing Hypertrophic obstructive cardiomyopathy.

NECK: o Carotid pulse (edge of adam’s apple and move back)

Pulse character- valvular lesions cause it to be abnormal

Places to Listen Aortic: 2nd intercostal space, midclavicular line RHS Pulmonary: 2nd inercostal space, lateral to sternum LHS Tricuspid: 4th intercostal space, lateral to sternum LHS Mitral: 5th intercostal space, midclavicular line LHS

Altered Heart sounds Splitting of Heart sounds (LUB SPLAT): Extra sound after S2 is called P2, Normal finding in inspiration Loud S1 (LUUBB!dub) Mitral stenosis- narrowed valve, shuts quicker, louder sound Soft S1 (lubDUB) Mitral regurg, valve not completely closed Soft S2 Aortic stenosis (reduced valve movement) Wide fixed splitting of S2 ASD Prosthetic heart sounds Metallic clicking sound

Brief systolic murmurs Mitral regurgitation and aortic stenosis

Places to Listen Aortic: 2nd intercostal space, midclavicular line RHS Pulmonary: 2nd inercostal space, lateral to sternum LHS Tricuspid: 4th intercostal space, lateral to sternum LHS Mitral: 5th intercostal space, midclavicular line LHS

Altered Heart sounds Splitting of Heart sounds (LUB SPLAT): Extra sound after S2 is called P2, Normal finding in inspiration Loud S1 (LUUBB!dub) Mitral stenosis- narrowed valve, shuts quicker, louder sound Soft S1 (lubDUB) Mitral regurg, valve not completely closed Soft S2 Aortic stenosis (reduced valve movement) Wide fixed splitting of S2 ASD Prosthetic heart sounds Metallic clicking sound

Brief systolic murmurs Mitral regurgitation and aortic stenosis

NOISES

Opening snapo Mitral stenosiso High pitched snap after S2

Ejection clicko Aortic valve openingo Aortic stenosiso Heard in aortic area after 1st heart sound

Mid-systolic clicko Mitral valve prolapsingo Halfway through systole, pressure in ventricles risen to such a level to prolapse the mitral valve

Pericardial friction rub

NOISES

Opening snapo Mitral stenosiso High pitched snap after S2

Ejection clicko Aortic valve openingo Aortic stenosiso Heard in aortic area after 1st heart sound

Mid-systolic clicko Mitral valve prolapsingo Halfway through systole, pressure in ventricles risen to such a level to prolapse the mitral valve

Pericardial friction rub

READING AN ECG

1. Check NAME, DATE, TIME2. Examine ECG in relation to previous ECGs (St changes can be fixed or dynamic)3. Always interpret it in CONTEXT to the clinical situation.

ABOUT THE ECG

The ECG represents electrical activity, primarily from the L.Ventricle, as it has more muscle mass than the RV. The ECG therefore tells you little about the RV. This is important as RV infarcts can occur, and can be missed if you don’t request specific RHS leads. They have a high rate of death, so important not to miss them. Suspect RV INFARCTS in patients who are VERY HYPOTENSIVE with little in the way of ST CHANGES in the ECG, or minor ST

READING AN ECG

1. Check NAME, DATE, TIME2. Examine ECG in relation to previous ECGs (St changes can be fixed or dynamic)3. Always interpret it in CONTEXT to the clinical situation.

ABOUT THE ECG

The ECG represents electrical activity, primarily from the L.Ventricle, as it has more muscle mass than the RV. The ECG therefore tells you little about the RV. This is important as RV infarcts can occur, and can be missed if you don’t request specific RHS leads. They have a high rate of death, so important not to miss them. Suspect RV INFARCTS in patients who are VERY HYPOTENSIVE with little in the way of ST CHANGES in the ECG, or minor ST

READING AN ECG

If you were to treat fast AF that was broad with DIGOXIN or BETA-BLOCKER, you can make AF worse. They act on AV NODE ONLY! If you block the AVNODE in the presence of an accessory pathway, the only way the beat can get to the ventricles is the

accessory pathway.

BUNDLE BRANCH BLOCKS

Impulse travels down the bundle of His, and divides intoo RIGHT BUNDLE BRANCH (one fascicle)o LEFT BUNDLE BRANCH (two fascicles)

Left anterior fascicle

READING AN ECG

If you were to treat fast AF that was broad with DIGOXIN or BETA-BLOCKER, you can make AF worse. They act on AV NODE ONLY! If you block the AVNODE in the presence of an accessory pathway, the only way the beat can get to the ventricles is the

accessory pathway.

BUNDLE BRANCH BLOCKS

Impulse travels down the bundle of His, and divides intoo RIGHT BUNDLE BRANCH (one fascicle)o LEFT BUNDLE BRANCH (two fascicles)

Left anterior fascicle

ECG and TERRATORIES

I AVR V1 V4

II AVL V2 V5

III AVF V3 V6

INFERIOR: II, III, AVF (the bottom L) RIGHT CORONARYSEPTAL: V1, V2 Proximal LADANTERIOR: V3, V4 LAD

ECG and TERRATORIES

I AVR V1 V4

II AVL V2 V5

III AVF V3 V6

INFERIOR: II, III, AVF (the bottom L) RIGHT CORONARYSEPTAL: V1, V2 Proximal LADANTERIOR: V3, V4 LAD

BASIC INTERPRETATION AND REGIGNITION ECG

RATE

RHYTHEM

AXIS

P WAVES

P-R INTERVAL

QRS COMPLEX


RATE

RHYTHEM

AXIS

P WAVES

P-R INTERVAL

QRS COMPLEX


Q WAVES

Should be 2 SMALL SQUARES DOWN and ONE ACROSS In the lateral leads, its fine for them to be big (V5, V6, AVL, 1) If they’re BIG ANYWHRE ELSE

o Abnormal: scar tissue in heart after a MI

R, and S WAVES

Used to predict LV HYPERTROPHY


Q WAVES

Should be 2 SMALL SQUARES DOWN and ONE ACROSS In the lateral leads, its fine for them to be big (V5, V6, AVL, 1) If they’re BIG ANYWHRE ELSE

o Abnormal: scar tissue in heart after a MI

R, and S WAVES

Used to predict LV HYPERTROPHY


CARDIAC ARREST RHYTHEMS

SHOCKABLEo VFo VT

NON-SHOCKABLE- need to reverse the cause of the arrest, and start CPRo PEAo ASYSTOLEo P wave ASYSTOLE: only p waves, can respond to cardiac pacing

ATRIAL FLUTTER

WENKEBACH

1st DEGREE BLOCK

3rd DEGREE BLOCK

LBBB

RBBB

VT

VF

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Cardiology