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CARDIOVASCULAR SYSTEM
Juliet Ver-Bareng, M.D., FPSP
Outline• Physiologic properties of the heart Electrical properties
< Excitability< Automaticity and Rhythmicity< ConductivityMechanical properties< Contractility< Distensibility
• Regulation of cardiac activity Neural controlHumoral control
Circulation• Role of the blood vessels
• Hemodynamics
• Blood Pressure determination
• Microcirculation – fluid exchange
• Factors affecting venous return
• Regulation of blood flow
• Regulation of blood pressure
Functions of the heart1. Generating blood pressure
- contraction of heart is responsible for movement of blood through the blood vessels
2. Routing blood to two circulation
- pulmonary and systemic circulation
3. Ensuring one way blood flow - presence of valves (AV and semilunar valves)
4. Regulating blood flow
- change in heart rate and force of contraction to match blood delivery to the changing metabolic needs of the tissues
Physiologic Properties of the heart
• Electrical Properties
- Excitability = bathmotropy
- Automaticity and Rhythmicity = chronotropy
- Conductivity = dromotropy
• Mechanical Properties
- Contractility = inotropy
- Distensibility = lucidotropy
Types of ion channels in the heartType Heart tissue
Na+ fast channels Atrial and ventricular myocardial cells, Purkinje fibers, AV nodal
Ca++ slow channels Atrial and ventricular myocardial cells, Purkinje,fibers SA nodal cells, AV nodal cells
K+ channels: Inwardly rectifying Delayed Transient outward
Atrial and ventricular myocardial cells, Purkinje fibersAtrial and ventricular myocardial cells, Purkinje,fibers SA nodal cells, AV nodal cellsAtrial myocardial cells, Purkinje,fibers
Pacemaker channels: “Funny” currents Hyperpolarizing currents
Purkinje fibersSA nodal cells and AV nodal cells
Ligand- operated channels: Ca++ activated nonspecific ATP sensitive K+ current Ach sensitive K+
current
Ventricular myocardial cells, Purkinje fibers
Atrial and ventricular myocardial cells
Atrial myocardial cells, Purkinje,fibers SA nodal cells, AV nodal cells
Resting membrane potential- the difference in ionic charge across the membrane of the cell = -70 to -9o mV- resting membrane potential is permeable to K+, and is relatively impermeable to other ions- maintenance of this electrical gradient is due to the: Na+- K+ pump and the Na+- Ca++ exchange mechanism
Electrical Properties A. Excitability – bathmotropy
SA node, AV node Myocardia, Purkinje system Slow response AP Fast response AP
Phases of fast response AP
4 = Resting Membrane Potential
0 = Rapid Depolarization
1 = Initial Repolarization
2 = Plateau
3 = Repolarization
Phases of fast response APPhase 0 - Rapid depolarization
- due to opening of the fast Na+ channels and the
subsequent rapid increase in the membrane conductance to
Na+ (gNa
) and a rapid influx of Na+ ions into the cell
The fast Na+ channel
made up of two gates at rest
m gate closed
h gate open
Upon electrical stimulation of the cell, the m gate opens
quickly while simultaneously the h gate closes slowly
For a brief period of time, both gates are open and Na+ can
enter the cell across the electrochemical gradient
Phases of fast response AP
Phase 1 – Initial repolarization - occurs with the inactivation of the fast Na+ channels - the transient net outward current causing the small downward deflection of the action potential is due to the movement of K+ and Cl- ions - Cl- ions movement across the cell membrane results from the change in membrane potential, from K+ efflux, and is not a contributory factor to the initial repolarization ("notch").
Phases of fast response AP
Phase 2- Plateau phase
- sustained by a balance between inward movement of Ca2+ (ICa) through L-type calcium channels and outward movement of K+ through the slow delayed rectifier potassium channels, Iks.
Phases of fast response APPhase 3 - Rapid Repolarization phase - L-type Ca2+ channels close, while the slow delayed rectifier (IKs) K+ channels are still open - this ensures a net outward current, corresponding to negative change in membrane potential, thus allowing more types of K+ channels to open - this net outward, positive current (equal to loss of positive charge from the cell) causes the cell to repolarize - the delayed rectifier K+ channels close when the membrane potential is restored to about -80 to -85 mV
Slow response AP
Phases
4 - Spontaneous depolarization
0 - Triggered depolarization
3 - Repolarization
Phases of slow response APPhase 4 – Spontaneous Depolarization
- Prepotential
- Slow diastolic depolarization• depolarization by themselves• the resting potential of a pacemaker cell
(-60mV to -70mV) is caused by;
= a continuous outflow or "leak" of K+ through ion channel proteins in the membrane that surrounds the cells
= a slow inward flow of Na+, called the funny current
= an inward flow of calcium• This relatively slow depolarization continues until the
threshold potential is reached• Threshold is between -40mV and -50mV
Phases of slow response APPhase 0 – Upstroke
- Triggered depolarization
- The SA and AV node do not have fast sodium channels like neurons, and the depolarization is mainly caused by a slow influx of calcium ions
- The calcium is let into the cell by voltage-sensitive calcium channels that open when the threshold is reached.
Phases of slow response AP
Phase 3 - Repolarization
• The Ca++channels are rapidly inactivated, soon after they open
• Sodium permeability is also decreased
• Potassium permeability is increased, and the efflux of potassium (loss of positive ions) slowly repolarizes the cell
Ion channel inhibitor/blocker• Na+ channel = phase 0 (fast response
- Tetrodotoxin
• Ca++ channel = phase 0 (slow response AP) and phase 2 (fast response AP)
- Verapamil
- Nifidipine
- Manganese
• K+ channel = phase 3
- Amiodarone
Refractory period
• Absolute refractory period
- duration when Na
channel is closed
• Relative refractory period
- m gate closing and
h gate opening
• Super normal period
- membrane potential close to the RMP
effective refractory period (ERP)
• absolute refractory period (ARP) of the cell
• during the ERP, stimulation of the cell by an adjacent cell undergoing depolarization does not produce new, propagated AP → nontetanization of the heart
• ERP acts as a protective mechanism in the heart by preventing multiple, compounded action potentials from occurring → limits the frequency of depolarization and therefore heart rate.
Electrical PropertiesB. Automaticity and Rhythmicity =
Chronotropy
- rate and rhythm
prepotential = phase 4
Heart RateNormal range
Bradycardia – vagal stimulation
Tachycardia – sympathetic effect
Vagal tone
Heart Rate at Rest
Age Group Beats per Minute
Newborn 140
Young Child 100-120
Adult 60-100
Mechanism of change in heart ratePrepotential:
RMP
TP
Slope
RMP TP Slope
Parasympathetic ↓ ↓
Sympathetic ↓
Automaticity Pacemaker Discharge rate
1. SA node = 70 – 80 beats/min
= primary pacemaker
2. AV node = 40 – 60 beats/min
3. Purkinje fibers = 30 – 40 beats/min
Ectopic beat – successful impulses coming from other pacemaker cells and not from SA node
Arrhythmia• when the heart rate is too fast or too slow or
when the electrical impulses travel in abnormal pathways is the heartbeat considered abnormal
An arrhythmia may occur for one of several reasons:
• Instead of beginning in the sinus node, the heartbeat begins in another part of the heart
• The sinus node develops an abnormal rate or rhythm
• A patient has a heart block
Abnormal Heart RhythmsCondition Symptoms Possible causes
Tachycardia HR > 100 bpm Elevated body temperature, excessive sympathetic stimulation
Bradycardia HR < 60 bpm Athletes: increased SV, excessive vagal stimulationCarotid sinus stimulation
Sinus arrhythmia HR varies with respiration Ischemia, inflammation, cardiac failure
Paroxysmal atrial tachycardia
Sudden increase in HR to 95 – 150 bpm P wave precedes QRS complex
Excessive sympathetic stimulation, increased cardiac permeability to Ca++
Atrial flutter As many as 300 P waves and 125 QRS complexes/min
Ectopic beats in the atria
Atrial fibrillation No P waves, complex normal QRS complex and T waves
Ectopic beat in the atria
Symptoms of Arrhythmia • Heartbeats are fast or slow, regular or irregular or
short or long • Person feels dizzy, light-headed, faint or even
loses consciousness • Person is experiencing chest pain, shortness of
breath or other unusual sensations along with the palpitations
• Palpitations happen when the patient is at rest or only during strenuous or unusual activity
• Palpitations start and stop suddenly or gradually
Electrical PropertiesC. Conductivity = DromotropyConducting tissues:1. SA node2. AV node3. Internodal tract4. Interatrial tract or Bachmann’s bundle5. Atrial muscles6. Bundle of His7. Bundle branches8. Purkinje fibers9. Ventricular muscles
Tissue Diameter (μm)
Conduction velocity (m/sec)
SA node 2 – 7 0.05
Atrial muscles 8 – 10 0.3 – 0.5
Internodal tract 16 – 20 1.0
AV node Variable 0.02 – 0.05
Purkinje fibers 70 – 80 2.0 – 4.0
Ventricular muscles
10 - 16 <1.0
Conduction time
Conduction of impulses• Physiologic delay – occurs at the AV node
Mechanisms:
1.Size of the fibers - small
a. interatrial tracts - enter the AV node
b. His-nodal tract – leaves AV node
2.Contains fewer gap junctions
Significance: allows time for ventricular filling
Conduction of impulses
Fastest conduction velocity - purkinje fibers
Mechanism: fibers have the largest diameter
Significance: ensures an almost simultaneous contraction of ventricles
Characteristics of conduction
Mechanism1. One way direction ARP 2. Decremental sizes of fibers
3. Indefatigable ARP
ECG
P wave QRS T wave
complex
Basic Information derived from ECG tracings
1. Heart rate
2. Origin of excitation
3. Rhythm = regular or irregular
4. Conduction velocity = PR interval
= normal, delayed or blocked
5. Mean Electrical Axis
6. Primary cardiac impairment = ST segment
7. Blood supply = large Q wave, ST segment and T wave
EKG
ECG
Large boxes are used to estimate heart rateMeasure from QRS to QRS
1 large box = 300 bpm2 large boxes = 150 bpm3 large boxes = 100 bpm4 large boxes = 75 bpm5 large boxes = 60 bpm
EKGNormal Sinus Rhythm (NSR) • originates in the SA node and follows the appropriate
conduction pathways. • rate is normal, and the rhythm is regular• every beat has a P wave followed by QRS complex
• EKG CriteriaRate: 60-100 bpm
Rhythm: Regular P waves: look the same and originate from the same locus (SA node) PR interval: 0.12 - 0.20 sec QRS: 0.08 -0.12 sec, narrow
EKG: Heart BlockFirst degree: regular rhythm PR interval > 0.12 sec
Second degree: Mobitz I: Wenkebach: Rhythm: Irregular
PR interval: Progressive lengthening followed by dropped beat
QRS's appear to occur in groups. Mobitz II: PR interval: Constant on conducted complexes until a sudden block of AV conduction = P wave is abruptly not followed by a QRS
Third degree: P wave: Independent P waves and QRS's (AV dissociation)
QRS: wide (>0.12 sec) and slower (30-40 bpm) with ventricular escape rhythm.
EKG
Limb leads Precordial leads
Mean Electrical Axis
-30° to +110° limb leads
Mean Electrical AxisLead with the tallest QRS complex
Perpendicular to the lead with equipotential QRS complex
Complimentary Leads:
I and aVF
II and aVL
III and aVR
Mechanical PropertiesA. Contractility – Inotropy Cardiac wall
Sarcomere length = 2.2 – 2.6 μm
Excitation-Contraction Coupling
Contractility = Inotropy
Systole = ejection of blood into the circulation
Systole = contraction
• Stroke volume = amount of blood ejected per contraction (beat)
• Cardiac output = amount of blood ejected per minute
Inotropism(+) = greater force of contraction → more blood
ejected
= results from an increased Ca++ concentration
- sympathetic stimulation = via β2 receptors
- epinephrine and norepinephrine
- cardiac glycosides (digitalis)
(-) = weaker force of contraction → less blood ejected
- parasympathetic stimulation
- hypoxia
- acidosis
Diastole = ventricular filling
Diastole = relaxation
= Lucidotropy
• End Diastolic Volume (EDV) – amount of blood contained in the ventricle at the end of diastole
• End Systolic Volume (ESV) – amount of blood left in the ventricle at the end of systole
• SV = EDV - ESV
Frank-Starling Law of the heart
- relationship between the initial length of the ventricular myocardia at the end of diastole and the force of contraction
= initial length - dependent on the EDV
= force of contraction → SV
- ability of the heart to change its force of contraction and therefore stroke volume in response to changes in venous return
Cardiac cycle
Cardiac cycle
Cardiac cycle
• Phase 1 = Atrial systole
• Phase 2 = Isovolumetric contraction
• Phase 3 = Rapid ejection
• Phase 4 = Reduced ejection
• Phase 5 = Isovolumetric relaxation
• Phase 6 = Rapid filling
• Phase 7 = Reduced filling
Heart sounds• S1
= closure of semilunar valves
aortic and pulmonic component
= isovolumetric relaxation
= sounds like “dub”
• S2
= closure of semilunar valves
aortic and pulmonic component
= isovolumetric relaxation
= sounds like “dub”
Heart sounds
• S3
- during rapid filling
• S4
- during atrial systole
Not normal in adults
Murmur – turbulent blood flow• Valvular defect
• Congenital abnormalities
Patent Ductus Arteriosus
Septal defect: ASD VSD
Valve Abnormality Timing of murmur
Semilunar valves
StenosisInsufficiency
SystolicDiastolic
AV valves StenosisInsufficiency
DiastolicSystolic
Effects of valvular lesions on circulation
• Reduction of cardiac output
• Additional cardiac work = due to extra volume load
• Backflow of blood is produced
Pressure Volume Loop Pressure (mm Hg) Points
A = opening AV valves
D C B = closure AV valves
SV C = opening of SL valves
D = closure of SL valves
A B
Volume (ml)
Lines
AB = Ventricular filling
BC = Isovolumetric contraction
CD = Ejection
DA = Isovolumetric relaxation
Cardiac OutputCO = SV X HR
Factors affecting cardiac function1. Preload2. Afterload3. Contratility4. Heart rate
Ejection Fraction = SV/EDV x 100 ≥ 55%
Preload = End Diastolic Volume
Regulation of cardiac activity
1. Intrinsic control – autoregulation
= regulation of SV
2. Extrinsic regulation
= regulation of heart rate
Autoregulation (SV = EDV – ESV)
1. Homeometric autoregulation = ↑ contractility →↓ ESV → ↑ SV
Systole
Diastole
2. Heterometric autoregulation = ↑ EDV →
↑ SV
= Frank-Starling’s Law of the heart
Extrinsic regulation of the heart = effect on Heart Rate
• Neural1. Extrinsic nerves to the heart vagal tone2. Cardiac centers: CIC and CAC3. Higher centers: cerebral cortex, limbic system4. Cardiac reflexes Baroreceptor - bradycardia Chemoreceptor Bainbridge Somatic afferent hot temperature – tachycardia cold temperature - bradycardia
Nerve supply to the heart• Parasympathetic nervous system – vagus
Right vagus = SA node, AV node, Atrial
muscles
Left vagus = AV node, Atrial muscle, SA
node
• Sympathetic nervous system
Right nerve = SA node, AV node, Atrial
muscles and Ventricular muscles
Left nerve = AV node, SA node, Atrial
muscles and Ventricular muscles
Nerve supply to the heart• Parasympathetic nervous system – vagus
Right vagus = SA node, AV node, Atrial
muscles
Left vagus = AV node, Atrial muscle, SA
node
• Sympathetic nervous system
Right nerve = SA node, AV node, Atrial
muscles and Ventricular muscles
Left nerve = AV node, SA node, Atrial
muscles and Ventricular muscles
Baroreceptors
• Marey’s Law Sinoaortic reflex
• Stimulus = high BP
• Receptors = carotid and aortic sinuses
• Afferent nerve = IX and X nerves
• Center = medulla
• Efferent nerve = X nerve
• Effector = SA node
• Effect = slowing HR
Chemoreceptors• Peripheral
Stimulus = hypoxia
Receptors = carotid and aortic bodies
Effect = increase in HR
• Central
Stimulus = high H+ in CSF
Receptor = medulla
Effect = increase in HR
Extrinsic regulation of the heart
• Humoral Tachycardia Bradycardia
1. Hormones
Epinephrine, NE Acetylcholine
2. Ions
Ca++ (Ca ++ rigor) K+ (K+ inhibition)
2. Gases
↑ CO2 ↓ O2
CIRCULATION• Pulmonary = from
RV to the lungs for
Oxygenation
• Systemic = from
LV to different organs
of the body
Blood Vessels
Functions of blood vessels
• Aorta – windkessel vessel• Large arteries – conducting vessels• Medium arteries – distributing vessels• Small arteries and arterioles – resistance
vessels • Capillaries – exchange vessels• Veins = capacitance vessels• Vena cava = conduits
Distribution of blood at rest
60 – 70 % veins and venules
10 – 12% pulmonary circulation
8 – 11% heart
10 – 12% arteries
4 - 5% capillaries
HEMODYNAMICS• Blood Flow (Q) = amount of blood from point
1 to point 2 in one minute = Poiseuille’s Equation = ml/min Q = ΔP/R R = 8 η l η = viscocity π r4 l = vessel length r = vessel radius Q = π ΔP r4
8 η l
HEMODYNAMICS• Character of flow = Reynold’s Number (Re # = ρ V D η ρ = blood density V = velocity of blood flow D = vessel diameter
> Laminar or Streamlined = flow of components of blood runs parallel to the wall of blood vessel
> Turbulent = flow of components of blood runs tangential to the wall
producing eddy currents
Hemodynamics• Wall Tension (T) Laplace’s Law
T = Pr
P = transmural pressure
r = vessel radius
Relationship of velocity of blood flow and total cross sectional area
Blood PressureQ = ΔP/R ΔP = Q x R BP = CO x TPR
Methods:1 Palpatory2 Auscultatory3 Oscillometric
SPDP
Korotkoff sounds
Components of BP
Arterial Pressure
• Pulse Pressure = SP – DP
• Mean Arterial Pressure
MAP = DP + 1/3PP
Categories for Blood Pressure Levels in Adults (in mmHg)
The ranges in the table apply to most adults (aged 18 and older) who don't have short-term serious illnesses
CategorySystolicPressure
DiastolicPressure
Normal < 120 And < 80
Prehypertension 120–139 Or 80–89
High blood pressure
Stage 1 140–159 Or 90–99
Stage 2 ≥ 160 Or ≥ 100
.
Risk factors of developing hypertension
• Family history of high blood pressure, heart disease, or diabetes• Age greater than 55• Overweight• Not physically active (sedentary)• Alcohol excessive drinking• Smoking• Food high in saturated fats or sodium use• Race• Gender• Certain medications such as NSAIDs, cocaine decongestants
Composition of microcirculation• ArteriolesMetarterioles
• Capillaries
• Venules
• Terminal lymphatic vessels
Fluid Exchange = governed by Starling’s forces
Filtration occurs mainly through the intercellular junctions of the small pore system
As formulated is Starling’s hypothesis:
- the fluid filtered across a capillary membrane is proportional to the net filtration pressure
- the sum of hydrostatic pressures and the colloidal osmotic pressure
- expressed as:
Vf = kf [(Pc - Pif) - (πc - πif)]
or = kf [(Pc+ πif) - (πc+ Pif)]
Fluid exchange
Veins• Capacitance vessels
• Reservoir of blood
• Low pressure
• Low resistance
Factors affecting Venous Return• Muscle contraction - rhythmical contraction of limb muscles
as occurs during normal locomotory activity (walking, running, swimming) = promotes venous return by the muscle pump mechanism
• Decreased venous compliance - following Sympathetic activation of veins, increases central venous pressure and promotes venous return indirectly by augmenting cardiac output through the Frank-Starling mechanism = increases the total blood flow through the circulatory system
• Respiratory activity - during respiratory inspiration, the decrease in right atrial pressure = increases the venous return
• Vena cava compression - increases vena cava resistance which occurs when the thoracic vena cava becomes compressed during a Valsalva maneuver or during late pregnancy = decreases return
• Gravity - the effects on venous return when a person stands up, the hydrostatic forces cause the venous pressure in the dependent limbs to increase = venous return decreases
Regulation of blood flow• Local regulation
1. Intrinsic
a. Myogenic theory
b. Endothelial derived =Nitric Oxide,
Endothelin, Thromboxane
2. Metabolic
a. Oxygen demand
> active hyperemia - ↑ O2 consumption
> reactive hyperemia – hypoxia due
previous occlusion of blood supply
b. Vasodilator agents = H+, histamine, kinins
Extrinsic regulation of blood flow• Neural Sympathetic tone Vascular centers: VCC and VDC Cardiovascular reflexes: Baroreceptor = ↓ TPR• Humoral 1. Hormones Vasodilators : ACh, Epinephrine Vasoconstrictors: Epinephrine, NE, Angiotensin, ADH, Serotonin 2. Ions Ca++ – vasoconstriction H+ and K+ - vasodilation 3. Gases ↑CO2 and ↓O2 - vasodilation
Delayed regulation of blood flow
• Opening of collaterals
- blood flowing to more blood vessels
• Angiogenesis
- formation of more arteries
Neural mechanisms• ANS on vessel caliber
- sympathetic tone - parasympathetic = vasodilatation
• Vasomotor centers - medulla- Vasoconstrictor center- Vasodilator center
• Higher centers- cerebral cortex- limbic system
• Vasomotor reflexes- baroreceptor- chemorecpetor- somatosympathetic
Humoral mechanismsVasoconstrictor agents Vasodilator agents
Epinephrine (on alpha receptors)
Epinephrine (on beta receptors)
Angiotensin Acetylcholine
Vasopressin Histamine
Serotonin Prostaglandin
Endothelin 1 ANP
Calcium Nitric oxide
Thromboxane Ions = H+, K+
CO2
Low O2
Bradykinin
Lactic acid
BP regulation - Onset of action
• Immediate
Cardiovascular reflexes
CNS ischemic effect• Intermediate
Capillary fluid shift
Renin-Angiotensin system• Delayed
Aldosterone
Renal vascular system
Effect of :• Acute pain → increased sympathetic
stimulation• Deep pain → increased parasympathetic
stimulation
Vasoconstriction Vasodilation• pH decreased increased• Temperature low high
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