CARDIAC CYCLE New for Student

7/28/2019 CARDIAC CYCLE New for Student

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Prof.dr.Hardi Darmawan, MPH&TM, FRSTM

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The Cardiac Cycle

Electrical events of the heart

(measured by ECG)

Mechanical Events

(contraction & relaxation of the heart)

Refers to

period from the start of one heart beat

next heart beat.

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The Steps of the cardiaccycle

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Atrial Systole

Isovolumetric ventricular contraction

Rapid ventricular ejection

Reduced ventricular ejection

Isovolumetric ventricular relaxation

Rapid ventricular filling

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1. Ventricular filling

2. Isovolumetric contraction

3. Ventricular ejection

4. Isovolumetric relaxation

5. Mitral valve opens

6. Mitral valve closes

7.Aortic valve opens

8. Aortic valve closes

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Cardiac CyclePhases:

1. Isovolumetric contraction-

period between mitral valve

closure and aortic valve

opening; period of highest

oxygen consumption

2. Systolic ejection-period betweenaortic valve opening and closing

3. Isovolumetric relaxation-period

between aortic valve closing

and mitral valve opening4. Rapid filling-period just after

mitral valve opening

5. Slow filling-period just before

mitral valve closure.


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Cardiac Cycle

Sounds:

S1 mitral and tricuspid valveclosure.

S2 aortic and pulmonary valveclosure.

S3 at end of rapid ventricularfilling.

S4 high atrial pressure/ stiffventricle.

S3 is associated with dilated CHF.

S4 (atrial kick) is associated witha hypertrophic ventricle.


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Cardiac Cycle

a wave atrial contraction

c wave RV contraction

(tricuspid valve bulging

into atrium)

v wave increased atrial

pressure due to filling

against closed tricuspid

valve.

Jugular venous distention is

seen in right heart failure.


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CARDIAC

CYCLE


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An example of a normal jugular venous pulse tracing


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The major features of a left ventricular

pressure-volume loop


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Step

Step

No. Mechanism Important Points

Ventricular Contraction (Systole)

AV Valve

Closure

1 Ventricular contraction causes

increased ventricular

pressure.

Normal aortic systolic

pressure: 120 mm Hg.

Normal pulmonary artery

systolic pressure: 15-18 mmHg.

2 When ventricular pressure

exceeds atrial pressure, AV

valves close.

Iso-

volumetric

Contraction

3 Closed AV valves isolate

ventricles from atria

Arterial diastolic pressure is

the lowest arterial pressure.

It occurs just before onset ofventricular ejection.

4 Ventricular volume staysconstant while ventricular

pressure rises.

SUMMARY OF THE CARDIAC CYCLE

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Step Step No. Mechanism Important Points


Ventricular

Ejection5 When ventricular pressure

exceeds arterial pressure

semilunar valves open.

Arterial systolic pressure is

the peak arterial pressure.

It occurs at the end of rapid

ejection.

Right ventricular ejection

occurs before left becausepressure in pulmonary artery

is low compared to that in

aorta.

6 Ejection starts, and arterial

volume and pressure begin to

increase.

7 Rapid ejection: two thirds of

stroke volume ejected during

first third of systole (ventricular

pressure > aortic pressure).

8 Reduced ejection: one third ofstroke volume ejected during

last two thirds of systole

(ventricular pressure < aortic

pressure).

9 Ventricles relax.

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Step StepNo.

Mechanism Important Points


Semilunar

Valve

Closure

10 Closure of aortic and

pulmonic valves prevents flow

of blood back into ventricles.

Incisura: notch on descending

limb of aortic pressure curve

produced by closure of aorticvalve, indicates end of

ventricular systole.

Ventricular Relaxation (Diastole)

Iso-

volumetric

Relaxation

11 Ventricles relax and

ventricular pressure rapidly

falls without change in

ventricular volume.

Systemic arterial pressure

declines as blood continues to

flow.

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StepStep

No.Mechanism Important Points

Ventricular Relaxation (Diastole)

AV Valve

Opening

12 Rapid filling: high atrial pressure

(due to continued venous returnduring ventricular systole) causes

initial rapid passive ventricular

filling (80% of blood volume).

Normal diastolic pressure in

aorta: 80 mm Hg. Normal diastolic pressure

pulmonary artery: 8-10 mmHg.

Tachycardia (>180 bpm) results

in decreased CO; ventricular

filling time is markedly reduced,

which lowers VEDV and SV.

Atrial contraction is notessential for ventricular filling,

as evidenced by adequate

ventricular filling in patients

without atrial contraction (eg,

atrial fibrillation or heart block).

Contribution of atrial

contraction to ventricular

volume is more important when

HR is rapid and duration of

diastasis is short (eg, mitral

stenosis).

13 Pressure in atria and ventricles

decreases and ventricular

relaxation continues during rapidfilling.

14 Slow filling ordiastasis: as blood

continues to return to heart,atrial

and ventricular pressures slowly

rise.

15 Ventricular filling of blood stops

shen ventricles reach their volume

limit.

16 Atrial contraction forces blood into

ventricles to complete ventricular

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II. The Heart As A Pump

A. The Cardiac Cycle

1. Diastole constitudes 2/3 of the cycle

(filling and isovolumetric contraction).

Aortic pressure is higher than

ventricular (aortic valve closed).

2. Systole accounts for 1/3 of the

cardiac cycle (ejection andisovolumetric relaxation)


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Cardiac Output (CO)Cardiac output = (stroke volume) x (heart rate)

Fick Principle

Mean arterial = cardiac x total peripheral

Similar to Ohms law:

Voltage = (current) x (resistance)

MAP = systolic + 2/3 diastolic

Pulse pressure = systolic diastolic

Pulse pressure = stroke volume

During exercise, CO initially

as a result of an in SV.

After prolonged exercise,

CO as a result of an in

HR.

If HR is too high, diastolic filling

is incomplete and CO

(e.g., ventricular

tachycardia)

Rate of O2 consumption

Arterial O2 content venous O2 content

CO =


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CO

HR

SV = = EDV - ESV

EF =

SV

EDV

X 100% (normal 55-80%)


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Calculations of Stroke Volume,

Cardiac Output & Ejection Fraction


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Cardiac Output Variables

Stroke volume affected byContractility, Afterload, andPreload. Increased SV when

preload, afterload, or

contractility.

Contractility (and SV) with :

1. Catecholamines ( activity of

Ca2+ pump in sarcoplasmic

reticulum)

2. intracellular calcium

3. extracellular sodium

4. Digitalis ( intracellular Na+,

resulting in Ca2+)

SV CAP.

Stroke volume in anxiety,exercise, andpregnancy.

A failing heart has strokevolume.


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Cardiac Output Variables

Contractility (and SV)

with:

1. 1 blockade

2. Heart failure3. Acidosis

4. Hypoxia/ hypercapnea

Myocardial O2 demand is

by:

1. afterload ( diastolic

BP)

2. contractility

3. heart rate

4. heart size ( walltension)


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Cardiac Function Curve

(Frank Starling Curve)


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Diagram of normal blood pressures

within heart chambers and great vessels


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HEART SOUNDSSound Cause of

Sound

Events

S1 Closure of AVvalves.

Just after onset of ventricular contraction.

Signals onset of ventricular systole.

S2 Closure of

semilunar valves.

Signals end of systole and onset of ventricular diastole.

Normal splitting: during inspiration, increased venous

return causes prolongation of right ventricular EF and an

increased separation between aortic valve closure (A2)and pulmonic valve closure (P2).

Aortic valve closes first because ejection rate from left

ventricle is higher than that from right ventricle.

Paradoxical splitting occurs if splitting of S2 decreases

during inspiration, indicating P2 precedes A2.

Delayed aortic valve closure indicates a disease processaffecting left ventricle (LBBB, aortic stenosis).

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HEART SOUNDS

Sound Cause of

Sound

Events

S3 Rapid, passive

ventricular filling.

At start of ventricular diastole.

Heard best at apex.

Usually not heard in adults but may be heard in children

or patients with LVE

S4 Forcing of

additional blood

into distended

ventricle.

Atrial contraction.

Occasionally heard in healthy individuals.

Individuals with CHF have triple sound called gallop

rhythm.

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ATRIAL PRESSURE CHANGES

VIA JUGULAR VENOUS TRACINGWave Timing of Wave Cause of Wave

a Atrial contraction at end of

ventricular diastole.

Small amount of blood regurgitates into great

veins.

Venous inflow stops, causing rise in venous

pressure

c Isovolumetric contraction Rise in atrial pressure produced by bulging of

AV valves into atria.

v Ventricular diastole Rise in atrial pressure before AV valves open

during diastole

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Valvular Lesions And Cardiac MurmursType Of

LesionFunction Murmur

Possible ECG

ChangeClinical Significance

Aortic

Stenosis

Creates high-

resistance area thatforces left ventricle to

generate high

pressures to eject

blood through

narrowed orifice.

Crescendo-

decrescendo(diamond-shape)

systolic ejection

murmur.

LVH, LBBB Ventricular systolic pressure

much higher than systolicpressure in respective artery

is pathognomonic.

May lead to LVH and LVE.

Aortic

Insuffi-

ciency or

Regur-

gitation

Blood flows back into

left ventricle during

diastole , reducing

effective CO.

Diastole

decrescendo, often

high-pitched,

blowing murmur that

begins with A2

LVH, with

narrow, deep

Q waves.

High systolic pressures

associated with low diastolic

pressures, leading to large

pulse pressure (>100 mmHg),

reflected by water-hammer or

Corrigan pulses.

Causes left ventricular

dilation, which leads to LVE.

PulmonaryStenosis Creates high-resistance are that

forces right ventricle to

generate high

pressure to eject blood

through narrowed

orifice.

Systolic ejectioncrescendo-

decrescendo

murmur, often with

harsh quality.

RVH, rightatrial

abnormality.

Usually congential, may beacquired with hypertrophic

cardiomyopathy.

May led to RVH and RVE

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Valvular Lesions And Cardiac MurmursType Of

LesionFunction Murmur

Possible ECG

ChangeClinical Significance

PulmonaryInsuffi-

ciency or

Regur-

gitation

Blood flows back intoright ventricle during

diastole, reducing

input to lungs.

Diastoledecrescendo, often

high-pitched,

blowing murmur that

begins with

pulmonic valve

closure (P2)

RVH Usually associated withpulmonary hypertension.

Causes right ventricular

dilation, which leads to

RVE.

Mitral ValveStenosis

Impedes filling of leftventricle, allowing

pressure gradient to

develop between left

atrium and left

ventricle during

diastole

Presystolic or earlydiastolic crescendo

murmur with low-

pitched rumble.

Heard on atrial

contraction and

rapid passive

ventriccular filling.

Left Atrialabnormality, atrial

fibrillation.

RVH if

associated with

pulmonary artery

hypertension

May led to pulmonaryedema (high pulmonary

venous pressures), left atrial

enlargement, or atrial

fibrillation.

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RIGHT VENTRICLE (RV)

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Clinical Correlations

RV (Right Ventricle)

RV Failure RV afterload

RV Failure :

1. Corpulmonale2. Intrinsic lung diseases, Pulmonary arterial

hypertension (PAH)

3. Acute cor pulmonale

RV dilation caused by thrombopulmonary embolism

4. Chronic corpulmonale

Due to

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Clinical Correlations (2)

Chronic corpulmonale RV hypertrophy RV enlargement

RV Failure

PAH

PAH > 30 mmHg

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PAH

vasculitis

Idiopathic(primary

PAH)

ChronicPulmonary

Emboli

ChronicLung

Disease

Emphysema

EisenmengerSyndrome(VICE)

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Cli i l Fi di /


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Clinical Findings /

Manifestations RUQ discomfort hepatomegaly

nutmeg pattern (chronic passive

congestion)

Peripheral edema (RV Failure ankleswelling)

Pulmonary edema

Jugular vein & portal vein distention Splenomegaly

ascites

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Cli i l Fi di /


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Clinical Findings /

Manifestations (2) Pleural effusion

Palpable parasternal heave

S4 heart sound (atrial gallop)

Tricuspid valve murmur

Ascent to high altitudes

contraindication due to hypoxic

pulmonary vasocontriction

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LEFT VENTRICLE (LV)

FAILURE (MYOCARDIAL

INFARCTION)

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LV Failure myocardial infarction (MI) LV hypertrophy dilation

LV Failureblood congestion pulmonary edema with wet coughing

Transferrin Hb leak congestedcapillaries phagocytosed bymacrophages in alveoli heart failurecells.

LV Failure COP kidneyperfusion A. Tubular necrosis

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General Features


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Over weight Poor diet

Angina left arm (referred arm)

Nausea

Profuse sweating, cold, clammy skin

(stress-induced catecholamines

epinephrine and norepinephrine; fromadrenal medulla stimulate sweat

glands )

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Clinical Manifestations


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Peripheral vasocontrictions, dyspnea,orthopnea, rales (cardiac asthma)

Pulmonary weight pressure (left atrial

press 30 mm vs 5mm Hg) Ejection fraction (0.35 vs 0.55)

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Clinical Manifestations (2)


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Nitroglycerin Adrenergic antagonist (propanolol,

blocker)

tachycardia

hypertension

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Treatment

relieve


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Streptokinase TPA (Tissue Plasminogen

Activator)

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Treatment (2)

Infarcted tissue

< 6 hr of MI

Atropine - Bradycardia

Heparinization warfarin :

- Ventricular aneurysms- Thrombopulmonary embolisms

- Deep Vein thrombosis (DVT)


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Thank you

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CARDIAC CYCLE New for Student