Prof.dr.

Hardi Darmawan, MPH&TM, FRSTM

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.

The Steps of the cardiac cycle

Atrial Systole

Isovolumetric ventricular contraction

Rapid ventricular ejection

Reduced ventricular ejection

Isovolumetric ventricular relaxation

Rapid ventricular filling

1. 2. 3. 4. 5. 6.

7.
8.

Ventricular filling Isovolumetric contraction Ventricular ejection Isovolumetric relaxation Mitral valve opens Mitral valve closes Aortic valve opens Aortic valve closes

Cardiac Cycle
Phases: 1. Isovolumetric contractionperiod between mitral valve closure and aortic valve opening; period of highest oxygen consumption 2. Systolic ejection-period between aortic valve opening and closing 3. Isovolumetric relaxation-period between aortic valve closing and mitral valve opening 4. 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 valve closure. S2 aortic and pulmonary valve closure. S3 at end of rapid ventricular filling. S4 high atrial pressure/ stiff ventricle. S3 is associated with dilated CHF. S4 (atrial kick) is associated with a 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.

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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SUMMARY OF THE CARDIAC CYCLE

Step Step No. Mechanism Important Points

Ventricular Contraction (Systole) AV Valve Closure 1 Ventricular contraction causes increased ventricular pressure. When ventricular pressure exceeds atrial pressure, AV valves close. Closed AV valves isolate ventricles from atria Ventricular volume stays constant while ventricular pressure rises. Normal aortic systolic pressure: 120 mm Hg. Normal pulmonary artery systolic pressure: 15-18 mm Hg. Arterial diastolic pressure is the lowest arterial pressure. It occurs just before onset of ventricular ejection.

Isovolumetric Contraction

3 4

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SUMMARY OF THE CARDIAC CYCLE

Step
Ventricular Ejection

Step No.
5

Mechanism
When ventricular pressure exceeds arterial pressure semilunar valves open.

Important Points
Arterial systolic pressure is the peak arterial pressure. It occurs at the end of rapid ejection. Right ventricular ejection occurs before left because pressure in pulmonary artery is low compared to that in aorta.

Ventricular Contraction (Systole)

Ejection starts, and arterial volume and pressure begin to increase.

Rapid ejection: two thirds of stroke volume ejected during first third of systole (ventricular pressure > aortic pressure). Reduced ejection: one third of stroke volume ejected during last two thirds of systole (ventricular pressure < aortic pressure). Ventricles relax.

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SUMMARY OF THE CARDIAC CYCLE

Step

Step No.
10

Mechanism

Important Points

Ventricular Contraction (Systole)

Semilunar Valve Closure

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 aortic valve, indicates end of ventricular systole.

Ventricular Relaxation (Diastole)

Isovolumetric Relaxation

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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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Step

Step No.
12

Mechanism

Important Points

Ventricular Relaxation (Diastole)

AV Valve Opening

Rapid filling: high atrial pressure (due to continued venous return during ventricular systole) causes initial rapid passive ventricular filling (80% of blood volume). Pressure in atria and ventricles decreases and ventricular relaxation continues during rapid filling. Slow filling or diastasis: as blood continues to return to heart,atrial and ventricular pressures slowly rise. Ventricular filling of blood stops shen ventricles reach their volume limit. Atrial contraction forces blood into ventricles to complete ventricular filling.

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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 not essential 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).

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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 and isovolumetric relaxation)

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Cardiac Output (CO)

Cardiac output = (stroke volume) x (heart rate)
Fick Principle
Rate of O2 consumption

CO =
Arterial O2 content venous O2 content

During exercise, CO initially as a result of an in SV. After prolonged exercise, CO as a result of an in HR.

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

If HR is too high, diastolic filling is incomplete and CO (e.g., ventricular tachycardia)

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CO SV = HR = EDV - ESV

SV

EF = 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 by Contractility, Afterload, and Preload. 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, and pregnancy. A failing heart has stroke volume.

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Cardiac Output Variables

Contractility (and SV) with: 1. 1 blockade 2. Heart failure 3. Acidosis 4. Hypoxia/ hypercapnea Myocardial O2 demand is by: 1. afterload ( diastolic BP) 2. contractility 3. heart rate 4. heart size ( wall tension)

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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 SOUNDS
Sound
S1 S2

Cause of Sound
Closure of AV valves. Closure of semilunar valves.

Events
Just after onset of ventricular contraction. Signals onset of ventricular systole. 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 process affecting left ventricle (LBBB, aortic stenosis).

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HEART SOUNDS
Sound
S3

Cause of Sound
Rapid, passive ventricular filling.

Events
At start of ventricular diastole. Heard best at apex. Usually not heard in adults but may be heard in children or patients with LVE Atrial contraction. Occasionally heard in healthy individuals. Individuals with CHF have triple sound called gallop rhythm.

S4

Forcing of additional blood into distended ventricle.

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ATRIAL PRESSURE CHANGES VIA JUGULAR VENOUS TRACING

Wave
a

Timing of Wave
Atrial contraction at end of ventricular diastole.

Cause of Wave
Small amount of blood regurgitates into great veins. Venous inflow stops, causing rise in venous pressure Rise in atrial pressure produced by bulging of AV valves into atria. Rise in atrial pressure before AV valves open during diastole

c v

Isovolumetric contraction Ventricular diastole

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Valvular Lesions And Cardiac Murmurs

Type Of Lesion Aortic Stenosis

Function
Creates highresistance area that forces left ventricle to generate high pressures to eject blood through narrowed orifice. Blood flows back into left ventricle during diastole , reducing effective CO.

Murmur
Crescendodecrescendo (diamond-shape) systolic ejection murmur.

Possible ECG Change LVH, LBBB

Clinical Significance
Ventricular systolic pressure much higher than systolic pressure in respective artery is pathognomonic. May lead to LVH and LVE.

Aortic Insufficiency or Regurgitation

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. Usually congential, may be acquired with hypertrophic cardiomyopathy. May led to RVH and RVE

Pulmonary Stenosis

Creates highresistance are that forces right ventricle to generate high pressure to eject blood through narrowed orifice.

Systolic ejection crescendodecrescendo murmur, often with harsh quality.

RVH, right atrial abnormality.

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Valvular Lesions And Cardiac Murmurs

Type Of Lesion Pulmonary Insufficiency or Regurgitation Function Blood flows back into right ventricle during diastole, reducing input to lungs. Murmur Diastole decrescendo, often high-pitched, blowing murmur that begins with pulmonic valve closure (P2) Presystolic or early diastolic crescendo murmur with lowpitched rumble. Heard on atrial contraction and rapid passive ventriccular filling. Possible ECG Change RVH Clinical Significance Usually associated with pulmonary hypertension. Causes right ventricular dilation, which leads to RVE.

Mitral Valve Stenosis

Impedes filling of left ventricle, allowing pressure gradient to develop between left atrium and left ventricle during diastole

Left Atrial abnormality, atrial fibrillation. RVH if associated with pulmonary artery hypertension

May led to pulmonary edema (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
Due to

RV afterload

RV Failure : 1. Corpulmonale 2. Intrinsic lung diseases, Pulmonary arterial hypertension (PAH) 3. Acute cor pulmonale

RV dilation caused by thrombopulmonary embolism

4. Chronic corpulmonale

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Clinical Correlations (2)

Chronic corpulmonale
RV hypertrophy RV enlargement RV Failure PAH

PAH > 30 mmHg

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vasculitis

Eisenmenger Syndrome (VICE)

Idiopathic (primary PAH)

PAH
Emphysema Chronic Pulmonary Emboli Chronic Lung Disease
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Clinical Findings / Manifestations

RUQ discomfort hepatomegaly nutmeg pattern (chronic passive congestion) Peripheral edema (RV Failure ankle swelling) Pulmonary edema Jugular vein & portal vein distention Splenomegaly ascites

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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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General Features
LV Failure myocardial infarction (MI) LV hypertrophy dilation LV Failure blood congestion pulmonary edema with wet coughing Transferrin Hb leak congested capillaries phagocytosed by macrophages in alveoli heart failure cells. LV Failure COP kidney perfusion A. Tubular necrosis

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Clinical Manifestations
Over weight Poor diet Angina left arm (referred arm) Nausea Profuse sweating, cold, clammy skin (stress-induced catecholamines epinephrine and norepinephrine; from adrenal medulla stimulate sweat glands )

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Clinical Manifestations (2)

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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Treatment
Nitroglycerin Adrenergic antagonist (propanolol, relieve blocker) tachycardia hypertension

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Treatment (2)
Streptokinase TPA (Tissue Plasminogen Activator)

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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