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 cardiac
cycle

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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 Cycle
Phases:
1. Isovolumetric contraction-
period 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.

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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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 SUMMARY OF THE CARDIAC CYCLE

Step
Step Mechanism Important Points
No.
Ventricular Contraction (Systole)
AV Valve 1 Ventricular contraction causes Normal aortic systolic
Closure increased ventricular pressure: 120 mm Hg.
pressure. Normal pulmonary artery
2 When ventricular pressure systolic pressure: 15-18 mm
exceeds atrial pressure, AV Hg.
valves close.
Iso- 3 Closed AV valves isolate Arterial diastolic pressure is
volumetric ventricles from atria the lowest arterial pressure.
Contraction It occurs just before onset of
4 Ventricular volume stays
constant while ventricular ventricular ejection.
pressure rises.

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 SUMMARY OF THE CARDIAC CYCLE
Step Step No. Mechanism Important Points
Ventricular Contraction (Systole)
Ventricular 5 When ventricular pressure Arterial systolic pressure is
Ejection exceeds arterial pressure the peak arterial pressure.
semilunar valves open. It occurs at the end of rapid
6 Ejection starts, and arterial ejection.
volume and pressure begin to Right ventricular ejection
increase. occurs before left because
pressure in pulmonary artery
7 Rapid ejection: two thirds of is low compared to that in
stroke volume ejected during aorta.
first third of systole (ventricular
pressure > aortic pressure).
8 Reduced ejection: one third of
stroke volume ejected during
last two thirds of systole
(ventricular pressure < aortic
pressure).
9 Ventricles relax.

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SUMMARY OF THE CARDIAC CYCLE

Step
Step Mechanism Important Points
No.
Ventricular Contraction (Systole)
Semilunar 10 Closure of aortic and Incisura: notch on descending
Valve pulmonic valves prevents flow limb of aortic pressure curve
Closure of blood back into ventricles. produced by closure of aortic
valve, indicates end of
ventricular systole.

Ventricular Relaxation (Diastole)

Iso- 11 Ventricles relax and Systemic arterial pressure
volumetric ventricular pressure rapidly declines as blood continues to
Relaxation falls without change in flow.
ventricular volume.

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 Step
Step Mechanism Important Points
No.
Ventricular Relaxation (Diastole)
AV Valve 12 Rapid filling: high atrial pressure Normal diastolic pressure in
Opening (due to continued venous return aorta: 80 mm Hg.
during ventricular systole) causes Normal diastolic pressure
initial rapid passive ventricular pulmonary artery: 8-10 mmHg.
filling (80% of blood volume). Tachycardia (>180 bpm) results
in decreased CO; ventricular
13 Pressure in atria and ventricles filling time is markedly reduced,
which lowers VEDV and SV.
decreases and ventricular
relaxation continues during rapid Atrial contraction is not
essential for ventricular filling,
filling. as evidenced by adequate
ventricular filling in patients
14 Slow filling or diastasis: as blood
without atrial contraction (eg,
continues to return to heart,atrial atrial fibrillation or heart block).
and ventricular pressures slowly Contribution of atrial
rise. contraction to ventricular
volume is more important when
15 Ventricular filling of blood stops HR is rapid and duration of
shen ventricles reach their volume diastasis is short (eg, mitral
limit. stenosis).
16 Atrial contraction forces blood into
ventricles to complete ventricular
filling.
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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 During exercise, CO initially
CO = as a result of an in SV.
Arterial O2 content venous O2 content After prolonged exercise,
CO as a result of an in
HR.
Mean arterial = cardiac x total peripheral
If HR is too high, diastolic filling
Similar to Ohms law: is incomplete and CO
Voltage = (current) x (resistance) (e.g., ventricular
MAP = systolic + 2/3 diastolic tachycardia)
Pulse pressure = systolic diastolic
Pulse pressure = stroke volume

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 CO
SV = = EDV - ESV
HR

SV

EF = X 100% (normal 55-80%)

EDV

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 Calculations of Stroke Volume,
Cardiac Output & Ejection Fraction

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 Cardiac Output Variables
Stroke volume affected by SV CAP.
Contractility, Afterload, and
Preload. Increased SV when
preload, afterload, or Stroke volume in anxiety,
contractility. exercise, and
pregnancy.
Contractility (and SV) with :
A failing heart has stroke
1. Catecholamines ( activity of
volume.
Ca2+ pump in sarcoplasmic
reticulum)
2. intracellular calcium
3. extracellular sodium
4. Digitalis ( intracellular Na+,
resulting in Ca2+)

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 Cardiac Output Variables

Contractility (and SV)

with: Myocardial O2 demand is
by:
1. 1 blockade
1. afterload ( diastolic
2. Heart failure
BP)
3. Acidosis
2. contractility
4. Hypoxia/ hypercapnea
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 Cause of Events
Sound
S1 Closure of AV Just after onset of ventricular contraction.
valves. Signals onset of ventricular systole.
S2 Closure of Signals end of systole and onset of ventricular diastole.
semilunar valves. 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 Cause of Events
Sound
S3 Rapid, passive At start of ventricular diastole.
ventricular filling. Heard best at apex.
Usually not heard in adults but may be heard in children
or patients with LVE
S4 Forcing of Atrial contraction.
additional blood Occasionally heard in healthy individuals.
into distended Individuals with CHF have triple sound called gallop
ventricle. rhythm.

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 ATRIAL PRESSURE CHANGES
VIA JUGULAR VENOUS TRACING
Wave Timing of Wave Cause of Wave
a Atrial contraction at end of Small amount of blood regurgitates into great
ventricular diastole. 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 Murmurs
Type Of Possible ECG
Function Murmur Clinical Significance
Lesion Change
Aortic Creates high- Crescendo- LVH, LBBB Ventricular systolic pressure
Stenosis resistance area that decrescendo much higher than systolic
forces left ventricle to (diamond-shape) pressure in respective artery
generate high systolic ejection is pathognomonic.
pressures to eject murmur. May lead to LVH and LVE.
blood through
narrowed orifice.

Aortic Blood flows back into Diastole LVH, with High systolic pressures
Insuffi- left ventricle during decrescendo, often narrow, deep associated with low diastolic
ciency or diastole , reducing high-pitched, Q waves. pressures, leading to large
Regur- effective CO. blowing murmur that pulse pressure (>100 mmHg),
gitation begins with A2 reflected by water-hammer or
Corrigan pulses.
Causes left ventricular
dilation, which leads to LVE.

Pulmonary Creates high- Systolic ejection RVH, right Usually congential, may be
Stenosis resistance are that crescendo- atrial acquired with hypertrophic
forces right ventricle decrescendo abnormality. cardiomyopathy.
to generate high murmur, often with May led to RVH and RVE
pressure to eject harsh quality.
blood through
narrowed orifice.

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 Valvular Lesions And Cardiac Murmurs
Type Of Possible ECG
Function Murmur Clinical Significance
Lesion Change
Pulmonary Blood flows back into Diastole RVH Usually associated with
Insuffi- right ventricle during decrescendo, often pulmonary hypertension.
ciency or diastole, reducing high-pitched, Causes right ventricular
Regur- input to lungs. blowing murmur that dilation, which leads to
gitation begins with RVE.
pulmonic valve
closure (P2)

Mitral Valve Impedes filling of left Presystolic or early Left Atrial May led to pulmonary
Stenosis ventricle, allowing diastolic crescendo abnormality, atrial edema (high pulmonary
pressure gradient to murmur with low- fibrillation. venous pressures), left atrial
develop between left pitched rumble. RVH if enlargement, or atrial
atrium and left Heard on atrial associated with fibrillation.
ventricle during contraction and pulmonary artery
diastole rapid passive hypertension
ventriccular filling.

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RIGHT VENTRICLE (RV)

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Clinical Correlations
RV (Right Ventricle)
Due to
RV Failure 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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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,
blocker) relieve

tachycardia
hypertension

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 Treatment (2)
Streptokinase
TPA (Tissue Plasminogen Infarcted tissue
Activator) < 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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