Cardiac Cycle

Everything that happens in a cardiac cycle is indicated.

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Rapid ejection

Final rapid repolarization

Resting membrane potential and diastolic depolarization

Rapid filling

Resting membrane potential and diastolic depolarization

Upstroke or rapid depolarization

Early rapid repolarization

Plateau

Atrial contraction

Isovolumetric contraction

Rapid ejection

Reduced ejection

Isovolumetric relaxation

Rapid filling

Reduced filling

Reduced ejection

Atrial contraction

Isovolumetric contraction

Rapid ejection

Isovolumetric relaxation

Rapid filling

Isovolumetric relaxation

Rapid ejection

Isovolumetric contraction

Atrial contraction

Reduced filling

Isovolumetric relaxation

Cardiac Cycle

It is the precise cycle of a heart beat. It has two cycles - diastole (from Greek dia 'apart' + stellein 'to place') in which the heart muscle relaxes and fills with blood; and systole (from Greek sustellein 'to contract') in which the heart muscle contracts and pumps out the blood. A healthy heart beats 70-75 times per minute and a beat completes in about 0.8 seconds. Here, I show the Wiggers Diagram that depicts volume and pressure changes in aorta, atria and ventricles, along with electrical and sound activity. To know more about how the heart chambers synchronize to pump blood, see The Heart, Part 1 - Under Pressure: Crash Course A&P #25 and The Heart, Part 2 - Heart Throbs: Crash Course A&P #26.

CONCEPT CHECK

Heart is made of cardiomyocytes (cardiac muscle cells) that are mononucleated unlike skeletal muscle cells, and are rich in mitochondria that produces ample ATP to make them resist constant fatigue of a pumping heart.

Functionally, they are divided into contractile cells which make most of the heart structure and are involved in contraction and relaxation through force and pressure; and conducting cells that generate electrical impulses and spread action potentials that regulate the rhythmic beating.

ELECTRICAL CONDUCTION PATHWAY IN THE HEART

1. Cardiac pacemaker cells produce rhythmic action potentials (see this) creating the electrical impulses that we observe on electrocardiogram (ECG). They are located at the sinoatrial (SA) node, an area in the right atrium, which acts as the natural primary pacemaker.

2. Impulse runs through atrial internodal tracts - anterior, middle and posterior - that connect SA node to the atrioventricular (AV) node. If SA node somehow fails to generate the beat, an ectopic secondary pacemaker created at the AV node creates the ECG signals. This conduction in AV node is slow enough to allow the filling of ventricles with blood.

3. The Bachman's bundle activates the left atrium electrically during a normal sinus rhythm.

4. The Bundle of His is the collection of heart muscles that transmits the electrical impulse from AV node through bundle branches towards Purkinje fibres that provide electrical conduction in the ventricles.

Aortic Pressure

It is the blood pressure at the root of aorta, the biggest artery in the body that originates from left ventricle in an arch like shape and moves down to the abdomen. It supplies oxygenated blood to the systemic circulation (everything except lungs). We measure the blood pressure using a sphygmomanometer at the brachial artery near the arm which is at the same level as the aorta.

AORTIC PRESSURE DURING THE CARDIAC CYCLE

Phase 1 (atrial contraction) - atrioventricular (A-V) valves open and semilunar valves close - at this point, AP reduces due to forward reflow of recoiled blood from the previous cycle.
Phase 2 (isovolumetric contraction) - all valves closed - AP reduces linearly as closing of AV valves has negligible effect on AP.
Phase 3 (rapid ejection) - aortic and pulmonic valves open; AV valves close - AP increases rapidly due to blood inflow.
Phase 4 (reduced ejection) - aortic and pulmonic valves open; AV valves close - AP falls at the onset of ventricular repolarization that reduces tension and pressure in ventricles.
Phase 5 (isovolumetric relaxation) - all valves closed - there is a slight increase in AP with a dicrotic notch due to a small blood backflow into ventricles
Phase 6 (rapid filling) - A-V valves open - AP starts to decline once the backflow in aorta is stabilized, owing to the relaxation of adjacent ventricles.
Phase 7 (reduced filling) - A-V valves open - AP continues to decline owing to the closed aortic valve that separates ventricular pressure build-up from AP

Atrial Pressure

Wiggers diagram depicts the left atrial pressure (LAP). It is directly correlated to the pulmonary wedge pressure (PWP) that measures the pressure after wedging a pulmonary catheter with an inflatable balloon in one of the pulmonary arteries.

LEFT ATRIAL PRESSURE DURING THE CARDIAC CYCLE

Phase 1 (atrial contraction) - atrioventricular (A-V) valves open and semilunar valves close - LAP increases slightly due to increase in the venous pressure, although there is no backflow of blood in the vena cavas due to the inertial milking effect (Systolic compression of coronary vessels with partial or complete decompression during diastole). This is shown by the a-wave followed by the x-descent.

Phase 2 (isovolumetric contraction) - all valves closed - mitral (semilunar) valves close. It creates a bulge in the leaflets back into the left atrium. This slightly increases LAP, denoted by a c-wave, and followed by an x'-descent.

Phase 3 (rapid ejection) - aortic and pulmonic valves open; AV valves close - LAP decreases as the ventricles empty the blood while mitral valves bulge out to expand the atrium. This reduces the LAP. Following incoming venous blood then slowly increases LAP.

Phase 4 (reduced ejection) - aortic and pulmonic valves open; AV valves close - LAP continues to increase due to continued venous return from lungs.

Phase 5 (isovolumetric relaxation) - all valves closed - LAP continues to rise due to incoming venous return. It reaches a peak before the mitral valve opens, called a v-wave.

Phase 6 (rapid filling) - A-V valves open - blood flows out of the atrium after mitral valve opens, thereby reducing LAP, denoted by a y-descent.

Phase 7 (reduced filling) - A-V valves open - in late diastole, the rate of filling of ventricles with blood decreases. This leads to a gradual rise in LAP due to same venous return with decreased blood outflow in the atria.

Ventricular Pressure

Wiggers diagram depicts the left ventricular pressure (LVP). LVP is less than aortic pressure during most of the cardiac cycle. Only during systole, pressures equal and aortic valve opens.

LEFT VENTRICULAR PRESSURE DURING THE CARDIAC CYCLE

Phase 1 (atrial contraction) - atrioventricular (A-V) valves open and semilunar valves close - blood flows passively through open mitral valves from atria to ventricles. As such, atrial contraction accounts for only 10% of left ventricular filling.

Phase 2 (isovolumetric contraction) - all valves closed - rate of pressure increase is maximized owing to closing of mitral valves. On a cellular level, this is referred to as excitation-contraction coupling (ECC) in which an action potential triggers myocytes to contract and subsequently relax.

Phase 3 (rapid ejection) - aortic and pulmonic valves open; AV valves close - blood flows from left and right ventricles into aorta and pulmonary arteries respectively. LVP is slightly greater than AP, and an energy gradient propels blood into aorta. The gradient is small, but also is the resistance to flow. AP and pulmonary arterial pressures reach peak in this phase, with maximum blood outflow velocity.

Phase 4 (reduced ejection) - aortic and pulmonic valves open; AV valves close - LVP falls slightly below the AP, but blood continues to flow due to the inherited kinetic energy.

Phase 5 (isovolumetric relaxation) - all valves closed - LVP decreases isovolumetrically, and falls below LAP at the end of this phase.

Phase 6 (rapid filling) - A-V valves open - it is the onset of passive ventricular filling. Mitral valves open and blood flows in, but ventricles are still undergoing relaxation. Upon complete relaxation, LVP begins to increases owing to inflowing blood pressure.

Phase 7 (reduced filling) - A-V valves open - about 90% of ventricular filling occurs till late diastole. Continuous filling increases LVP, but also decreases pressure gradient across AV valves. This lowers blood flow and waits for next cardiac cycle through atrial contraction.

Ventricular Volume

Wiggers diagram depicts the left ventricular volume (LVV). The performance of ventricles is measured in terms of

(1) End-diastolic volume (EDV)

(2) End-systolic volume (ESV)

(3) Stroke volume (SV = EDV - ESV), and

(4) Ejection fraction (EF = SV / EDV)

LEFT VENTRICULAR VOLUME DURING THE CARDIAC CYCLE

Phase 1 (atrial contraction) - atrioventricular (A-V) valves open and semilunar valves close - when atria contract, an increased force is generated that increases the blood flow across the mitral valve by increasing the pressure gradient. This is called an atrial kick, and maximizes the left ventricular end-diastolic volume (LVEDV).

Phase 2 (isovolumetric contraction) - all valves closed - LVV remains constant for the period between closing of the mitral valve and opening of the aortic valve. The volume is averaged to get end-diastolic volume (EDV).

Phase 3 (rapid ejection) - aortic and pulmonic valves open; AV valves close - rapid ejection of blood causes rapid decline in LVV.

Phase 4 (reduced ejection) - aortic and pulmonic valves open; AV valves close - reduced ejection of blood causes reduced rate of decline of LVV.

Phase 5 (isovolumetric relaxation) - all valves closed - The end-systolic volume (ESV) of blood that remains in the left ventricle (LVESV) between closing of aortic valve and opening of mitral valve is ~50 ml. The stroke volume is ~70 ml.

Phase 6 (rapid filling) - A-V valves open - it is the onset of passive ventricular filling. Mitral valves open and blood flows in that rapidly increases LVV.

Phase 7 (reduced filling) - A-V valves open - it is the diastasis (middle stage of diastole) stage of ventricular filling, where the initial passive ventricular filling slows, but before the atria contract to complete the active filling.

Electrocardiogram (ECG)

An electrocardiogram (ECG or EKG) records electrical signals in the heart in a non-invasive manner to detect cardiac problems.

It is commonly used to detect

Arrhythmias - abnormal heart rhythms
Myocardial infarction - heart attack due to disrupted coronary blood flow
Cardiomyopathy - abnormal blood pumping
Coronary artery disease (CAD) - limited blood flow due to plaque obstruction

An ECG may be recommended when a person feels chest pain (angina), dizziness, lightheadedness or confusion, heart palpitations, rapid pulse, shortness of breath, and weakness, fatigue or a decline in ability to exercise.

SIGNIFICANCE OF WAVES DETECTED BY AN E.C.G.

P wave - atrial depolarization

QRS complex - atrial repolarization and ventricular depolarization

T wave - ventricular repolarization

U wave - papillary muscle repolarization

Note: U wave and atrial repolarization wave in QRS complex are not easily observable.

CONSTRUCTION OF AN E.C.G. APPARATUS

10 electrodes are attached to the body to form 12 ECG leads. For further details on the types of electrode systems and their positioning, visit life-in-the-fast-lane page on ECG lead positioning. We also calculate the common virtual electrode called Wilson's central terminal (Vw) as

Vw = 1/3 (RA + LA + LL)

While V1 - V6 are measured as is, other 6 leads (I, II, III, aVF, aVL, aVR) are calculated vectorially as indicated in the figures

I = LA - RA
II = LL - RA
III = LL - LA
aVF (augmented vector foot) = 3/2 (LL - Vw )
aVR (augmented vector right) = 3/2 (RA - Vw )
aVL (augmented vector left) = 3/2 (LA - Vw )

Phonocardiogram (PCG)

A PCG plots high-fidelity sounds and murmurs of the heart on a phonocardiograph. These sounds are generated when heart valves open or close.

The first heart sound (S1), also described as 'lub', is produced by the closure of AV valves. It is made up of M1 (mitral valve closure) that slightly precedes T1 (tricuspid valve closure) at the beginning of ventricular contraction or systole. The sound detected is a result of the reverberation in blood due to blocking of flow reversal by the AV valves.

Splitting of S1 is caused by the delay of T1 sound with respect to M1. This is an indication of right bundle branch block (RBBB).

The second heart sound (S2), also described as 'dub', is produced by the closure of semilunar valves at the junction of ventricular systole and diastole. It is made up of A2 (aortic valve closure) that precedes P2 (pulmonary valve closure).

Splitting of S2 is caused by the delay of P2 sound with respect to A2. This is an indication of RBBB, pulmonary stenosis, and atrial septal defect.

The third heart sound (S3), also described as 'lub-dub-ta' or 'slosh-ing-in' or 'Kentucky' gallop, is a rare sound that indicates heart failure or volume overload. It is a low frequency sound of the back-and-forth oscillation of the blood between ventricular walls. It is heard only after the ventricles are fully filled (onset of diastasis) and under tension to cause reverberation.

The fourth heart sound (S4), also described as 'ta-lub-dub' or 'a-stiff-wall' or 'Tennessee' gallop, is a low-frequency pathologic sound that indicates valvular aortic stenosis, or hypertrophic cardiomyopathy. It occurs just after atrial contraction at the end of diastole.

Bell can listen to low frequency S3 and S4 sounds

Drum can listen to high frequency S1 and S2 sounds

Cardiac Action Potential

An action potential is a reversible change of the membrane potential caused by a sequential activation of several ion currents. These currents are generated by the diffusion of ions down their electrochemical gradient.

It is relevant to understand that depolarization means less negative charge inside the cell and repolarization means more negative charge inside the cell than before.

There are 3 types of cardiac action potentials found in heart cells.