2.3 Cardiac Anatomy, Electrophysiology, and Hemodynamic Control

Cardiac Anatomy, Electrophysiology, and Hemodynamic Control

Prescribing safe and effective exercise in clinical physical therapy requires an intimate understanding of cardiovascular anatomy, cardiac electrophysiology, and hemodynamic regulation. Whether monitoring an inpatient during early Phase I cardiac rehabilitation following an acute myocardial infarction or treating a patient with chronic hypertension in an outpatient orthopedic clinic, physical therapists must accurately interpret vital signs, recognize electrocardiographic (ECG) warning flags, and understand the hemodynamic determinants of cardiovascular performance.

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1. Gross Cardiac Anatomy, Chambers, and Valvular Mechanics

The heart is a muscular dual-pump situated within the middle mediastinum, encased by the fibroserous pericardial sac. It consists of four distinct muscular chambers and four unidirectional fibrous valves.

The Four Chambers

1. Right atrium (RA): Receives systemic venous return through the superior and inferior venae cavae and venous return from the myocardium through the coronary sinus. Landmarks include the pectinate muscles, crista terminalis and fossa ovalis. The sinoatrial (SA) node is near the superior vena cava–right atrial junction.
2. Right ventricle (RV): A thin-walled chamber that curves around the left ventricle and pumps into the lower-pressure pulmonary circulation. Its trabeculae include the moderator band, which carries part of the right bundle branch toward the anterior papillary muscle.
3. Left atrium (LA): The posterior chamber receives oxygenated blood from the pulmonary veins, typically four, with variants. The pectinate muscles are largely confined to the appendage, a common site of thrombus in atrial fibrillation.
4. Left ventricle (LV): A thick-walled chamber that ejects blood into the systemic circulation. The orientation of myocardial fibers changes gradually across its wall. This arrangement contributes to systolic twist, and early diastolic untwisting contributes to ventricular filling.

Heart Valves and Acoustic Mechanics

• Atrioventricular (AV) Valves:
  • Tricuspid Valve: Situated between RA and RV, featuring three cusps (anterior, posterior, septal).
  • Mitral (Bicuspid) Valve: Situated between LA and LV, featuring two cusps (anterior and posterior).
  • Chordae tendineae connect the leaflets to papillary muscles. As the ventricle contracts, these structures restrain leaflet prolapse. The pressure gradient drives valve closure.
• Semilunar Valves:
  • Aortic Valve: Located at the left ventricular outflow tract, comprising three pocket-like semilunar cusps (right coronary, left coronary, and non-coronary cusps). Immediately superior to the cusps lie the sinuses of Valsalva, from which the coronary arteries arise.
  • Pulmonic valve: Located at the right ventricular outflow tract. Its three semilunar cusps prevent backflow from the pulmonary trunk.
  • Decelerating ejection and reversal of the arterial-to-ventricular pressure gradient bring the semilunar cusps together at the end of ejection.

Acoustic Heart Sounds

• First heart sound ($S_1$): Vibrations associated with AV valve closure mark the onset of ventricular systole. Listen near the apex for the mitral component and along the lower left sternal border for the tricuspid component.
• Second heart sound ($S_2$): Associated with aortic and pulmonic valve closure at the transition to diastole. Its components are best assessed near the upper sternal borders.
• Physiological splitting of $S_2$: In spontaneous inspiration, greater right-sided filling and a longer right ventricular ejection interval delay pulmonic closure. Aortic closure can occur slightly earlier. The gap between $A_2$ and $P_2$ widens on inspiration and usually narrows on expiration.
• Third heart sound ($S_3$): A low-frequency sound during rapid early ventricular filling. It can occur physiologically in younger people and can also accompany elevated filling pressures or volume overload.
• Fourth heart sound ($S_4$): A low-frequency sound during late filling as the atrium contracts. It can accompany a stiff ventricle and requires an effective atrial contraction.

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2. Coronary Arterial Perfusion and Ischemic Territories

Myocardial tissue is perfused by the right and left coronary arteries, which originate from the root of the ascending aorta just superior to the aortic valve cusps.

Left Coronary Artery (LCA) System

The left main coronary artery usually divides into the left anterior descending (LAD) and left circumflex (LCx) arteries. The right coronary artery (RCA) follows the right atrioventricular groove and gives off branches to the right ventricle. The origin of the posterior descending artery (PDA) is used to describe dominance. It usually arises from the RCA and can arise from the LCx in left-dominant anatomy. Nodal arterial supply also varies.

Inferior ST elevation with greater elevation in III than II and reciprocal depression in aVL supports an RCA culprit. The pattern is a localization clue and the artery is confirmed in the acute coronary assessment. In a patient with acute symptoms, activate the urgent cardiac response.

Diastolic Coronary Flow

Flow to the left ventricular myocardium is greatest during diastole. Systolic contraction compresses intramyocardial vessels, especially in the subendocardium, and relaxation relieves that compression as the aortic pressure continues to drive flow. Systolic flow can contribute, and the timing differs by coronary territory. A faster heart rate shortens diastolic time and increases demand, which can expose limited coronary flow reserve.

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3. Cardiac Electrophysiology and Conduction Pathways

Coordinated mechanical pumping relies on rapid electrical depolarization traveling through specialized cardiac conduction pathways.

Sinoatrial (SA) node
        │
        ▼
Right atrial myocardium ── Bachmann bundle ──► Left atrial myocardium
        │
        ▼
Atrioventricular (AV) node  [slower conduction]
        │
        ▼
Bundle of His
        ├──► Right bundle branch ──► Right ventricular Purkinje network
        └──► Left bundle branch  ──► Left ventricular Purkinje network

The Conduction Pathway

1. Sinoatrial (SA) node: The usual pacemaker. Several mechanisms contribute to spontaneous diastolic depolarization, including the hyperpolarization-activated HCN channels that carry the mixed sodium and potassium current $I_f$. The observed resting sinus rate reflects autonomic input as well as nodal automaticity.
2. Atrioventricular (AV) node: Located in the region of the triangle of Koch. Slow conduction helps coordinate atrial contraction before ventricular activation. Junctional tissue can generate an escape rhythm if sinus impulses fail to arrive.
3. Bundle of His and bundle branches: The penetrating His bundle crosses the insulating fibrous skeleton and leads to the right and left bundle branches. The left branch distributes impulses through a variable fascicular network.
4. Purkinje network: Rapid conduction delivers activation to much of the ventricular endocardium before it spreads through ventricular muscle. Distal escape rhythms are generally slower than junctional escape rhythms.

Normal Surface Electrocardiogram (ECG) Waves and Intervals

• P wave: Represents atrial depolarization. In sinus rhythm, the impulse starts in the SA node.
• PR interval: From P-wave onset to QRS onset. A typical adult interval is 120–200 ms, or three to five small boxes at 25 mm/s. A value over 200 ms with 1:1 conduction is termed first-degree AV block or AV delay.
• QRS complex: Represents ventricular depolarization. A QRS of at least 120 ms is wide in adults. Assess morphology and rhythm to distinguish bundle branch block, a ventricular rhythm and other causes.
• ST segment: From the J point to T-wave onset. It is usually near the baseline. Horizontal or downsloping depression can suggest ischemia in the appropriate setting. Baseline ECG, symptoms, leads and test protocol affect interpretation.
• T wave: Represents ventricular repolarization.
• QT interval: From QRS onset to T-wave end. QTc adjusts for heart rate. The AHA ECG standard describes adult QTc greater than 450 ms in men or at least 460 ms in women as prolonged. Correction method and QRS duration affect interpretation. Prolongation can increase the risk of torsades de pointes.

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4. The Mechanical Cardiac Cycle (Wiggers Sequence)

One teaching model groups the Wiggers sequence into five phases. Read the pressure relationships across each valve and follow the volume within one ventricle.

1. Atrial systole: Atrial contraction adds to ventricular filling late in diastole. The ventricle reaches its end-diastolic volume (EDV). The atrial contribution varies with rate, loading and ventricular relaxation and stiffness.
2. Isovolumetric contraction: Ventricular pressure exceeds upstream atrial pressure and closes the AV valve ($S_1$). It is still below the pressure in the downstream artery, so the outlet valve stays closed. In the normal left ventricle, both the mitral and aortic valves are closed and volume stays approximately at EDV.
3. Ejection: When LV pressure exceeds aortic pressure, the aortic valve opens. The right ventricle ejects when its pressure exceeds pulmonary arterial pressure. The pressures at opening depend on the measured arterial pressures for that beat. Rapid and reduced ejection leave the end-systolic volume (ESV).
4. Isovolumetric relaxation: As ejection ends and ventricular pressure falls below arterial pressure, semilunar valve closure marks $S_2$. In the left ventricle both valves are again closed, and pressure falls at nearly constant ESV.
5. Early filling and diastasis: Once ventricular pressure drops below atrial pressure, the AV valve opens. Rapid filling follows, then slower filling as pressures approach one another. Diastasis shortens as heart rate rises.

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5. Hemodynamics and Stroke Volume Determinants

Cardiovascular function is quantified by fundamental hemodynamic equations:

$\text{Cardiac Output (CO)} = \text{Heart Rate (HR)} \times \text{Stroke Volume (SV)}$

$\text{Stroke Volume (SV)} = \text{End-Diastolic Volume (EDV)} - \text{End-Systolic Volume (ESV)}$

$\text{Ejection Fraction (EF)} = \frac{\text{SV}}{\text{EDV}} \times 100\%$

Worked example: EDV 120 mL and ESV 50 mL give SV 70 mL/beat and EF $70/120 \times 100\% \approx 58\%$. At 70 beats/min, CO is $4{,}900$ mL/min, or 4.9 L/min. The numbers describe an example beat at rest. With mitral regurgitation, some of the ejected LV volume goes into the left atrium. With aortic regurgitation, some volume returns to the LV during diastole. In each case, calculate net output using the effective forward volume delivered per beat.

Report LVEF with its measurement method. The Saudi Heart Association classifies established heart failure by LVEF as reduced at 40% or less, mildly reduced at 41%–49%, or preserved at 50% or more. The AHA/ACC/HFSA framework explicitly requires evidence of elevated filling pressures in the mildly reduced and preserved groups. Combine EF with the clinical assessment and other tests for heart failure.

Determinants of Stroke Volume

Stroke volume (EDV − ESV)
├─ Preload: end-diastolic myocardial stretch
├─ Afterload: load opposing ventricular ejection
└─ Contractility: myocardial force-generating state at a given load

1. Preload: End-diastolic stretch depends on filling and ventricular properties. EDV can serve as an index of preload in a simplified model. At comparable afterload and contractility, greater filling can increase stroke volume through Frank–Starling length-dependent activation, which includes increased myofilament calcium sensitivity. The size of the response varies across patients and loading conditions.
2. Afterload: The ventricle ejects against arterial pressure and pulsatile impedance, and outflow obstruction can add load. Resistance, arterial compliance and ventricular geometry all matter. For a thin-walled spherical approximation, wall stress is $\sigma \approx Pr/(2h)$, with transmural pressure $P$, chamber radius $r$ and wall thickness $h$. Holding other terms fixed, higher pressure or a larger radius raises estimated stress. A thicker wall lowers it in this model. Real ventricular geometry limits this estimate. At comparable preload and contractility, a sudden rise in afterload tends to reduce stroke volume.
3. Contractility: The force-generating state changes with intracellular calcium handling and myofilament properties. Sympathetic $\beta_1$ stimulation increases calcium availability for contraction and also accelerates relaxation. At comparable loading, higher contractility tends to reduce ESV and increase SV.

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6. Blood Pressure Regulation and Autonomic Control

For mean flow through a vascular bed, the driving pressure is the upstream minus the downstream pressure. In the systemic circuit the upstream pressure is MAP and the downstream pressure is mean right atrial pressure (RAP):

$\text{SVR} = \frac{\text{MAP}-\text{RAP}}{\text{CO}}$

Rearranging gives $\text{MAP} = \text{RAP} + \text{CO}\times\text{SVR}$. Omitting RAP is an approximation when it is small relative to MAP. With pressure in mmHg and CO in L/min, resistance is in mmHg·min/L (Wood units). Multiply by 80 to express it in dyn·s/cm⁵. Pulmonary vascular resistance uses $(\text{mPAP}-\text{PAWP})/\text{CO}$, with mean pulmonary arterial pressure (mPAP) and pulmonary arterial wedge pressure (PAWP). The calculation uses mean pressures and the flow through the corresponding circuit. In steady circulation without a shunt, mean systemic and pulmonary flow are equal.

MAP is the time average of arterial pressure over the beat. A common cuff-pressure estimate is:

$\text{MAP} \approx \text{DBP} + \frac{1}{3}(\text{SBP}-\text{DBP})$

For 120/80 mmHg, the estimate is $80 + 40/3 \approx 93.3$ mmHg. If mean RAP is 3.3 mmHg and CO is 5 L/min, estimated SVR is $90/5=18$ Wood units or 1,440 dyn·s/cm⁵. The cuff estimate depends on waveform shape and can differ from measured MAP, especially at altered heart rates or in abnormal hemodynamic states.

Rapid Neural Control: The Arterial Baroreceptor Reflex

Stretch-sensitive arterial baroreceptors in the carotid sinus and aortic arch signal through the glossopharyngeal (CN IX) and vagus (CN X) nerves, respectively. When arterial pressure falls, such as during venous pooling on standing:

1. Less arterial stretch reduces afferent input to the nucleus tractus solitarius (NTS) in the medulla.
2. Sympathetic activity increases and cardiac vagal activity decreases.
3. The heart generally beats faster and more forcefully, and arteriolar and venous constriction help support pressure and venous return.

Long-Term Humoral Control: The Renin-Angiotensin-Aldosterone System (RAAS)

Low renal perfusion pressure, reduced tubular sodium chloride delivery to the macula densa or renal sympathetic stimulation can increase renin secretion by juxtaglomerular cells.

• Renin cleaves liver-derived angiotensinogen to angiotensin I.
• Angiotensin-converting enzyme (ACE), expressed on vascular endothelium including the pulmonary circulation, converts angiotensin I to angiotensin II.
• Angiotensin II can constrict arterioles and stimulate thirst and aldosterone release from the adrenal zona glomerulosa.
• Aldosterone increases renal sodium reabsorption, including through regulation of epithelial sodium channels and sodium–potassium pumps in the distal nephron. Sodium retention can support extracellular volume and blood pressure.

Clinical Physical Therapy Application: The Rate-Pressure Product (RPP)

The rate-pressure product (RPP) is heart rate multiplied by systolic pressure. It is an indirect index of myocardial oxygen demand. For example, 128 beats/min × 168 mmHg gives 21,504 beats·mmHg/min. A service using values scaled by 100 would report 215.0 on that scale. Record the convention. Use the individual’s exercise-test response to inform the prescribed intensity. New chest symptoms call for immediate clinical assessment.