1.1 Cardiovascular Physiology, Hemodynamics & Ischemic Heart Disease

1.1 Cardiovascular Physiology, Hemodynamics & Ischemic Heart Disease

A mastery of cardiovascular physiology, intracardiac pressure dynamics, and coronary perfusion mechanics is essential for perioperative hemodynamic management during general, regional, and monitored anesthesia care. This section provides an in-depth review of cardiac performance determinants, vascular resistance calculations, coronary physiology, and anesthetic strategies for ischemic heart disease.

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1. Determinants of Cardiac Output & The Cardiac Cycle

Cardiac output ($CO$) is the volume of blood pumped by the heart per unit time, defined as:

$CO = HR \times SV$

• Normal Resting Cardiac Output: $4.0 - 8.0 \text{ L/min}$
• Cardiac Index ($CI = CO / BSA$): $2.5 - 4.0 \text{ L/min/m}^2$
• Normal Stroke Volume ($SV$): $60 - 100 \text{ mL/beat}$

Stroke volume represents the volume ejected per contraction ($SV = EDV - ESV$) and is governed by three interrelated mechanical variables: preload, afterload, and contractility.

+-------------------------------------------------------------------------+
|                        DETERMINANTS OF STROKE VOLUME                    |
+-------------------+-----------------------------+-----------------------+
| Preload           | Afterload                   | Contractility         |
| (End-Diastolic    | (Ventricular Wall Stress    | (Inotropy / Chemical  |
| Fiber Length)     | During Systolic Ejection)   | State of Myocardium)  |
+-------------------+-----------------------------+-----------------------+

The Frank-Starling Mechanism

The Frank-Starling law states that the force of myocardial contraction is directly proportional to the initial length of the cardiac muscle fibers (sarcomere stretch).

• Optimal Sarcomere Length: Approximately $2.2 ,\mu\text{m}$, allowing maximal overlap between actin and myosin cross-bridges.
• Physiologic Principle: Increased end-diastolic volume (EDV) increases myocardial stretch, resulting in a more forceful contraction and increased stroke volume up to a physiologic limit.
• Curve Shifts: Inotropic agents (epinephrine, calcium, dopamine) shift the Starling curve upward and to the left (greater SV at lower filling pressures). Volatile anesthetics, propofol, beta-blockers, acidosis, hypercapnia, and myocardial ischemia shift the curve downward and to the right.

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2. Preload, Afterload & Ventricular Wall Stress

Preload Dynamics & Ventricular Compliance

Preload is the myocardial wall tension at the end of diastole, clinically approximated by end-diastolic volume (EDV) or end-diastolic pressure (EDP).

• Right Ventricular Preload: Central Venous Pressure (CVP: $2 - 6 \text{ mmHg}$).
• Left Ventricular Preload: Pulmonary Artery Occlusion Pressure (PAOP/PCWP: $6 - 12 \text{ mmHg}$) or Left Ventricular End-Diastolic Area (LVEDA via transesophageal echocardiography).
• Ventricular Compliance ($\Delta V / \Delta P$): In a non-compliant or hypertrophied ventricle (e.g., severe aortic stenosis, chronic hypertension, acute myocardial ischemia), small increases in end-diastolic volume produce steep, disproportionate spikes in LVEDP. Conversely, a dilated, compliant ventricle accommodates large volume increases with minimal pressure elevation.

Afterload & Laplace's Law

Afterload represents the tension or stress in the ventricular wall during systolic ejection. Laplace's Law defines myocardial wall stress ($\sigma$) as:

$\sigma = \frac{P \times r}{2h}$

Where:

• $P = \text{Intraventricular systolic pressure}$
• $r = \text{Ventricular internal radius (chamber dimension)}$
• $h = \text{Ventricular wall thickness}$

Clinical Applications of Laplace's Law:

1. Concentric Hypertrophy (Pressure Overload, e.g., Aortic Stenosis, HTN): Parallel replication of sarcomeres increases wall thickness ($h$), which normalizes wall stress ($\sigma$) in the face of elevated intracavitary pressure ($P$).
2. Eccentric Hypertrophy (Volume Overload, e.g., Aortic/Mitral Regurgitation): Series replication of sarcomeres dilates the chamber radius ($r$), which significantly increases wall stress ($\sigma$) and accelerates myocardial oxygen consumption.

Hemodynamic Formulas & Normal Values

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3. Coronary Physiology & Perfusion Dynamics

Coronary Blood Flow (CBF)

• Resting coronary blood flow is approximately $225 - 250 \text{ mL/min}$ ($4 - 5%$ of total cardiac output), or $75 - 80 \text{ mL}/100\text{g}/\text{min}$.
• Resting myocardial oxygen consumption ($MVO_2$) is $8 - 10 \text{ mL } O_2/100\text{g}/\text{min}$.
• Oxygen Extraction Ratio: The myocardium has the highest basal oxygen extraction of any organ in the body ($65 - 75%$, coronary sinus $SvO_2 \approx 30%$, $PvO_2 \approx 20 \text{ mmHg}$). Because basal extraction is near-maximal, the heart cannot compensate for increased metabolic demand by extracting more oxygen; increased demand must be met almost entirely by an increase in coronary blood flow.

Coronary Perfusion Pressure (CPP)

$CPP_{LV} = DBP - LVEDP$

         Aortic Root Pressure (Diastolic BP)
                         |
                         v
        [Coronary Vascular Bed]
                         ^
                         |
         Left Ventricular Cavity Pressure (LVEDP)

• Left Ventricle Perfusion Timing: During systole, high intramyocardial tissue pressure exceeds aortic systolic pressure, compressing intramural vessels and halting flow. Consequently, $80 - 85%$ of left ventricular coronary perfusion occurs during diastole.
• Right Ventricle Perfusion Timing: RV peak systolic pressure ($25 \text{ mmHg}$) is significantly lower than systemic systolic pressure ($120 \text{ mmHg}$). Therefore, the RV is perfused continuously during both systole and diastole ($CPP_{RV} = MAP - CVP$).
• Coronary Autoregulation: Maintains stable CBF across perfusion pressures of $60 - 140 \text{ mmHg}$. Flow is primarily regulated by local metabolic byproducts (adenosine, nitric oxide, prostaglandins, interstitial $H^+$, $K^+$, $CO_2$).

Determinants of Myocardial Oxygen Balance

+------------------------------------+-------------------------------------+
|      MYOCARDIAL OXYGEN SUPPLY      |       MYOCARDIAL OXYGEN DEMAND      |
+------------------------------------+-------------------------------------+
| 1. Diastolic Blood Pressure (DBP)  | 1. Heart Rate (MOST CRITICAL)       |
| 2. Diastolic Perfusion Time (HR)   | 2. Afterload / Systolic Wall Stress |
| 3. Low LVEDP (reduced backpressure)| 3. Myocardial Contractility         |
| 4. Arterial Oxygen Content (CaO₂)  | 4. Preload / End-Diastolic Radius   |
| 5. Coronary Vascular Patency       |                                     |
+------------------------------------+-------------------------------------+

NCE Clinical Pearl — Heart Rate is King: Tachycardia exerts a devastating two-fold penalty on myocardial oxygen balance:

1. It exponentially shortens diastolic filling time, drastically reducing coronary oxygen supply.
2. It directly increases the number of contractions per minute, dramatically increasing oxygen demand.

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4. Ischemic Heart Disease (IHD) & Coronary Pathophysiology

Mechanisms of Ischemia: Flow-Limiting Stenosis & Coronary Steal

• Critical Stenosis: A reduction in luminal diameter of $\ge 70%$ (or $\ge 50%$ of the Left Main coronary artery) limits maximal coronary flow reserve during stress.
• Coronary Steal Syndrome: Occurs in the presence of localized coronary artery stenosis with collateral vessels supplying an ischemic region. When a potent coronary arteriolar vasodilator (e.g., adenosine, dipyridamole, high-dose isoflurane) is administered, resistance vessels in the non-ischemic myocardium dilate widely, lowering local vascular resistance. Because the vessels in the ischemic bed are already maximally dilated by endogenous metabolites, blood is diverted away from the ischemic subendocardium and toward the non-ischemic zone.

Hemodynamic Goals for Patients with Coronary Artery Disease

NCE Exam Trap — Phenylephrine vs. Ephedrine in Severe CAD: In a hypotensive CAD patient with baseline tachycardia ($HR = 95 \text{ bpm}$), Phenylephrine (pure $\alpha_1$-agonist) is preferred over Ephedrine. Phenylephrine raises SVR and DBP (improving $CPP$), and induces a reflex vagal reduction in heart rate (prolonging diastole and lowering $MVO_2$). Ephedrine increases heart rate and contractility via $\beta_1$ stimulation, exacerbating myocardial ischemia.