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Huppert’s Notes: Pathophysiology and Clinical Pearls for Internal Medicine

Chapter 1­01: Anatomy and Physiology in Cardiology

CARDIAC ANATOMY
FIGURE 1.1

Cardiac chambers, valves, and major vessels.

CARDIAC ELECTROPHYSIOLOGY
Cardiac electrical conduction system: Sinoatrial (SA) node (1° pacemaker) → Atrioventricular (AV) node (stalls conduction; can also act as a
backup pacemaker with rate of 40–60 bpm) → Bundle of His → Right/left bundle → Purkinje fibers → Ventricle

Pacemaker cells (SA/AV node cells) automatically create electrical impulses that trigger myocyte cells (atrial/ventricular cells)

­ Pacemaker action potential is described using three phases (Phases 0, 3, and 4). It is automatic and initiated by a slow inward Ca2+ current.
The maximum diastolic potential (analogous to resting membrane potential) is ∼−55 mV (Figure 1.2)

­ Myocyte action potential is described using five phases (Phases 0–4). It is automatic and triggered by a fast inward Na+ current. The resting
membrane potential is −90 mV, determined by K+ conductance and equilibrium potential (Figure 1.3)

FIGURE 1.2

Cardiac pacemaker cell action potential.

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 membrane potential is −90 mV, determined by K+ conductance and equilibrium potential (Figure 1.3)
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FIGURE 1.2
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Cardiac pacemaker cell action potential.

FIGURE 1.3

Cardiac myocyte action potential.

TABLE 1.1
Hemodynamic Calculations Used Clinically

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Volume Calculations
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SV = EDV – ESV
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TABLE 1.1
Hemodynamic Calculations Used Clinically

Volume Calculations

SV = EDV – ESV

SV = CO/HR

EF = SV/EDV = (EDV − ESV)/EDV. Normal 55–70%.

Pressure Calculations

MAP = (SBP + [2 × DBP])/3. Normal 65–100 mmHg.

MAP = CO × SVR

mPAP = (PASP + [2 × PADP])/3. Normal <20 mmHg.

Resistance Calculations

Ohm’s Law: V = IR; R = V/I

SVR = (MAP − RAP) × 80/CO. Normal 800–1200 dynes × cm−5.

PVR = (mPAP − PCWP)/CO. Normal <3 Wood units.

Flow Calculations

CO = HR × SV. Normal 4–8 L/min.

CO = VO2/(CaO2 − CvO2)

CO = VO2/(Hgb × 13.6 × [PaO2 − MvO2]). Fick Principle.

CI = CO/BSA. Normal 2.4–4 L/min/m2.

Abbreviations: Stroke volume (SV), End­diastolic volume (EDV), End­systolic volume (ESV), Cardiac output (CO), Heart rate (HR), Ejection fraction (EF), Mean arterial
pressure (MAP), Systolic blood pressure (SBP), Diastolic blood pressure (DBP), Systemic vascular resistance (SVR), Mean pulmonary artery pressure (mPAP),
Pulmonary artery systolic pressure (PASP), Pulmonary artery diastolic pressure (PADP), Voltage (V), Current (I), Resistance (R), Right atrial pressure (RAP), Pulmonary
vascular resistance (PVR), Pulmonary capillary wedge pressure (PCWP), Heart rate (HR), Stroke volume (SV), Oxygen consumption (VO2), Arteriovenous oxygen
difference (CaO2 − CvO2), Hemoglobin (Hgb), Partial pressure of oxygen (PaO2), Myocardial volume oxygen (MvO2), Cardiac index (CI), Body surface area (BSA)

DETERMINANTS OF CARDIAC FUNCTION

Preload: Myocardial stretch before contraction (i.e., the end­diastolic length of the cardiac fibers), which affects the force of contraction

­ Proxy: End­diastolic volume (EDV), end­diastolic pressure (EDP)

­ Frank­Starling
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Afterload: Force to push against. Two types: Wall stress and vascular resistance
DETERMINANTS OF CARDIAC FUNCTION
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Preload: Myocardial stretch before contraction (i.e., the end­diastolic length of the cardiac fibers),
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by: affects the force of contraction

­ Proxy: End­diastolic volume (EDV), end­diastolic pressure (EDP)

­ Frank­Starling curve: ↑Venous return → ↑SV + ↑CO

Increases preload: ↑Blood volume, exercise, sympathetic (reduced venous compliance), ↓HR (longer filling time)

Afterload: Force to push against. Two types: Wall stress and vascular resistance

­ Proxy = systemic or pulmonary vascular resistance, ventricular wall stress

­ Wall stress = (pressure × radius) / (2 × wall thickness); ↑ Wall stress = ↑ O2 demand

­ Systemic vascular resistance (SVR) (component of LV afterload) = (MAP − RAP) / CO

Increases LV afterload: Hypertension, aortic stenosis, systolic heart failure (↑ Wall stress)

­ Pulmonary vascular resistance (PVR) (component of RV afterload) = (mPAP − PAWP) / CO

Increases RV afterload: PE, pulmonary arterial hypertension

Contractility: Inherent ability of the myocardium to contract independent of preload or afterload

­ Proxy: None (SV, CO, EF provide an impression; however, all are affected by preload/afterload)

Increases contractility: Sympathetic (catecholamine via β1 receptor), inotropic drugs (e.g., dobutamine via B1 receptor, digoxin via
↑intracellular Ca2+), tachycardia (via Ca2+ buildup)

Decreases contractility: Parasympathetic (ACTH via M2 receptor), beta blocker/calcium channel blocker, CHF/MI, acidosis,
hypoxia/hypercapnia

There are three ways to increase stroke volume (i.e., the width of a pressure­volume loop; Figure 1.4):

­ Increased preload → ↑SV (Frank­Starling)

­ Decreased afterload → ↑SV (increases linearly along the end­systolic pressure­volume relationship [ESPVR])

­ Increased contractility → ↑SV (increased slope of ESPVR line)

FIGURE 1.4

Pressure volume loop of the cardiac cycle and impact of preload, afterload, and inotropy.

A) Cardiac pressure­volume loop and key physiologic events. B) Interactions between preload and afterload at constant inotropy. C) Interdependent
effects of changes in afterload. D) Interdependent effects of changes in inotropy.

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Pressure volume loop of the cardiac cycle and impact of preload, afterload, and American
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A) Cardiac pressure­volume loop and key physiologic events. B) Interactions between preload and afterload at constant inotropy. C) Interdependent
effects of changes in afterload. D) Interdependent effects of changes in inotropy.

PHASES OF THE CARDIAC CYCLE

Diastole:

­ Atrial pressure > ventricular pressure → Tricuspid and mitral valves open → Filling

­ Contraction: Atrial pressure < ventricular pressure → Tricuspid and mitral valves close → S1

Mitral valve snaps before the tricuspid valve because the LV contracts first (but normally heard as just one sound)

S1 is loudest at the apex (fifth intercostal space, mid­clavicular line)

Systole:

­ ↑Ventricular pressure in isovolumetric contraction until ventricular pressure > pulmonary artery/aortic pressure → Pulmonic and aortic
valves open → Ejection

­ End of ejection: Ventricular pressure falls → Pulmonic and aortic valves close → S2

Aortic sound occurs before the pulmonic sound because the aortic pressure is higher

S2 is loudest at the base (upper sternal border)

“Split S2”: The close of the aortic valve (A2) and the close of the pulmonary valve (P2) are not synchronized and become wider during
inspiration (i.e. widened A2P2) because ↓intrathoracic pressure → ↑Venous return → Longer RV emptying time → Pulmonic valve closes
later → P2 comes later

EXTRA HEART SOUNDS

S 3 (Ventricular gallop): OVERLOAD; early diastolic sound, listen with the stethoscope’s bell

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­ Differential diagnosis: Can be normal in patients age <35 yr or in pregnancy. Otherwise, specific sign of decompensated heart failure (92%
specificity for LVEDP >15 mmHg and BNP >100 pg/mL)
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EXTRA HEART SOUNDS Access Provided by:

S 3 (Ventricular gallop): OVERLOAD; early diastolic sound, listen with the stethoscope’s bell

­ Turbulent flow of blood hitting an overfilled ventricle

­ Differential diagnosis: Can be normal in patients age <35 yr or in pregnancy. Otherwise, specific sign of decompensated heart failure (92%
specificity for LVEDP >15 mmHg and BNP >100 pg/mL)

S 4 (Atrial gallop/kick): STIFF VENTRICLE; late diastolic sound, listen with the stethoscope’s diaphragm

­ Atrium pushing blood against a stiff ventricle

­ Differential diagnosis: Always pathologic – ventricular hypertrophy (secondary to HTN), heart failure

FIGURE 1.5

The cardiac cycle. This image depicts the relationship between various cardiac parameters over the course of a single cardiac cycle, including
cardiac filling (black), ECG findings (dark green), heart sounds (purple), aortic pressure (light blue), left ventricular pressure (dark blue), left atrial
pressure (green), ventricular volume (royal blue), and jugular venous pulse (lime).

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CENTRAL
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Hill. All RightsPRESSURE (CVP)
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a wave: atrial contraction
FIGURE 1.5

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The cardiac cycle. This image depicts the relationship between various cardiac parameters over the course of a single cardiac cycle, including
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cardiac filling (black), ECG findings (dark green), heart sounds (purple), aortic pressure (light blue), left ventricular pressure (dark blue), left atrial
pressure (green), ventricular volume (royal blue), and jugular venous pulse (lime).

CENTRAL VENOUS PRESSURE (CVP) WAVEFORM / JUGULAR VENOUS PULSE (JVP)

a wave: atrial contraction

c wave: RV contraction (closed tricuspid valve bulging into the atrium)

x descent: Atrial relaxation and downward displacement of the closed tricuspid valve during ventricular contraction

v wave: Increased RA pressure during systole because passive filling against a closed tricuspid valve

y descent: Tricuspid valve opens and emptying blood from RA fills RV

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