Chapter 4 Cardiovascular Physiology
Clinical note: Pulse pressure may be increased in conditions such as hyperthyroidism (increased systolic pressure and decreased diastolic pressure) and aortic regurgitation (increased systolic pressure and decreased diastolic pressure) and decreased in conditions such as aortic stenosis (decreased systolic pressure).
Clinical note: In certain circumstances, S1 may be accentuated. This occurs when the valve leaflets are “slammed” shut in early systole from a greater than normal distance because they have not had time to drift closer together. Three conditions that can result in an accentuated S1 are a shortened PR interval, mild mitral stenosis, and high cardiac-output states or tachycardia.
4-2 A, Relationship of splitting of S2 to respiration in normal subjects. B, Reversed splitting of S2 associated with delayed aortic closure, most commonly caused by left bundle branch block (LBBB). C, Fixed splitting of S2 characteristic of severe pulmonary hypertension. A2, Aortic valve closure; P2, pulmonic valve closure; PA, pulmonic artery; S1, first heart sound.
(From Fowler NO: Diagnosis of Heart Disease. New York: Springer-Verlag; 1991, p 31.)
Clinical note: Paradoxical or “reversed” splitting occurs when S2 splitting occurs with expiration and disappears on inspiration. Moreover, in paradoxical splitting, the pulmonic valve closes before the aortic valve, such that P2 precedes A2. The most common cause is left bundle branch block (LBBB). In LBBB, depolarization of the left ventricle is impaired, resulting in delayed left ventricular contraction and aortic valve closure.
Clinical note: An S4 usually indicates decreased ventricular compliance (i.e., the ventricle does not relax as easily), which is commonly associated with ventricular hypertrophy or myocardial ischemia. An S4 is almost always present after an acute myocardial infarction. It is loudest at the apex with the patient in the left lateral decubitus position (lying on their left side).
where oxygen consumption is monitored by analysis of expired air, mixed venous blood is sampled by inserting a catheter into the pulmonary artery, and arterial blood is obtained from any peripheral artery.
Clinical note: If the heart muscle is not contracting efficiently (e.g., after a myocardial infarction), the EF may be decreased. If the ejection fraction is equal to or less than 40%, patients are said to have systolic heart failure. Multiple studies have shown that these patients benefit from taking angiotensin-converting-enzyme inhibitors (ACE inhibitors), which reduce pathologic ventricular remodeling in heart failure. Note that some patients may have a “preserved” ejection fraction on echocardiography but still have heart failure; in these cases, they would have diastolic heart failure.
4-4 Stroke volume versus preload. Atrial pressure at ventricular end diastole correlates with ventricular end diastolic volume and pressure and is often used as a surrogate marker of preload. Note that cardiac output increases from point A to point B as the preload increases.
4-5 Stroke volume versus contractility. For any given end diastolic volume (A), addition of a positive inotropic agent (e.g., epinephrine) increases stroke volume and cardiac output by increasing contractility (B). Similarly, addition of a negative inotropic agent (e.g., antagonist of circulating epinephrine or norepinephrine) decreases stroke volume and cardiac output by decreasing contractility (C). Note that in heart failure, a new preload “set point” (D) is established to optimize cardiac output.
(From Lilly LS: Pathophysiology of Heart Disease, 3rd ed. Philadelphia: Lippincott Williams & Wilkins; 2003, Fig. 9-5A.)
Clinical note: The presence of an inspiratory S2 split on cardiac auscultation can be explained by increased venous return to the right atrium during inspiration, which increases the EDV and necessitates a longer systole to eject the additional blood into the pulmonary artery. Pulmonary vascular resistance also decreases somewhat during inspiration, which decreases the pulmonary back pressure needed to close the pulmonic valve. These two factors delay closure of the pulmonary valve during inspiration.
Clinical note: Measurement of atrial pressures can be helpful in determining the cause of various cardiac disorders. Elevated right atrial and pulmonary artery pressures can often be appreciated on examination by simply looking for jugular venous distention or by performing echocardiography. However, a more invasive procedure, using a pulmonary wedge device or Swan-Ganz catheter, is required to evaluate left atrial pressure. This catheter is inserted into a peripheral vein and threaded through the venous circulation until it becomes “wedged” in one of the small branches of the pulmonary artery. Equilibration of blood from the pulmonary veins then allows an indirect measurement of left atrial pressure.
4-12 Pressure-volume changes in aortic stenosis. Ao, Aorta; AV, atrioventricular; IVC, inferior vena cava; LA, left atrium; LV, left ventricle; LVH, left ventricular hypertrophy; MV, mitral valve; PA, pulmonary artery; PMI, point of maximal impulse; PV, pulmonary valve; RA, right atrium, RV, right ventricle; SV, stroke volume; SVC, superior vena cava; TV, tricuspid valve.
(B, From Goljan EF: Rapid Review Pathology, 3rd ed. Philadelphia: Mosby; 2010, Fig. 10-18.)
Pathology note: In some individuals, the aortic valve is congenitally bicuspid. These bicuspid valves are predisposed to early calcification and stenosis, often causing significant aortic stenosis in individuals in their late 40s or early 50s. More commonly, aortic stenosis in elderly people is caused by calcification of the normal tricuspid valve, a condition known as senile calcific aortic stenosis. Another cause of aortic stenosis is rheumatic fever, but this disease is becoming rare in developed nations because of the use of antibiotics.
Clinical note: A stenotic aortic valve increases the rate of blood flow through the aortic valve, producing turbulent flow and consequently a systolic ejection murmur (while blood is being ejected across the valve).
4-13 A and B, Pathologic and clinical findings often seen with aortic regurgitation. Ao, Aorta; AV, atrioventricular; IVC, inferior vena cava; LA, left atrium; LV, left ventricle; LVH, left ventricular hypertrophy; MV, mitral valve; PA, pulmonary artery; PV, pulmonary valve; RA, right atrium, RV, right ventricle; SVC, superior vena cava; TV, tricuspid valve.
(A, From Damjanov I: Pathophysiology. Philadelphia: Saunders; 2008, Fig. 4-53; B, from Goljan EF: Rapid Review Pathology, 3rd ed. Philadelphia: Mosby; 2010, Fig. 10-19.)
Pathology note: Aortic regurgitation may involve several different pathogenetic mechanisms. The most common causes are connective tissue defects that weaken the supporting aortic and valvular structures (e.g., Marfan syndrome, Ehlers-Danlos syndrome) and inflammatory diseases of the heart and/or aorta (e.g., endocarditis, syphilitic aortitis).
4-14 Schematic of mitral stenosis illustrating some of the pathologic anatomic and hemodynamic changes that may occur. Ao, Aorta; AV, aortic valve; IVC, inferior vena cava; LA, left atrium; LV, left ventricle; LVH, left ventricular hypertrophy; MV, mitral valve; PA, pulmonary artery; PH, pulmonary hypertension; PV, pulmonary valve; RA, right atrium; RV, right ventricle; RVH, right ventricular hypertrophy; SVC, superior vena cava; TV, tricuspid valve.
(From Goljan EF: Rapid Review Pathology, 3rd ed. Philadelphia: Mosby; 2010, Fig. 10-14.)
Pathology note: Rheumatic fever remains the most common cause of mitral stenosis. Symptoms of mitral stenosis (dyspnea, exercise intolerance) usually develop about 20 years after an acute episode of rheumatic fever.
(A, From Damjanov I: Pathophysiology. Philadelphia: Saunders; 2008, Fig. 4-55; B, from Talley N, O’Connor S: Clinical Examination, 5th ed. Philadelphia: Elsevier; 2006, Fig. 3-40.)