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SECTION II
Cardiovascular Disease
2 Structure and Function of the Normal
Heart and Blood Vessels, 4
3 Evaluation of the Patient With Cardio-
vascular Disease, 10
4 Diagnostic Tests and Procedures in the
Patient With Cardiovascular Disease, 24
5 Heart Failure and Cardiomyopathy, 43
6 Congenital Heart Disease, 55
7 Valvular Heart Disease, 64
8 Coronary Heart Disease, 77
9 Cardiac Arrhythmias, 99
10 Pericardial and Myocardial Disease, 123
11 Other Cardiac Topics, 131
12 Vascular Diseases and Hypertension, 139
3
2
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Structure and Function of the Normal
Heart and Blood Vessels
Nicole L. Lohr, Ivor J. Benjamin
DEFINITION
The circulatory system comprises the heart, which is connected in
series to the arterial and venous vascular networks. These vascular networks are arranged in parallel and connect at the level of the capillaries
(Fig. 2.1). The heart is composed of two atria, which are low-pressure
capacitance chambers that function to store blood during ventricular
contraction (systole) and then fill the ventricles with blood during
ventricular relaxation (diastole). The two ventricles are high-pressure
chambers responsible for pumping blood through the lungs (right
ventricle) and to the peripheral tissues (left ventricle). The left ventricle is thicker than the right, in order to generate the higher systemic
pressures required for perfusion.
There are four cardiac valves that facilitate unidirectional blood
flow through the heart. Each of the four valves is surrounded by a
fibrous ring, or annulus, that forms part of the structural support of
the heart. Atrioventricular (AV) valves separate the atria and ventricles. The mitral valve is a bileaflet valve that separates the left atrium
and left ventricle. The tricuspid valve is a trileaflet valve that separates
the right atrium and right ventricle. Thin, fibrous connective tissue
(chordae tendineae) attaches the ventricular aspects of these valves to
the papillary muscles of their respective ventricles for proper opening
of the valves. Additional valves include the aortic valve that separates
the left ventricle from the aorta, and the pulmonic valve that separates
the right ventricle from the pulmonary artery.
A thin, double-layered membrane called the pericardium surrounds the heart. The inner, or visceral, layer adheres to the outer
surface of the heart, also known as the epicardium. The outer layer
is the parietal pericardium, which attaches to the sternum, vertebral
column, and diaphragm to stabilize the heart in the chest. Between
these two membranes is a pericardial space filled with a small amount
of fluid (<50 mL). This fluid serves to lubricate contact surfaces and
limit direct tissue-surface contact during myocardial contraction. A
normal pericardium exerts minimal external pressure on the heart,
thereby facilitating normal movement of the interventricular septum
during the cardiac cycle. Too much fluid in this space (i.e., pericardial effusion) can cause impaired ventricular filling and abnormal septal movement. (Please refer to Chapter 68, “Pericardial Diseases,” in
Goldman-Cecil Medicine, 26th Edition).
CIRCULATORY PATHWAY
The purpose of the circulatory system is to bring deoxygenated blood,
carbon dioxide, and other waste products from the tissues to the lungs
for disposal and reoxygenation (see Fig. 2.1A). Deoxygenated blood
drains from peripheral tissues through venules and veins, eventually
entering the right atrium through the superior and inferior venae cavae
during ventricular systole. Venous drainage from the heart enters the
right atrium through the coronary sinus. During ventricular diastole,
the blood in the right atrium flows across the tricuspid valve and into
the right ventricle. Blood in the right ventricle is ejected across the
pulmonic valve and into the main pulmonary artery, which bifurcates
into the left and right pulmonary arteries and perfuses the lungs. After
multiple bifurcations, blood reaches the pulmonary capillaries, where
carbon dioxide is exchanged for oxygen across the alveolar-capillary
membrane. Oxygenated blood then enters the left atrium from the
lungs via the four pulmonary veins. Blood flows across the open mitral
valve and into the left ventricle during diastole and is ejected across
the aortic valve and into the aorta during systole. The blood reaches
various organs, where oxygen and nutrients are exchanged for carbon
dioxide and metabolic wastes, and the cycle begins again.
The heart receives its blood supply through the left and right coronary arteries, which originate in outpouchings of the aortic root called
the sinuses of Valsalva. The left main coronary artery is a short vessel that bifurcates into the left anterior descending (LAD) and the left
circumflex (LCx) coronary arteries. The LAD supplies blood to the
anterior and anterolateral left ventricle through diagonal branches
and to the anterior interventricular septum through septal perforator
branches. The LAD travels anteriorly in the anterior interventricular
groove and terminates at the cardiac apex. The LCx traverses posteriorly in the left AV groove (between left atrium and left ventricle) to
perfuse the lateral aspect of the left ventricle (through obtuse marginal
branches) and the left atrium. The right coronary artery (RCA) courses
down the right AV groove to the crux of the heart, the point at which
the left and right AV grooves and the inferior interventricular groove
meet. The RCA gives off branches to the right atrium and acute marginal branches to the right ventricle.
The blood supply to the diaphragmatic and posterior aspects of the
left ventricle varies. In 85% of individuals, the RCA bifurcates at the
crux to form the posterior descending coronary artery (PDA), which
travels in the inferior interventricular groove to supply the inferior
left ventricle and the inferior third of the interventricular septum, and
the posterior left ventricular (PLV) branches. This course is termed a
right-dominant circulation. In 10% of individuals, the RCA terminates
before reaching the crux, and the LCx supplies the PLV and PDA. This
course is termed a left-dominant circulation. In the remaining individuals, the RCA gives rise to the PDA and the LCx gives rise to the PLV
in a co-dominant circulation.
CONDUCTION SYSTEM
The sinoatrial (SA) node is a collection of specialized pacemaker cells,
1 to 2 cm long, located in the right atrium between the superior vena
cava and the right atrial appendage (see Fig. 2.1B). The SA node is supplied by the SA nodal artery, which is a branch of the RCA in about
60% of the population and a branch of the LCx in about 40%. An
4
CHAPTER 2 Structure and Function of the Normal Heart and Blood Vessels
A
B
Sinoatrial node
Atrioventricular
bundle branch
branch
bundle branch
5
Head, upper extremities
Superior
vena cava
Pulmonary
artery
Coronary
circulation
Ostium
of coronary
sinus
Right atrium
Right ventricle
Inferior
vena cava
“Capacitance”
function of the
venous system
Venous valves
“Resistance” function
of the arterial system
node
Right bundle
branch
Fig. 2.1 (A) Schematic representation of the systemic and pulmonary cir-
culatory systems. The venous system contains the greatest amount of
blood at any one time and is highly distensible, accommodating a wide
range of blood volumes (high capacitance). The arterial system is composed of the aorta, arteries, and arterioles. Arterioles are small muscular
arteries that regulate blood pressure by changing tone (resistance). (B) A
schematic representation of the cardiac conduction system.
electrical impulse originates in the SA and is conducted to the AV node
by internodal tracts within the atria.
Pulmonary
circulation
Abdominal
Lower extremities
Purkinje fibers
Bronchial
arteries
Aorta
Left
atrium
Left
ventricle
viscera
Aorta
Bundle of His
Main left
Anterior
fascicle of left
Posterior fascicle
of left bundle
The AV node is a critical electrical interface between the atria
and ventricles, because it facilitates electromechanical coupling. The
AV node is located at the inferior aspect of the right atrium, between
the coronary sinus and the septal leaflet of the tricuspid valve. The
AV node is supplied by the AV nodal artery, which is a branch of
the RCA in about 90% of the population and a branch of the LCx in
10%. Electrical impulse conduction slows through the AV node and
continues to the ventricles by means of the His-Purkinje system. The
increased impulse time through the AV node allows for adequate ventricular filling.
The bundle of His extends from the AV node down the membranous interventricular septum to the muscular septum, where it
divides into the left and right bundle branches, finally terminating
in Purkinje cells, which are specialized cells that facilitate the rapid
propagation of electrical impulses. The Purkinje cells directly stimulate myocytes to contract. The right bundle and the left bundle are
supplied by septal perforator branches from the LAD. The distal
and posterior portion of the left bundle has an additional blood
supply from the AV nodal artery (PDA origin); for that reason, it
is more resistant to ischemia. Conduction can be impaired at any
point, from ischemia, medications (e.g., β-blockers, calcium channel blockers), infection, or congenital abnormalities. (Please refer
to Chapter 55, “Principles of Electrophysiology,” in Goldman-Cecil
Medicine, 26th Edition.)
NEURAL INNERVATION
The autonomic nervous system is an integral component in the regulation of cardiac function. In general, sympathetic stimulation increases
the heart rate (HR) (chronotropy) and the force of myocardial contraction (inotropy). Sympathetic stimulation commences in preganglionic neurons located within the superior five or six thoracic segments
of the spinal cord. They synapse with second-order neurons in the
cervical sympathetic ganglia and then propagate the signal through
cardiac nerves that innervate the SA node, AV node, epicardial vessels,
and myocardium. The parasympathetic system produces an opposite
physiologic effect by decreasing HR and contractility. Its neural supply
originates in preganglionic neurons within the dorsal motor nucleus
of the medulla oblongata, which reach the heart through the vagus
nerve. These efferent neural fibers synapse with second-order neurons
located in ganglia within the heart that terminate in the SA node, AV
node, epicardial vessels, and myocardium to decrease HR and contractility. Conversely, afferent vagal fibers from the inferior and posterior
aspects of the ventricles, the aortic arch, and the carotid sinus conduct
sensory information back to the medulla, which mediates important
cardiac reflexes.
MYOCARDIAL STRUCTURE
The proper cellular organization of cardiac tissue (myocardium)
is critical for the generation of efficient myocardial contraction.
Disruptions in this structure and organization lead to cardiac dyssynchrony and arrhythmias, which cause significant morbidity and
mortality. Atrial and ventricular myocytes are specialized, branching
muscle cells that are connected end to end by intercalated disks. These
disks aid in the transmission of mechanical tension between cells. The
myocyte plasma membrane, or sarcolemma, facilitates excitation and
contraction through small transverse tubules (T tubules). Subcellular
features specific for myocytes include increased mitochondria number
for production of adenosine triphosphate (ATP); an extensive network
of intracellular tubules, called the sarcoplasmic reticulum, for calcium
storage; and sarcomeres, which are myofibrils comprised of repeating
units of overlapping thin actin filaments and thick myosin filaments
and their regulatory proteins troponin and tropomyosin. Specialized
myocardial cells form the cardiac conduction system (described earlier) and are responsible for the generation of an electrical impulse and
6 SECTION II Cardiovascular Disease
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Depolarization Repolarization
+
2+
-Ca
Na
exchange pump
Ca
Ca
2+
-ATPase
2+
Ca
2+
SR
2+
Ca
+
Na
Ca2+ storageCa2+ release
T tubule
2+
Ca
Myosin
M
ATP
Fig. 2.2 Calcium dependence of myocardial contraction. (1) Electrical depolarization of the myocyte results
in an influx of Ca2+ ions into the cell through channels in the T tubules. (2) This initial phase of calcium entry
stimulates the release of large amounts of Ca2+ from the sarcoplasmic reticulum (SR). (3) The Ca2+ then binds
to the troponin-tropomyosin complex on the actin filaments, resulting in a conformational change that facilitates the binding interaction between actin and myosin. In the presence of adenosine triphosphate (ATP), the
actin-myosin association is cyclically dissociated as the thick and thin filaments slide past each other, resulting in contraction. (4) During repolarization, the Ca2+ is actively pumped out of the cytosol and sequestered
in the SR. ATPase, Adenosine triphosphatase; M, mitochondrion.
Actin
Ca
2+
SR Ca
ATPase
M
2+
+
Na
ATP
organized propagation of that impulse to cardiac myocytes, which, in
turn, respond by mechanical contraction.
is derived from ATP. During contraction, ATP promotes dissociation
of myosin from actin, thereby permitting the sliding of thick filaments
past thin filaments as the sarcomere shortens.
MUSCLE PHYSIOLOGY AND CONTRACTION
Calcium-induced calcium release is the primary mechanism for myocyte contraction. When a depolarizing stimulus reaches the myocyte,
it enters special invaginations within the sarcolemma called T tubules.
These specialized channels open in response to depolarization, permitting calcium flux into the cell (Fig. 2.2). The sarcoplasmic reticulum closely proximates the T tubules, and the initial calcium current
triggers the release of large amounts of calcium from the sarcoplasmic reticulum into the cell cytosol. Calcium then binds to the calcium-binding regulatory subunit, troponin C, on the actin filaments
The force of myocyte contraction is regulated by the amount of free
calcium released into the cell by the sarcoplasmic reticulum. More calcium allows for more frequent actin-myosin interactions, producing
a stronger contraction. On repolarization of the sarcolemmal membrane, intracellular calcium is rapidly and actively resequestered into
the sarcoplasmic reticulum, where it is stored by various proteins,
including calsequestrin, until the next wave of depolarization occurs.
Calcium is also extruded from the cytosol by various calcium pumps
in the sarcolemma. The active removal of intracellular calcium by ATP
ion pumps facilitates ventricular relaxation, which is necessary for
proper ventricular filling during diastole.
of the sarcomere, resulting in a conformational change in the troponin-tropomyosin complex. The myosin binding site on actin is now
exposed, to facilitate binding of actin-myosin cross-bridges, which are
necessary for cellular contraction. The energy for myocyte contraction
Circulatory Physiology and the Cardiac Cycle
The term cardiac cycle describes the pressure changes within each cardiac chamber over time (Fig. 2.3). This cycle is divided into systole,
CHAPTER 2 Structure and Function of the Normal Heart and Blood Vessels
CO = SV ×HR
Time (sec)
Pressure (mm Hg)
7
120
100
Fig. 2.3 Simultaneous electrocardiogram (ECG) and pressure tracings
obtained from the left atrium (LA), left ventricle (LV), and aorta and the
jugular venous pressure during the cardiac cycle. (For simplification,
pressures on the right side of the heart have been omitted. Normal
right atrial (RA) pressure closely parallels that of the LA, and right ventricular and pulmonary artery pressures are timed closely with their
corresponding left-sided counterparts; they are reduced only in magnitude. Normally, closure of the mitral and aortic valves precedes closure
of the tricuspid and pulmonic valves, whereas valve opening reverses
this order. The jugular venous pulse lags behind the RA pulse.) During
the course of one cardiac cycle, the electrical (ECG) events initiate and
therefore precede the mechanical (pressure) events, and the latter precede the auscultatory events (heart sounds) that they themselves produce (red boxes). Shortly after the P wave, the atria contract to produce
the a wave. The QRS complex initiates ventricular systole, followed
shortly by LV contraction and the rapid buildup of LV pressure. Almost
immediately, LV pressure exceeds LA pressure, closing the mitral valve
and producing the first heart sound. After a brief period of isovolumic
contraction, LV pressure exceeds aortic pressure and the aortic valve
opens (AVO). When the ventricular pressure once again falls to less than
the aortic pressure, the aortic valve closes to produce the second heart
sound and terminate ventricular ejection. The LV pressure decreases
during the period of isovolumic relaxation until it drops below LA pressure and the mitral valve opens (MVO). See text for further details.
the period of ventricular contraction, and diastole, the period of ventricular relaxation. Each cardiac valve opens and closes in response
to pressure gradients generated during these periods. At the onset of
systole, ventricular pressures exceed atrial pressures, so the AV valves
passively close. As myocytes contract, the intraventricular pressures
rise initially, without a change in ventricular volume (isovolumic
Systole Diastole
80
60
40
20
Aorta
Left
ventricle
LA
a
LV
0
Jugular
pulse
a
ECG
0.0 0.1 0.2 0.3 0.4 0.5 0.6 0.7
P
Q
R
Isovolumic
contraction
AVO
MVO
v
y
c
x
Heart
3421
sounds
c
S
x
T
Isovolumic
relaxation
v
y
contraction), until they exceed the pressures in the aorta and pulmonary artery. At this point, the semilunar valves open, and ventricular
ejection of blood occurs. When intracellular calcium levels fall, ventricular relaxation begins; arterial pressures exceed intraventricular
pressures, so the semilunar valves close. Ventricular relaxation initially
does not change ventricular volume (isovolumic relaxation). At the
point at which intraventricular pressures fall below atrial pressures, the
AV valves open. This begins the rapid and passive ventricular filling
phase of diastole, during which blood in the atria empties into the ventricles. At the end of diastole, active atrial contraction augments ventricular filling. When the myocardium exhibits increased stiffness due
to age, hypertension, diabetes, or heart failure, the early passive phase
of ventricular filling is decreased. To compensate for the reduction in
passive ventricular filling, there is reliance on atrial contraction to sufficiently fill the ventricle during diastole. A pathologic consequence of
atrial fibrillation, a disease in which the atrium does not contract, is
that patients often have worse symptoms because this additional ventricular filling is lost.
Pressure tracings obtained from the periphery complement the
hemodynamic changes exhibited in the heart. In the absence of valvular disease, there is no impediment to blood flow moving from the ventricles to the arterial beds, so the systolic arterial pressure rises sharply
to a peak. During diastole, no further blood volume is ejected into the
aorta, so the arterial pressure gradually falls as blood flows to the distal
tissue beds and elastic recoil of the arteries occurs.
Atrial pressure can be directly measured in the right atrium, but
the left atrial pressure is indirectly measured by occluding a small pulmonary artery branch and measuring the pressure distally (the pulmonary capillary wedge pressure). An atrial pressure tracing is shown in
Fig. 2.3. It is composed of several waves. The a wave represents atrial
contraction. As the atria subsequently relax, the atrial pressure falls,
and the x descent is seen on the pressure tracing. The x descent is interrupted by a small c wave, generated as the AV valve bulges toward the
atrium during ventricular systole. As the atria fill from venous return,
the v wave is seen, after which the y descent appears as the AV valves
open and blood from the atria empties into the ventricles. The normal ranges of pressures in the various cardiac chambers are shown in
Table 2.1.
Cardiac Performance
The amount of blood ejected by the heart each minute is referred to as
the cardiac output (CO). It is the product of the stroke volume (SV),
which is the amount of blood ejected with each ventricular contraction, and the HR:
The cardiac index is a way of normalizing the CO to body size. It is the
CO divided by the body surface area and is measured in L/min/m2. The
normal CO is 4 to 6 L/min at rest and can increase fourfold to sixfold
during strenuous exercise.
The main determinants of SV are preload, afterload, and contractility (Table 2.2). Preload is the volume of blood in the ventricle at the
end of diastole; it is primarily a reflection of venous return. Venous
return is determined by the plasma volume and the venous compliance. Clinically, intravenous fluids increase preload, whereas diuretics
or venodilators such as nitroglycerin decrease preload. When the preload is increased, the ventricle stretches, and the ensuing ventricular
contraction becomes more rapid and forceful, because the increased
sarcomere length facilitates actin and myosin cross-bridge kinetics
by means of an increased sensitivity of troponin C to calcium. This
phenomenon is known as the Frank-Starling relationship. Ventricular
filling pressure (ventricular end-diastolic pressure, atrial pressure, or
8 SECTION II Cardiovascular Disease
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TABLE 2.1 Normal Values for Common
Hemodynamic Parameters
Heart rate 60-100 beats/min
Pressures (mm Hg)
Central venous ≤9
Right atrial ≤9
Right ventricular
Systolic 15-30
End-diastolic ≤9
Pulmonary arterial
Systolic 15-30
Diastolic 3-12
Pulmonary capillary wedge ≤12
Left atrial ≤12
Left ventricular
Systolic 100-140
End-diastolic 3-12
Aortic
Systolic 100-140
Diastolic 60-90
Resistance
Systemic vascular resistance 800-1500 dynes-sec/cm
Pulmonary vascular resistance 30-120 dynes-sec/cm
Cardiac output 4-6 L/min
Cardiac index 2.5-4 L/min
−5
−5
pulmonary capillary wedge pressure) is frequently used as a surrogate
measure of preload.
Afterload is the force against which the ventricles must contract to
eject blood. The main determinants of afterload are the arterial pressure and the dimensions of the left ventricle. As the arterial blood pressure increases, the amount of blood that can be ejected into the aorta
decreases. Wall stress, a significant and often overlooked determinant
of afterload, is directly proportional to the size of the ventricular cavity
and inversely proportional to the ventricular wall thickness (Laplace’s
law). Diuretics reduce the increased wall stress associated with pathologic dilatation in cardiomyopathy by decreasing left ventricular
volume and size. In addition, ventricular wall hypertrophy is a compensatory mechanism to reduce afterload caused by systemic hypertension. Drugs that treat hypertension, such as angiotensin-converting
enzyme (ACE) inhibitors and hydralazine, reduce blood pressure (BP)
and thereby reduce afterload.
Contractility, or inotropy, represents the force of ventricular con-
traction in the presence of constant preload and afterload. Inotropy is
regulated at a cellular level through stimulation of catecholaminergic
(epinephrine, norepinephrine, and dopamine) receptors, intracellular
signaling cascades (phosphodiesterase inhibitors), and intracellular
calcium levels (affected by levosimendan and, indirectly, by digoxin).
Many antihypertensive medications (e.g., β-blockers, calcium channel
antagonists) interfere with adrenergic receptor activation or intracellular calcium levels, which can decrease the strength of ventricular
contractions. (Please refer to Chapter 47, “Cardiac and Circulatory
Function,” in Goldman-Cecil Medicine, 26th Edition.)
Physiology of the Coronary Circulation
The normally functioning heart maintains equilibrium between the
amount of oxygen delivered to myocytes and the amount of oxygen
consumed by them (myocardial oxygen consumption, or Mvo2).
If a myocyte works harder because it is contracting with increased
TABLE 2.2 Factors Affecting Cardiac
Performance
Preload (Left Ventricular Diastolic Volume)
Total blood volume
Venous (sympathetic) tone
Body position
Intrathoracic and intrapericardial pressures
Atrial contraction
Pumping action of skeletal muscle
Afterload (Impedance Against Which the Left Ventricle
Must Eject Blood)
Peripheral vascular resistance
Left ventricular volume (preload, wall tension)
Physical characteristics of the arterial tree (elasticity of vessels or presence
of outflow obstruction)
Contractility (Cardiac Performance Independent of Preload
or Afterload)
Sympathetic nerve impulses
Increased contractility
Circulating catecholamines
Digitalis, calcium, other inotropic agents
Increased heart rate or post-extrasystolic augmentation
Anoxia, acidosis
Decreased contractility
Pharmacologic depression
Loss of myocardium
Intrinsic depression
Heart Rate
Autonomic nervous system
Temperature, metabolic rate
Medications, drugs
frequency (HR), with increased intensity (contractility), or against an
increased load (wall stress), then it will use more oxygen and its Mvo2
will increase. In order to meet this increase in demand for more oxygen, the heart will have to either increase blood flow or increase its
efficiency in extracting oxygen. The heart is unique in that its oxygen
extraction is almost maximal at resting conditions. Therefore, increasing blood flow is the only reasonable means of increasing oxygen
supply.
Microvascular blood flow in the coronary circulation is impaired
during systole because the intramyocardial blood vessels are compressed by contracting myocardium. Therefore, most coronary flow
occurs during diastole. Accordingly, the diastolic pressure is the
major pressure driving flow within the coronary circulation. Systolic
pressure impedes intramyocardial arterial blood flow but augments
venous flow. On a clinical note, tachycardia is particularly detrimental because coronary flow is reduced when the diastolic filling time is
abbreviated, and the Mvo2 increases with increasing HR. In order to
sustain constant perfusion to the myocardium, coronary blood flow is
maintained constant over a wide range of pressures in a process called
autoregulation.
In response to a change in Mvo2, the coronary arteries dilate or
constrict, which changes the vascular resistance and thereby appropriately changes flow. This regulation of arterial resistance occurs at the
arterioles and is mediated by several factors. Adenosine, a metabolite
of ATP, is released during contraction and acts as a potent vasodilator.
CHAPTER 2 Structure and Function of the Normal Heart and Blood Vessels
R =8ηL /
πr
4
F =ΔP/R = ΔPπr4/8 ηL
9
Other consequences of myocardial metabolism, such as decreased oxygen tension, increased carbon dioxide, hydrogen peroxide, acidosis,
and hyperkalemia, also mediate coronary vasodilation. The endothelium produces several potent vasodilators, including nitric oxide and
prostacyclin. Nitric oxide is released by the endothelium in response
to acetylcholine, thrombin, adenosine diphosphate (ADP), serotonin,
bradykinin, platelet aggregation, and an increase in shear stress (called
flow-dependent vasodilation). Finally, the coronary arteries are innervated by the autonomic nervous system, and activation of sympathetic
neurons mediates vasoconstriction or vasodilation through α- or β-re-
ceptors, respectively. Parasympathetic neurons from the vagus nerve
secrete acetylcholine, which mediates vasodilation. Vasoconstricting
factors, notably endothelin, are produced by the endothelium and may
be important in conditions such as coronary vasospasm. (Please refer
to Chapter 47, “Cardiac and Circulatory Function,” in Goldman-Cecil
Medicine, 26th Edition.)
Physiology of the Systemic Circulation
The normal cardiovascular system delivers appropriate blood flow to
each organ of the body under a wide range of conditions. This regulation is achieved by maintaining BP through adjustments in cardiac
output and tissue blood flow resistance by neural and humoral factors.
Poiseuille’s law generally describes the relationship between pressure and flow in a vessel. Fluid flow (F) through a tube is proportional
(proportionality constant = K) to the pressure (P) difference between
the ends of the tube:
K is equivalent to the inverse of resistance to flow (R); that is, K = 1/R.
Resistance to flow is determined by the properties of both the fluid
and the tube. In the case of a steady, streamlined flow of fluid through
a rigid tube, Poiseuille found that these factors determine resistance:
Where r is the radius of the tube, L is its length, and η is the viscosity
of the fluid. Notice that changes in radius have greater influence than
changes in length, because resistance is inversely proportional to the
fourth power of the radius. Poiseuille’s law incorporates the factors
influencing flow, so that:
Therefore, the most important determinants of blood flow in the cardiovascular system are ΔP and r4. Small changes in arterial radius can
cause large changes in flow to a tissue or organ. Practically, systemic
vascular resistance (SVR) is the total resistance to flow caused by
changes in the radius of resistance vessels (small arteries and arterioles)
of the systemic circulation. The SVR can be calculated as the pressure
drop across the peripheral capillary beds (mean arterial pressure − right
atrial pressure) divided by the blood flow across the beds (i.e., SVR =
BP/CO). It is normally in the range of 800 to 1500 dynes-sec/cm−5.
The autonomic nervous system alters systemic vascular tone
through sympathetic and parasympathetic innervation as well as metabolic factors (local oxygen tension, carbon dioxide levels, reactive oxygen species, pH) and endothelium-derived signaling molecules (NO,
endothelin). Neural regulation of BP occurs by means of constitutive
and reflex changes in autonomic efferent outflow to modulate cardiac
chronotropy, inotropy, and vascular resistance.
The baroreflex loop is the primary mechanism by which BP is neurally modulated. Baroreceptors are stretch-sensitive nerve endings that
are distributed throughout various regions of the cardiovascular system. Those located in the carotid artery (e.g., carotid sinus) and aorta
are sometimes referred to as high-pressure baroreceptors and those in
the cardiopulmonary areas as low-pressure baroreceptors. After afferent
impulses are transmitted to the central nervous system, the signals are
integrated, and the efferent arm of the reflex projects neural signals
systemically through the sympathetic and parasympathetic branches
of the autonomic nervous system. In general, an increase in systemic
BP increases the firing rate of the baroreceptors. Efferent sympathetic
outflow is inhibited (reducing vascular tone, chronotropy, and inotropy), and parasympathetic outflow is increased (reducing cardiac
chronotropy). The opposite occurs when BP decreases. (Please refer
to Chapter 47, “Cardiac and Circulatory Function,” in Goldman-Cecil
Medicine, 26th Edition.)
Physiology of the Pulmonary Circulation
Like the systemic circulation, the pulmonary circulation consists of a
branching network of progressively smaller arteries, arterioles, capillaries, and veins. The pulmonary capillaries are separated from the alveoli
by a thin alveolar-capillary membrane through which gas exchange
occurs. The partial pressure of oxygen (Po2) is the main regulator of
pulmonary blood to optimize blood flow toward well-ventilated lung
segments and away from poorly ventilated segments.
SUGGESTED READINGS
Berne RM, Levy MN: Physiology: part IV. The cardiovascular system, ed 7, St.
Louis, 2017, Elsevier.
Guyton AC, Hall JE: Textbook of medical physiology, ed 13, St. Louis, 2015,
Elsevier.
3
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Evaluation of the Patient With
Cardiovascular Disease
James Kleczka, Noura M. Dabbouseh
DEFINITION AND EPIDEMIOLOGY
Cardiovascular disease is a major cause of morbidity and mortality around the world, and its spectrum is wide-reaching. Included in
this population of patients are people with coronary artery disease
(CAD), congestive heart failure, stroke, hypertension, peripheral arterial disease, atrial fibrillation and other arrhythmias, valvular disease,
and congenital heart disease. The impact of cardiovascular disease is
unmistakable: It is the leading cause of death in both males and females
in the United States, with reports estimating that heart disease accounts
for between one in three and one in four deaths. It accounted for more
inpatient hospital days in the years of 1990-2009 than other disorders
such as chronic lung disease and cancer. The high number of inpatient
days associated with cardiovascular disease led to a total economic cost
of more than $297 billion in the year 2008 alone. In 2011, an estimated
$316.6 billion in health care costs and lost productivity was attributable to heart disease and stroke.
Given these facts, the proper evaluation of a patient with cardiovascular disease is imperative in order to potentially decrease an individual’s morbidity and mortality and potentially impact health care
expenditures. An understanding of the basics of the pathophysiology
of heart disease as well as a thorough history and detailed physical
examination are required to accurately assess and manage patients
with cardiovascular disease.
PATHOLOGY
The term cardiovascular disease encompasses a wide array of patient
problems. The heart’s circulation, myocardium, rhythm, valves, and
pericardial structures may be affected, as can the arterial or venous
vascular systems. Coronary artery disease (CAD), discussed in depth in
Chapter 8, is a leading cause of morbidity and mortality. While many
patients do have silent CAD or asymptomatic coronary atherosclerosis, this still impacts patient morbidity. At presentation, patients with
symptomatic CAD may have stable angina or an acute coronary syndrome, further stratified into unstable angina (UA), non–ST segment
elevation myocardial infarction (NSTEMI), or ST segment elevation
myocardial infarction (STEMI). The initial presentation for some
patients with CAD is sudden cardiac death, the result of arrhythmia
often caused by atherosclerosis of the coronary vasculature.
Congestive heart failure is the end result of many cardiac disorders
and has been historically classified as systolic or diastolic in etiology.
More recently, the terms heart failure with reduced ejection fraction
(HFrEF) and heart failure with preserved ejection fraction (HFpEF),
which is often due to diastolic dysfunction, have gained widespread
acceptance. In patients with ventricular enlargement or systolic dysfunction, the term cardiomyopathy is appropriate whether or not a patient
has clinically demonstrated signs of heart failure. Various forms of
cardiomyopathy may lead to systolic dysfunction and a decline in ejection fraction. Without proper management, this will inevitably lead to
alterations in hemodynamics that result in development of pulmonary
vascular congestion, edema, and a decline in functional capacity, all
symptoms of clinical heart failure. Diastolic dysfunction can be present
with systolic dysfunction and is often the result of uncontrolled hypertension or infiltrative disorders such as hemochromatosis or amyloidosis. Various forms of heart failure are further discussed in Chapter 5.
Stroke is caused by cerebral hypoperfusion, which can result from
such problems as carotid disease, thromboembolism, or emboli
of infectious origin. A more detailed discussion can be found in
Chapter 118.
Peripheral arterial disease (PAD), addressed in Chapter 12, includes
such entities as aneurysms of the ascending, descending, and abdominal aorta and its branches; aortic or peripheral arterial dissection;
carotid disease; and atherosclerosis of branch vessels of the aorta and
vessels in the limbs. PAD is often present in patients with CAD.
Atrial fibrillation and hypertension (see Chapter 9) are not
uncommon and increase in prevalence with age. Although they are
not typically the primary cause of mortality, these problems often
predispose to other causes of cardiovascular disease mortality, such
as stroke and heart failure. Arrhythmias other than atrial fibrillation are also common and can lead to significant morbidity and
mortality.
Valvular heart disease may lead to cardiomyopathy and is found in
all age groups.
Congenital heart disease includes a wide variety of disorders, ranging
from valve abnormalities and coronary anomalies to cardiomyopathy
and other structural abnormalities including shunts and malformations of the cardiac chambers. With advances in surgical techniques
and medical therapy, life expectancy has improved significantly for
patients with congenital heart disease. Congenital heart disease is discussed further in Chapter 6.
CLINICAL PRESENTATION
Technologic advancements have allowed for specialized testing to assist
in the diagnosis of cardiovascular diseases. We now rely on such tests
as angiography, ultrasound scanning, and advanced imaging modalities such as high-resolution computed tomography and magnetic
resonance imaging to determine how to manage an individual case.
However, these techniques should be used not as a primary method of
assessment but rather to supplement the findings from a thorough history and physical examination. Despite the availability of rather costly
imaging techniques and laboratory tests, a relatively inexpensive but
detailed history and physical examination is a clinician’s strongest tool
in helping to establish a diagnosis.
10
CHAPTER 3 Evaluation of the Patient With Cardiovascular Disease
TABLE 3.1 Cardiovascular Causes of Chest Pain
11
Condition Location Quality Duration
Angina Retrosternal region: radi-
ates to or occasionally
isolated to neck, jaw,
shoulders, arms (usually
left), or epigastrium
Myocardial infarction Same as angina Same as angina, although
Pericarditis Left of the sternum; may
radiate to neck or left
shoulder, often more
localized than pain of
myocardial ischemia
Aortic dissection Anterior chest; may radi-
ate to back, interscapular region
A patient who is given the opportunity to outline his or her symptoms in his or her own words can help lead a clinician toward the right
diagnosis. For example, many patients who deny chest pain when
asked specifically about this symptom will go on to describe the symptom of chest pressure, which patients often feel is distinct from “pain.”
Gathering further historical details such as provoking factors (e.g.,
activity, extreme emotional stress, or rest or unprovoked symptoms),
Pressure, squeezing,
tightness, heaviness,
burning, indigestion
more severe
Sharp, stabbing, knifelike Lasts many hours to days;
Excruciating, tearing,
knifelike
<2-10 min Precipitated by exertion,
Variable; usually >30 min Unrelieved by rest or
may wax and wane
Sudden onset, unrelenting Usually occurs in setting
disease such as pneumonia, gastrointestinal pathology such as gastroesophageal reflux, or musculoskeletal pain related to chest wall trauma.
Issues with organs in the abdominal cavity such as the gallbladder or
pancreas can also cause chest pain. It is therefore very important to
characterize the pain in terms of location, quality, quantity, duration,
radiation, aggravating and alleviating factors, and associated symp-
toms. These details will help determine the origin of the pain.
location, quality, intensity, and radiation of the symptom is imperative
when taking a thorough history. One should delve into aggravating or
alleviating factors and whether there are other symptoms that accompany the primary symptom. It is also important to note the pattern of
the symptom in terms of stability or progression in intensity or frequency over time. An assessment of functional status should always be
a part of the history in a patient with cardiovascular disease; a recent
decline in exercise tolerance can help determine severity of disease.
A detailed past medical history and review of systems are necessary
in order to understand if the cardiovascular condition is isolated or
part of a syndrome. For example, a patient may have arrhythmias in
the setting of hyperthyroidism. Rheumatologic disorders often affect
the heart. And cancer can increase the risk of thromboembolism, of
pericardial effusion and, with some therapies, cardiomyopathy. A
comprehensive list of medications must be reviewed, and a social history must be taken detailing alcohol use, smoking, and occupational
history. Patients should also be questioned regarding major risk factors such as hypertension, hyperlipidemia, and diabetes mellitus. A
thorough family history is needed, not only to identify such entities as
early-onset CAD but also to assess for other potentially inherited disorders, such as familial cardiomyopathy or arrhythmic disorders (e.g.,
long-QT syndrome).
cal angina pectoris. Angina is often described as tightness, pressure,
burning, or squeezing discomfort that patients may not identify
as true pain. Patients frequently describe angina as a sensation of
“bricks on the center of the chest” or an “elephant standing on the
chest.” Angina is more common in the morning, and the intensity
may be affected by heat or cold, emotional stress, or eating. This discomfort is typically located in the substernal region or left side of the
chest. Anginal pain may radiate to other parts of the body, such as
the left shoulder and arm (particularly the ulnar aspect), the neck,
the jaw, or the epigastrium. Pain that radiates to the back may raise
suspicion for aortic dissection. Anginal chest pain is usually brought
on with exertion, in particular with more intense activity or walking
up inclines, in extremes of weather, or after large meals. It is typically
brief in duration, lasting 2 to 10 minutes, and frequently resolves
with rest or administration of nitroglycerine within 1 to 5 minutes.
Associated symptoms often include nausea, diaphoresis, dyspnea,
palpitations, and dizziness. Patients typically report a stable pattern
of angina that is relatively predictable and reproducible with a given
amount of exertion. When this pain begins to increase in frequency
and severity or occurs with lesser amounts of exertion or at rest, one
must then consider unstable angina. Anginal pain that occurs at rest
with increased intensity and lasts longer than 30 minutes may repre-
Chest Pain
Chest pain is one of the cardinal symptoms of cardiovascular disease,
but it may also be present in many noncardiovascular diseases (Tables
sent acute myocardial infarction (MI). Some patients endorse a feeling of doom when suffering an MI. Angina-like pain at rest may also
occur with coronary vasospasm and noncardiac chest pain.
3.1 and 3.2). Chest pain may be caused by cardiac ischemia but also
may be related to aortic pathology such as dissection, pulmonary
be confused with angina pectoris (see Table 3.2). Pain associated
Aggravating or
Alleviating Factors
cold weather, or emotional stress; relieved
by rest or nitroglycerin;
variant (Prinzmetal)
angina may be unrelated to exertion, often
early in the morning
nitroglycerin
Aggravated by deep
breathing, rotating
chest, or supine position; relieved by sitting
up and leaning forward
of hypertension or
predisposition, such as
Marfan syndrome
Associated
Symptoms or Signs
Dyspnea; S3, S4, or
murmur of papillary
dysfunction during pain
Dyspnea, nausea,
vomiting, weakness,
diaphoresis
Pericardial friction rub
Murmur of aortic insuffi-
ciency; pulse or blood
pressure asymmetry;
neurologic deficit
Myocardial ischemia due to obstructive CAD often leads to typi-
There are several other potential causes of chest pain that may
12 SECTION II Cardiovascular Disease
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TABLE 3.2 Noncardiac Causes of Chest Pain
Condition Location Quality Duration
Pulmonary
embolism (chest
pain often not
present)
Pulmonary
hypertension
Pneumonia with
pleurisy
Spontaneous
pneumothorax
Musculoskeletal
disorders
Herpes zoster Dermatomal
Esophageal reflux Substernal or
Peptic ulcer Epigastric,
Gallbladder
disease
Anxiety states Often localized
Substernal or
over region
of pulmonary
infarction
Substernal Pressure; oppressive — Aggravated by effort Pain usually associated with dyspnea; signs
Located over
involved area
Unilateral Sharp, well localized Sudden onset;
Variable Aching, well localized Variable Aggravated by movement;
distribution
epigastric;
may radiate to
neck
substernal
Right upper
quadrant;
epigastric
over precordium
Pleuritic (with pulmo-
nary infarction) or
angina-like
Pleuritic — Aggravated by breathing Dyspnea, cough, fever, bronchial breath
Sharp, burning Prolonged None Vesicular rash appears in area of discomfort
Burning, visceral
discomfort
Visceral burning,
aching
Visceral Prolonged Spontaneous or after meals Right upper quadrant tenderness may be
Variable; location
often moves from
place to place
Sudden onset
(minutes to
hours)
lasts many
hours
10-60 min Aggravated by large meal,
Prolonged Relief with food, antacid —
Varies; often
fleeting
Aggravating or
Alleviating Factors Associated Symptoms or Signs
Aggravated by deep
breathing
Aggravated by breathing Dyspnea; hyperresonance and decreased
history of exertion or injury
postprandial recumbency;
relief with antacid
Situational Sighing respirations; often chest wall
Dyspnea, tachypnea, tachycardia; hypoten-
sion, signs of acute right ventricular heart
failure, and pulmonary hypertension with
large emboli; pleural rub; hemoptysis
with pulmonary infarction
of pulmonary hypertension
sounds, rhonchi, egophony, dullness to
percussion, occasional pleural rub
breath and voice sounds over involved
lung
Tender to palpation or with light pressure
Water brash
present
tenderness
with acute pericarditis is typically sharp, is located to the left of the
sternum, and radiates to the neck, shoulders, and back. This may
be rather severe pain that is present at rest and can last for hours.
It typically improves with sitting up and forward and worsens with
inspiration. Oftentimes history of causative viral prodrome can be
elicited.
Acute aortic dissection usually causes sudden onset of severe tearing chest pain that radiates to the back between the scapulae or to
the lumbar region. Typically, there is a history of hypertension, and
pulses may be asymmetric between the extremities. A murmur of
aortic regurgitation may also be heard. Pain associated with pulmonary embolism is also acute in onset and is usually accompanied by
shortness of breath. This pain is typically pleuritic, worsening with
inspiration.
Dyspnea
Dyspnea is another hallmark symptom of cardiovascular disease,
but it is also a primary symptom of pulmonary disease. It is defined
as an uncomfortable heightened awareness of breathing. This can be
an entirely normal sensation in individuals performing moderate to
extreme exertion, depending on their level of conditioning. When
it occurs at rest or with minimal exertion, dyspnea is considered
abnormal. Dyspnea may accompany a large number of noncardiac
conditions such as anemia due to a lack of oxygen-carrying capacity,
pulmonary disorders such as obstructive or restrictive lung disease and
asthma, obesity due to an increased work of breathing and restricted
filling of the lungs, and deconditioning. In the cardiovascular patient,
dyspnea may be caused by ventricular dysfunction, either systolic or
diastolic; CAD and resultant ischemia; a large pericardial effusion
causing impaired filling and resulting depressed cardiac output (cardiac tamponade); or valvular heart disease that, when severe, can lead
to a drop in cardiac output. In cases of left ventricular dysfunction and
valvular disease, the mechanism of dyspnea often involves increased
intracardiac pressures that lead to pulmonary vascular congestion.
Fluid then leaks into the alveolar space, impairing gas exchange and
causing dyspnea.
Breathing difficulties can also be secondary to a low-output state
without pulmonary vascular congestion. Patients often notice dyspnea
with exertion, but it can also occur at rest in patients with severe cardiac disease. Shortness of breath at rest is also a symptom in patients
with pulmonary edema, large pleural effusions, anxiety, or pulmonary
embolism. A patient with left ventricular systolic or diastolic failure
may describe the acute onset of breathing difficulty when sleeping.
This problem, called paroxysmal nocturnal dyspnea (PND), is caused
by pulmonary edema that is redistributed in a prone position; it is usually secondary to left ventricular failure. These patients often notice the
acute onset of dyspnea followed by coughing roughly 2 to 4 hours after
going to sleep. This can be a very uncomfortable feeling, and it leads
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