Miller Cardiac Physiology

Question 1

Cardiac output is determined by

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the heart rate, myocardial contractility, and preload and afterload

Question 2

The majority of cardiomyocytes consist of myofibrils, which are rodlike bundles that form the contractile elements within the cardiomyocyte.

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Question 3

basic working unit of contraction is the

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sarcomere

Question 4

Action potentials have four phases in the heart.

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Question 5

key player in cardiac excitation-contraction coupling is the ubiquitous second messenger …

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calcium

Question 6

β-Adrenoreceptors stimulate chronotropy, inotropy, lusitropy, and dromotropy.

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notropy: contraction of myocardium (sometimes refers to contractility)

Lusitropy: relaxation of myocardium

Chronotropy: firing of sinoatrial node (sometimes refers to heart rate)

Dromotropy: conduction velocity of atrioventricular node

Question 7

The basic anatomy of the heart consists of two atria and two ventricles that provide two separate circulations in series.

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Question 8

The pulmonary circulation is a _ and receives output from the ___ and its chief function is __.

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a low-resistance and high-capacitance vascular bed, receives output from the right side of the heart, and its chief function is bidirectional gas exchange

Question 9

The left side of the heart provides output for the __ and it functions to ___ and to remove__ from various tissue beds.

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systemic circulation. It functions to deliver oxygen (O 2 ) and nutrients and to remove carbon dioxide (CO 2 ) and metabolites from various tissue beds.

Question 10

The cardiac cycle is the sequence of electrical and mechanical events during the course of a single heartbeat.

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Question 11

The sinoatrial (SA) node is usually the

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pacemaker; it can generate impulses at the greatest frequency and is the natural pacemaker.

Question 12

As blood accumulates in the atria, atrial pressure increases until it exceeds the pressure within the ventricle, and the AV valve opens. Blood passively flows first into the ventricular chambers, and such flow accounts for approximately 75% of the total ventricular filling. 3 The remainder of the blood flow is mediated by active atrial contraction or systole, known as the atrial kick

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Question 13

The first part of ventricular systole is known as isovolumic or isometric contraction

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Question 14

Ventricular ejection is divided into the rapid ejection phase and the reduced ejection phase. During the rapid ejection phase, forward flow is maximal, and pulmonary artery and aortic pressure is maximally developed. In the reduced ejection phase, flow and great artery pressure taper with progression of systole. Pressure in both ventricular chambers decreases as blood is ejected from the heart, and ventricular diastole begins with closure of the pulmonic and aortic valves. The initial period of ventricular diastole consists of the isovolumic (isometric) relaxation phase. This phase is concomitant with repolarization of the ventricular myocardium and corresponds to the end of the T wave on the ECG. The final portion of ventricular diastole involves a rapid decrease in intraventricular pressure until it decreases to less than that of the right and left atria, at which point the AV valve reopens, ventricular filling occurs, and the cycle repeats itself.

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Question 15

The architecturally complex structure of the LV thus allows maximal shortening of myocytes, which results in increased wall thickness and the generation of force during systole

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Question 16

Regional wall thickness is a commonly used index of myocardial performance that can be clinically assessed, such as by perioperative echocardiography or magnetic resonance imaging.

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Question 17

In contrast to the ellipsoidal form of the LV, the RV is crescent shaped

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Question 18

Systolic performance of the heart is dependent on loading conditions and contractility.

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Question 19

Diastole is ventricular relaxation, and it occurs in four distinct phases: (1) isovolumic relaxation; (2) the rapid filling phase (i.e., the LV chamber filling at variable left ventricular pressure); (3) slow filling, or diastasis; and (4) final filling during atrial systole.

Answer 19

The isovolumic relaxation phase is energy dependent. During the auxotonic relaxation (phases 2 through 4), ventricular filling occurs against pressure. It encompasses a period during which the myocardium is unable to generate force, and filling of the ventricular chambers takes place. The isovolumic relaxation phase does not contribute to ventricular filling. The greatest amount of ventricular filling occurs in the second phase, whereas the third phase adds only approximately 5% of total diastolic volume and the final phase provides 15% of ventricular volume from atrial systole.

Question 20

Whereas systolic dysfunction is a reduced ability of the heart to eject, diastolic dysfunction is a decreased ability of the heart to fill

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Question 21

Many different factors influence diastolic function: magnitude of systolic volume, passive chamber stiffness, elastic recoil of the ventricle, diastolic interaction between the two ventricular chambers, atrial properties, and catecholamines.

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Question 22

Preload is defined as the ventricular load at the end of diastole, before contraction has started.

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left ventricular volume such as pulmonary wedge pressure or central venous pressure are used to estimate preload. 3 With the development of transesophageal echocardiography, a more direct measure of ventricular volume is available.

Question 23

in the heart, an increase in end-diastolic volume is the equivalent of an increase in myocardial stretch; therefore, according to the Frank-Starling law, increased stroke volume is generated.

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Question 24

Afterload is defined as systolic load on the LV after contraction has begun.

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Aortic compliance is an additional determinant of afterload. 1 Aortic compliance is the ability of the aorta to give way to systolic forces from the ventricle. Changes in the aortic wall (dilation or stiffness) can alter aortic compliance and thus afterload. Examples of pathologic conditions that alter afterload are aortic stenosis and chronic hypertension. Both impede ventricular ejection, thereby increasing after load. In clinical practice, the measurement of systolic blood pressure is adequate to approximate afterload, provided that aortic stenosis is not present.

Question 25

Laplace’s law states that wall stress (σ) is the product of pressure (P) and radius (R) divided by wall thickness (h) 3 : σ=P×R/2h

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Question 26

For example, in aortic stenosis, afterload is increased. The ventricle must generate a much higher pressure to overcome the increased load opposing systolic ejection of blood. To generate such high performance, the ventricle increases its wall thickness (left ventricular hypertrophy). By applying Laplace’s law, increased left ventricular wall thickness will decrease wall stress, despite the necessary increase in left ventricular pressure to overcome the aortic stenosis ( Fig. 20-4 ). 10 In a failing heart, the radius of the LV increases, thus increasing wall stress

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Question 27

Each Frank-Starling curve specifies a level of contractility, or the inotropic state of the heart, which is defined as the work performed by cardiac muscle at any given end-diastolic fiber.

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Factors that modify contractility are exercise, adrenergic stimulation, changes in pH, temperature, and drugs such as digitalis. The ability of the LV to develop, generate, and sustain the necessary pressure for the ejection of blood is the intrinsic inotropic state of the heart.

Question 28

Pressure-volume loops, albeit requiring catheterization of the left side of the heart, are currently the best way to determine contractility in an intact heart ( Fig. 20-6 ). 10 The pressure-volume loop represents an indirect measure of the Frank-Starling relationship between force (pressure) and muscle length (volume).

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Question 29

Ejectionfraction=(LVEDV−LVESV)/LVEDV

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Question 30

Cardiac output is the amount of blood pumped by the heart per unit of time ( Q˙ )

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and is determined by four factors: two factors that are intrinsic to the heart—heart rate and myocardial contractility—and two factors that are extrinsic to the heart but functionally couple the heart and the vasculature—preload and afterload.

Question 31

Heart rate is defined as the number of beats per minute and is mainly influenced by the autonomic nervous system. Increases in heart rate escalate cardiac output as long as ventricular filling is adequate during diastole

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Contractility can be defined as the intrinsic level of contractile performance that is independent of loading conditions. Contractility is difficult to define in an intact heart because it cannot be separated from loading conditions. 8 15 For example, the Frank-Starling relationship is defined as the change in intrinsic contractile performance, based on changes in preload

Question 32

The Fick principle is based on the concept of conservation of mass such that the O 2 delivered from pulmonary venous blood (q 3 ) is equal to the total O 2 delivered to pulmonary capillaries through the pulmonary artery (q 1 ) and the alveoli (q 2 )

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Question 33

baroreceptor reflex: The baroreceptor reflex is responsible for the maintenance of arterial blood pressure.

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This reflex is capable of regulating arterial pressure around a preset value through a negative-feedback loop ( Fig. 20-19 ). 75 76 In addition, the baroreceptor reflex is capable of establishing a prevailing set point for arterial blood pressure when the preset value has been reset because of chronic hypertension.

Question 34

Changes in arterial blood pressure are monitored by circumferential and longitudinal stretch receptors located in the carotid sinus and aortic arch. The nucleus solitarius, located in the cardiovascular center of the medulla, receives impulses from these stretch receptors through afferents of the glossopharyngeal and vagus nerves. The cardiovascular center in the medulla consists of two functionally different areas; the area responsible for increasing blood pressure is laterally and rostrally located, whereas the area responsible for lowering arterial blood pressure is centrally and caudally located. The latter area also integrates impulses from the hypothalamus and the limbic system. Typically, stretch receptors are activated if systemic blood pressure is greater than 170 mm Hg. The response of the depressor system includes decreased sympathetic activity, leading to a decrease in cardiac contractility, heart rate, and vascular tone. In addition, activation of the parasympathetic system further decreases the heart rate and myocardial contractility. Reverse effects are elicited with the onset of hypotension.

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Question 35

Chemoreceptor Reflex Chemosensitive cells are located in the carotid bodies and the aortic body. These cells respond to changes in pH status and blood O 2 tension. At an arterial partial O 2 pressure (PaO 2 ) of less than 50 mm Hg or in conditions of acidosis, the chemoreceptors send their impulses along the sinus nerve of Hering (a branch of the glossopharyngeal nerve) and the tenth cranial nerve to the chemosensitive area of the medulla. This area responds by stimulating the respiratory centers and thereby increasing ventilatory drive. In addition, activation of the parasympathetic system ensues and leads to a reduction in heart rate and myocardial contractility. In the case of persistent hypoxia, the CNS will be directly stimulated, with a resultant increase in sympathetic activity.

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Question 36

Bainbridge Reflex The Bainbridge reflex 80 81 82 is elicited by stretch receptors located in the right atrial wall and the cavoatrial junction. An increase in right-sided filling pressure sends vagal afferent signals to the cardiovascular center in the medulla. These afferent signals inhibit parasympathetic activity, thereby increasing the heart rate. Acceleration of the heart rate also results from a direct effect on the SA node by stretching the atrium. The changes in heart rate are dependent on the underlying heart rate before stimulation

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Question 37

Bezold-Jarisch Reflex The Bezold-Jarisch reflex responds to noxious ventricular stimuli sensed by chemoreceptors and mechanoreceptors within the left ventricular wall by inducing the triad of hypotension, bradycardia, and coronary artery dilatation. 75 The activated receptors communicate along unmyelinated vagal afferent type C fibers. These fibers reflexively increase parasympathetic tone. Because it invokes bradycardia, the Bezold-Jarisch reflex is thought of as a cardioprotective reflex. This reflex has been implicated in the physiologic response to a range of cardiovascular conditions such as myocardial ischemia or infarction, thrombolysis, or revascularization and syncope. Natriuretic peptide receptors stimulated by endogenous ANP or BNP may modulate the Bezold-Jarisch reflex. Thus the Bezold-Jarisch reflex may be less pronounced in patients with cardiac hypertrophy or atrial fibrillation. 83

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Question 38

Valsalva Maneuver Forced expiration against a closed glottis produces increased intrathoracic pressure, increased central venous pressure, and decreased venous return. Cardiac output and blood pressure will be decreased after the Valsalva maneuver. This decrease will be sensed by baroreceptors and will reflexively result in an increase in heart rate and myocardial contractility through sympathetic stimulation. When the glottis opens, venous return increases and causes the heart to respond by vigorous contraction and an increase in blood pressure. This increase in arterial blood pressure will, in turn, be sensed by baroreceptors, thereby stimulating the parasympathetic efferent pathways to the heart.

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Question 39

Cushing Reflex The Cushing reflex is a result of cerebral ischemia caused by increased intracranial pressure. Cerebral ischemia at the medullary vasomotor center induces initial activation of the sympathetic nervous system. Such activation will lead to an increase in heart rate, arterial blood pressure, and myocardial contractility in an effort to improve cerebral perfusion. As a result of the high vascular tone, reflex bradycardia mediated by baroreceptors will ensue.

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Question 40

Oculocardiac Reflex The oculocardiac reflex is provoked by pressure applied to the globe of the eye or traction on the surrounding structures. Stretch receptors are located in the extraocular muscles. Once activated, stretch receptors will send afferent signals through the short- and long-ciliary nerves. The ciliary nerves will merge with the ophthalmic division of the trigeminal nerve at the ciliary ganglion. The trigeminal nerve will carry these impulses to the gasserian ganglion, thereby resulting in increased parasympathetic tone and subsequent bradycardia. The incidence of this reflex during ophthalmic surgery ranges from 30% to 90%. Administration of an antimuscarinic drug such as glycopyrrolate or atropine reduces the incidence of bradycardia during eye surgery (also see Chapter 84 ).

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