Cardiovascular Physiology - 2nd Edition

Educational Objectives

Describe the mechanisms and functions of the heart and cardiovascular system.

Summary

Cardiovascular Physiology

Alina Grigore, MD, Associate Professor of Anesthesiology, and Director, Division of Cardiothoracic Anesthesiology, University of Maryland School of Medicine, Baltimore, MD

Basic anatomy of the heart: 2 atria and 2 ventricles provide 2 separate circulations in series; atria act as reservoirs for venous blood, with small pumping action to assist ventricular filling; ventricles are the major pumping chambers that deliver blood to the pulmonary and systemic circulation; right side supplies pulmonary circulation (low resistance and high capacitance bed); left side generates output to the systemic circulation (high resistance vascular bed); left ventricle is the driving force to the cardiovascular system to supply oxygen and nutrients and remove metabolic waste by undergoing a cycle of contraction and relaxation called the cardiac cycle

Cardiac cycle: during the initial portion, an electrical signal is generated in the “pacemaker cell,” which is distributed through the heart by means of an electrical conduction system; systole — in response to electrical stimulation, the myocardium of the first atria and then the ventricles undergo contraction; diastole — sequential relaxation; this cycle of compressing the blood in the ventricles during systole followed by the filling of ventricles during diastole induces pressure changes in the ventricles that cause 1-way valves in the heart to close at different intervals of the cardiac cycle; the result of pumping blood into the arteries by ventricles undergoing systole is the generation of blood pressure, the primary driving force for the flow of blood through the body; the cardiac cycle begins with excitation of the myocardium, leading to a sequence of mechanical events, with the final result of building a pressure gradient and generation of stroke volume during systole

Systole: represents a rapid increase in cardiac pressure followed by a rapid decrease in volume

Diastole: represents a rapid decrease in pressure followed by an increase in volume

Phases of the cardiac cycle: isovolemic contraction — represents the beginning of myocardial shortening; ejection phase — begins with an opening of the aortic volume and generates stroke volume and cardiac output; isovolemic relaxation — represents early ventricular relaxation; diastolic filling — begins with the opening of the mitral valve

Cardiac output: product of stroke volume and heart rate; systolic performance of the heart is dependent on loading conditions and contractility

Sarcomere: fundamental contractile unit of cardiac muscle; sarcomeres are arranged in parallel cross-striated bundles of thin and thick fibers; thin fibers are made of acting tropomyosin and troponin complex; thick fibers are made of myosin and supporting proteins; sarcomeres are connected in a series, producing characteristic shortening and thickening of the long and short axis of each myocyte

Systolic function of the heart: exists between closure of the mitral valve and the start of contractility and ejection of blood from the heart

Primary purpose: generate stroke volume and cardiac output

Stroke volume: determined by preload, afterload and contractility

Preload: represents the ventricular load at the end of diastole and equals the ventricular wall stress at the end of diastole; determined by ventricular end-diastolic volume, end-diastolic pressure, and wall thickness; there is a linear relationship between sarcomere length and myocardial force, first described by Starling

Starling’s law of the heart: energy of contraction of the muscle is related or proportional to the initial length of the muscle fiber; as ventricular end-diastolic volume increases and stretches the muscle fibers, the energy of contraction and stroke volume also increase to a point of overstretching, when stroke volume may actually increase, as happens in the failing heart; cardiac output will also increase or decrease in parallel with stroke volume if there is no change in heart rate

Factors affecting preload: total blood volume, body position, intrathoracic pressure, intrapericardial pressure, venous stone, pumping action of skeletal muscles and atrial contrition to the ventricular filling; total body volume is approximately 70 to 75 mL/kg (distributed between compartments, 15% intrathoracic and 85% extrathoracic)

Afterload: systolic load of the left ventricle after contraction has begun; determined by the ventricular wall stress during systole and by aortic compliance (also called impedance)

Ventricular wall stress: Law of Laplace — product of systolic pressure generated by a ventricle; radius of the ventricle divided by 2 times ventricular wall thickness

Impedance: systemic circulation that opposes ventricular ejection and pulsatile blood flow

Stroke volume: determined by Ohm’s law, which states that flow is the ratio between pressure (generated by the left ventricle during systole) and resistance (resistance encountered by the flow [ie, systemic vascular resistance])

Systemic vascular resistance: difference between mean arterial pressure and right atrial pressure divided by cardiac output; contractility — intrinsic property of the myocardial fibers that determines the amount of work the heart can perform at a given load; determined by availability of intracellular calcium released from the sarcoplasmic reticulum, which binds to troponin, displacing tropomyosin from the active binding sites on actin and forming actin-myosin cross-bridges; all inotropic positive agents have the final pathway to increasing intracellular calcium level

Ejection fraction: most common method to measure contractility; ratio between stroke volume and end-diastolic volume; calculated by means of transesophageal echocardiography in transgastric short-axis view by the simplified formula of end-diastolic volume or area minus end-systolic volume or area divided by end-diastolic volume or area; normal value — 55%; disadvantage of using ejection fraction for assessment of contractility is that the parameter is preload dependent

Change in pressure over change in time (DP/DT): ratio of change of pressure over time during the isovolemic phase of contraction; another index used to assess ventricular contractility (also preload dependent); DP/DT can be measured invasively by using an intracardiac catheter with a manometer for pressure measurements or non-invasively by Doppler echocardiography; normal values — >1200 mm Hg for normal left ventricle

Ventricular elastance: ratio of ventricular pressure over volume; low independent indices of measurements of ventricular contractility, measured at the end of systole

Heart rate: second major determinant of cardiac output; controlled by cardiac conduction system, central nervous system, and autonomic nervous system; primary determinant of heart rate lies within the cardiac conduction system (rate of slow depolarization of the sinoatrial node); neural mechanism exerts some control over the natural heart rate by controlling the conduction velocity of the atrioventricular node; normal resting heart rate — 70 beats per minute; mainly controlled by the vagal tone; loss in vagal tone leads to faster heart rate (seen in transplanted, denervated hearts; there is a relationship between heart rate and contractility (trapstep or Baldwich phenomenon); increased heart rate leads to increased level of intracellular calcium and increased contractility; heart rate is the major determinant of myocardial oxygen consumption

Diastolic function of the heart: diastole is ventricular relaxation and occurs in 4 distinct phases (isovolemic relaxation, rapid filling, slow filling or diastasis, and filling during atrial contraction)

Isovolemic phase (myocardial relaxation): occurs between closure of the aortic valve and opening of the mitral valve; phase of rapid fall in the left ventricular pressure as the ventricle relaxes without change in volume; sarcoplasmic uptake of intracellular calcium release during systole allows the myocardium to relax and generate decreased intraventricular pressure; when left ventricular pressure drops below atrial pressure, the mitral valve opens and the early filling phase of diastole begins, which accounts for 70% to 75% of total left ventricular stroke volume; after left ventricular and left atrial pressures have equalized, the mitral valve remains open and pulmonary venous return continues to flow through the left atrium to the left ventricle (diastasis), accounting for 5% of left ventricular stroke volume

Atrial systole: final phase of diastole; accounts for the remaining 15% to 20% of total left ventricular stroke volume; diastolic function can be measured by peaking spontaneous rate of decline in left ventricular pressure (DP/DT) or by the constant isovolemic decline in left ventricular pressure (Kendall τ coefficient) measured by Doppler echocardiography; ventricular compliance can also be evaluated by the pressure volume relationship; diastolic dysfunction can be present in the absence of systolic dysfunction and can be encountered in 50% of patients diagnosed with congestive heart failure

Blood flow: the heart is the only organ that furnishes its own blood supply; myocardial blood supply is from the right and left coronary arteries, which run over the surface of the heart giving branches to the endocardium (inner layer of the myocardium)

Venous drainage: occurs primarily by means of coronary sinus into the right atrium; small portion of blood flows directly into the ventricles through Thebesian veins, delivering unoxygenated blood to the systemic circulation

Oxygen extraction by the tissues: dependent on consultation and delivery; left ventricular perfusion — occurs during diastole; determined by the gradient between aortic diastolic pressure and left ventricular end diastolic pressure, which defines coronary perfusion pressure; right ventricular perfusion — occurs during both systole and diastole; more consistent during the cardiac cycle because pressures generated by the right ventricle during systole are lower than pressures generated by the left ventricle

Poiseuille’s law: coronary blood flow is directly proportional to coronary perfusion pressure and to the fourth power of the radius of the vessel; coronary blood flow is inversely proportional to vessel length and blood viscosity; coronary blood flow is 25 mL/minute and represents 5% of cardiac output; increased heart rate reduces the time for diastolic filling and can reduce the myocardial blood flow, causing ischemia; the normal heart extracts 75% to 80% of arterial oxygen content; the myocardium is the greatest extraction organ in the body; majority of oxygen demand is derived from the development of left ventricular pressure during isovolemic contraction, increasing myocardial contractility, which enhances oxygen consumption; heart rate remains the primary determinant of oxygen consumption; maximum cardiac oxygen extraction occurs in the resting condition; balancing oxygen demands occurs primarily through enhanced coronary blood flow and constant hemoglobin concentration

Coronary reserve: difference between maximal and resting coronary blood flow; sympathetic β-adrenergic receptor activation in adenosine dilates the coronary arteries; metabolically induced coronary vasodilation may redistribute blood away from the ischemic zone through coronary collateral vessels and can lead to coronary steal syndrome; left ventricular subendocardium is exposed to higher pressures during systole and is more susceptible to myocardial ischemia; subendocardial ischemia can occur when there is an acute decrease in systemic diastolic pressure or an acute increase in left ventricular diastolic pressure without acute occlusion of the coronary artery; myocardial infarction can occur in the absence of coronary thrombosis, emboli, or stenosis; alternatively, transmural ischemia is more likely to occur in the presence of acute coronary occlusion

Summary:

Right ventricle: a low-pressure chamber that cannot tolerate large changes in pressure and volume; perfused during systole and diastole

Left ventricle: a high-pressure chamber that can accommodate large increases in blood pressure without change in stroke volume; perfused during diastole

Stroke volume: equal for both ventricles; stroke work is 5 to 7 times higher for the left ventricle

Cardiac output: amount of blood pumped by the heart per unit of time; the product of heart rate and stroke volume; determinants of cardiac output are preload, afterload, contractility, and heart rate; can be calculated by multiplying the mean arterial pressure by 80 and dividing it by cardiac output; can be measured by thermodilution technique as well as by fixed principle; fixed principle — based on the concept of conservation of mass such that the oxygen delivered from pulmonary venous blood is equal to the oxygen delivered to pulmonary capillaries through the pulmonary artery and alveoli; requires knowledge of total body oxygen consumption, which can be calculated by the metabolic cart indirect calorimetry method in the intensive care unit; normal range — 5 to 6 L/minute; for stroke volume 60 to 90 mL/minute

Cardiac index: cardiac output divided by body surface area

Heart is auto-excitatory: action potentials are formed spontaneously at regular intervals in specialized cells called “pacemaker cells”; these cells are arranged in a network that enables signals to be conducted throughout the myocardium from their point of origin; 4 major structures are found within the conduction network

Sinoatrial node: located in the right atrial wall near the junction with the superior vena cava; contains pacemaker cells that undergo spontaneous depolarization at a higher rate than any other pacemaker cells in the heart; the sinoatrial node sets the basic tempo for heart contraction, the sinus rhythm (often referred to as “the pacemaker of the heart”); action potentials originating in the sinoatrial node are conducted rapidly through both atria by means of tracks of pacemaker cells

Atrioventricular node: located in the medial wall of the right atrium near its junction with the right ventricle; the atrioventricular node contains the only pacemaker cells that leak out to the ventricles; electrical signals originating in the sinoatrial node and passing through the atria can normally be conducted only to the ventricles through the atrioventricular node; pacemaker cells in the atrioventricular node have low conduction velocities, thus electrical signals pass through this region slowly; once the signal passes through the atrioventricular node, it is transferred to the atrioventricular bundle (ie, Bundle of His)

Bundle of His: conducts the signal through the interventricular septum toward the apex of the heart; soon after entering the interventricular septum, the atrioventricular bundle bifurcates into 2 separate branches; conduction of the electrical signal through the interventricular septum coupled with the slow conduction velocity of the atrioventricular node causes atrioventricular delay (the time from generation of atrial action potential to the time of transmission to the ventricular myocardium in generating ventricular contraction); the delay ensures that atrial systole is complete at the onset of ventricular systole; once the signal reaches the apex of the heart, it is conducted to the lateral walls of the ventricle through branched tracks of pacemaker cells, called Purkinje fibers, which distribute the electrical signal to the ventricular myocardium; electrical changes occurring during the cardiac cycle can be monitored from the surface of the body by electrocardiogram

Electrocardiogram: normal electrocardiogram recording associated with a single cardiac cycle contains 3 distinctive wave forms; P wave — generated when the atria depolarize as the action potential wave spreads out from the sinoatrial node; QRS complex — consists of Q, R, and S waves and is triggered by the depolarization of the ventricles just before ventricular systole; during the QRS complex, the atria undergo repolarization as a result of the small electrical disturbance but atrial repolarization is masked by the massive change in extracellular charge caused by ventricular depolarization; T wave — triggered by the repolarization of the ventricles at the end of ventricular systole; a number of important intervals can be measured from electrocardiogram recording; a simple measure of the duration of cardiac cycle is measured as the time that elapses between a particular point in one cardiac cycle to the same point in the next cardiac cycle (eg, from R wave to R wave); PR interval — indicates the duration of time that atria are depolarized, which is roughly equal to the duration of atrial systole; PR interval also indicates how long it takes for the electrical signal to travel from the atria to the ventricles (called the atrioventricular delay); RT interval — ventricles remain in a depolarized state; duration of the interval is roughly the duration of ventricular asystole, which is the amount of time required for blood to be ejected into systemic circulation; TR interval — indicates how long ventricles remain in a polarized state between depolarization, corresponding to the duration of ventricular diastole; ST interval — the important diagnostic interval; may become elevated as a result of recent myocardial infarction or depressed in individuals with coronary ischemia; electrocardiogram shows heart rate and rhythm and can indicate myocardial damage but provides no information about the adequacy of contraction; pulseless electrical activity — electromechanical disassociation; normal electrical complexes can exist in the absence of cardiac output; electrical signals recorded on an electrocardiogram are caused by intermittent periods where the myocardium undergoes action potential; action potentials trigger the ventricles to contract for a period of time and then relax; series of 1-way valves prevent backflow of the blood from the ventricles into the atria during systole and from the atria into the ventricles during diastole; closure of the valves can be heard during the cardiac cycle; the first sound produced is caused by closure of atrioventricular valves at the beginning of ventricular asystole when pressure in the ventricles exceeds atrial pressure; second sound is generated at the beginning of ventricular diastole when ventricular pressure falls below arterial pressure, causing closure of aortic and pulmonary valves

Cardiac cycle and arterial blood pressure: flow of blood through the cardiovascular system is driven by the pressure difference between one segment of a blood vessel circuit and the next; blood pressure drops sequentially throughout the circuit; blood at one point will flow to the next, where the pressure is lower; contractions of the heart elevate blood pressure high enough so that blood can be propelled through the entire circuit; arteries play a particularly important role in ensuring adequate blood flow through the cardiovascular system; arteries serve as pressure reservoirs; the elastic walls of the arteries expand during ventricular asystole to accommodate the influx of fresh blood and then compress back on blood during ventricular diastole (maintaining relatively high blood pressure even when ventricular blood pressure has dropped to near zero); ensures that blood flows constantly throughout the cardiovascular system during the entire cardiac cycle; blood pressure in the arteries oscillates during the cardiac cycle

Systolic blood pressure: pressure in the arteries during ventricular asystole; similar to that of blood in the ventricles during this period

Diastolic blood pressure: pressure in the arteries during ventricular relaxation or diastole; somewhat lower although not nearly as low as pressure in the ventricles at this time

Pulse pressure: difference in pressure between systole and diastole; a useful diagnostic measure for cardiovascular health

Mean arterial pressure: average blood pressure in the arteries throughout the cardiac cycle; calculated as the sum of 2 times diastolic pressure plus systolic pressure divided by 3

Systemic vascular resistance: the difference between mean arterial blood pressure and mean right atrial pressure times 80 divided by cardiac output; normal values are between 700 and 1600 dyne/cm⁵; short-duration regulation of mean arterial pressure occurs through the arteriole and to a lesser extent through intracardiac baroreceptors

Arterial baroreceptors: located at the bifurcation of the common carotid arteries and in the aortic arch; acute rise in blood pressure activates baroreceptors through a stretching mechanism, increasing afferent conduction to the carotid sinus nerve, which is centrally transmitted by the glossopharyngeal nerve; glossopharyngeal nerve — first synapses in the nucleus tractus solitarius; postsynaptic neuron activates the vagal motor nucleus and nucleus ambiguus, causing a reduction in heart rate; low-pressure baroreceptors located in the vena cava, right atrium, right ventricle, and pulmonary vein respond to the crisis in right atrial filling pressure by activating sympathetic tone in the arterial vasculature

Bezold-Jarisch reflex: causes a vagal depressive response, with a decrease in heart rate and mean arterial pressure when ventricular and atrial vagal afferents are activated by volume overload; myocardial ischemia stimulates sympathetic afferents, which causes tachycardia, an increase in mean arterial pressure; α-adrenoreceptors mediate most sympathetic nerve vascular response; β-adrenoreceptors modulate sympathetic innervation of the adrenal gland; mean arterial pressure is an important diagnostic measure to identify chronic hypertension; blood pressure can change based on activity levels or on body position (eg, when a person is standing, blood will tend to be drawn into the lower extremities with the force of gravity; the heart would need to pump harder to recover blood into the liver and the brain against the force of gravity, thus blood pressure would become elevated); if a person is reclining, blood tends to pool in the abdomen and thorax, and the effect of gravity becomes less; the heart does not need to pump the blood as forcefully to ensure adequate circulation; blood pressure will tend to become lower

Cardiovascular fitness: blood flow through the cardiovascular system is adjusted to meet the demands of tissues; during high levels of activity, cardiac output elevates, usually as a result of an increase in both components of cardiac output (heart rate and stroke volume); both heart rate and stroke volume are normally elevated during exercise; relative contribution of each can differ substantially based on cardiovascular fitness; if an individual exercises regularly, the number of myofibrils in the cardiac muscle cells tend to increase and the ventricle can contract more forcefully during systole and increase stroke volume; as a result, heart rate does not increase as much during exercise to generate the same degree of cardiac output (enables individuals to exercise regularly, to sustain the same level of exercise for a longer period of time, to recover more quickly from exercise, and to be able to compensate for changes in circulation in a more effective way) blood flow gets redistributed to the muscles

Cerebral circulation: the brain is approximately 2% of total body weight and receives 15% of cardiac output; cerebral blood flow is 45 to 55 mL/100 g brain/minute (reflecting the high metabolic rate of the brain; cerebral oxygen consumption is 3.5 mL/100 g brain/minute (accounts for 20% of total body oxygen consumption at rest); cerebral blood flow is maintained at a constant level when arterial blood pressure varies between 50 and 150 mm Hg; autoregulation of cerebral blood flow is shifted to the right in patients with a history of severe hypertension and is inhibited by hypercarbia and a higher concentration of volatile anesthetics; cerebral blood flow increases linearly 1 to 2 mL/100 g brain/minute for each 1 mm Hg increase in arterial carbon dioxide concentration

Spinal cord perfusion pressure: gradient between mean arterial pressure or right atrial pressure and cerebrospinal fluid pressure; normal values — 60 to 90 mm Hg

Pulmonary circulation: a low-pressure system compared with systemic circulation; gravity affects ventilation/perfusion ratio in the lung; in the upper one-third of the lung (zone 1), the ventilation/perfusion ratio is higher than in zones where ventilation exceeds perfusion (ie, dead space ventilation); in the middle region of the lung (zone 2), the ventilation/perfusion ratio is close to 1, which is a good ventilation perfusion balance; in the lower third of the lung (zone 3), the ventilation/perfusion ratio is <1, indicating poor ventilation with good perfusion (ie, shunting area); hypoxia triggers hypoxic pulmonary vasoconstriction, which shunts the blood away from poorly ventilated regions, thus improving arterial oxygen saturation; pulmonary vascular resistance — the difference between mean pulmonary arterial pressure and capillary wedge pressure divided by cardiac output times 80; normal values are between 20 and 130 dyne/cm⁵

Renal circulation: kidneys have a high metabolic rate, with oxygen extraction <10% as a result of renal perfusion, which exceeds metabolic requirements; blood flow under resting conditions is 20% of cardiac output; renal blood flow remains constant between 75 and 175 mm Hg and becomes pressure dependent above or below this range

Hepatic blood flow: the liver receives 25% of cardiac output; three-quarters of this cardiac output goes to the portal blood flow, and the remaining one-quarter goes to the liver; mean portal venous pressure is 10 mm Hg, mean arterial hepatic pressure is 90 mm Hg; the liver contains 60% of total body volume and is an important volume reservoir that can be mobilized rapidly in response to hypovolemia-induced sympathetic stimulation

Splanchnic circulation: poorly autoregulated in contrast to other organs; splanchnic blood flow under resting conditions is 24% of cardiac output; and metabolic autoregulation is provided by adenosine

Uterine blood flow: difference between uterine arterial and venous pressure divided by uterine vascular resistance; normal flows are around 100 mL/minute; and can increase to 700 to 900 mL/minute during pregnancy

Muscle and skin blood flow: under resting conditions is 24% and 9%, respectively; maximum exercise increases muscle blood flow to 88% of cardiac output at the expense of all other organs except coronary blood flow, which remains constant at 5% of cardiac output under any degree of physical exercise

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