CARDIOVASCULAR ANATOMY AND PHYSIOLOGY

CV ANATOMY AND PHYSIOLOGY

OUTLINESFunctional Anatomy of the HeartPhysiology of the HeartCardiac cyclePressure Volume loop

3ANATOMIC LOCATION OF THE HEART

In mediastinum behind sternum and pointing left, lying on the diaphragmIt weighs 250-350 gm (about 1 pound)

The RV free wall occupies a more right-sided, anterior position within the mediastinum compared with the position of the thicker-walled LV that is located in a left-sided, posterior orientation 3

PERICARDIUM

Pericardiumis a double-walled sac containing theheartand the roots of thegreat vessels. 4

PERICARDIUM

LAYERS OF THE HEART

COMPONENT OF MYOCARDIUM

The left and right atria consist of two, thin overlying sheaths of muscle oriented at right angles to each other. The two thicker-walled ventricles consist of three interdigitating muscle layers: the deep sinospiral, the superficial sinospiral, and the superficial bulbospiral muscles

The two outer muscle layers are oriented obliquely from the base of the heart to the apex. Constriction of these fibers shortens the longitudinal axis of the left ventricle (LV) by moving the base toward the apex. The circumferential deep sinospiral muscles reduce the LV diameter synchronous contraction of the LV muscles shortens the long axis of the heart, decreases the circumference of the LV chamber, and lifts the apex toward the anterior chest wall. This latter action produces the familiar palpable point of maximum impulse, which is normally located in the fifth or sixth intercostal space in the midclavicular line.

Ventricular volume ejection. Contraction characteristics and modes of emptying. The volumes ejected by each ventricle is equal but the left ventricle requires a more circumferential muscular wall to eject its volume at a pressure that is approximately 4 to 5 times greater than that in the right ventricle.

During contraction, the RV moves toward the interventricular septum with a bellows-like action. The atrioventricular (AV) groove P.211separating the right atrium and RV shortens toward the apex during contraction. This anatomic configuration permits the more flexible RV wall to eject a large volume of blood with a minimal amount of shortening.7

8HEART INNERVATIONSympatheticIncreases rate and force of contractionsParasympathetic (branches of Vagus n.)Slows the heart rate

FUNCTIONAL ANATOMY OF THE HEART4 chambers - 2 atria - 2 ventricle2 pairs valves - Semilunar valves - AV valves2 systemsPulmonarySystemic

The RV and LV are the major cardiac pumping chambers, but the atria play critically important supporting roles. The atria function as reservoirs, conduits, and contractile chambers and facilitate the transition between continuous, low-pressure venous to phasic, high-pressure arterial blood flow.

Efficient pumping action of the heart requires two pairs of unidirectional valves. One pair is located at the outlets of the RV and LV (pulmonic and aortic valves, respectively). These three-leaflet valves operate passively with changes in pressure gradients. The aortic valve leaflets do not flatten against the aortic wall during LV ejection because a modest dilation of the aortic root located immediately distal to each leaflet establishes an eddy current of blood flow. These dilated regions are termed the sinuses of Valsalva and permit blood flow through the right and left main coronary arteries whose openings are located in the aortic wall directly behind the valve cusps. The AV valves separating the atria from the ventricles are the tricuspid and mitral valve on the right and left sides of the heart, respectively. The mitral valve is the only cardiac valve with two leaflets. Both tricuspid and mitral valves are thin, fibrous structures that are supported by chordae tendinae attachments to papillary muscles that are part of the ventricular musculature and contract during systole. The tricuspid and mitral valves open and close with alternations in the pressure gradients between the corresponding atrial and ventricular chambers9

FLOW PATTERN

The LV pumps blood from the low-pressure venous into the high-pressure arterial system. The right ventricle (RV) receives venous blood from the right atrium via the superior and inferior vena cavae at low pressure (2 to 10 mm Hg) and oxygen saturation (60 to 75%). The RV is crescent-shaped and contains embryologically distant inflow and outflow tracts that contract in a peristaltic sequence to propel blood into the pulmonary arterial tree. Blood flow through the pulmonary circulation functions primarily as a gas exchanger, providing for the elimination of carbon dioxide (CO2; a major product of cellular metabolism) and the uptake of oxygen (O2). The pulmonary vasculature is characterized by lower pressure than the systemic circulation and has shorter, larger-bore blood vessels with relatively thinner walls than systemic resistance vessels. Thus, the pulmonary circulation is a low-pressure, low-resistance system into which the RV transfers blood. The LV is capable of tolerating large increases in arterial pressure without a substantial reduction in stroke volume; the RV may acutely decompensate with even modest increases in pulmonary vascular resistance.

During contraction, LV pressure increases from end-diastolic values of 10 to 12 mm Hg to a peak pressure of 120 to 140 mm Hg during systole. The peak pressures generated by the LV reflect the requirement to circulate blood through the high-resistance systemic circulation that is composed of thicker blood vessels containing larger quantities of vascular smooth muscle than their counterparts in the pulmonary arterial tree. Resistance to blood flow is especially high in small arterioles and precapillary vessels, and blood flow in these vessels requires that the LV generate higher perfusion pressure than the RV. The volume of blood pumped by RV and LV is identical (stroke volume), but the pressure-volume work (stroke work) performed by the LV is 5 to 7 times greater than that of the RV. Left ventricular ejection is associated with a wall tension gradient from the apex to the base of the heart (aortic outflow tract), thereby producing the intraventricular gradient required to transfer stroke volume from the LV into the aorta.10

CARDIAC CYCLE

Single heart beat

Electrical events (ECG)

Mechanical event

The cardiac cycle is the sequence of electrical and mechanical events during the course of a single heartbeat. (1) the electrical events of a single cardiac cycle represented by the electrocardiogram (ECG) and (2) the mechanical events of a single cardiac cycle represented by left atrial and left ventricular pressure pulses correlated in time with aortic flow and ventricular volume.[11

CARDIAC CYCLEElectrical event

Electrical events of the pacemaker and the specialized conduction system are represented by the ECG at the body surface

It is the result of differences in electrical potential generated by the heart at sites of the surface recording.

The action potential initiated at the SA node is propagated to both atria by specialized conduction tissue, and it leads to atrial systole (contraction) and the P wave of the ECG. At the junction of the interatrial and interventricular septa, specialized atrial conduction tissue converges at the atrioventricular (AV) node, which is connected distally to the His bundle. The AV node is an area of relatively slow conduction, and a delay between atrial and ventricular contraction normally occurs at this locus. The PR interval can be used to measure the delay between atrial and ventricular contraction at the level of the AV node. From the distal His bundle, an electrical impulse is propagated through large left and right bundle branches and finally to the Purkinje system fibers, which are the smallest branches of the specialized conduction system. Finally, electrical signals are transmitted from the Purkinje system to individual ventricular cardiomyocytes. The spread of depolarization to the ventricular myocardium is manifested as the QRS complex on the ECG. Depolarization is followed by ventricular repolarization and appearance of the T wave on the ECG12

CARDIAC CYCLEMechanical eventSystoleisovolemic contraction, rapid ejection and slower ejection

Diastole isovolumic relaxation, early filling, diastasis, and atrial systole.

Left ventricular systole is commonly divided into three parts: isovolumic contraction, rapid ejection, and slower ejection.

Closure of both the tricuspid and mitral valves occurs when RV and LV pressures exceed corresponding atrial pressure and is the source of the first heart sound.

Isovolumic contraction is the interval between closure of the mitral valve and the opening of the aortic valve. Left ventricular volume remains constant during this period of the cardiac cycle.

The rate of increase of LV pressure (dP/dt, an index of myocardial contractility) reaches its maximum during isovolumic contraction. True isovolumic contraction does not occur in the RV because the sequential nature of inflow followed by outflow tract RV contraction. Pressure in the aortic root declines to its minimum value immediately before the aortic valve opens.

Rapid ejection occurs when LV pressure exceeds aortic pressure and the aortic valve opens. Approximately two thirds of the LV end-diastolic volume is ejected into the aorta during this rapid ejection phase of systole. Aortic dilation occurs in response to this rapid increase in volume as the kinetic energy of LV contraction is transferred to the systemic arterial circulation as potential energy.

The normal LV end-diastolic volume is about 120 mL. The average ejected stroke volume is 80 mL, and the normal ejection fraction is approximately 67%. A decrease in ejection fraction below 40% is typically observed when the myocardium is affected by ischemia, infarction, or cardiomyopathic disease processes (e.g., myocarditis, amyloid infiltration).

Contractile dysfunction may also occur as a result of chronic pressure or volume overload, diabetes, or hypothyroidism. As aortic pressure peaks and resists further LV ejection, transfer of further stroke volume slows and eventually stops. During this period of slower ejection, aortic pressure may briefly exceed LV pressure. The reversal of the pressure gradient between the aortic root and the LV causes the aortic valve to close, thereby producing the second heart sound (S2).

Diastole is divided into four phases in the LV: isovolumic relaxation, early filling, diastasis, and atrial systole.

Isovolumic relaxation defines the period between aortic valve closure and mitral valve opening during which LV volume remains constant. LV pressure falls precipitously as the myofilaments relax.

When LV pressure falls below left atrial pressure, the mitral valve opens, and blood volume stored in the left atrium rapidly enters the LV driven by the pressure gradient between these chambers. This early-filling phase of diastole accounts for approximately 70 to 75% of total LV stroke volume available for the subsequent contraction. Delays in LV relaxation occur as a consequence of aging or disease process (e.g., myocardial ischemia) and may attenuate early ventricular filling.

After left atrial and LV pressures have equalized, the mitral valve remains open and pulmonary venous return continues to flow through the left atrium into the LV. This phase of diastole is known as diastasis, during which the left atrium functions as a conduit. Tachycardia progressively shortens and may completely eliminate this phase of diastole.

Diastasis accounts for no more than 5% of total LV end-diastolic volume under normal circumstances.

The final phase of diastole is atrial systole. Contraction of the left atrium contributes the remaining blood volume (approximately 15 to 20%) used in the subsequent LV systole. Disease processes known to reduce LV compliance (e.g., myocardial ischemia, pressure-overload hypertrophy) attenuate early filling and increase the importance of atrial systole to overall LV filling. Thus, loss of normal sinus rhythm may precipitate catastrophic decreases in cardiac output in patients with symptomatic coronary artery disease, critical aortic stenosis, or poorly controlled chronic essential hypertension

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CARDIAC CYCLE

CARDIAC OUTPUTAmount of blood pumped by the heart per minute. CO = HR x SV CI = HR x SV x BSA Cardiac output (Q) directly proportional to pressure (P) and inversely proportional to peripheral vascular resistant (R) Ohm law: Q = P/R

Cardiac output is the amount of blood pumped by the heart per minute. It is the product of heart rate and stroke volume and may be normalized to the body surface area (cardiac index). Cardiac output (Q) is directly related to pressure (P) and inversely related to peripheral vascular resistance (R) using an equation analogous to Ohm's law: Q = P/R. 15

CARDIAC OUTPUTCO is a function of PRELOAD, AFTERLOAD, MYOCARDIAL CONTRACTILITY and HRPreload: LV end-diastolic volumeFrank sterling lawAfterload: Aortic pressure Distensibility of the aorta, Resistance of the peripheral arterial vasculature

Cardiac output is a function of preload, afterload, myocardial contractility (inotropic state), and heart rate.Preload is defined by LV end-diastolic volume in the intact heart and reflects the stretch of ventricular myofilaments produced by this end-diastolic volume immediately before the onset of contraction. According to Starling's law, the force of LV contraction and volume of blood ejected from the chamber during systole (stroke volume) is directly related to the end-diastolic myofilament length, and hence, the end-diastolic volume.Thus, the ventricular myocardium behaves similar to skeletal muscle in that an increase in initial stretch determines the subsequent force of contraction. Afterload may be simplistically represented as the aortic pressure against which the LV must propel blood. The distensibility of the aorta, the resistance of the peripheral arterial vasculature, and the actions of reflected waves on the central aortic circulation are the principle determinants of afterload.

Systemic vascular resistance (the ratio of pressure to cardiac output, P/Q) is the most commonly used nonparametric expression of peripheral resistance and is primarily affected by autonomic nervous system activity. For example, an increase in sympathetic nervous system tone produces vasoconstriction of peripheral resistance arterioles through activation of 1-adrenoceptors in vascular smooth muscle, thereby augmenting afterload. A brief, large increase in afterload may cause a transient decrease in stroke volume, but a compensatory increase in preload during successive cardiac cycles restores cardiac output by increasing LV force of contraction16

CARDIAC OUTPUTMYOCARDIAL CONTRACTILITYInotropic state (autonomic and pharmacologic)HEART RATEDeterminant of myocardial oxygen consumption

Inotropic state is the intrinsic force of myocardial contraction independent of changes in preload, afterload, or heart rate. The number of cross bridges between the contractile elements and the relative sensitivity of the contractile elements to activator Ca2+ play important roles in determining inotropic state. In the intact heart, a positive inotropic effect is reflected by an increase in pressure-volume work at each end-diastolic volume. Such an increase in inotropic state may occur in response to an increase in cardiac sympathetic nerve activity through stimulation of 1-adrenoceptors. Pharmacologic increases in contractility may be produced by drugs that activate 1-adrenoceptors (e.g., dobutamine) or by those that prevent metabolism of the intracellular second messenger cyclic adenosine monophosphate (cAMP; e.g., milrinone)

Cardiac output is also influenced by heart rate. The primary determinant of myocardial oxygen consumption is heart rate because the heart completes an entire cycle with each beat, and hence, the more frequently the heart performs pressure-volume work, the more oxygen must be consumed. The upper and lower limits of heart rate may influence cardiac output. At low heart rates (except in trained athletes), there simply may not be adequate cardiac output to meet the body's oxygen requirements, deliver substrates for metabolism, or remove products of cellular metabolism. In contrast, at high heart rates, particularly in patients with heart disease, there may not be adequate diastolic filling time to maintain cardiac output and coronary artery perfusion, the latter of which is particularly dependent on duration of diastole. Thus, shortened diastolic time during profound tachycardia may reduce stroke volume and cardiac output, contribute to hypotension, and decrease the duration of coronary perfusion. Such events may cause acute myocardial ischemia or infarction17

FRANK STERLING LAW

Starling's law, the force of LV contraction and volume of blood ejected from the chamber during systole (stroke volume) is directly related to the end-diastolic myofilament length, and hence, the end-diastolic volume.Thus, the ventricular myocardium behaves similar to skeletal muscle in that an increase in initial stretch determines the subsequent force of contraction

Frank-Starling relationship. The relationship between sarcomere length and tension developed in cardiac muscles is shown. In the heart, an increase in end-diastolic volume is the equivalent of an increase in myocardial stretch; therefore, according to Starling's law, increased stroke volume is generated.

The Frank-Starling relationship is an intrinsic property of myocardium by which stretching of the myocardial sarcomere results in enhanced myocardial performance for subsequent contractions Otto Frank first noted in 1895 that in skeletal muscle, the change in tension was directly related to its length and that in the heart, as pressure changed, a corresponding change in volume occurred.[8] E. H. Starling, using an isolated heart-lung preparation as a model, observed in 1914 that the mechanical energy set free on passage from the resting to the contracted state is a function of the length of the muscle fiber.[9] If a strip of cardiac muscle is mounted in a muscle chamber under isometric conditions and stimulated at a fixed frequency, an increase in sarcomere length results in an increase in twitch force. Starling concluded that the increased twitch force was the result of a greater interaction of muscle bundles18

CELULAR AND MOLECULAR BIOLOGY OF CARDIAC MUSCLE CONTRACTIONInitiationAction potential via pacemaker cells to conduction fibersExcitation-Contraction Coupling1. Starts with CICR (Ca2+ induced Ca2+ release)AP spreads along sarcolemmaT-tubules contain voltage gated L-type Ca2+ channels which open upon depolarizationCa2+ entrance into myocardial cell and opens RyR (ryanodine receptors) Ca2+ release channelsRelease of Ca2+ from SR causes a Ca2+ sparkMultiple sparks form a Ca2+ signalSpark Gif

CELULAR AND MOLECULAR BIOLOGY OF CARDIAC MUSCLE CONTRACTIONExcitation-Contraction Coupling contCa2+ signal (Ca2+ from SR and ECF) binds to troponin to initiate myosin head attachment to actinContractionSame as skeletal muscle, butStrength of contraction variesSarcomeres are not all or none as it is in skeletal muscleThe response is graded!Low levels of cytosolic Ca2+ will not activate as many myosin/actin interactions and the opposite is trueLength tension relationships existStrongest contraction generated when stretched between 80 & 100% of maximum (physiological range)What causes stretching?The filling of chambers with blood

CELULAR AND MOLECULAR BIOLOGY OF CARDIAC MUSCLE CONTRACTIONRelaxationCa2+ is transported back into the SR andCa2+ is transported out of the cell by a facilitated Na+/Ca2+ exchanger (NCX)As ICF Ca2+ levels drop, interactions between myosin/actin are stoppedSarcomere lengthens

PRESSURE VOLUME LOOP

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