CV Anatomy

CARDIOVASCULAR ANATOMY AND PHYSIOLOGY

CARDIOVASCULAR ANATOMY AND PHYSIOLOGY

OUTINESIntroductionBasic anatomy of the heartPhysiology of intact heart

INTRODUCTIONWilliam Harvey (1628)The modern concept of circulation and that the heart is the generator for the circulation

William Harvey as an Englishphysician. He was the first to describe completely and in detail thesystemic circulationand properties ofbloodbeing pumped to the brain and body by theheart

Since that time, the field of cardiac physiology has developed to now include the physiology of the heart as a pump, cellular and molecular biology of the cardiomyocyte, and regulation of cardiac function by neural and humoral factors.

we now appreciate that physiology of the heart is only a component of the interrelated and integrated cardiovascular and circulatory physiology.3

HEART ANATOMYLocationLayersChambers Innervation Blood supply

HEART ANATOMYLocation

The adult human heart has a mass of between 250 and 350grams and is about the size of a fist.It is locatedinside the thoracic cavity. anteriorto the vertebral column andposteriorto the sternum 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

5

HEART ANATOMYLayers

6

HEART ANATOMYLayers

HEART ANATOMY4 Chambers - 2 atria - 2 ventricle2 Pairs valves - Semilunar valves - AV valves2 SystemsPulmonarySystemic

Heart consists of two atria and two ventricles that provide two separate circulations in series. The pulmonary circulation, 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. The left side of the heart provides output for the systemic circulation. It functions to deliver oxygen and nutrients and remove CO2 and metabolites from various tissue beds.

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 chambers

8

HEART ANATOMYPacemaker and specialized conduction systems SA Node, AV nodes, Bundle of his and purkinje fibers

Autonomic innervationSympathetics and Parasympathetics

9

HEART ANATOMYBlood supply

HEART ANATOMY

PHYSIOLOGY OF THE HEARTTo understand the mechanical performance of the intact heart, it is important to have knowledge :1.Cardiac cycle 2.Determinants of ventricular function

To understand the mechanical performance of the intact heart, it is important to have knowledge of the phases of the cardiac cycle and determinants of ventricular function

12

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.13

CARDIAC CYCLEElectrical event of the pacemakers and specialized conduction syste are represented by ECG

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 ECG14

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

15

CARDIAC CYCLESYSTOLICIsovolemic contraction:Interval between closure of the mitral valve and the opening of the aortic valve. Volume are constantRapid ejection:Left ventricular pressure > Aortic pressureAortic valve open2/3rd of LVEDV ejectedSlower ejectionFlow and great artery pressure taper with progression

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).

16

CARDIAC CYCLEDiastoleIsovolemic contraction The interval between closure of the mitral valve and the opening of the aortic valvevolume are constantRapid fillingLV < LA, Mitral valve open, 70-75% of total LEVDDiastasisLA and LV pressure equalized, MV remain open, atria as conduit. 5% of total LVEDAtrial systoleremaining 15-20%, loss in AF

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

17

CARDIAC CYCLEMechanical

18

CARDIAC CYCLE

SYSTOLIC FUNCTIONDescription of systolic function of LV

Factors influence systolic function:Loading conditionPreload and afterload2. Contractility

The heart provides the driving force for delivering blood throughout the cardiovascular system to supply nutrients and remove metabolic waste. Because of the complexity of RV anatomy, the traditional description of systolic function is usually limited to the LV.

Systolic performance of the heart is dependent on loading conditions and contractility. Preload and afterload are two interdependent factors extrinsic to the heart that govern cardiac performance20

PRELOAD AND AFTERLOADPreloadLV end-diastolic vol and stretch of vent myofilament before contraction

Starling describe linear relationship exists between sarcomere length and myocardial force

Afterload Aortic pressure against which the LV must propel blood.

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.

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 afterload

Echocardiography can estimate aortic impedance noninvasively by determining aortic blood flow at the time of its maximal increase. In more general clinical practice, measurement of systolic blood pressure is adequate to approximate afterload, provided that aortic stenosis is not present.21

PRELOAD AND AFTERLOADWall stress that is present at the end of diastole and during LV ejection

LAW of LAPLACE:Wall stress = Pressure(P) x Radius(r) 2 wall thickness(h)The most relevant indices that account for changes in myocardial oxygen demand

Preload and afterload can be thought of as the wall stress that is present at the end of diastole and during LV ejection, respectively. Wall stress is a useful concept because it includes preload, afterload, and the energy required to generate contraction. Wall stress and heart rate are probably the two most relevant indices that account for changes in myocardial oxygen demand. The law of Laplace states that wall stress () is the product of pressure (P) and radius (R) divided by wall thickness (h)

22

WALL STRESSThickness of the LV muscle is an important modifier of wall stress

Thickness of the LV muscle is an important modifier of wall stress. For example, in aortic stenosis, afterload is increased. The ventricle has to generate far higher pressure to overcome the increased load opposing systolic ejection of blood. To generate such high performance, the ventricle increases its wall thickness (LV hypertrophy). By applying Laplace's law, increased LV wall thickness will decrease wall stress despite the necessary increase in LV pressure to overcome the aortic stenosis .In a failing heart, the radius of the LV increases, thus increasing wall stress.23

FRANK STARLING RELATIONSHIPIntrinsic property of myocardium

Myocardial sarcomere stretching results in enhanced myocardial performance

Increase in cross-bridging is equivalent to an increase in muscle performance.

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

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

Electron microscopy has demonstrated that sarcomere length (2.0 to 2.2m) is positively related to the amount of actin and myosin cross-bridging and that there is an optimal sarcomere length at which the interaction is maximal.This concept is based on the assumption that the increase in cross-bridging is equivalent to an increase in muscle performance. Although this theory continues to hold true for skeletal muscle, the force-length relationship in cardiac muscle is more complex. When comparing force-strength relationships between skeletal and cardiac muscle, it is noteworthy that the reduction in force is only 10% even if cardiac muscle is at 80% sarcomere length. The cellular basis of the Frank-Starling mechanism is still being investigated and will be discussed briefly later.

A common clinical application of Starling's law is the relationship of left ventricular end-diastolic volume (LVEDV) and stroke volume. The Frank-Starling mechanism may remain intact even in a failing heart.[10] However, ventricular remodeling after injury or in heart failure may modify the Frank-Starling relationship.24

FRANK STARLING RELATIONSHIPInotropic or contractilityWork performed by cardiac muscle at any given end-diastolic fiber

Factors that modify:ExerciseAdrenergic stimulationTemperaturepHDrugs such as digitalis

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. Factors that modify contractility will create a family of Frank-Starling curves with different contractility.

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

25

PRESSURE VOLUME LOOPIndirect measurement of frank starling relationship between force (pressure) and muscle length (volume).

To measure the intrinsic contractile activity of an intact heart, several strategies have been attempted with varying success. 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.The pressure-volume loop represents an indirect measure of the Starling relationship between force (pressure) and muscle length (volume). Clinically, the most commonly used noninvasive index of ventricular contractile function is the ejection fraction, which is assessed by echocardiography, angiography, or radionuclide ventriculography.26

HEART RATEDeterminant of myocardial oxygen consumption

Higher HR: increase cardiac cycles in turn result in increase energy and oxygen consumption

Lower HR: decrease of CO

27

CELULAR CARDIAC PHYSIOLOGY

With depolarization of cardiac cell. A small amount of calcium enter the the cell and triggers the release of additional calcium from intracellular storage sites ( sacoplasmic reticulum)> the calcium binds to troponin, tropomyosin is displaced from the active binding site on actin, and actin myosin crossbridges are formed.

All agents with positive inotropic properties such as the caecholamines, have in common that they increase intracellular calcium. Where as negative inotropes have the opposite effect28

SYSTOLIC FUNCTIONPeriod existing between closure of the mitral valve and start of contraction to the end of ejection of blood from heart

Purpose: ejection of the blood into the circulation via generation of pressure gradient

Has been used to determine outcome and therapeutic effectiveness for years

30

SYSTOLIC FUNCTIONCardiac OutputAmount of blood flowing into circulation per minute.CO = SV x HRPrimary determinant of CO are the HR and SVSecondary factors are venous return, SVR, peripheral oxygen use, total blood vol, respiration and body position

SYSTOLIC FUNCTIONNormal CO: 5 6 L/min in a 70kgSV : 60-80 ml/beat and HR: 80/min

CO is highly variable in normal healthy individual being able to increase up to 25-30 L/min during high metabolic demand

SYSTOLIC FUNCTIONCardiac index (CI) used to compare different sizes of individuals CI = (SV x HR) / BSANormal values: 2.5 3.5 L/min/m2

SYSTOLIC FUNCTIONStroke VolumeAmount of blood ejected by ventricle with each single contraction

Determinant of SV are preload, afterload and contractility

SYSTOLIC FUNCTIONPreloadVentricular wall stress at end diastole

Determine by: ventricular EDV, end diastolic pressure (EDP) and wall thickness

SYSTOLIC FUNCTIONTo apply preload principle, adjustment are made:Substituting ventricular volume for preload stressVentricular volume closely approximate muscle fibers length. Substituting ventricular press to ventricular volumeLAP, PAOP or PCWP ,PADP,RAP and CVP are often used to substitutes for LVEDP and LVEDV

36

SYSTOLIC FUNCTIONFactors that affecting preload:Total blood volume, body position, intrathoracic pressure, intrapericardial pressure, venous tone, pumping action of skeletal muscles and the atrial contribution to ventricular filling

Measurements:LVEDV: TEELVEDP: LAP, PCWP, PADP and CVP (can cause missleading

SYSTOLIC FUNCTIONFrank starling relation of chamber diastolic length

SYSTOLIC FUNCTIONAfterload Systolic ventricular wall stress is the burden that the RV or LV wall has to shoulder for ejecting its SV. Laplace law: wall stress = Pressure x Diameter / wall thickness

Second major determinant of the mechanical properties of cardiac muscle fibers and performance of the intact heart

39

SYSTOLIC FUNCTIONMeasurements of afterloadWall stressImpedanceEffective arterial elastanceSystolic intraventricular pressureSystemic vascular resistancePulmonary vascular resistance

SYSTOLIC FUNCTIONImpedance Afterload: external or extracardiac forces(impedance) present in systemic circulation that oppose ventricular ejection and pulsatile flow.

SVR = MAP- RAPOhm law : Q = P/RP = Q x RResistance is determined by arteriolar resistance (SVR)SVR= (MAP-RAP)/CO

SYSTOLIC FUNCTIONFactors that decreasing contractilityParasympathetic stimulationSympathetic inhibition Administration of beta adrenergic blocking dx, slow calcium channel blockers and myocardial depressantsMyocardial ischemia and infarctionIntrinsic myocardial disease such as cardiomyopathiesHypoxia and acidosis

SYSTOLIC FUNCTIONContractilityAmount of work that the heart can perform at given load

Factors increasing contractilitySympathetic stimulationParasympathetic inhibition producing increased HRAdministration of positive inotropic drugs such as digitalis

SYSTOLIC FUNCTIONMeasurement of contractilityIsovolemic contraction phase indicesPrototype: dP/dt (mmHg/s)Ejection phase indicesEF = SV/EDVLoad-independent indicesEnd systolic points measured during rapid decrease in preload

Indices of contractility can be classified according to the phase of the cardiac cycle during which they are obtained

44

SYSTOLIC FUNCTION

SYSTOLIC FUNCTIONHeart rateMost variable determinants of overall cardiac function

HR controlled by: Cardiac conduction system, CNS, and autonomic system

HR can increase contractility of the heartTreppe or step (Bowditch) phenomenomeThis is due to increase in the level of intracellular calcium

DIASTOLIC FUNCTIONMost important focus of cardiac physiologySeen in 40%-50% of patient with CHF

Determinant of diastolic functionMyocardial relaxatioinPassive ventricular fillingAtrial or active filling

DIASTOLIC FUNCTIONMyocardial relaxationKey determination of the length and amount of early passive ventricular filling

Relaxation relies on the use of energy and ATP to drive the Calcium from the cells into the SR. its an energy dependent process

DIASTOLIC FUNCTIONAtrial or active fillingIn the presence of severe diastolic dysfunction, atrial kick become essential to maintained SV and CO.If normal SR not maintained, atrial kick cannot function in its supportive role.Reestablishment of normal SR by cardioversion or sequential pacing can reverse the CHF symptoms