Cardiac Physiology




Key Points




  • 1.

    The cartilaginous skeleton, myocardial fiber orientation, valves, blood supply, and conduction system of the heart determine its mechanical capabilities and limitations.


  • 2.

    The cardiac myocyte is engineered for contraction and relaxation, not protein synthesis.


  • 3.

    The cardiac cycle is a highly coordinated, temporally related series of electrical, mechanical, and valvular events.


  • 4.

    A time-dependent, two-dimensional projection of continuous pressure and volume during the cardiac cycle creates a phase space diagram that is useful for the analysis of systolic and diastolic function of each cardiac chamber in vivo.


  • 5.

    Each cardiac chamber is constrained to operate within its end-systolic and end-diastolic pressure-volume relationships when contractile state and compliance are constant.


  • 6.

    Heart rate, preload, afterload, and myocardial contractility are the main determinants of pump performance.


  • 7.

    Preload is the quantity of blood that a cardiac chamber contains immediately before contraction begins, and afterload is the external resistance to emptying with which the chamber is confronted after the onset of contraction.


  • 8.

    Myocardial contractility is quantified using indices derived from pressure-volume relationships, isovolumic contraction, and the ejection phase.


  • 9.

    Diastolic function is the ability of a cardiac chamber to effectively collect blood at a normal filling pressure.


  • 10.

    Left ventricular diastole is a complicated sequence of temporally related, heterogeneous events; no single index of diastolic function completely describes this period of the cardiac cycle.


  • 11.

    Left ventricular diastolic dysfunction is a primary cause of heart failure in as many as 50% of patients.


  • 12.

    The pericardium exerts important restraining forces on chamber filling and is a major determinant of ventricular interdependence.



The heart is an electrically self-actuated, phasic, variable-speed hydraulic pump composed of two dual-component, elastic, muscular chambers, each consisting of an atrium and a ventricle connected in series that simultaneously provide an equal quantity of blood to the pulmonary and systemic circulations. All four chambers of the heart are responsive to the stimulation rate, muscle stretch immediately before contraction (ie, preload), and the forces resisting further muscle shortening after contraction has begun (ie, afterload). The heart efficiently provides its own energy supply through an extensive coronary circulation.


The heart rapidly adapts to changing physiologic conditions by altering its inherent mechanical properties (ie, Frank-Starling mechanism) and by responding to neurohormonal and reflex-mediated signaling. Overall performance is determined by the contractile characteristics of the atria and ventricles (ie, systolic function) and by the ability of its chambers to effectively collect blood at normal filling pressures before the subsequent ejection (ie, diastolic function). This innate duality implies that heart failure may occur as a consequence of abnormalities in systolic or diastolic function.




Functional Implications of Gross Anatomy


Structure


The heart’s anatomy determines many of its major mechanical capabilities and limitations. The annuli of the valves, the aortic and pulmonary arterial roots, the central fibrous body, and the left and right fibrous trigones form the heart’s skeletal foundation. This flexible, strong, cartilaginous structure is located at the superior aspect (ie, base) of the heart. It provides support for the translucent, macroscopically avascular valves, resists the forces of developed pressure and blood flow within the chambers, and provides a site of insertion for superficial subepicardial muscle.


The left atrium (LA) and right atrium (RA) are composed of two relatively thin, orthogonally oriented layers of myocardium. The walls of the right ventricle (RV) and left ventricle (LV) are thicker (approximately 5 and 10 mm, respectively) than those of the atria and consist of three muscle layers: interdigitating deep sinospiral, superficial sinospiral, and superficial bulbospiral.


The RV is located in a more right-sided, anterior position than the LV within the mediastinum. Unlike the thicker-walled, ellipsoidal LV that propels oxygenated blood from the pulmonary venous circulation into the high-pressure systemic arterial vasculature, the thinner-walled, crescentic RV pumps deoxygenated venous blood into a substantially lower-pressure, more compliant pulmonary arterial tree.


Valves


Two pairs of valves ensure unidirectional blood flow through the right and left sides of the heart. The pulmonic and aortic valves are trileaflet structures located at the RV and LV outlets, respectively, and they operate passively with changes in hydraulic pressure. The pulmonic valve leaflets are identified by their anatomic positions (ie, right, left, and anterior), whereas the name of each aortic valve leaflet is derived from the presence or absence of an adjacent coronary ostium. The pulmonic and aortic valves open as a consequence of RV and LV ejection, respectively.


The thin, flexible, and very strong mitral valve separates the LA from the LV. The mitral valve is an oval, hyperbolic paraboloid (ie, saddle-shaped structure) containing two leaflets, identified as anterior and posterior on the basis of their anatomic locations. The valve leaflets coapt in a central curve, with the anterior mitral leaflet forming the convex border.


The functional integrity of the mitral valve apparatus is crucial to overall cardiac performance. The apparatus ensures unidirectional blood flow from the LA to the LV by preventing regurgitant flow into the LA and proximal pulmonary venous circulation.


Blood Supply


Blood flow to the heart is supplied by the left anterior descending coronary artery (LAD), the left circumflex coronary artery (LCCA), and right coronary artery (RCA). Most blood flow to the LV occurs during diastole, when aortic blood pressure exceeds the LV pressure, establishing a positive pressure gradient in the coronary arteries, all three of which contribute to the LV’s blood supply. Acute myocardial ischemia resulting from a critical coronary artery stenosis or abrupt occlusion causes a predictable pattern of LV injury based on the known distribution of blood supply. The LAD and its branches (including septal perforators and diagonals) supply the medial one-half of the LV anterior wall, the apex, and the anterior two-thirds of the interventricular septum. The LCCA and its obtuse marginal branches supply the anterior and posterior aspects of the lateral wall, whereas the RCA and its distal branches supply the medial portions of the posterior wall and the posterior one-third of the interventricular septum.


The coronary artery that supplies blood to the posterior descending artery (PDA) defines the right or left dominance of the coronary circulation. Right dominance (ie, PDA supplied by the RCA) is observed in approximately 80% of patients, whereas left dominance (ie, PDA supplied by the LCCA) occurs in the remainder.


In contrast to the LV, coronary blood flow to the RA, LA, and RV occurs throughout the cardiac cycle because systolic and diastolic aortic blood pressures exceed the pressures within these chambers. The RCA and its branches supply most of the RV, but the RV anterior wall also may receive blood from branches of the LAD. RV dysfunction may occur because of RCA or LAD ischemia.


Conduction


The mechanism by which the heart is electrically activated plays a crucial role in its mechanical performance. The sinoatrial (SA) node is the primary cardiac pacemaker if marked decreases in firing rate, conduction delays or blockade, or accelerated firing of secondary pacemakers (eg, atrioventricular (AV) node, bundle of His) do not occur. The anterior, middle, and posterior internodal pathways transmit the initial SA node depolarization rapidly through the RA myocardium to the AV node ( Table 4.1 ). A branch (ie, Bachmann bundle) of the anterior internodal pathway also transmits the SA node depolarization from the RA to the LA across the atrial septum.



Table 4.1

Cardiac Electrical Activation Sequence




































Structure Conduction Velocity (m/s) Pacemaker Rate (beats/min)
SA node <0.01 60–100
Atrial myocardium 1.0–1.2 None
AV node 0.02–0.05 40–55
Bundle of His 1.2–2.0 25–40
Bundle branches 2.0–4.0 25–40
Purkinje network 2.0–4.0 25–40
Ventricular myocardium 0.3–1.0 None

AV , Atrioventricular; SA, sinoatrial.

From Katz AM. Physiology of the Heart. 3rd ed. Philadelphia: Lippincott Williams & Wilkins; 2001.


The bundle of His pierces the connective tissue insulator of the cartilaginous cardiac skeleton and transmits the AV depolarization signal through the right and left bundle branches to the RV and LV myocardium, respectively, by an extensive Purkinje network located within the inner one-third of the ventricular walls. The bundle of His, the bundle branches, and the Purkinje network are composed of His-Purkinje fibers that ensure rapid, coordinated distribution of depolarization. This electrical configuration facilitates synchronous ventricular contraction and coordinated ejection.


Artificial cardiac pacing (eg, epicardial RV pacing) bypasses the normal conduction system and produces dyssynchronous LV activation. This dyssynchrony causes uncoordinated contraction that may reduce global LV systolic function, and it is a frequent cause of a new regional wall motion abnormality after cardiopulmonary bypass in cardiac surgical patients. This type of contractile dyssynchrony is also associated with chronic RV apical pacing (eg, for treatment of sick-sinus syndrome or an AV conduction disorder) and is known to cause detrimental effects on LV chamber geometry and function. Recognition of the key relationship between a normal electrical activation sequence and LV contractile synchrony forms the basis for the successful use of cardiac resynchronization therapy in some patients with heart failure.




Functional Implications of Gross Anatomy


Structure


The heart’s anatomy determines many of its major mechanical capabilities and limitations. The annuli of the valves, the aortic and pulmonary arterial roots, the central fibrous body, and the left and right fibrous trigones form the heart’s skeletal foundation. This flexible, strong, cartilaginous structure is located at the superior aspect (ie, base) of the heart. It provides support for the translucent, macroscopically avascular valves, resists the forces of developed pressure and blood flow within the chambers, and provides a site of insertion for superficial subepicardial muscle.


The left atrium (LA) and right atrium (RA) are composed of two relatively thin, orthogonally oriented layers of myocardium. The walls of the right ventricle (RV) and left ventricle (LV) are thicker (approximately 5 and 10 mm, respectively) than those of the atria and consist of three muscle layers: interdigitating deep sinospiral, superficial sinospiral, and superficial bulbospiral.


The RV is located in a more right-sided, anterior position than the LV within the mediastinum. Unlike the thicker-walled, ellipsoidal LV that propels oxygenated blood from the pulmonary venous circulation into the high-pressure systemic arterial vasculature, the thinner-walled, crescentic RV pumps deoxygenated venous blood into a substantially lower-pressure, more compliant pulmonary arterial tree.


Valves


Two pairs of valves ensure unidirectional blood flow through the right and left sides of the heart. The pulmonic and aortic valves are trileaflet structures located at the RV and LV outlets, respectively, and they operate passively with changes in hydraulic pressure. The pulmonic valve leaflets are identified by their anatomic positions (ie, right, left, and anterior), whereas the name of each aortic valve leaflet is derived from the presence or absence of an adjacent coronary ostium. The pulmonic and aortic valves open as a consequence of RV and LV ejection, respectively.


The thin, flexible, and very strong mitral valve separates the LA from the LV. The mitral valve is an oval, hyperbolic paraboloid (ie, saddle-shaped structure) containing two leaflets, identified as anterior and posterior on the basis of their anatomic locations. The valve leaflets coapt in a central curve, with the anterior mitral leaflet forming the convex border.


The functional integrity of the mitral valve apparatus is crucial to overall cardiac performance. The apparatus ensures unidirectional blood flow from the LA to the LV by preventing regurgitant flow into the LA and proximal pulmonary venous circulation.


Blood Supply


Blood flow to the heart is supplied by the left anterior descending coronary artery (LAD), the left circumflex coronary artery (LCCA), and right coronary artery (RCA). Most blood flow to the LV occurs during diastole, when aortic blood pressure exceeds the LV pressure, establishing a positive pressure gradient in the coronary arteries, all three of which contribute to the LV’s blood supply. Acute myocardial ischemia resulting from a critical coronary artery stenosis or abrupt occlusion causes a predictable pattern of LV injury based on the known distribution of blood supply. The LAD and its branches (including septal perforators and diagonals) supply the medial one-half of the LV anterior wall, the apex, and the anterior two-thirds of the interventricular septum. The LCCA and its obtuse marginal branches supply the anterior and posterior aspects of the lateral wall, whereas the RCA and its distal branches supply the medial portions of the posterior wall and the posterior one-third of the interventricular septum.


The coronary artery that supplies blood to the posterior descending artery (PDA) defines the right or left dominance of the coronary circulation. Right dominance (ie, PDA supplied by the RCA) is observed in approximately 80% of patients, whereas left dominance (ie, PDA supplied by the LCCA) occurs in the remainder.


In contrast to the LV, coronary blood flow to the RA, LA, and RV occurs throughout the cardiac cycle because systolic and diastolic aortic blood pressures exceed the pressures within these chambers. The RCA and its branches supply most of the RV, but the RV anterior wall also may receive blood from branches of the LAD. RV dysfunction may occur because of RCA or LAD ischemia.


Conduction


The mechanism by which the heart is electrically activated plays a crucial role in its mechanical performance. The sinoatrial (SA) node is the primary cardiac pacemaker if marked decreases in firing rate, conduction delays or blockade, or accelerated firing of secondary pacemakers (eg, atrioventricular (AV) node, bundle of His) do not occur. The anterior, middle, and posterior internodal pathways transmit the initial SA node depolarization rapidly through the RA myocardium to the AV node ( Table 4.1 ). A branch (ie, Bachmann bundle) of the anterior internodal pathway also transmits the SA node depolarization from the RA to the LA across the atrial septum.



Table 4.1

Cardiac Electrical Activation Sequence




































Structure Conduction Velocity (m/s) Pacemaker Rate (beats/min)
SA node <0.01 60–100
Atrial myocardium 1.0–1.2 None
AV node 0.02–0.05 40–55
Bundle of His 1.2–2.0 25–40
Bundle branches 2.0–4.0 25–40
Purkinje network 2.0–4.0 25–40
Ventricular myocardium 0.3–1.0 None

AV , Atrioventricular; SA, sinoatrial.

From Katz AM. Physiology of the Heart. 3rd ed. Philadelphia: Lippincott Williams & Wilkins; 2001.


The bundle of His pierces the connective tissue insulator of the cartilaginous cardiac skeleton and transmits the AV depolarization signal through the right and left bundle branches to the RV and LV myocardium, respectively, by an extensive Purkinje network located within the inner one-third of the ventricular walls. The bundle of His, the bundle branches, and the Purkinje network are composed of His-Purkinje fibers that ensure rapid, coordinated distribution of depolarization. This electrical configuration facilitates synchronous ventricular contraction and coordinated ejection.


Artificial cardiac pacing (eg, epicardial RV pacing) bypasses the normal conduction system and produces dyssynchronous LV activation. This dyssynchrony causes uncoordinated contraction that may reduce global LV systolic function, and it is a frequent cause of a new regional wall motion abnormality after cardiopulmonary bypass in cardiac surgical patients. This type of contractile dyssynchrony is also associated with chronic RV apical pacing (eg, for treatment of sick-sinus syndrome or an AV conduction disorder) and is known to cause detrimental effects on LV chamber geometry and function. Recognition of the key relationship between a normal electrical activation sequence and LV contractile synchrony forms the basis for the successful use of cardiac resynchronization therapy in some patients with heart failure.




Cardiac Myocyte Anatomy and Function


Ultrastructure


The myocyte contains large numbers of mitochondria that are responsible for the generation of high-energy phosphates (eg, adenosine triphosphate [ATP], creatine phosphate) required for contraction and relaxation ( Fig. 4.1 ). The sarcomere is the contractile unit of the cardiac myocyte. Its myofilaments are arranged in parallel, cross-striated bundles of thin fibers that contain actin, tropomyosin, and the troponin complex, and thick fibers that are primarily composed of myosin and its supporting proteins. Sarcomeres are connected in series, and the long and short axes of each myocyte simultaneously shorten and thicken, respectively, during contraction.


Sep 1, 2018 | Posted by in PAIN MEDICINE | Comments Off on Cardiac Physiology
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