Heart Physiol

Physiology of The Heart

M. Djauhari Widjajakusumah

Departemen Fisiologi

Fakultas Kedokteran Universitas Indonesia

Mohrman, Heller: Cardiovascular Physiology, 6th Edition 2006

Cardiovascular circuitry indicating the percentage distribution of cardiac output to various organ systems in a resting individual.

Figure 12.

Lauralee Sherwood, Human Physiology:

From Cells to Systems, 7th Ed, 2010

Major body fluid compartments with average volumes indicated for a 70-kg human. Total body water is about 60% of body weight.

Mohrman, Heller: Cardiovascular

Physiology, 6th Edition 2006

Lauralee Sherwood, Human Physiology: From Cells to Systems,

7th Ed, 2010

FIGURE 9-6 Organization of cardiac muscle fibers. Bundles of cardiac muscle fibers are arranged spirally around the ventricle. Adjacent cardiac muscle cells are joined end to end by intercalated discs, which contain two types of specialized junctions: desmosomes, which act as spot rivets mechanically holding the cells together; and gap junctions, which permit action potentials to spread from one cell to adjacent cells.

FIGURE 9-6 Organization of cardiac muscle fibers. Bundles of cardiac muscle fibers are arranged spirally around the ventricle. Adjacent cardiac muscle cells are joined end to end by intercalated discs, which contain two types of specialized junctions: desmosomes, which act as spot rivets mechanically holding the cells together; and gap junctions, which permit action potentials to spread from one cell to adjacent cells.

Specialized types of junctions

Desmosomes

Consist of a region between two adjacent cells where the apposed plasma membranes are separated by about 20 nm

Have a dense accumulation of protein at the cytoplasmic surface of each membrane and in the space between the two membranes

Protein fibers extend from the cytoplasmic surface of desmosomes into the cell and are linked to other desmosomes on the opposite side of the cell.

Desmosomes function to hold adjacent cells firmly together in areas that are subject to considerable stretching, such as in the skin.

The specialized area of the membrane in the region of a desmosome is usually disk-shaped, and these membrane junctions could be likened to rivets or spot-welds.

Vander et al.: Human Physiology: The Mechanism of Body Function, Eighth

Edition, 2001

Gap Junction

Structure in plasma membranes of cells that are in direct physical contact with one another

The two opposing plasma membranes come within 2 to 4 nm of each other, which allows specific proteins from the two membranes to join, forming small, protein-lined channels linking the two cells, linking the cytosols of adjacent cells

Allows cells to have direct communication by allowing small molecules to pass directly from the cytosol of one cell to the cytosol of an adjacent cell

Gap junctions coordinate the activities of adjacent cells by allowing chemical messengers to move from one cell to another

The small diameter of the channels (about 1.5 nm) limits what can pass between the cytosols of the connected cells to small molecules and ions, such as sodium and potassium, and excludes the exchange of large proteins

Heart muscle cells and smooth-muscle cells possess gap junctions, play a very important role in the transmission of electrical activity between the cells.

Despopoulos, Color Atlas of Physiology 5TH ed 2003 Thieme

FIGURE 9-8 Specialized conduction system of the heart and spread of cardiac excitation.

Human Physiology: From Cells to Systems,

Seventh Edition, Lauralee Sherwood, 2010

Impulse Transmission

AV delay AV node conduction: 0.09 sec Penetrating portion of AV bundle: 0.04 sec ------------------------------------

PR segment 0.13 sec

Atrial impulse conduction SA node Internodes AV node: 0.03 sec ------------------------------------

PR interval 0.16 sec

Conduction Velocity

Myocardium Atrium: 0.3 m/sec Ventricle: 0.5 m/sec

Special Conducting System Internodal pathways: 1 m/sec Transitional fibers: 0.02 m/sec AV Node: 0.05 m/sec Purkinje fibers (Bundles of His, terminal fibers): 1.5 - 4.0 m/sec

AV Node Slow Conduction

Small cells Thin cell membrane slow conduction velocity

Resting Em < Myocardium resting Em Small amplitude of action potential slow conduction

velocity

Few intercalated disc Great intercellular electrical resistance slow conduction

velocity

Purkinje Fiber

Fiber diameter > myocardium diameter Conduction velocity > conduction velocity in myocardium

Smaller intercalated disc electrical resistance Conduction velocity > conduction velocity in myocardium

Figure 15-19 Typical action potentials (in millivolts) recorded from cells in the ventricle (A), SA node (B), and atrium (C). Sweep velocity in B is one-half that in A or C. (From Hoffman BF, Cranefield PF: Electrophysiology of the heart, New York, 1960, McGraw-Hill.)

Richard E. Klabunde 2012, Cardiovascular PhysiologyConcepts

Fig 2-2. Time course of membrane potential and ion permeability changes that occur during "fast response" (left) and "slow response" (right) action potentials

Mohrman & Heller: Cardiovascular Physiology, 6th Ed 2006

Figure 22. Action potentials from these cell types are referred to as "fast response"

and "slow response" action potentials, respectively.

Panel A: fast response action potentials are characterized by a rapid depolarization (phase 0) with a substantial overshoot (positive

inside voltage), a rapid reversal of the overshoot potential (phase 1), a long plateau (phase 2), and a repolarization (phase 3) a stable, high (ie, large negative) resting membrane potential (phase

4).

Panel B: the slow response action potentials are characterized by a slower initial depolarization phase, a lower amplitude overshoot, a shorter and less stable plateau phase, and a repolarization to an unstable, slowly depolarizing "resting" potential. The unstable resting potential seen in pacemaker cells with slow response action potentials is variously referred to as the phase 4 depolarization, diastolic depolarization, or pacemaker potential.


Figure 22 Panels C and D

The resting phase

o The membranes of both types of cells are more permeable to K+ than to Na+ or Ca2+. Em resting are close to the potassium equilibrium potential (of 90 mV)

The slow depolarization phase in the pacemaker-type cells

o A progressive decrease in the membranes permeability to K+ during the resting phase

o The permeability to Na+ increases slightly. The gradual increase in the Na+/K+ permeability ratio will cause the membrane potential to move slowly away from the K+ equilibrium potential (90 mV) in the direction of the Na+ equilibrium potential

o Third, an increase in the permeability of the membrane to calcium ions, which results in an inward movement of positively charged ions and also contributes to the diastolic depolarization.


FIGURE 2.5 Changes in ion conductances associated

with a ventricular myocyte action potential.

Phase 0 (depolarization) primarily is due to the rapid increase in sodium conductance (gNa+) accompanied by a fall in potassium conductance (gK+)

The initial repolarization of phase 1 is due to opening of special potassium channels (Ito)

Phase 2 (plateau) primarily is due to an increase in slow inward calcium conductance (gCa++) through L-type Ca++ channels

Phase 3 (repolarization) results from an increase in gK+ and a decrease in gCa++

Phase 4 is a true resting potential that primarily reflects a high gK+. ERP, effective refractory period.

Richard E. Klabunde 2012, Cardiovascular PhysiologyConcepts

Changes in Na+ and K+ conductance during the action potential in giant squid axon. The dashed line represents the action potential superimposed on the same time coordinate. Note that the initial electrotonic depolarization initiates the change in Na+ conductance, which in turn adds to the depolarization. (Modified from Hodgkin AL: Ionic movements and electrical activity in giant nerve fibers. Proc R Soc Lond Ser B 1958;143:1.)

Figure 102 Rhythmical discharge of a sinus nodal fiber. Also, the sinus nodal action potential is compared with that of a ventricular muscle fiber.

Guyton & Hall: Textbook of Med Physiol 11th ed, 2006

Figure 15-20 Mechanisms involved in the changes in frequency of pacemaker firing. In A, a reduction in the slope (from a to b) of slow diastolic depolarization diminishes the firing frequency. In B, an increase in the threshold potential (from TP-1 to TP-2) or an increase in the magnitude of the resting potential (from a to d) also diminishes the firing frequency. (From Hoffman BF, Cranefield PF: Electrophysiology of the heart, New York, 1960, McGraw-Hill.)

Mohrman & Heller: Cardiovascular Physiology,

6th Ed 2006

Richard E. Klabunde 2012, Cardiovascular Physiology Concepts

Figure 15-2 Time relationships between the developed force and the changes in transmembrane potential in a thin strip of ventricular muscle. (Redrawn from Kavaler F, Fisher VJ, Stuckey JH: Bull NY Acad Med 41:592, 1965.)

Cardiac versus Skeletal Muscle AP

Refractory Period

Atrium Ventricle

Absolute refractory period 0.15 sec 0.25 - 0.30 sec

Relative refractory period 0.03 sec 0.05 sec ------------------------------------ --------------------------------------------------------------

0.18 sec 0.30 - 0.35 sec

Diagram of the changes in pressure and velocity as blood flows through the systemic circulation. TA, total cross-sectional area of the vessels, which increases from 4.5 cm2 in the aorta to 4500 cm2 in the capillaries (Table 301). RR, relative resistance, which is highest in the arterioles.

Ganong Review of Med Physiol 22nd ed,

2005

The mean arterial pressure is the average pressure driving blood forward into the tissues throughout the cardiac

cycle.

Mean arterial pressure is not the halfway value between systolic and diastolic pressure.

Arterial pressure remains closer to diastolic than to systolic pressure for a longer portion of each cardiac cycle.

At resting heart rate, about two thirds of the cardiac cycle is spent in diastole and only one third in systole.

Berne, et al: Physiology, 5th ed, 2007


Seventh Edition Lauralee Sherwood, 2010


Seventh Edition Lauralee Sherwood,

2010

Control of Cardiac Output

Cardiac output

Heart rate Stroke volume

Parasympathetic activity

Sympathetic activity (and epinephrine)

End-diastolic volume

Venous return

+ +

+ + +

+

+

_ Extrinsic control

Intrinsic control

Intrinsic control

Contractility

Peripheral resistance

vasoconstriction

arterioles

+

Extrinsic control Human Physiology:

From Cells to Systems, Seventh Edition, Lauralee Sherwood, 2010

Factors that Increase Cardiac Output

Cardiac output = Stroke Volume X Heart Rate

Cardiac muscle SA Node

End-Diastolic Volume Epinephrine & Norepinephrine Acetylcholine

Venous return Adrenal Med & Sympathetic Nerve Activity

Parasympathetic Nerve Activity

Muscle Pump & Respiratory Pump

Cardio-Accelerator & Vasomotor Centers (Medulla)

Cardio-Inhibitory Center (Medulla)

Exercise Stress Low Blood Pressure

Ganongs Review of Medical Physiology, 23rd ed, 2010

Blood Pressure : Neural Regulation

Blood Pressure

Baroreceptors

Cardiovascular Centers

Blood Vessels Heart Heart

sympathetic output parasympathetic output

Blood Pressure

output

Heart Rate (SA Node)

Stroke volume

Heart Rate (SA Node)

vasoconstriction

Blood Pressure : Hormonal Regulation

Blood pressure Baroreceptors

In kidneys Secretion of renin

Blood Angiotensin II

activated

Posterior pituitary ADH released

CV Center sympathetic output

Adrenal Cortex Aldosterone

released

Blood Vessels vasoconstriction

Kidneys water

reabsorption

Adrenal Medulla Epinephrine

released

Kidneys water

reabsorption

Sensory nerve fibers

Blood Vessels vasoconstriction

Heart

Heart rate (SA node)

Baroreceptors

In arch of aorta & carotid sinuses.

Output

Stroke volume (Cardiac muscle) Blood pressure

Basic pathways involved in the medullary control of blood pressure. The vagal efferent pathways that slow the heart are not shown. The putative neurotransmitters in the pathways are indicated in parentheses. Glu, glutamate; GABA,-aminobutyric acid; Ach, acetylcholine; NE, norepinephrine; IML, intermediolateral gray column; NTS, nucleus of the tractus solitarius; CVLM, IVLM, RVLM, caudal, intermediate, and rostral ventrolateral medulla; IX and X, glossopharyngeal and vagus nerves.

Figure 317.

Ganongs Review of Medical Physiology 22nd, 2006

+ +

+

+

+

+

+ + +

Components of the arterial baroreceptor reflex pathway. nts, nucleus tractus solitarius; rvlm, rostral ventrolateral medullary group; rn, raph nucleus; na, nucleus ambiguus; ??, incompletely mapped integration pathways that may also involve structures outside the medulla. Lange Cardiovascular Physiology, 2006 The McGraw-Hill Companies.

Nucleus ambiguus: The nucleus of origin of motor fibers of the vagus, glossopharyngeal, and aaccessory nerves that suplay the striated muscles of the larynx and pharynx. (Dorlands Illustrated Medical Dictionary 27th ed, 1988 W.B.Saunders Company)

Lauralee Sherwood, Human Physiology: From Cells to Systems, 7th Ed, 2010

Lange Cardiovascular Physiology, 2006 The McGraw-Hill Companies

Terima kasih

Physiology of The HeartSlide Number 2Mohrman, Heller: Cardiovascular Physiology, 6th Edition 2006Slide Number 4Slide Number 5Slide Number 6Slide Number 7Slide Number 8Slide Number 9Slide Number 10Slide Number 11Specialized types of junctionsSlide Number 13Gap Junction Slide Number 15Slide Number 16Slide Number 17Slide Number 18Slide Number 19Slide Number 20Slide Number 21Slide Number 22Slide Number 23Impulse TransmissionConduction VelocityAV Node Slow ConductionPurkinje FiberSlide Number 28Slide Number 29Slide Number 30Slide Number 31Slide Number 32Slide Number 33Slide Number 34Slide Number 35Slide Number 36Slide Number 37Slide Number 38Slide Number 39Slide Number 40Slide Number 41Slide Number 42Slide Number 43Slide Number 44Refractory PeriodSlide Number 46Slide Number 47Slide Number 48Slide Number 49Slide Number 50Slide Number 51Slide Number 52Slide Number 53Slide Number 54Slide Number 55Slide Number 56Slide Number 57Slide Number 58Slide Number 59Slide Number 60Human Physiology: From Cells to Systems,Seventh EditionLauralee Sherwood, 2010Slide Number 62Slide Number 63Slide Number 64Control of Cardiac OutputSlide Number 66Factors that Increase Cardiac OutputSlide Number 68Slide Number 69Blood Pressure : Neural RegulationBlood Pressure : Hormonal RegulationSlide Number 72Slide Number 73Slide Number 74Slide Number 75Slide Number 76Slide Number 77Slide Number 78Slide Number 79Slide Number 80Slide Number 81Slide Number 82Slide Number 83Slide Number 84

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Heart Physiol