CARDIOVASCULAR PHYSIOLOGY

(G Edward Morgan Jr., et all) Fariz Wajdi Latuconsina

JANTUNG

Secara anatomis 1 organ, secara fungsional 2 pompa Masing-masing memiliki atrium dan ventrikel Atrium conduits and priming pumps Ventrikel major pumping chambers Masing-masing ruangan (atrium dan ventrikel) di pisahkan oleh katup yang mencegah terjadinya aliran yang tidak sesuai

JANTUNG
The right ventricle receives systemic venous (deoxygenated) blood and pumps it pulmonary circulation The left ventricle receives pulmonary venous (oxygenated) blood and pumps it the systemic circulation. The normal pumping action of the heart is the result of a complex series of electrical and mechanical events.

OTOT JANTUNG
Consists of specialized striated muscle in a connective tissue skeleton. Can be divided atrial, ventricular, and specialized pacemaker and conducting cells

CARDIAC ACTION POTENTIALS

The myocardial cell membrane is normally permeable to K+ but is relatively impermeable to Na+ Movement of K+ out of the cell and down its concentration gradient results in a net loss of positive charges from inside the cell The resting membrane potential represents the balance between two opposing forces The normal ventricular cell resting membrane potential is 80 to 90 mV

CARDIAC ACTION POTENTIALS

PHASE 0 1 2 3 4 NAME Upstroke Early rapid repolarization Plateau Final repolarization Resting potential EVENT Activation (opening) of fast Na+ channels Inactivation of Na+ channel and transient increase in K+ permeability Activation of slow Ca2+ channels Inactivation of Ca2+ channels and increased permeability to K+ Normal permeability restored (atrial and ventricular cells) CELLULAR ION MOVEMENTS Na+ in and decreased permeability to K+ K+ out (ITo) Ca2+ in K+ out K+ out Na+ in

Diastolic repolarization

Intrinsic slow leakage of Ca2+ into cells that spontaneously depolarize

Ca2+ in

CARDIAC ACTION POTENTIALS

INITIATION & CONDUCTION OF THE CARDIAC IMPULSE

The cardiac impulse normally originates in the sinoatrial (SA) node The impulse generated at the SA node is normally rapidly conducted across the atria and to the AV node. The lower fibers of the AV node combine to form the common bundle of His. This specialized group of fibers passes into the interventricular septum before dividing into left and right branches to form the complex network of Purkinje fibers that depolarizes both ventricles.

ELECTROCARDIOGRAM
Terdiri dari beberapa kejadian gelombang defleksi dari suatu gelombang isoelektrik. Defleksi positif pertama gel P. Sebagai konsekuensi dari atrial depolarization Kejadian elektris pertama dalam jantung dimulai dari SA node. Gelombang P kemudian diikuti beberapa saat dimana gelombang kembali menjadi isoelektrik. Disini gelombang sudah mulai berjalan manuju AV node, bundle of his, RBB & LBB hingga serat purkinje PR interval adalah durasi sejak dimulainya depolarisasi atrium (awal gel P) hingga dimulainya depolarisasi ventrikel (QRS kompleks) Kompleks QRS merekam potensial aksi yang terjadi ketika gelombang depolarisasi didistribusikan keseluruh ventrikel.

ELECTROCARDIOGRAM
Segmen ST interval diantara akhir kompleks QRS dan awal gel T. bersifat isoelektrik karena seluruh otot ventrikel telah terdepolarisasi. Juga menggambarkan fase plateu pada potensial aksi jantung Repolarisasi ventrikel menimbulkan gelombang T yang menunjukkan akhir dari fase 2 dan 3 dari potensial aksi jantung. Interval QT adalah durasi diantara permulaan depolarisasi ventrikel (kompleks QRS) hingga penyelesaian repolarisasi ventrikel (akhir gel T)

ELECTROCARDIOGRAM

MECHANISM OF CONTRACTION
Myocardial cells contract as a result of the interaction of two overlapping, rigid contractile proteins, actin and myosin Cell shortening occurs when the actin and myosin are allowed to fully interact and slide over one another Regulatory proteins tropomyosin + troponin

MECHANISM OF CONTRACTION

INNERVATION OF THE HEART (parasympathetic)

Parasympathetic innervation arises in the motor nucleus of the vagus and the nucleus ambiguous in the medulla Parasympathetic fibers primarily innervate the atria and conducting tissues Acetylcholine is the neurotransmitter responsible for parasympathetic nervous system activation through nicotinic and muscarinic receptors Acetylcholine acts on specific cardiac muscarinic receptors (M2) to produce negative chronotropic, dromotropic, and inotropic effects

INNERVATION OF THE HEART (sympathetic)

widely distributed throughout the heart originate in the thoracic spinal cord (T1T4) cervical ganglia (stellate) cardiac nerves Norepinephrine release causes positive chronotropic, dromotropic, and inotropic effects primarily through activation of 1adrenergic receptors 2-adrenergic receptors (found primarily in atria) activation increases heart rate and, to a lesser extent, contractility 1-Adrenergic receptors have a positive inotropic effect

INNERVATION OF THE HEART

The afferent innervation of the heart consists of mechanoreceptors with primarily vagal afferent pathways and receptors with spinal afferent pathways. Activation of the ventricular receptors by nociception or stretch, a vagal depressor response decrease in heart rate and mean arterial pressure (the Bezold-Jarisch reflex).

CARDIAC CYCLE
1. Atrial Systole 2. Isometric Contraction 3. Ejection 4. Isometric Relaxation 5. Filling

DETERMINANTS OF VENTRICULAR PERFORMANCE

factors affecting systolic and diastolic functions can be differentiated: Systolic function involves ventricular ejection, Diastolic function is related to ventricular filling. Systolic function Cardiac output Cardiac output volume of blood pumped by heart per minute

CARDIAC OUTPUT
CO=SV X HR
HR (Heart Rate)
Intrinsic function of SA Node Modified by autonomic, humoral, and local factor Normal HR = 118 bpm (0.57 ) vagal HR (stimulation M2 cholinergic receptor) Sympathetic HR (1 2 adrenergic receptor) Blood volume pumped per contraction determined by three major factors: preload, afterload, and contractility CI = CO BSA

CI (Cardiac Index)
Normal: 2.5 4.2 L/min/m2 Relatively insensitive measurements of ventricular performance

BSA (Body Surface Area)

Obtained from nomograms based on height and weight

SV (Stroke Volume)

PRELOAD
Preload is muscle length prior to contraction Ventricular preload end-diastolic volume Generally dependent on ventricular filling relationship between CO and left ventricular end-diastolic volume Starlings law of the heart

Determinants of Ventricular Filling Factors:

Venous return Blood volume (BV) Distribution of BV (posture, intrathoracic pressure, pericardial pressure, venous tone) Rhythm (atrial contraction) Heart Rate

Diastolic Function and Ventricular Compliance ventricular compliance ventricular end-diastolic volume Factor affecting ventricular compliance:
Those related to the rate of relaxation (early diastolic compliance) hypertrophy, ischemia, and asynchrony Passive stiffness of ventricles (late diastolic compliance) hypertrophy and fibrosis Extrinsic factor pericardial disease, overdistention of the contralateral ventricle, airway or pleural pressure, tumor, etc)

metabolic activity venous tone venous return HR (>120 bpm in adults) Ventricular filling

AFTERLOAD
the tension against which the muscle must contract commonly equated with either ventricular wall tension during systole or arterial impedance to ejection Systolic intraventricular pressure is dependent on the force of ventricular contraction; the viscoelastic properties of the aorta, its proximal branches, and blood (viscosity and density); and systemic vascular resistance (SVR) = 80

MAP = mean arterial pressure (mmHg) CVP = central venous pressure (mmHg)

CONTRACTILITY
Cardiac contractility (inotropism) is the intrinsic ability of the myocardium to pump in the absence of changes in preload or afterload Contractility is related to the rate of myocardial muscle shortening, which is in turn dependent on intracellular calcium Contractility can be altered by neural, humoral, or pharmacological influences Sympathetic nervous system activity most important effect on contractility Sympathomimetic drugs and secretion of epinephrine from the adrenal glands similarly increase contractility via 1-receptor activation Myocardial contractility is depressed by anoxia, acidosis, depletion of catecholamine stores within the heart, and loss of functioning muscle mass as a result of ischemia or infarction

Wall Motion Abnormalities

When the ventricular cavity does not collapse symmetrically or fully, emptying becomes impaired abnormalities may be due to ischemia, scarring, hypertrophy, or altered conduction

Valvular Dysfunction
Valvular dysfunction can involve any one of the four valves in the heart and can lead to stenosis, regurgitation (incompetence), or both

ASSESSMENT OF VENTRICULAR FUNCTION

Assessment of Systolic Function Ejection Fraction the fraction of the end-diastolic ventricular volume ejected =

EDV left ventricular diastolic volume ESV end-systolic volume

SYSTEMIC CIRCULATION
Secara fungsional dibagi arteri, arteriol, kapiler, dan vena Arteri saluran bertekanan tinggi yang menyuplai organ Arteriol pembuluh kecil yang secara langsung memperdarahi dan mengatur aliran darah kapiler Kapiler pembuluh berdinding tipis tempat terjadinya pertukaran nutrisi antara darah dan jaringan Vena mengembalikan darah menuju jantung

DISTRIBUTION OF BLOOD VOLUME

HEART PULMONARY CIRCULATION SYSTEMIC CIRCULATION Arterial

7% 9%

15%

Capillary Venous

5% 64%

Factors influence blood flow

Mechanism of local and metabolic control (Autoregulation)

Endothelium-derived factors

Autonomic control of the systemic vasculature

Autoregulation
Most tissue beds regulate their own blood flow (autoregulation) Arterioles generally dilate in response to reduced perfusion pressure or increased tissue demand arterioles constrict in response to increased pressure or reduced tissue demand due to both an intrinsic response of vascular smooth muscle to stretch and the accumulation of vasodilatory metabolic byproducts

Endothelium-derived Factors

Include:
Vasodilator (NO, prostacyclin (PGI2)) Vasoconstrictor (endothelins, thromboxane A2) anticoagulants (eg, thrombomodulin, protein C) fibrinolytics (tissue plasminogen activator) factors that inhibit platelet aggregation (nitric oxide and PGI2)

Autonomic Control Of The Systemic Vasculature

control of the vasculature is primarily sympathetic Sympathetic fibers innervate all parts of the vasculature except for capillaries Their principal function is to regulate vascular tone Variations of arterial vascular tone serve to regulate blood pressure and the distribution of blood flow to the various organs, whereas variations in venous tone alter venous return to the heart

Sympathetic-induced vasoconstriction (via 1adrenergic receptors) can be potent in skeletal muscle, kidneys, gut, and skin The most important vasodilatory fibers are those to skeletal muscle, mediating an increase in blood flow (via 2-adrenergic receptors) in response to exercise Vasodepressor (vasovagal) syncope, which can occur following intense emotional strain associated with high sympathetic tone, results from reflex activation of both vagal and sympathetic vasodilator fibers.

ARTERIAL BLOOD PRESSURE

Systemic blood flow is MAP = SVR X CO pulsatile in large arteries = + 3 because of the heart's cyclic Pulse pressure difference between activity; systolic and diastolic pressure by the time blood reaches the systemic capillaries, flow is continuous (laminar). The mean pressure in large arteries, which is normally about 95 mm Hg, falls nearly to zero in the large systemic veins that return blood to the heart.

CONTROL OF ARTERIAL BLOOD PRESSURE

Immediate Control: primarily the function of autonomic nervous system reflexes Sensed both centrally (in hypothalamic and brain stem areas) and peripherally by specialized sensors (baroreceptors) in arterial blood pressure sympathetic tone adrenal secretion of epinephrine + vagal activity Systemic Vasoconstriction, HR, contractility blood pressure. BP baroreceptor dischargeinhibiting systemic vasoconstriction and enhancing vagal tone

CONTROL OF ARTERIAL BLOOD PRESSURE

Intermediate Control In the course of a few minutes, sustained decreases in arterial pressure together with enhanced sympathetic outflow activate the reninangiotensinaldosterone system, increase secretion of argininevasopressin (AVP), and alter normal capillary fluid exchange Sustained changes in arterial blood pressure can also alter fluid exchange in tissues by their secondary effects on capillary pressures. Hypertension increases interstitial movement of intravascular fluid, whereas hypotension increases reabsorption of interstitial fluid. Such compensatory changes in intravascular volume can reduce fluctuations in blood pressure, particularly in the absence of adequate renal function

CONTROL OF ARTERIAL BLOOD PRESSURE

Long Term The effects of slower renal mechanisms become apparent within hours of sustained changes in arterial pressure. As a result, the kidneys alter total body sodium and water balance to restore blood pressure to normal. Hypotension results in sodium (and water) retention, whereas hypertension generally increases sodium excretion in normal individuals

ANATOMY AND PHYSIOLOGY OF CORONARY CIRCULATION

DETERMINANTS OF CORONARY PERFUSION

Coronary perfusion intermittent coronary perfusion pressure is usually determined by the difference between aortic pressure and ventricular pressure
= + Decreases in aortic pressure or increases in ventricular end-diastolic pressure can reduce coronary perfusion pressure. Increases in heart rate also decrease coronary perfusion because of the disproportionately greater reduction in diastolic time as heart rate increases

CONTROL OF CORONARY BLOOD FLOW

normally parallels myocardial metabolic demand Under normal conditions, changes in blood flow are entirely due to variations in coronary arterial tone (resistance) in response to metabolic demand Autonomic influences are generally weak Sympathetic stimulation generally increases myocardial blood flow because of an increase in metabolic demand and a predominance of 2-receptor activation Parasympathetic effects on the coronary vasculature are generally minor and are weakly vasodilatory

Myocardial oxygen balance

Myocardial oxygen demand is usually the most important determinant of myocardial blood flow. Relative contributions to oxygen requirements include basal requirements (20%), electrical activity (1%), volume work (15%), and pressure work (64%). The myocardium usually extracts 65% of the oxygen in arterial blood, compared with 25% in most other tissues Therefore, the myocardium (unlike other tissues) cannot compensate for reductions in blood flow by extracting more oxygen from hemoglobin. Any increases in myocardial metabolic demand must be met by an increase in coronary blood flow.

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