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CARDIAC PHYSIOLOGY
MODERATOR:DR.P. SRINIVASA RAO.PRESENTER:DR.M. MOUNIKA.
INTRODUCTION⚫ Heart is the principle vital organ.⚫ It functionally divides into right and left
pumps, consisting of an atrium and ventricle.
⚫ Right ventricle receives deoxygenated blood and pumps it to pulmonary circulation.
⚫ Left ventricle receives oxygenated blood and pumps it to systemic circulation.
⚫ Cardiac muscle - Involuntary striated muscle - Extensive branching - consists of INTERCALATED
DISCS and GAP JUNCTIONS.⚫ Heart is a MECHANICAL and FUNCTIONAL
SYNCITIUM.
CARDIAC ACTION POTENTIAL⚫ Normal ventricular Resting membrane
potential is -80mv to -90mv.⚫ In contrast with action potentials in axons, the
spike in cardiac action potentials is followed by a plateau phase that lasts for 0.2 to 0.3 sec.
⚫ Action potential for skeletal muscle and nerves is due to abrupt opening of voltage gated sodium channels , in cardiac muscle it is initiated by voltage gated sodium channels but maintained by voltage gated calcium channels.
CONDUCTING SYSTEM
PACE MAKER POTENTIAL⚫ It usually originates in SA node , a group of specialised
pace maker cells in the sulcus terminalis,located posteriorly at the junction of right atrium and the superior vena cava.
MECHANISM OF CONTRACTION
CARDIAC CYCLE
⚫ Cardiac cycle can be defined by both mechanical and electrical events
⚫ Systole-contraction⚫ Diastole-relaxation⚫ Cardiac cycle begins with initiation of
heart beat .
PHASES OF CARDIAC CYCLE:1.Atrial systole2.Isometric contraction3.Ejection4.Isometric relaxation5.filling
VENTRICULAR STRUCTURE AND FUNCTION⚫ VENTRICULAR STRUCTURE:⚫ The specific architectural order of the cardiac
muscles provides the basis for the heart to function as a pump.
⚫ The ellipsoid shape of the left ventricle (LV) is a result of the laminar layering of spiraling bundles of cardiac muscles
⚫ The orientation of the muscle bundle is longitudinal in the subepicardial myocardium and circumferential in the middle segment and again becomes longitudinal in the subendocardial myocardium .
⚫ this type of orientation allows the LV to eject blood in a corkscrew type motion beginning from the base and ending at the apex.
Cardiac Cycle
2 components:⚫ Diastole: Filling of the chamber⚫ Systole: Contraction of the chamber and
ejection of blood
Cardiac Output⚫ The amount of blood ejected from the
ventricle in one minute CO = SV x HR⚫ Elements of cardiac output:⚫ Stroke volume⚫ Amount of blood ejected from the
ventricle in one contraction SV=EDV-ESV⚫ Heart rate⚫ The number of cardiac cycles in one
minute
CARDIAC OUTPUT⚫ Ventricular function is often equated with
cardiac output(CO)⚫ To compensate with variations in body
size, it is often expressed in terms of cardiac index(CI)
CI=CO/BSABSA=Body surface area normal CI=2.5-4.2 lit/min/sq.mt
HEART RATE⚫ Heart rate(HR) is an intrinsic function of
SA node.⚫ Normal intrinsic heart rate of young
adults is about 90-100beats/min.⚫ Usually decreases with age based on
formula: normal intrinsic HR=118
beats/min-(0.57*age)⚫ Decreased HR-M2 cholinergic receptors.⚫ Increased HR-Beta-1adrenergic
receptors.
DETERMINATION OF STROKE VOLUME:
⚫ Preload: Amount of blood delivered to the chamber.
⚫ Depends upon venous return to the heart.⚫ Also dependent upon the amount of blood
delivered to the ventricle by the atrium.⚫ Heart rate and Rhythm also affects preload.⚫ Contractility : The efficiency and strength
of contraction⚫ Frank Starling’s Law⚫ Afterload : Resistance to forward blood
flow by the vessel walls
FRANK-STARLING LAW
⚫ Other factors determining stroke volume includes: Wall motion abnormalities
Valvular dysfunction
PRESSURE-VOLUME RELATIONSHIP
⚫ It is used to demonstrate how changes in preload and afterload affect stroke volume,ESV and EDV.
⚫ A drop in preload- decrease SV,ESV,EDV.⚫ Eg: clamping of IVC.⚫ An increase in afterload-increase in end
systolic pressure and volume, decrease in SV.
Autonomic Nervous SystemSympathetic Nervous System⚫ Extensively innervates the SA node and
ventricular cells⚫ Increase in heart rate⚫ Increase in conduction and contractility in
the ventriclesParasympathetic Nervous System⚫ Innervates the SA and AV nodes⚫ Decreases heart rate⚫ Decreases conduction times through the AV
node
The Vascular System⚫ The vascular system is composed of the
systemic and pulmonary circulation.⚫ Both systems consist of arteries,
capillaries and veins.⚫ Arterial system: away from the heart⚫ Venous system: capillary beds to heart⚫ Anatomical differences of arteries and
veins
FACTORS CONTRIBUTING TO ARTERIAL BLOOD PRESSURE:
⚫ BP = CO x TPR⚫ Cardiac Pump⚫ Blood Volume⚫ Peripheral Resistance⚫ Elasticity of Arterial Walls⚫ Viscosity of Blood
⚫ Mean arterial pressure(MAP):proortionate to the product of systemic vascular resistance and cardiac output.
⚫ MAP=diastolic pressure+1/3pulse pressure
Control of arterial blood pressure⚫ Regulated by series of immediate
,intermediate and long term control.⚫ Immediate control includes: 1.Barorecetor reflexes. 2.Chemoreceptor reflexes. 3.Brain(CNS) Ischaemic responses.⚫ Intermediate control includes:Hormonal
control: 1.catecholamines 2.Renin–angiotensin–aldosterone system
3.vasopressin
⚫ Long term control includes: - Renal body fluid control systems:
i.Kidneys alter total body water and sodium balance to restore blood pressure to normal.
ii. hypotension-sodium retention hypertension-sodium excretion
Inhalational agents⚫ Nitrous oxide—used safely for cardiac pts.⚫ Halothane—B blocking action,BP
decreased,sensitises heart to adr,ventricular arrhythmias.so not to be used in cardiac pts.
⚫ Isoflurane—”controlled hypotension”,cardiac output best maintained. “Coronary steal “ phenomenon.
⚫ Desflurane—similar to isoflurane but no coronary steal phenomenon.
⚫ sevoflurane—cardiac output minimally depressed.
Intravenous anaesthetics
⚫ Barbiturates—⚫ Thiopentone and methohexitone.—⚫ Hypotension,direct depression of the
vasomotor centre.,direct myocardial depressant.increase in heart rate (compensatory mechanism)
⚫ Nonbarbiturates⚫ Propofol—hypotension.⚫ Etomidate—most cardiovascular stable.⚫ Ketamine — tachycardia ,hypertension ,
DOC in shock.
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