2Action potential in cardiac muscle fiber is prolonged why ?? Action potential caused by two types of channels:Fast sodium channelsSlow calcium channels / calcium- sodium channels --- responsible for plateau portion of action potential –slow to open and remain open for longImmediately after action potential permeability of membrane for potassium decreases thus preventing early return of action potential to resting level
3SA node action potential Resting membrane potential millivoltsFast sodium channels are inactivated.Atrial action potential is slower to develop and return to resting level is also slowSodium ions tend to leak inside and potential rises in positive directionWhen it reaches to -40mv ,sodium calcium channels become activatedSodium calcium channel inactivate after milliseconds and large number of potassium channels open ---- terminate action potentialPotassium channels remain open longer leading to hyperpolarization
5Draw and label action potential in ventricular muscle ??
6Action potential in ventricular muscle Resting membrane potential mvPhase rapid influx of positive sodium ionsPhase slight repolarization due to slight efflux of potassium ionsPhase opening of slow sodium calcium channels, plateau phasePhase late repolarization phasecessation of influx of sodium and calcium, efflux of potassiumPhase cell is at rest and Na K pump will restore resting membrane potential
7Refractory period of cardiac muscle DefinitionThe time interval during which a normal cardiac impulse cannot re-excite an already excited area of cardiac muscle fiber.TypesAbsolute - The time period during which the heart fibers will not contract in response to a stimulus whatever its strength may be.0.25 to 0.30 secRelative The myocardial fibers can be stimulated to contract but the stimulus needed will be of much greater intensity.0.05 secRefractory period of atria is shorter than for ventricles
8How impulse spreads in cardiac muscle fibers ?? Self excitation of sinus nodal fibersTransmission of impulse through atria by using anterior, middle and posterior internodal pathwaysAv nodal delayRapid transmission through the purkinje systemOne way conduction through the AV bundleDistribution of purkinje fibers in ventricles – right and the left bundle branch
9Enlist properties of cardiac muscle. Functional SyncytiumRhythmicityConductivityExcitability Or ContractilityContractilityAll Or None LawStair Case Phenomena Or TreppeFrank Starling LawRefractory PeriodCardiac Muscle Tone
10Explain Excitation contraction coupling in cardiac muscle fiber
11Define preload and afterload ?? The degree of tension on the muscle when it begin to contract is called PRELOAD. It is end diastolic pressure.AFTERLOADThe pressure in the aorta leading from the ventricle. This corresponds to systolic pressure.
12How pumping of heart is regulated ? Frank Starling LawWithin physiological limits the heart pumps all the blood that return to it by veinsNervous regulationSympatheticIncrease in heart rateStrength of contractionParasympatheticSlows the heart rateStrength of contraction decreases by 20-30%
13Effect of potassium and calcium ions on heart function K heart is dilated and flaccidslows the heart ratecan block conduction of cardiac impulseCausehigh K depolarizes the resting membrane potential ,causing potential to be less negativeMembrane potential decreases so intensity of action potential decreases ,making the contraction weaker.
15Define End Diastolic Volume During diastole volume of ventricles increases from 70 to 120 ml. This volume is called end diastolic volume.Stroke volumeThe volume of blood ejected with each beat is called stroke volume .End Systolic VolumeThe volume of blood remaining in each ventricle at the end of systole is called end systolic volume. It is normally ml.Ejection fractionThe fraction of end diastolic volume that is ejected is called ejection fraction. Usually 60%
16Draw the left ventricular pressure and volume changes ??
22Heart sounds First heart sound Produced due to closure of AV ( tricuspid and mitral) valvesSound is produced due to vibration of taut valves after closure , along with vibration of walls of heart and major vesselsSecond heart soundSudden closure of semilunar valvesThird heart soundDue to oscillation of blood back and forth between walls of ventriclesFourth heart soundContraction of atria and inrush of blood into ventricles
23Heart block1.Prolonged P-R (or P-Q) Interval i.e. First Degree Heart BlockPR interval increases to greater than 0.20 sec2.Second Degree Heart BlockPR interval becomes greater than 0.45 sec ,action potential is sometimes strong enough to pass and sometimes not giving dropped beats in ECG.3.Complete A-V Block (Third degree Block)Complete block of impulse from atria into ventricles .4.Incomplete Intraventricular block i.e. Electrical Alternans.Impulse conduction blocked in peripheral ventricular purkinje system
24Cardiac arrest Definition: Treatment: Cessation of all rhythmical impulses of the heart. May occur during deep anesthesia or severe myocardial diseases.Treatment:Cardiopulmonary resuscitation is quite successful in re-establishing a normal heart rhythm
25How blood flow is regulated ? Acute controlVasodilator theoryOxygen lack /nutrient lack theoryAcute metabolic control of blood flowReactive hyperemiaActive hyperemiaAutoregulationMetabolicMyogenic theory
26Write a short note on reactive hyperemia ? When blood supply to tissue or organ is blocked for few seconds to hours and then unblocked ,blood flow through tissues increases four to seven times normal. This phenomenon is called reactive hyperemia.CAUSEManifestation of local metabolic blood flow regulationLack of blood flow causes accumulation of vasodilatorsExtra blood flow tries to repay the deficit that has occurred
27Long term regulation Long term regulation Change in tissue vascularity Role of OxygenRole of Vascular Endothelial Growth Factor or angiogenic Factors-VEGFFibroblast growth factorAngiogenin
28Define edema. Enlist the starling forces DefinitionPresence of excess fluid in tissue spaces of body is called edema.
33When person stands from lying position how blood pressure is regulated? Baroreceptor reflexReceptorBaroreceptors of carotid sinus and aortaAfferentsGlossopharyngealVagusCentreTractus solitarius of medullaEfferentsThrough ANS to the circulationEffectIncrease in blood pressure back to normal
34Define cardiac output. Enlist factors effecting venous return ? The quantity of blood pumped into the aorta each minute by the heart is called cardiac output.Factors affecting venous returnContraction force of left ventricleGravitySkeletal muscle pumpVenous valvesRespiratory pump
36Define shock. Give its classification Generalized inadequate blood flow to through the body, to the extent that tissues are damaged because of lack of oxygen and other nutrients.ClassificationCirculatory ShockBy decreased cardiac outputWithout decreased cardiac outputHemorrhagic Shock(Hypovolemic Shock)Neurogenic ShockAnaphylactic ShockSeptic Shock
37What are the compensatory reactions activated by hemorrhage ??
38Clinical presentation of shock Fast thready pulsecold sweating on foreheaddecreased mentationdry tongue andsunken eyes
39A 45 year old man was brought to accident and emergency department A 45 year old man was brought to accident and emergency department. He had a road traffic accident. He was bleeding profusely. On examination systolic blood pressure was 60 mmHg, pulse was 108 /min, weak and thready. Skin was pale and extremities were cold. What is the most likelyDiagnosisExplain the underlying pathophysiologyWhat is the underlying cause forTachycardiaCold and pale extremities
41TachycardiaSympathetic stimulationCold and pale extremitiesvasoconstriction
42Write short note on cardiogenic shock ? Circulatory shock syndrome caused by inadequate cardiac pumping is called cardiogenic shock or cardiac shock.ExplanationDamage to heartInadequate pumpingCoronary blood supply also reducedHeart becomes weakerArterial pressure falls moreShock worsens
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