1. HEART
About Disease.co Team

2. Action potential in cardiac muscle fiber is prolonged why ??
Action potential caused by two types of channels:
Fast sodium channels
Slow calcium channels / calcium- sodium channels --- responsible for plateau portion of action potential –slow to open and remain open for long
Immediately after action potential permeability of membrane for potassium decreases thus preventing early return of action potential to resting level

3. SA node action potential
Resting membrane potential millivolts
Fast sodium channels are inactivated.
Atrial action potential is slower to develop and return to resting level is also slow
Sodium ions tend to leak inside and potential rises in positive direction
When it reaches to -40mv ,sodium calcium channels become activated
Sodium calcium channel inactivate after milliseconds and large number of potassium channels open ---- terminate action potential
Potassium channels remain open longer leading to hyperpolarization

4. Draw and label action potential in SA node

5. Draw and label action potential in ventricular muscle ??

6. Action potential in ventricular muscle
Resting membrane potential mv
Phase rapid influx of positive sodium ions
Phase slight repolarization due to slight efflux of potassium ions
Phase opening of slow sodium calcium channels, plateau phase
Phase late repolarization phase
cessation of influx of sodium and calcium, efflux of potassium
Phase cell is at rest and Na K pump will restore resting membrane potential

7. Refractory period of cardiac muscle
Definition
The time interval during which a normal cardiac impulse cannot re-excite an already excited area of cardiac muscle fiber.
Types
Absolute - 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 sec
Relative The myocardial fibers can be stimulated to contract but the stimulus needed will be of much greater intensity.
0.05 sec
Refractory period of atria is shorter than for ventricles

8. How impulse spreads in cardiac muscle fibers ??
Self excitation of sinus nodal fibers
Transmission of impulse through atria by using anterior, middle and posterior internodal pathways
Av nodal delay
Rapid transmission through the purkinje system
One way conduction through the AV bundle
Distribution of purkinje fibers in ventricles – right and the left bundle branch

9. Enlist properties of cardiac muscle.
Functional Syncytium
Rhythmicity
Conductivity
Excitability Or Contractility
Contractility
All Or None Law
Stair Case Phenomena Or Treppe
Frank Starling Law
Refractory Period
Cardiac Muscle Tone

10. Explain Excitation contraction coupling in cardiac muscle fiber

11. Define preload and afterload ??
The degree of tension on the muscle when it begin to contract is called PRELOAD. It is end diastolic pressure.
AFTERLOAD
The pressure in the aorta leading from the ventricle. This corresponds to systolic pressure.

12. How pumping of heart is regulated ?
Frank Starling Law
Within physiological limits the heart pumps all the blood that return to it by veins
Nervous regulation
Sympathetic
Increase in heart rate
Strength of contraction
Parasympathetic
Slows the heart rate
Strength of contraction decreases by 20-30%

13. Effect of potassium and calcium ions on heart function
K heart is dilated and flaccid
slows the heart rate
can block conduction of cardiac impulse
Cause
high K depolarizes the resting membrane potential ,causing potential to be less negative
Membrane potential decreases so intensity of action potential decreases ,making the contraction weaker.

14. CALCIUM
calcium spastic contraction
calcium cardiac flaccidity

15. Define End Diastolic Volume
During diastole volume of ventricles increases from 70 to 120 ml. This volume is called end diastolic volume.
Stroke volume
The volume of blood ejected with each beat is called stroke volume .
End Systolic Volume
The volume of blood remaining in each ventricle at the end of systole is called end systolic volume. It is normally ml.
Ejection fraction
The fraction of end diastolic volume that is ejected is called ejection fraction. Usually 60%

16. Draw the left ventricular pressure and volume changes ??

17. Mechanical events during cardiac cycle
Isovolumetric contraction
Rapid ventricular ejection
Slow ventricular ejection
Isovolumetric ventricular relaxation
Rapid ventricular filling
Slow ventricular filling
Atrial systole

18. Draw and label right atrial pressure changes ?
Jugular venous pressure (JVP)

22. Heart sounds First heart sound
Produced due to closure of AV ( tricuspid and mitral) valves
Sound is produced due to vibration of taut valves after closure , along with vibration of walls of heart and major vessels
Second heart sound
Sudden closure of semilunar valves
Third heart sound
Due to oscillation of blood back and forth between walls of ventricles
Fourth heart sound
Contraction of atria and inrush of blood into ventricles

23. Heart block
1.Prolonged P-R (or P-Q) Interval i.e. First Degree Heart Block
PR interval increases to greater than 0.20 sec
2.Second Degree Heart Block
PR 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

24. Cardiac 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

25. How blood flow is regulated ?
Acute control
Vasodilator theory
Oxygen lack /nutrient lack theory
Acute metabolic control of blood flow
Reactive hyperemia
Active hyperemia
Autoregulation
Metabolic
Myogenic theory

26. Write 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.
CAUSE
Manifestation of local metabolic blood flow regulation
Lack of blood flow causes accumulation of vasodilators
Extra blood flow tries to repay the deficit that has occurred

27. Long term regulation Long term regulation Change in tissue vascularity
Role of Oxygen
Role of Vascular Endothelial Growth Factor or angiogenic Factors-
VEGF
Fibroblast growth factor
Angiogenin

28. Define edema. Enlist the starling forces
Definition
Presence of excess fluid in tissue spaces of body is called edema.

29. Starling forces

30. Short term regulation of blood pressure
Baroreceptor reflex
Chemoreceptor reflex
Volume reflex
Bainbridge reflex
CNS ischemic response

31. Long term regulation of blood pressure
Renal blood volume pressure control
Renin Angiotensin
Aldosterone

32. Renin angiotensin system

33. When person stands from lying position how blood pressure is regulated?
Baroreceptor reflex
Receptor
Baroreceptors of carotid sinus and aorta
Afferents
Glossopharyngeal
Vagus
Centre
Tractus solitarius of medulla
Efferents
Through ANS to the circulation
Effect
Increase in blood pressure back to normal

34. Define 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 return
Contraction force of left ventricle
Gravity
Skeletal muscle pump
Venous valves
Respiratory pump

35. Vasomotor reflexes
Force from front
Blood volume

36. Define 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.
Classification
Circulatory Shock
By decreased cardiac output
Without decreased cardiac output
Hemorrhagic Shock
(Hypovolemic Shock)
Neurogenic Shock
Anaphylactic Shock
Septic Shock

37. What are the compensatory reactions activated by hemorrhage ??

38. Clinical presentation of shock
Fast thready pulse
cold sweating on forehead
decreased mentation
dry tongue and
sunken eyes

39. A 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 likely
Diagnosis
Explain the underlying pathophysiology
What is the underlying cause for
Tachycardia
Cold and pale extremities

40. Hypovolemic shock Diagnosis Hypovolemic shock Pathophysiology
Hemorrhage
Hypovolemia
Decreased systemic filling pressure
Decreased venous return
Decreased cardiac output
Decreased blood pressure
Decreased systemic blood flow

41. Tachycardia
Sympathetic stimulation
Cold and pale extremities
vasoconstriction

42. Write short note on cardiogenic shock ?
Circulatory shock syndrome caused by inadequate cardiac pumping is called cardiogenic shock or cardiac shock.
Explanation
Damage to heart
Inadequate pumping
Coronary blood supply also reduced
Heart becomes weaker
Arterial pressure falls more
Shock worsens

43. Thank you For visiting our site
About Disease.co Team