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  • 1. Cardiovascular physiology Moderator : Dr V. Chandak Dr. Tarun Yadav
  • 2. Heart Heart is functionally divided into right and left pumps each consisting of an atrium & a ventricle. The atria serve as both conduits and priming pumps, whereas the ventricles act as the major pumping chambers. The right ventricle receives systemic venous (deoxygenated) blood and pumps into the pulmonary circulation Left ventricle receives pulmonary venous (oxygenated) blood and pumps it into the systemic circulation. Four valves normally ensure unidirectional flow through each chamber.
  • 3. specialized striated muscle self-excitatory nature Serial low-resistance connections (intercalated disks) between individual myocardial cells. Electrical activity spreads via specialized conduction pathways. The normal absence of direct connections between the atria and ventricles except through the atrioventricular (AV) node delays conduction and enables atrial contraction to prime the ventricle.
  • 4. CARDIAC ACTION POTENTIALS Myocardial cell membrane is permeable to K+ but is relatively impermeable to Na+. Na+–K+ATPase concentrates K+ intracellularly in exchange for extrusion of Na+ out. Intracellular Na+ concentration is kept low, whereas intracellular K+ concentration is kept high. Relative impermeability to calcium also maintains a high extracellular to cytoplasmic calcium gradient. Movement of K+ out & down its concentration gradient results in a net loss of positive charges from inside the cell. An electrical potential is established, with the inside of the cell negative with respect to the extracellular environment.
  • 5. The resting membrane is the balance between two opposing forces: the movement of K+ down its concentration gradient and the electrical attraction of the negatively charged intracellular space for the positively charged potassium ions. –80 to –90 mV When the cell membrane potential becomes less negative and reaches a threshold value, a characteristic action potential (depolarization) develops.
  • 6. The action potential raises the membrane potential of the myocardial cell to +20 mV. Spike in cardiac action potentials is followed by a plateau phase that lasts .2– .3 s Action potential is due to the opening of both fast sodium channels (the spike) and slower calcium channels (the plateau).
  • 7. Cardiac Cycle The cardiac cycle is traditionally defined based on events occurring before, during, and after LV contraction. (0.8 sec) Left ventricular systole is commonly divided into three parts: isovolumic contraction, rapid ejection, and slower ejection.
  • 8. Isovolumic Contraction Isovolumic contraction is the interval between closure of the mitral valve and the opening of the aortic valve. Left ventricular volume remains constant during this period of the cardiac cycle. The rate of increase of LV pressure reaches its maximum during isovolumic contraction. Pressure in the aortic root declines to its minimum value immediately before the aortic valve opens.
  • 9. Rapid Ejection Rapid ejection occurs when LV pressure exceeds aortic pressure and the aortic valve opens. Approximately two thirds of the LV end-diastolic volume is ejected into the aorta during this rapid ejection phase of systole. Aortic dilation occurs in response to this rapid increase in volume as the kinetic energy of LV contraction is transferred to the systemic arterial circulation as potential energy. The compliance of the aorta and proximal great vessels determines the amount of potential energy that can be stored and subsequently released to the arterial vasculature during diastole. The normal LV end-diastolic volume is about 120 mL. The average ejected stroke volume is 80 mL, and the normal ejection fraction is approximately 67%.
  • 10. Slow ejection During the period of slower ejection, aortic pressure may briefly exceed LV pressure. The reversal of the pressure gradient between the aortic root and the LV causes the aortic valve to close, thereby producing the second heart sound (S2)
  • 11. Diastole is divided into four phases in the LV: isovolumic relaxation, early filling, diastasis, and atrial systole
  • 12. Isovolumic relaxation defines the period between aortic valve closure and mitral valve opening during which LV volume remains constant. LV pressure falls precipitously as the myofilaments relax.
  • 13. Early Filling When LV pressure falls below left atrial pressure, the mitral valve opens, and blood volume stored in the left atrium rapidly enters the LV driven by the pressure gradient between these chambers. This early-filling phase of diastole accounts for approximately 70 to 75% of total LV stroke volume available for the subsequent contraction.
  • 14. Diastasis After left atrial and LV pressures have equalized, the mitral valve remains open and pulmonary venous return continues to flow through the left atrium into the LV. This phase of diastole is known as diastasis, during which the left atrium functions as a conduit. Diastasis accounts for no more than 5% of total LV end-diastolic volume under normal circumstances.
  • 15. Atrial systole The final phase of diastole is atrial systole. Contraction of the left atrium contributes the remaining blood volume (approximately 15 to 20%) used in the subsequent LV systole.
  • 16. Cardiac output DEFINATION  Cardiac output : vol of blood pumped by heart per minute. It is measure of ventricular systolic function. C.O = S V HR  Stroke volume: vol of blood pumped per contraction  Cardiac index : C I = C O / BSA normal value 2.5 to 4.2 l / min / m2
  • 17. DETERMINANTS OF C .O Intrinsic factors Heart rate Contractility Extrinsic factors Pre load After load
  • 18. Heart rate No of beats per minute C .O directly proportional to HR HR is intrinsic function of SA node HR is modified by autonomic, humoral, local factors Enhanced vagal activity decrease HR Enhanced sympathetic activity increase HR
  • 19. Contractility Intrinsic ability of myocardium to pump in absence of changes in preload and after load Factors modifying contractility are exercise, adrenergic stimulation, changes in Ph, temperature, drugs, ischemia anoxia.
  • 20. Frank starling relationship Relation between sarcomere length and myocardial force States that if cardiac muscle is stretched it develops greater contractile tension Increase in venous return increases contractility and CO Clinical application is relation between LVEDV and SV
  • 21. Tension Frank straling relationship Length (= preload)
  • 22. HOW TO ASSESS CONTRACTILITY ? Pressure volume loops Noninvasive like echocardiography, vetriculography EF = (LVEDV – LVESV)/ LVEDV NORMAL – 60 6%
  • 23. PRELOAD Defined as ventricular load at the end of diastole before contraction has started In clinical practice PCWP or CVP are used to estimate preload
  • 24. Determinants of preload Venous return Blood volume Heart rate Atrial contraction
  • 25. AFTERLOAD Defined as systolic load on LV after contraction has began Aortic compliance is determinant of afterload e.g. AS or chronic hypertension both impede ventricular ejection Measurement of afterload DONE BY echocardiography systolic BP or SVR
  • 26. AFTERLOAD Wall stress: Laplace law states that wall stress is product of pressure and radius divided by wall thickness wall stress= P R/ 2H RV load depends on PVR.
  • 27. CARDIAC WORK External work( stroke work) is work done to eject blood under pressure. stroke work= SV P Internal work is work done to change shape of heart for ejection. Wall stress directly proportional to internal work Both internal work and external work consume oxygen
  • 28. Wall motion abnormalities Valvular dysfunction
  • 29. Methods to measure CO Fick principal Thermodilution Dye dilution Ultrasonography Thoracic bioimpedance
  • 30. Pressure volume loop
  • 31. Anatomy and physiology of coronary circulation Rt coronary artery - arises from anterior aortic sinus - supply RA, RV, inferior wall of LV, (60% ) SA node, (80%) AV node Posterior descending artery - 80% branch of RCA (rt dominant circulation) - 20% branch of LCA ( lt dominant circulation) - supplies interventricular septum and inferior wall
  • 33. Left coronary artery arises from posterior aortic sinus supply LA, LV, most of interventricular septum Left anterior descending septum and anterior wall Left circumflex lateral wall
  • 34. Venous drianage Coronary sinus great cardiac vein middle cardiac vein small cardiac vein oblique vein Anterior cardiac vein Venae cordae minimae
  • 36. Determinants of coronary perfusion Coronary perfusion is intermittent compared to continous in other organs CPP = Aortic diastolic pressure – LVEDP LV is perfused entirely during diastole RV is perfused during both systole & diastole
  • 37. Autoregulation of coronary blood flow Coronary blood flow = 250 ml/min at rest Myocardium regulates its blood supply between 50 to 170 mmhg Metabolic control Neurohumoral control
  • 38. Neurohumoral control When blood pressure decreases Blood flow decreases Vascular smooth muscle relaxation Blood flow increases
  • 39. Metabolic control When blood flow decreases Metabolites accumulate Vasodilatation occurs Blood flow increases
  • 40. Myocardial oxygen balance Myocardium extracts 65% 02 in arterial blood compared to 25% in most other tissues Cannot compensates for reduction in blood flow by extracting more 02 from Hb Any increase in demand must be met by an increase in coronary blood flow
  • 41. Myocardial 02 supply & demand Supply HR coronary perfusion pressure arterial 02 content coronary vessel diameter
  • 42. Myocardial 02 supply & demand Demand basal requirement HR wall tension contractility
  • 43. Systemic circulation Arteries (wind kessel vessels) Arterioles (resistance vessels) Capillaries Veins ( capacitance vessels)
  • 44. Normal distribution of blood volume Heart Pulmonary circulation Systemic circulation Arteries Capillaries Veins 7% 9% 15% 5% 64%
  • 45. Autoregulation Defination Ability of organ to maintain constant blood flow over wide range of perfusion pressure Mechanism metabolic myogenic
  • 46. Arterial blood pressure Mean arterial pressure MAP = DP + PP/3
  • 47. Control of arterial blood pressure Immediate control Intermediate control Long term control
  • 48. Immediate control Minute to minute control of BP central sensors Peripheral baroreceptor( stretch receptors) aortic carotid Chemoreceptor
  • 49. Intermediate control After few minutes of sustained decrease in BP Renin angiotensin aldosteron system ANP Altered capillary permiability
  • 50. Renin angiotensin aldosterone system
  • 51. Atrial Natriuretic Peptide Produced by the atria of the heart. Stretch of atria stimulates production of ANP. – Antagonistic to aldosterone and angiotensin II. – Promotes Na+ and H20 excretion in the urine by the kidney. – Promotes vasodilation.
  • 52. Long term control After hours of sustained change in BP Sodium and water retension
  • 53. Cardiac reflexes Baroreceptor reflex Chemoreceptor reflex Bainbridge reflex Bezold jarish reflex Valsalva maneuver Occulocardiac reflex
  • 54. Baroreceptor reflex ↑ BP ↑ BR in carotid sinus & aortic arch Sinus nerve & Aortic nerve IX & X nerve N. solitarius ↑ vagal tone ↓ HR
  • 55. Chemoreceptor reflex ↓pO2 ↑ pCO2 & ↓pH ↑ CR in carotid body & aortic arch Sinus nerve & Aortic nerve IX & X nerve ↑ Respiratory centre ↑ ventilatory drive
  • 56. Bainbridge reflex Venous engorgement of atria & great veins Stimulation of stretch receptors X nerve CVS center medulla ↓ Vagal tone ↑ HR
  • 57. Bezold jarish reflex Ischemia Receptors in LV X nerve Reflex bradycardia, Hypotension & coronary artery dilation
  • 58. Valsalva maneuver Forced expiration against closed glottis ↑ Intrathoracic pressure → ↑CVP → ↓ V.R → ↓ CO &BP → sensed by BR → ↑ HR & contractility When glottis opens ↑ VR → ↑ contractility → ↑ BP →sensed by BR → ↓ HR & BP
  • 59. Occulocardiac reflex Pressure on eye long & short ciliary nvs ciliary ganglion gasserion ganglia ↑ PNS → BRADYCARDIA
  • 60. Thank you www.anaesthesia.co.in anaesthesia.co.in@gmail.com