CARDIAC PHYSIOLOGY and anaesthesia considerations .pptx

Cardiac physiology and anaesthesia considerations

1. CARDIAC PHYSIOLOGY Presenter- Dr. Shivangi Khanna Moderator-Dr. Anjum Saiyed

2. FUNCTIONS OF CARDIOVASCULAR SYSTEM Transport and distribute essential substances to the tissues. Remove metabolic byproducts. Adjustment of oxygen and nutrient supply in different physiologic states. Regulation of body temperature. Humoral communication.

3. CARDIOVASCULAR SYSTEM HEART (PUMP) VESSELS (DISTRIBUTION SYSTEM) REGULATION AUTOREGULATION NEURAL HORMONAL RENAL-BODY FLUID CONTROL SYSTEM

4. PRESSURES IN HEART CHAMBERS:

5. CARDIOVASCULAR MECHANICS

6. CARDIAC CYCLE The cardiac cycle describes a highly coordinated, temporally related series of electrical,mechanical and valvular events.

7. CARDIAC CYCLE The cardiac cycle is the sequence of electrical and mechanical events during the course of a single heartbeat.

8. Phases of the cardiac cycle: Isovolumic contraction 0.05sec Maximal ejection 0.1sec Start of relaxation and reduced ejection 0.15sec Isovolumic relaxation 0.1sec Rapid filling 0.1sec Slow filling ( diastasis ) 0.2sec Atrial systole or booster 0.1sec TOTAL TIME FOR ONE CARDIAC CYCLE-0.8SEC LV systole-0.3sec LV diastole 0.5 sec

9. VENTRICULAR STRUCTURE The LV is ellipsoid in shape The myofibrils are longitudinal in the subepicardial layer, circumferential in the middle segment and again longitudinal in the subendocardial layer. The ellipsoid shape causes regional differences in the myocardial thickness and cross sectional radius of the LV. This helps in accomodating variable loading conditions of the LV This type of anatomy also helps in a corkscrew manner of contraction of the LV from base to apex, thus allowing maximal shortening of myofibrils Release of this contraction also causes a suction for filling of the LV

10. VENTRICULAR STRUCTURE cont… The RV is crescent shaped, so much of the contractile force is recruited from the LV based septum Scaffold: supports the heart and adjacent vessels M/o cross linked collagen fibres - type I (thick ) and type III (thin) Elastic fibres lie in close proximity to the collagen fibres

11. CARDIAC VOLUMES Stroke Volume: The volume of blood pumped with each heartbeat it is determined by Preload: gives the volume of blood that the ventricle has available to pump Contractility : the force that the muscle can create at the given length Afterload : the arterial pressure against which the muscle will contract. SV=EDV-ESV EDV (End Diastolic Volume)- amount of blood collected in a ventricle during diastole ESV(End Systolic Volume)- amount of blood remaining in a ventricle after contraction Ejection fraction: the fraction of EDV pumped with each heart beat EF=SV/EDV Most commonly used non invasive index of cardiac contractile function Assessed by echocardiography, angiography, radionuclide ventriculography .

12. VENTRICULAR FUNCTION SYSTOLIC FUNCTION: dependant upon Heart rate preload afterload Contractility Systolic interaction ( interventricular septum) DIASTOLIC FUNCTION: Depends upon

13. PRELOAD Preload :  Preload is the ventricular load at end of diastole. This value is related to right atrial pressure. The most important determining factor for preload is venous return .

14. AFTERLOAD Afterload :  Afterload is the systolic load of the ventricle after the contraction has begun Afterload for the left ventricle is determined by aortic pressure Afterload for the right ventricle is determined by pulmonary artery pressure Assessment of afterload - Aortic impedence i.e. aortic pressure/aortic flow at an instant Clinically, SBP is adequately approximate to afterload . SVR is the most commonly used clinical estimate of LV afterload . SVR=(MAP-RAP)*80/CO dynes.sec.cm⁻⁵

15. FRANK STARLING PRINCIPLE: It is an intrinsic property of the myocardium by which stretch of the sarcomere results in enhanced myocardial performance for subsequent performances. Heart muscle expands to maximum during filling. Maximal length produces maximum tension on the muscle, resulting in forceful contraction. Therefore, greater filling (more volume entering the heart) produces greater ejection (more volume leaving). 2-2.2µm

16. FRANK STARLING PRINCIPLE CONT… This principle illustrates the relationship between cardiac output and left ventricular end diastolic volume (or the relationship between stroke volume and right atrial pressure.) It remains intact even in a failing heart Ventricular remodelling after injury or heart failure may modify it

17. FRANK STARLING PRINCIPLE CONT… Contractility : It is the inotropic state of the heart Work performed by the myocardium at any given end-diastolic fibre length Each FS curve specifies a level of contractility

18. PRESSURE VOLUME LOOPS Indirect method of measuring Frank Starling relationship Currently, the best way to assess contractility in an intact heart.

19. PRESSURE VOLUME LOOPS CONT… The filling curve of the LV moves along the End Diastolic Pressure-volume relationship curve The slope of the EDPVR curve is the reciprocal of ventricular compliance. The maximal pressure that can be developed by the ventricle at any given left ventricular volume is defined by the end-systolic pressure-volume relationship (ESPVR), which represents the inotropic state of the ventricle The PV loops change with changes in preload, afterload and inotropic state.

20. PRESSURE VOLUME LOOPS CONT… Effect of preload changes at constant inotropy : preload EDV SV( frank starling) This increase in SV is not as much as that seen in an isolated heart with constant afterload The CO and BP increase with increase in SV and any increase is partially offset

21. PRESSURE VOLUME LOOPS CONT… Effect of afterload changes at constant inotropy : afterload velocity of muscle contraction (frank starling) SV This decrease in SV is offset by the increase in EDV due to increased ESV

22. PRESSURE VOLUME LOOPS CONT… Effect of contractile state of the heart: The ratio of continuous pr. and volume of the LV during the cardiac cycle is called the ‘time varying elastance ’. Maximal elastance ( Emax ) occurs very close to the upper left corner of PV loop These Emax are linearly related and form the ESPVR, the slope of which is called the ‘end systolic elastance ’ ( Ees ). Alterations in contractile state are reflected in the Ees Clinically EF is the most common measure of LV contractility.

23. PRESSURE VOLUME LOOPS CONT… SYSTOLIC DYSFUNCTION DIASTOLIC DYSFUNCTION

24. CARDIAC WORK External work/stroke work: ejects blood under pressure Stroke work=SV×P P- pressure developed during ejection of blood Internal work: to change the shape of the heart wall stress is directly proportional to the internal work Efficiency of cardiac contraction: Cardiac efficacy=External work/Energy equivalent of O2 consumption

25. LAPLACE LAW σ =P×R/2h σ- wall stress P- Pressure R- radius of the ventricle h – thickness of the ventricle Wall stress and heart rate are probably the two most relevant factors that account for changes in myocardial oxygen demand Ellipsoid shape is responsible for the least amount of stress,therefore when the shape changes to spherical during contraction, the wall stress increases. When the afterload is increased, as in aortic stenosis , the increase in wall thickness of the LV offsets the increase in wall stress needed for generating enough pressure to maintain cardiac output

26. TREPPE: THE STAIRCASE EFFECT Aka Bowditch Effect In an isolated cardiac muscle, increase in frequency of stimulation induces an increase in the force of contraction At 150 to 180 stimuli per minute maximal contractile force is reached When this stimulation becomes extremely rapid, the force of contraction decreases. In a failing heart, this force frequency relationship may be less effective Pacing induced positive inotropic effects may be effective only upto a certain heart rate. Due to increased availability of calcium for binding to troponin C

27. PRESSURE VOLUME LOOPS CONT… Aortic stenosis

28. CARDIAC OUTPUT It is the amount of blood pumped by the heart per unit of time Determined by- Heart rate Myocardial contractility Preload Afterload Measurement of CO: Invasive methods Fick’s method Thermodilution method Dye dilution method Non invasive methods Esophageal doppler Transoesophageal Echocardiography Pulse contour CO Partial CO2 rebreathing Thoracic electrical bioimpedence

29. CARDIAC OUTPUT CONT… FICK’S METHOD: Concept- O2 delivered from the pulmonary venous blood(q3)is equal to the total O2 delivered to the pulmonary capillaries through the pulmonary artery(q1) and the alveolii (q2) q1+q2=q3 q1=Q×CpaO2 q1- amount of O2 delivered to pulmonary capillaries via pulmonary artery Q- total pulmonary arterial blood flow CpaO2- O2 concentration in pulmonary arterial blood q3=Q×CpvO2 q3- amount of O2 carried away from pulmonary venous blood Q- total pulmonary venous blood flow CpvO2- O2 concentration in pulmonary venous blood

30. CARDIAC OUTPUT CONT… q1+q2=q3 Q(CpaO2)+q2=Q(CpvO2) q2=Q{CpvO2-CpaO2) Q=q2/(CpvO2-CpaO2) CpaO2~ mixed venous systemic O2 CpvO2~peripheral arterial O2 Oxygen consumption=q2 Therefore, if CpaO2, CpvO2 and oxygen consumption are known, CO can be calculated it is considered the most accurate method available to evaluate patients with low cardiac output

31. CARDIAC OUTPUT CONT… THERMODILUTION TECHNIQUE: This method uses a special thermistor – tipped catheter(Swan- Ganz catheter) inserted from a central vein into the pulmonary artery. A cold solution of D/W 5% or normal saline (temperature 0 oC ) is injected into the right atrium from a proximal catheter port. This solution causes a decrease in blood temperature, which is measured by a thermistor placed in the pulmonary artery catheter. The decrease in temperature is inversely proportional to the dilution of the injectate .

32. CARDIAC OUTPUT CONT… The cardiac output can be derived from the modified Stewart-Hamilton conservation of heat equation most common approach in use today DYE DILUTION TECHNIQUE: Uses the same principle as thermodilution technique

33. PERICARDIUM Pericardium is less compliant than the myocardium. Fluid- 15-35 ml The slope of EDPVR increases as the pericardial pressure increases. Plays a crucial role in ventricular interdependance . RV filling RV pr and vol pr in pericardium compression of LV and reduced filling. SV and MAP. Constrictive pericarditis and pericardial tamponade cause pulsus paradoxus b/c of exaggerated effects of normal respiration

34. REGULATION OF CARDIAC FUNCTION

35. EXTRINSIC INNERVATION OF THE HEART Afferents: SYMPATHETIC- the paired superior, middle and inferior cardiac nerves from the cervical ganglia and those originating from the upper 4-5 thoracic ganglia PARASYMPATHETIC- the paired vagi Form the cardiac plexus Efferents : Through the C fibres , to the white rami , to bulbar center Responsible for perception of cardiogenic pain. Through Glossopharyngeal and Vagus nerves

36. EXTRINSIC INNERVATION OF THE HEART CONT…

37. EXTRINSIC INNERVATION OF THE HEART CONT… C fibres communicating rami brachial,cervical and intercostal nerves Referred type pain Due to metabolic changes in the myocardium causing irritation of the c fibres Area of distribution - a region including the mandible, neck, anterior and posterior surfaces of the thorax, the epigastrium and both the upper limbs ANGINA PECTORIS

38. NEURAL REGULATION Regulated by the two limbs of the ANS At rest, the major influence on the heart is parasympathetic. Sympathetic influence is more in the ventricles, than on the atria The supraventricular tissue receives significantly more intense vagal stimulation Both the neurotransmitters i.e. norepinephrine and acetylcholine are G- protein coupled receptors.

39. NEURAL REGULATION CONT.. Parasympathetic receptors: M2 receptors are mainly found in the mammalian heart Have action on-potassium channels calcium channels funny current phospholipase A2 phospholipase D tyrosine kinases M3 receptors are found mainly in the coronaries Ach- reduces pacemaker activity slows AV conduction decreases atrial contractile force exerts inhibitory modulation of ventricular contractile force

40. NEURAL REGULATION CONT.. Sympathetic receptors: All types of β receptors are found in the human heart. β 1 receptors are the predominant subtype in heart(both atria and ventricles) β 2 – atria>ventricles β 3- ventricles Both β 1 and β 2 act by Gs- cAMP pathway β 2 receptors have been found to be coupled with the Gi pathway to activate the non cAMP dependant signaling pathways.

41. NEURAL REGULATION CONT.. α₁ receptors- G protein coupled α₁ A, α₁ B, and α₁ D subtypes Both α₁ A and α₁ B are positive inotropic , but this is of minor importance They are coupled to phospholipase C, D and A₂. They increase the intracellular calcium and myocardial sensitivity to it. Cardiac hypertrophy is mediated by them, through Gq signaling α₂ receptors- Three subtypes α₂ A, α₂B and α₂C . Presynaptic inhibition of NE release.

42. HORMONAL REGULATION Cardiac hormones: Polypeptides secreted by cardiac tissues Natriuretic peptides Adrenomedullin Angiotensin II Aldosterone Natriuretic peptides: Atrial natriuretic protein- secreted from the atria B-type natriuretic peptide- from the venttricles Generate cGMP Cardiac endocrine response to pressure or volume overload Organogenesis of the embryonic heart and CVS Adrenomedullin : Accumulation of cAMP Positive inotropic and positive chronotropic Increase NO- potent vasodilator

43. HORMONAL REGULATION CONT.. Angiotensin II- key modulator of cardiac growth and function Two receptors- AT₁ and AT₂ AT₁ Predominant subtype Positive chronotropic and inotropic Cell growth and prol proliferation of myocytes and fibroblasts Release of growth factors, aldosterone and catecholamines Basis for treating heart failure with ACEI’s AT₂ Antiproliferative Most abundant in fetal heart Upregulated in response to injury and ischemia Aldosterone : Binds to mineralocorticoid receptors Increase expression and activity of- Na⁺/K ⁺ ATPase , Na⁺-K ⁺ cotransporter , Cl ⁻-HCO₃⁻ antiporter and Na⁺- H⁺antiporter Cardiac fibrosis- impairment of contractile function

44. CARDIAC REFLEXES

45. BARORECEPTOR REFLEX Receptors- circumferential and longitudinal stretch receptors in carotid sinus and aortic arch Activated by increase in BP (>170mmHg) Inhibited by decrease in BP Reflex is lost when BP<50mmHg Hormonal and sex differences might alter baroreceptor responses Volatile anaesthetics esp. Halothane inhibit the heart rate component CCBs, ACEIs or PDE inhibitors lessen the cardiovascular response due to effects on the peripheral vasculature CNS signaling pathways are also affected due to changes in calcium or angiotensin

46. CHEMORECEPTOR REFLEX Receptors- chemosensitive cells located in the carotid bodies and aortic body. Respond to changes in pH and blood O2 tension pO2<50 mmHg or acidosis sinus nerve of Hering (IX) and X CN chemosensitive area of medulla stimulation activation of respiratory center parasympathetic system Increased ventilatory reduced heart rate drive and contractility

47. BAINBRIDGE REFLEX BEZOLD ZARISCH REFLEX right atrial filling pressure stretch receptors in the rt. Atrial wall and cavoatrial junction Cardiovascular center in medulla Noxious stimuli to either ventricle associated with myocardial ischemia,profound hypovolemia , coronary reperfusion, aortic stenosis , neuraxial anesthesia associated with sympathetic blockade and “empty” ventricle vasovagal syncope Ventricular chemoreceptors and mechanoreceptors in LV wall Hypotension, bradycardia , parasympathetically induced coronary vasodilation , and inhibition of sympathetic outflow from vasomotor centers Less pronounced in hypertrophy or A fib because of modulation by ANP and BNP Vagal afferents Inhibition of parasympathetic system Increased heart rate Direct effect of stretch on SA node Vagal afferents type C

48. VALSALVA MANEUVER MULLER MANEUVER Forced expiration against closed glottis increased ICP increased CVP and decreased VR Carotid-afferent nerve of Hering ( glossopharyngeal ), Aortic- vagus Increased venous pressure in head, upper extremities, with decreased right heart venous return causing decreased blood pressure and cardiac output reflex increase in heart rate Inspiratory effort against a closed airway Decreased pleural pressure Right ventricular end-diastolic volume and left ventricular end-diastolic pressure increase, while left ventricular end-diastolic volume is unchanged or decreased, and ejection fraction is unchanged Müller maneuver may cause ventricular akinesis due to increased wall stress, increasing myocardial oxygen demand, or increased left ventricular transmural pressure, decreasing motion in nonfunctional ventricularmyocardium

49. CUSHING’S REFLEX OCULOCARDIAC REFLEX Increased cerebrospinal fluid (CSF) pressure compresses cerebral arteries Cerebral ischemia at vasomotor center Sympathetic system activation increase in arterial pressure, heart rate and contractility sufficient to reperfuse the brain Reflex bradycardia by baroreceptor reflex Traction on the extraocular muscles (more especially the medial rather than the lateral rectus) or pressure on the globe Ciliary ganglion gasserian ganglion Increased parasympathetic tone Bradycardia and hypotension Long and short ciliary nerves Ophthalmic division of trigeminal

50. REFERENCES Clinical anaesthesia – Barash , cullen , stoelting Kaplan’s cardiac anaesthesia Miller’s textbook of anaesthesia Nerves of the heart: a comprehensive review with a clinical point of view; Mario P. San MAURO,Facundo PATRONELLI: Neuroanatomy (2009) 8: 26–31 Measurement of cardiac output: Comparison of four different methodsN Kothari MD, T Amaria DNB, A Hegde MD, A Mandke MD, NV Mandke M.Ch. Lilavati Hospital & Research Center , Mumbai Editorial:The End-systolic Pressure-Volume Relation of the Ventricle: Definition,Modifications and Clinical Use,KIICHI SAGAWA, M.D. International Journal of Caring Sciences, 1(3):112–117Invasive and non-invasive methods for cardiac output measurement:Lavdaniti M Alexander Technological Educational Institute of Thessaloniki, Greece

51. Thank You