Cardiovascular Physiology and Pharmacology

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1 Cardiovascular Physiology and Pharmacology Peter Paal Perioperative Medicine, Barts Heart Centre St. Bartholomew s Hospital, Barts Healt NHS Queen Mary University of London and Department of Anaesthesiology and Intensive Care University Hospital Innsbruck, Austria

2 Thanks to Prof. Dr. W. Toller, MBA, DESA Head of the Division of Cardiovascular Anesthesiology Department of Anesthesiology and Intensive Care Medicine Medical University of Graz Austria

3 CARDIOVASCULAR PHYSIOLOGY

4 Myocardial contraction and Frank-Starling-Relationship

5 Actin-Myosin-Filaments

6 Troponin complex I = Inhibits interaction between actin and myosin when phosphorylated C = Ca 2+ binding Protein T = Tropomyosin-binding

7 Frank Starling law of the heart (Starling's law) Stroke volume in response to end- diastolic volume Volume stretches ventricular wall more forceful contraction Mechanism: Stretching increases affinity of troponin C for calcium greater number of actinmyosin cross-bridges form

8 Relation of resting sarcomere length on contractile force

9 Maximal force is generated with an initial sarcomere length of 2.2 µm Tension (%)

10 % Cell shortening Sensitivity of myofilaments for Ca Control 10 Desensitization Intracellular Ca2+ concentration (nm)

11 % Cell shortening Sensitivity of myofilaments for Ca Sensitization Control Intracellular Ca 2+ concentration (nm)

12 Relative Force Development Change of myofilament sensitivity to Ca 2+ 1,2 1,0 0,8 0,6 0,4 a b Temperature Protons ADP Phosphate 0,2 0, pca ( log[ca])

13 The cardiac cycle - Relation of Pressure against Volume

14 Left ventricular pressure-volume loop Stroke work = SV x Pressure

15 Sources of errors Does aortic pressure peak at end of systole? Does AV open when ventricular contraction begins? Volume change during isometric contraction? All valves closed at the onset of systole?

16 Systole Different Phases Isovolumetric contraction phase All valves closed Ejection phase Maximum ejection Reduced ejection

17 Diastole Different Phases Isovolumetric relaxation Ends with AV opening Rapid filling phase Diastasis Atrial systole Ends with start of systole 80% of the blood flows passively down to the ventricles

18 Duration (sec) of cardiac cycle phases in adult Isovolumetric contraction 0,05 Maximum ejection 0,09 Reduced ejection 0,13 Total systole 0,27 Protodiastole 0,04 Isovolumetric relaxation 0,08 Rapid inflow 0,11 Diastasis 0,19 Atrial systole 0,11 Total diastole 0,53 atz, Physiology of the Heart 2nd ed., p363; 1992 Raven press Heart Rate 75/min S:D = 1:2

19 Relationship of duration of systole + diastole with increasing heart rate

20 End-systolic and end-diastolic pressure-volume relationship Inotropy Lusitropy

21 Decreased contractility, increased end-diastolic volume

22 Vasoconstriction, fluid retention

23 Increased contractility, increased lusitropy

24 Wiggers Diagram - Relation of Pressures, Volume and ECG over Time

25 Aortic valve opens Aortic valve closes Wiggers- Diagram Mitral valve closes Mitral valve opens

26 Central venous pressure waveform atrial systole cusps bulge into atrium as AV closes Filling of atria; concomitant ventricular systole x y atrial relaxation; ventricle contracts, downward movement of base AV opens; rapid drainage into ventricle

27 Simultaneous plotting of ECG and central-venous pressure

28 Myocardial Perfusion, Oxygen Supply, Oxygen Demand

29 Anatomy of the coronary arteries Frank Netter, 1990

30 SYSTOLE DIASTOLE Arterial Blood Pressure Left Coronary Artery Flow 0 Flow Right Coronary Artery Flow 0 Flow

31 Main determinants of myocardial oxygen supply O 2 -Content of coronary blood Haemoglobin Coronary perfusion Coronary resistance Diastolic aortic pressure LVEDP Heart Rate Main natural mechanism to increase supply: Coronary vasodilation (!) Coronary oxygen extraction already maximal at rest!

32 Main determinants of myocardial oxygen demand Heart Rate Tachycardia increases oxygen demand Bradycardia decreases oxygen demand (e.g. b-blockers)

33 Relationship of duration of systole + diastole with increasing heart rate

34 Main determinants of myocardial oxygen demand Heart Rate Tachycardia increases oxygen demand Bradycardia decreases oxygen demand (e.g. b-blockers) Myocardial contractility Inotropes increase oxygen demand (e.g. epinephrine) b-blockers decrease oxygen demand

35 Effects of Milrinone or Levosimendan on Myocardial Oxygen Consumption Kaheinen, J Cardiovasc Pharmacol 43:555, 2004

36 Main determinants of myocardial oxygen demand Heart Rate Tachycardia increases oxygen demand Bradycardia decreases oxygen demand (e.g. b-blockers) Myocardial contractility Inotropes increase oxygen demand (e.g. epinephrine) b-blockers decrease oxygen demand Wall tension of the myocardium High wall tension increases oxygen demand Decrease of wall tension decreases oxygen demand

37 Wall tension of the myocardium Laplace s Law T = p x r 2h T = wall tension p = internal pressure r = internal radius h = wall thickness Increase in preload ± afterload increases wall tension e.g. Nitrates decrease wall tension Dilated cardiomyopathy increases wall tension Ventricular hypertrophy decreases wall tension

38 Same pressure, same stroke volume, higher wall stress

39 Cardiovascular Reflexes

40 Cardiovascular reflexes = neural feedback loops Afferent Activity Heart Vasculature Regulation and modulation of cardiac function CNS Vasomotor Center Efferent Activity

41 Cardiovascular reflexes Baroreceptor Reflex Bainbridge-Reflex Bezold-Jarisch-Reflex Valsalva Manoeuvre

42 Baroreceptor Reflex Definition Homeostatic mechanism for maintaining blood pressure Elevated blood pressure reflexively decreases heart rate + blood pressure Decreased blood pressure increases heart rate + blood pressure

43 Baroreceptors Afferents

44 Target: Solitary tract nucleus = vasomotor center Pressure sensing results in greater afferent activity which inhibits vasomotor center

45 Baroreceptor Reflex Efferents To heart Primarily governs rate To kidney To peripheral vasculature Primarily governs degree of vessel constriction Subdivisions Carotid baroreceptor reflex - Heart Aortic baroreceptor reflex - Vascular

46 Bainbridge-Reflex Definition Rapid intravenous infusion of volume produces tachycardia Tachycardia is reflex in origin Stretch receptors in the right and left atria Vagus nerve constitutes afferent limb Withdrawal of vagal tone primary efferent limb Bainbridge, The influence of venous filling upon the rate of the heart. J Physiol 50:65 84, 1915

47 Bezold-Jarisch-Reflex Definition Inhibition of sympathetic outflow to blood vessels and the heart Mediated by mechano- and chemosensitive receptors located in the wall of the ventricles Preservation of the heart Vasodilation during heart failure Hypotension Bradycardia Apnea possible Possible cause of profound bradycardia and circulatory collapse after spinal anesthesia Albert von Bezold ( ) and Adolf Jarisch Jr. ( )

48 The Valsalva Manoeuvre Test of Sympathetic nerve system function Parasympathetic nerve system function Straining by blowing into mouthpiece against a pneumatic resistance while maintaining a pressure of 40 mmhg for 15 sec

49 Four phases of the Valsalva Manoeuvre 1. BP via mechanical factors 2. BP (due to venous return); reflex HR and SVR return of BP despite SV 3. BP via mechanical factors after expiratory pressure is released 4. Venous return and SV (back to normal over several min), but PVR and CO cause BP and HR (reflex)

50 Four phases of the Valsalva Manoeuvre

51 CARDIOVASCULAR PHARMACOLOGY

52 Synthesis of dopamine, norepinephrine and epinephrine (1) Phenylalanine NH 2 CH 2 CH 2 COOH Tyrosine NH 2 HO CH 2 CH 2 COOH HO HO Dopa NH 2 CH 2 CH 2 COOH

53 Synthesis of dopamine, norepinephrine and epinephrine (2) HO Dopamin CH 2 CH 2 NH 2 HO HO Norepinephrine OH CH CH 2 NH 2 HO HO Epinephrine OH CH CH 2 NH CH 3 HO Dobutamine, Phenylephrine, Efedrine are synthetic!

54 Degradation of catecholamines Example: Dopamine

55 Catecholamines act by stimulating adrenergic receptors b-adrenergic receptors b 1 Cardiac stimulation (positive inotropic, lusitropic, chronotropic) Agonists, e.g. Isoprenaline, Dobutamine, Epinephrine Antagonists, e.g. Esmolol, Metoprolol, Atenolol, Bisoprolol, Carvedilol b 2 Smooth muscle relaxation, (increased myocardial contractility) Agonists, e.g. Salbutamol, Terbutalin, Salmeterol Antagonists, e.g. Propranolol b 3 Enhancement of lipolysis, smooth muscle relaxation Agonists + Antagonists, in development e.g. Solabegron

56 b 1 -Adrenoceptor Ca 2+ Dobutamine, Epinephrine G s A C Milrinone P ATP TnI Actin TnC camp PDE Protein Kinase A Ca 2+ Ca 2+ Sarc. Ret. Ca 2+ Myosin Ca 2+ PL ATP Ca 2+

57 Catecholamines act by stimulating adrenergic receptors a-adrenergic receptors a 1 Vasoconstriction, renal sodium retention, decreased gastrointestinal motility Agonists, e.g. Norepinephrine, Phenylephrine, Etilefrine, Metaraminol, Methoxamine, Epinephrine Antagonists, e.g. Phentolamine, Phenoxybenzamine, Prazosin, Labetalol, Carvedilol a 2 Central inhibition of sympathetic activity ( vasodilation, bradycardia) Agonists, e.g. Clonidine, Dexmedetomidine Antagonists, e.g. Phentolamine, Tolazoline

58 a1 a2 b G q G i G s Phospholipase C Adenylatecyclase Adenylatecyclase PIP 2 DAG ATP camp ATP camp IP 3 Ca 2+ Smooth muscle contraction Ca 2+ Inhibition of transmitter release Smooth muscle contraction Heart muscle contraction Smooth muscle relaxation glycogenolysis

59 Dopamine Stimulates Dopamine-Receptors at low doses (1 3 µg/kg/min) Various subtypes of Dopamine-receptors (D 1 -D 5 ) High receptor density in the proximal tubules of the kidney natriuresis, diuresis High receptor density in the pulmonary artery vasodilation Additionally stimulates b 1 -Receptors at moderate doses (3 10 µg/kg/min) Additionally stimulates a 1 -Receptors at high doses (> 10 µg/kg/min)

60 Effects of various catecholamines on different adrenergic receptors Cardiac b-receptors Vascular a-receptors Vascular b-receptors Norepinephrine Epinephrine Isoproterenol Dopamine Dobutamine ++ - (+) Phenylephrine Ephedrine

61 Comparison of clinical effects of inotropes Epinephrine, Norepinephrine Dopamine Dobutamine Milrinone Levosimendan Vasoconstriction Enhanced inotropy Increased heart rate Myocardial O 2 consumption Tachyarrhythmias Offset of action min hours hours - days

62 K + K + Digoxin 3 K + Na + 2 Na + Na + Ca 2+ ATPase Exchanger Ca 2+ Na + Na + Myosin TnI Actin TnC

63 Myocardial Contraction and Frank-Starling-Relationship The cardiac cycle- Relation of Pressure against Volume Wiggers Diagram- Relation of Pressures, Volume and ECG over Time Myocardial Perfusion, Oxygen Supply, Oxygen Demand Cardiovascular Reflexes Cardiovascular Pharmacology-Synthesis, Metabolism and Action of Catecholamines

64 Questions? Thank you!

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