CARDIAC PHYSIOLOGY 1.pdf............................................

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1. CARDIAC PHYSIOLOGY
PRESENTOR: DR.ESHVANTHNI.V
MODERATOR: DR.A.SARGUNARAJ

2. CORONARY CIRCULATION
•Right coronary arterysupplies:
1.Right atrium
2.Right ventricle
3.A small part of left ventricle near the posterior interventricular
groove
4.Posterior part of interventricular septum
5.Major portion of the conducting system of the heart

3. •Left coronary artery supplies:
1.Left atrium
2.Left ventricle
3.A small part of right ventricle near anterior interventricular groove
4.Anterior part of interventricular septum
5.A part of left branch of bundle of his
❑It has 2 branches:
•Anterior descending branch
•Left circumflex branch

5. •Coronoaryarteries are end artery
•Funtionalanastomoses are present which become active under
abnormal condition
•2 types of anastomosis:
Cardiac
anastamosis
•Branches of one coronary artery with
other
•Branches of coronary arteries and
branches of deep system of veins
Extracardiac
anastamosis
•Vasa vasoraof aorta
•Vasa vasoraof pulmonary artery
•Intrathoracic arteries
•Bronchial arteries
•Phrenic arteries

6. VENOUS DRAINAGE OF HEART
•Coronary sinus
•Great cardiac vein
•Anterior cardiac vein
•Arteriosinusoidal vessel
•Arterioluminal vessel
•Thebesianvessel

7. MYOCARDIUM
•Involuntary, striated muscle tissue in the heart between the
epicardium and the endocardium, its cells are called cardiomyocytes.
•Primary structural proteins are actin and myosin filaments
•Unlike skeletal muscles these filaments are branched, the cardiac T
tubules are larger, broader and fewer in number

8. •T tubules form dyads with the SR intercalated discs with permeable
junction
•Thus cardiomyocytesare functionally interconnected

9. CARDIAC ACTION POTENTIAL

10. EXCITATION CONTRACTION COUPLING
•Occurs in both cardiac and skeletal muscle when the action potential
spreads into the cell through transverse tubules
•Depolarisationof T tubule causes influx of calcium into the
sarcoplasm→binds to troponin →activates contraction of actin and
myosin filaments.
•It triggers an additional release of calcium from the SR into the
sarcoplasm.

11. CARDIAC CYCLE
Sequence of changes in the pressure and flow in the heart chambers
and blood vessels between 2 subsequent cardiac contractions.

12. ELECTRICAL EVENTS AND
ELECTROCARDIOGRAM
•ECG is the result of differences in electrical potential generated by the
heart
•SA node →AV node →His bundle →Purkinje system →
cardiomyocytes
•P wave →atrial systole
•PR interval →delay in atrial and ventricular contraction
•QRS complex →ventricular depolarization
•T wave →ventricular repolarization

13. MECHANICAL EVENTS
•Atrial systole –0.1 sec
•Ventricular systole –0.3 sec
-isovolumetricventricular contraction
-ventricular systole proper
•Ventricular diastole –0.5 sec
-protodiastole, isovolumetricventricular relaxation phase,
ventricular diastole proper & rapid filling phase due to atrial systole
•Atrial systole –0.7 sec

15. VR to right and left atria
Increase in atrial pressure > ventricular
pressure
Opening of AV valves
Blood flows passively into ventricular chamber
Onset of atrial systole or kick

16. Closure of AV valve
Isovolumetriccontraction of ventricles
Ventricular pressure > aortic & Pulmonary.Apressure
Opening of pulmonary and aortic valve
Ventricular ejection

17. Progressive fall in ventricular pressure
Closure of aortic and pulmonary valve
Isovolumetricrelaxation
Decreased ventricular pressure < atrial pressure
Opening of AV valves

18. NORMAL VOLUMES OF BLOOD IN VENTRICLE
•Atrial systole pushes final 20-25 ml blood (20%)
•After atrial contraction, 110-120 ml in each ventricle
•(end-diastolic volume)
•Contraction ejects ~70 ml (stroke volume output)
•Thus, 40-50 ml remain in each ventricle (End‐
•systolic volume)
•The fraction ejected is then ~60% (ejection fraction)

19. •Blood pressure in aorta is 80-120 mm Hg
•Blood pressure in pulmonary trunk is 8-25 mm Hg
•Ventricular pressure usually not increases during diastole
•Right Atrial pressure changes reflected in Jugular vein

20. CENTRAL VENOUS WAVEFORM
•a wave-atrial contraction
•c wave-ventricular systole, tricuspid bulging
•v wave-systolic filling of right atria
•x descent-atrial relaxation
•y descent-early ventricular filling

21. •“a-c” interval measures the time of conduction of the cardiac impulse
from the right atrium to the ventricles
•“a-c” interval is prolonged in cases of delayed conductivity in the AV
bundle which is an early sign of heart block
•In partial heart block, the number of “a” waves is greater than the
number of the “c” or “v” waves.
•In atrial fibrillation, the “a” wave is absent.

22. PRELOAD
•Ventricular load at the end of diastole, before contraction has started
•Pulmonary wedge pressure or central venous pressure is used to
measure preload
•When the HR & contractility remains constant , CO is directly
proportional to preload

23. AFTERLOAD
•Systolic load on LV after contraction has begun
•Aortic compliance is a determinant of afterload
•Measurement of afterload done by echocardiography and SBP

24. LAPLACE’S LAW
•States that wall stress is the product of pressure and radius divided
by wall thickness,
Wall stress=PR/2h
•Preload and afterload is the wall stress that is present at the end of
diastole and left ventricular ejection.

25. FRANK STARLING RELATIONSHIP
•Relationship between sarcomere length and myocardial force
•Stretching of myocardial sarcomere results in enhanced myocardial
performance i.eforce of contraction of ventricular muscle fibreis directly
proportional to its initial length

26. CONTRACTILITY
•Defined as the work performed by cardiac muscle at any end-diastolic
volume

27. •Pressure volume loops, requiring catheterization of the left side of the
heart , best way to determine the contractility in an intact heart.
•Pressure volume loop, an indirect measure of frank starling
relationship between force and muscle strength.
•Noninvasive index of ventricular contractile function isejection
fraction.
•EF= [LVEDV-LVESV]/LVEDV

28. CARDIAC WORK
•External work is work done to eject blood under pressure
•Stroke work= SV x P or [LVEDV-LVESV] x P
•Internal work is the work done to change shape of heart for ejection
•Wall stress directly proportional to internal work of the heart
•Cardiac efficiency=external work/energy equivalent of O2
consumption

29. HEART RATE AND FORCE FREQUENCY
RELATIONSHIP
•In isolated cardiac muscle, an increase in frequency of stimulation
induces an increase in force of contraction
•However when a stimulation becomes extremely rapid, the force of
contraction decreases.
•Pacing induced positive inotropic effect may be effective only uptoa
certain HR. In a failing heart, the force frequency relationship may be
less effective in producing a positive inotropic effect

30. CARDIAC OUTPUT
•Amount of blood pumped by the heart per unit of time
CO= SV x HR
•Determined by:-
•Intrinsic factor: HR & myocardial contractility
•Extrinsic factor: preload and afterload

31. •Heart rate-no.ofbeats per min, influenced by ANS
•Enhanced vagal activity decrease HR
•Enhanced sympathetic activity increase HR
•Stroke volume: volume of blood pumped per contraction
•Determined by: preload, afterload & contractility

32. Methods to measure CO
1.Thermodilutionmethod
2.Fick method
3.Echocardiography
❑Thermodilutionmethod
•Cold saline →arm vein →right atrium
•Change in temperature is inversely related to the amount of blood
flowing through the aorta

33. Direct Fick method
•FICK PRINCIPLE: amount of substance taken per min = [A-V] difference
of the substance x blood flow/min
•Diasdvantage-
1.Invasive procedure, risk of haemorrahge, infection
2.Patient is conscious, so CO may be higher
3.Ventricular fibrillation

34. CONTROL OF CARDIAC
FUNCTION

35. NEURAL REGULATION OF CARDIAC FUNCTION
•SNS provide positive chronotropic, inotropic and lusitropiceffects
[during exercise or stress]
•PNS has direct inhibitory effect on the atria and has a negative
modulatory effect on the ventricle [at rest]
•Parasympathetic innervation is by vagal nerve →activation of
muscarinic receptor →reduce pacemaker activity, slows AV
conduction, directly decrease atrial contractile force, inhibitory
modulation of ventricular contractile force

36. •Atria→innervated by both SNS & PNS
•Ventricles→principally by SNS
•SNS continually discharge at a slow rate maintaining a strength of
ventricular contraction 20-25%
•Maximal SNS stimulation→increase CO by 100% above normal
•Maximal PNS stimulation→decrease ventricular contractile strength
only by about 30%

37. HORMONAL CONTROL
•Hormones produced by cardiomyocytes:-
natriuretic peptide, adrenomedullin, aldosterone,
angiotensin II
•ANP & BNP are released from atria and ventricle in response to
stretch of the chamber wall
•Participate in homeostasis of body fluids, in regulation of BP and in
growth and development of cardiac tissue

38. •Adrenomedullin, a peptide hormone that increase level of cAMPand
has positive inotropic and chronotropic effect on the heart and is a
vasodilator.
•Angiotensin II stimulates AT1 receptors with positive inotropic and
chronotropic effect
•It also stimulate AT2 receptor which mediates cell growth and
proliferation of cardiomyocytes.
•Other hormones: growth hormone, thyroid hormone, sex steroid
hormone

39. SEX STEROID HORMONES AND THE HEART
•Premenopausal women has more intense cardiac contractility, lower
cardiovascular risk compared to men→estradiol
•2 types of estrogen receptors in heart
•Estrogen has vasodilatoryeffect
•In men, aromatase mediated conversion of testosterone to estrogen
maintains normal vascular tone

40. CARDIAC REFLEXES

41. BARORECEPTOR REFLEX
Increase in BP
Stimulation of BR in carotid
sinus and aortic arch
IX & X NERVE
N.solitarius
Increase in vagal tone

42. CHEMORECEPTOR REFLEX
Pao2<50mmhg or acidosis
Chemosensitivecells in carotid bodies and the aortic body
Sinus nerve of heringand X cranial nerve
Stimulates the respiratory centre
Increase the ventilator drive

43. •Activation of parasympathetic system→reduction in HR and
myocardial contractility
•Persistent hypoxia→CNSdirectly stimulated

44. BAINBRIDGE REFLEX
Increase in right side filling pressure
Stretch receptors in right atrial wall and the
cavoatrialjunction
Vagal afferent signals to medulla
Inhibit parasympathetic activity→increase HR

45. BEZOLD-JARISCH REFLEX
Ischemia or infarction, thrombolysis or
revascularization and syncope
Activation of chemoreceptors and
mechanoreceptors within the LV wall
Hypotension, bradycardia and coronary
artery dilatation

46. VALSALVA MANEUVER
•Forced expiration against a closed glottis→increase intrathoracic
pressure, CVP and decrease venous return
•Decrease in CO & BP
•Sensed by baroreceptor→sympathetic stimulation →increase in HR
& myocardial contractility
•When glottis opens-→increase in VR & BP
•Increase in BP→sensed by baroreceptor →stimulate
parasympathetic

47. CUSHING REFLEX
Increase in ICP
Cerebral ischemia at
VMC
Activation of SNS
Increase in HR, ABP &
myocardial contractility

48. OCULOCARDIAC REFLEX
Pressure on eye or traction of surrounding structures
Stretch receptors send afferent signals through short
and long ciliary nerves
Trigerminal.Ncarry impulse to gasserianganglion
Increase PNS→bradycardia

49. HEMODYNAMIC EQUATIONS
•CO= HR x SV [5-7L/MIN]
•CI = CO/BSA [2.4L/MIN]
•SV = EDV-ESV [1ML/KG or 70-90 ML]
•MAP = CO x SVR
•MAP = 2/3 DBP + 1/3 SBP [60-90MMHG]

50. REFERENCES
•Stoelting’spharmacology and physiology in anesthesiapractice ,5
th
edition
•Millers Anesthesia, 9
th
edition
•Barash, clinical anesthesia, 8th edition

51. THANK YOU