this is a ppt on cardiovasciular physiology .......

1. CARDIOVASCULAR PHYSIOLOGY -2
Presenter : Dr Rajesh Munigial
DM Cardiac Anaesthesia ( Trainee)
JNMC BELGAUM

2. TOPICS OF DISCUSSION
• Determinants of cardiac output
• Control of arterial blood pressure
• Cardiac reflexes
• Coronary physiology

3. CARDIAC OUTPUT
• Amount of blood pumped by each ventricle per minute into circulation
• 5-6lit/min
• It is a measure of systolic ventricular function
• Law of conservation of mass-
volume of blood ejected by left heart =volume of blood received by right heart
CARDIAC OUTPUT = Stroke Volume × Heart Rate

4. Determinants Of Cardiac Output

5. Determinants Of Cardiac Output

6. HEART RATE
• When stroke volume remains constant, cardiac output is directly
proportional to heart rate.
• Heart rate is an intrinsic function of the SA node (spontaneous
depolarization) but is modified by autonomic, humoral, and local
factors.
• The normal intrinsic rate of the SA node in young adults is about 90 to
100 beats/min, but it decreases with age

7. STROKE VOLUME
• Stroke volume is normally determined by three major factors: preload, afterload,
and contractility.
• Preload is muscle length prior to contraction, whereas afterload is the tension
against which the muscle must contract.
• Contractility is an intrinsic property of the muscle that is related to the force of
contraction but is independent of both preload and afterload.

8. PRELOAD
• Ventricular preload is end-diastolic volume, which is
generally dependent on ventricular filling.
• The relationship between cardiac output and left
ventricular enddiastolic volume was first described
by Starling.
• Frank starling law
(Described by Otto Frank and Ernest Starling )
 length  force of cardiac contraction
• When the heart rate and contractility remain
constant, cardiac output increases with increasing
preload until excessive end-diastolic volumes are
reached.

9. FRANK STARLING LAW

11. Significance
LVF causes accumulation of blood in LV

 Blood supply to vital organs

accumulation of blood in LV

operation of Frank Starling
mechanism

greater LV output

12. Estimation Of LV Preload

13. AFTERLOAD
• Afterload is defined as the additional load to which cardiac muscle is subjected
immediately after the onset of contraction.
• The mechanical forces to which the LV is subjected during ejection also may be used
to define LV afterload
• Left ventricular afterload is usually equated clinically with SVR, which is calculated
by the following equation:
Normal SVR is 900–1500 dyn · s cm–5

14. • Right ventricular afterload is mainly dependent on pulmonary vascular resistance
(PVR) and is expressed by the following equation:
Normal PVR is 50 to 150 dyn · s cm–5

15. Factors Affecting Afterload
• Wall stress
• Impedance
• Compliance
• Effective arterial resistance
• Systolic intraventricular pressure
• Systemic vascular resistance
• Pulmonary vascular resistance

16. LAPLACE LAW
• If the ventricle is assumed to be spherical, ventricular wall tension can be expressed
by Laplace’s law
where P is intraventricular pressure, R is the ventricular radius, and H is
wall thickness
• So , greater the volume of ventricle , more is the energy required for
contraction

17. IMPEDANCE
• Principal determinant of ventricular afterload that opposes phasic changes
in pressure and flow
• Most prominent in large arteries close to heart
• Opposing the pulsatile output of ventricles
• Influenced by
Compliance- force which opposes the rate of change in flow (pulsatile
flow)
Resistance- force which opposes the steady flow (non pulsatile flow)

18. Vascular Resistance
Resistance to flow in a hydraulic circuit
It is expressed by the relationship between pressure gradient across the circuit (∆ P) and
the rate of flow(Q)
∆ P∞ Q (Ohm’s law )
∆ P= Q×R, where
∆ P= Pressure, Q=Flow, R=Resistance
Applying Ohm’s law to CVS
SVR = MAP – RAP/ CO
PVR = PAP – LAP / CO
Clinical implication : Shift from a low CO/ high SVR to a more favourable high CO / low
SVR condition – by using vasodilators (heart failure)

19. Pleural Pressure
• Afterload (transmural) is affected by pleural pressure which acts on the outer surface of
heart
• -ve pleural pressure + ve pleural pressure
 
 Opposes ventricular emptying facilitates ventricular
emptying
 
  systolic blood pressure  systolic blood pressure

20. CONTRACTILITY
• Cardiac contractility (inotropy) is the intrinsic ability of the myocardium to pump in
the absence of changes in preload or afterload.
• Contractility is related to the rate of myocardial muscle shortening, which is, in
turn, dependent on the intracellular Ca 2+ concentration during systole.

21. Indices Of Left Ventricular Contractility

22. METHODS TO MEASURE CARDIAC OUTPUT
• Fick principal
• Thermodilution
• Dye dilution
• Ultrasonography
• Thoracic bioimpedance

23. ASSESMENT OF DIASTOLIC FUNCTION
• The ability of each chamber to efficiently fill with normal pressure is
essential to assure the best possible overall cardiac performance.
Determinants of LV diastolic function

24. ARTERIAL BLOOD PRESSURE
• Immediate control
• Intermediate control
• Long term control

25. Immediate Control
• Minute to minute control of BP
• central sensors
• Peripheral baroreceptor( stretch receptors)
aortic
carotid
• Chemoreceptor

26. RAAS (Renin Angiotensin Aldosterone System

27. ANP (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.

29. Long Term Control
• After hours of sustained change in BP
• Sodium and water retention (kidneys)

30. CARDIAC REFLEXES
• Baroreceptor reflex
• Chemoreceptor reflex
• Bainbridge reflex
• Bezold jarish reflex
• Valsalva maneuver
• Cushings reflex
• Occulocardiac reflex

31. BARORECEPTOR REFLEX
↑ BP

↑ BR in carotid sinus & aortic arch

Sinus nerve & Aortic nerve

IX & X nerve

N. solitarius

↑ vagal tone

↓ HR

32. CHEMORECEPTOR REFLEX
↓pO2 ↑ pCO2 & ↓pH

↑ CR in carotid body & aortic arch

Sinus nerve & Aortic nerve

IX & X nerve

↑ Respiratory centre

↑ ventilatory drive

33. BAINBRIDGE REFLEX
Venous engorgement of atria &
great veins

Stimulation of stretch receptors

X nerve

CVS center medulla

↓ Vagal tone

↑ HR

34. BEZOLD JARISH REFLEX
Ischemia

Receptors in LV

X nerve

Reflex bradycardia,
Hypotension & coronary
artery dilation

35. CUSHING’S REFLEX
↑ Intracranial pressure

Cerebral ischemia

↑ VMC

↑SNS - ↑BP

↑BR

↑CIC

↑Vagal tone

reflex bradycardia ↓ HR

36. OCCULOCARDIAC REFLEX

37. PHYSIOLOGY OF CORONARY CIRCULATION

38. CHARACTERISTIC FEATURES
• Coronary perfusion is intermittent compared to continuous in other
organs
• Blood flow is 250ml/min or 65-85ml/min/100gm of cardiac tissue
• 4-5% of cardiac output
• 02 consumption is very high , 70%extraction at rest.
• End arteries
• CPP = Aortic diastolic pressure – LVEDP
• Normal range 60-80mmhg

39. • Coronary flow is phasic
• LV is perfused entirely
during diastole
• RV is perfused during both
systole & diastole

40. AUTOREGULATION OF CORONARY
BLOOD FLOW
• Coronary blood flow = 250 ml/min at rest
• Myocardium regulates its blood supply between 50 to 170 mmhg

41. Endothelial Function
• Studies demonstrated that baseline values for myocardial oxygen consumption are much
smaller in the RV compared with the LV which is consistent with the disparity in pressure-
volume work between the chambers.
• RV blood flow (per 100 g tissue) is approximately two-thirds that of the LV.
• The RV’s smaller myocardial oxygen extraction indicates that blood flow is high relative to
oxygen consumption.
• This relative “overperfusion” of the RV has been attributed to a blunting of right coronary
vasoconstriction by NO (a coronary vasodilator) that is released tonically from the vascular
endothelium
• The RV is less susceptible than the LV to myocardial ischemia and infarction because of its
more favorable hemodynamic characteristics

42. NEUROHUMORAL CONTROL
When blood pressure decreases

Blood flow decreases

Vascular smooth muscle relaxation

Blood flow increases

43. METABOLIC CONTROL
When blood flow decreases

Metabolites accumulate(co2, ROS, NO, adenosine)

Vasodilatation occurs

Blood flow increases

44. CORONARY FLOW RESERVE
• Ratio of maximal to baseline coronary blood flow
• Assessed using reactive hyperemic response or coronary vasodilator
• 500–600% in normal left or right coronary circulation
• Reduced by coronary stenosis, ventricular hypertrophy, hemodilution, hypoxemia, hypercapnea, or
microvascular dysfunction
• Can be used to assess severity of coronary stenosis
• A decrease predisposes to demand-induced ischemia
Coronary flow reserve is exhausted when stenosis severity reaches approximately 90%

45. Clinical Aspects Of Coronary Flow Reserve
In the presence of an epicardial coronary stenosis (blood flow restriction), myocardial
ischemia can be inhibited by interventions that reduce myocardial oxygen demand,
such as those that decrease heart rate and myocardial contractility. This principle
forms the basis for the use of β-blockers in patients with coronary artery disease
. Analogously, an intentional increase in myocardial oxygen demand provoked with a
positive inotropic medication reproducibly causes regional wall motion abnormalities
indicative of ischemia when flow limiting coronary stenoses are present and is the
basis of dobutamine stress echocardiography

46. CORONARY STEAL – WHO IS STEALING WHAT ?

47. • Coronary steal occurs when
vasodilation causing an increase
in blood flow to well-perfused
myocardium is accompanied by a
decrease in flow to the collateral-
dependent region with
borderline perfusion and limited
vasodilator reserve

48. 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

49. Factors Affecting Myocardial Oxygen Demand
Supply Balance

51. REFERENCES
• Kaplan’s cardiac anaesthesia , 8th edition
• Morgan and Mikhail’s clinical anaesthesiology , 7th edition
• Heward SJ, Widrich J. Coronary Perfusion Pressure. [Updated 2023 Mar 16]. In:
StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024

52. Thank you !!!