Cardiovascular physiology

1. Cardiovascular Physiology

2. Preload
• Ventricular load at the end of diastole (end diastolic volume),
dependent on ventricular filling
• Frank-Starling’s Law: Stroke volume of LV will increase as LVEDV
increases due to myocyte stretch causing more forceful systolic
contraction
– Excessive filling can cause decrease in contraction
• Direct measurements from echocardiography

3. Factors Affecting Preload
• Blood volume
• Distribution of blood
– Posture
– Intrathoracic pressure (positive pressure ventilation)
– Pericardial pressure
– Venous tone
• Atrial contraction: absent (atrial fibrillation), ineffective (atrial flutter),
altered timing (junctional rhythms)
• Heart rate: greater decrease in diastole

4. Factors Affecting Preload
• LVEDP can be used as measure of preload if relationship between
ventricular volume and compliance is constant (however not linear)
• RV more compliant than LV, thinner wall
• Hypertrophy, ischaemia, fibrosis, asynchrony, pericardial disease,
increased airway and pleural pressure decrease compliance

5. Afterload
• Equates to ventricular wall tension during systole or arterial impedence
to ejection
• Laplace Law: Circumferential Stress = PR/2H
– P is intraventricular pressure
– R is ventricular radius
– H is wall thickness
• Arteriolar tone mainly dependent on SVR = 80X(MAP-CVP/CO)
• RV afterload dependent on PVR = 80X(PAP-LAP/CO)
– PCWP can be substituted as approximation for LAP

6. Contractility
• Contractility or inotropy is the intrinsic ability of the myocardium to
pump in the absence of changes in preaload or afterload
• Dependent on intracellular Ca2+
during systole
• SANS activity has most effect, noradrenaline from nerve terminals and
adrenaline from adrenals via β1-activation, also sympathomimetic drugs
• Depressed by hypoxia, acidosis, catecholamine depletion,
ischaemia/infarction

7. Contractility
• Most anaesthetics are negative inotropes
• Positive inotropes
– Digoxin: Na/K pump inhibitor
– Dobutamine: β1 agonist
– Norepinephrine: β1 and α1 agonist
– Milrinone: PDE inhibitor
– Dopamine: Dose dependent action
• SV increases with increase in preload and contractility and decreases
with increase in afterload

8. Heart Rate
• CO is directly proportional to HR, provided SV is constant
• Intrinsic function of SAN
• Normal intrinsic HR = 118 – (0.57 X Age)
• Slowed by vagal activity by activation of M2 receptors
• Increased by sympathetic activity through β1 receptors
• CO = SV X HR

9. Arterial supply: 2 Coronary arteries- RCA & LCA.

10. Artery & branches Supplied area
RCA: Posterior Descending (PDA)
Acute Marginal (AM)
Conus branches
• right atrium
• most of the right ventricle,
• a small part of the diaphragmatic aspect of left ventricle,
• part of left atrium, and
• posterior one-third of interventricular septum.
• SA node in 60%
• AV node in 85%
• Bundle of His, anterior papillary muscle
• Posterior papillary muscle (PDA)
LCA: Left circumflex (LCX)
Left Anterior Descending (LAD)
Obtuse Marginal (OM)
Diagonal (D1, D2, D3)
• most of left atrium.
• free wall of the left ventricle,
• a narrow strip of the right ventricle anteriorly,
• anterior two-thirds of ventricular septum
• SA node in 40% (LAD)
• AV node in 15% (LCX)
• Bundle of His, anterior papillary muscle
Coronary artery dominance: artery that supplies PDA
~70-85% Right dominant

11. Coronary blood flow
• ~70 ml/min/100 g of heart weight,
• 225-250ml/min,
• 4-5% of the total cardiac output.
• 70 % of the oxygen in the coronary arterial blood is extracted
• Myocardium regulates its own blood flow between 50-120 mmHg
CPP
• Increase in heart rate = decrease in diastole time

12. Phasic Changes in Coronary Blood Flow During Systole
and Diastole
Systole: aortic pressure and
intramyocardial pressure nearly
equal 》 occlusion of
intramyocardial vessel- no
coronary blood flow
Diastole: arterial diastolic
pressure>LVEDP 》 Ventricular
perfusion occurs

13. CONTROL OF CORONARY BLOOD FLOW
1. Local Muscle Metabolism/ myocardial metabolic demand
• Primary Controller
• local arteriolar vasodilation in response to the nutritional needs of cardiac muscle.
• Increased cardiac contraction 》 increased rate of coronary blood flow
• Oxygen Demand is a Major Factor
• increased oxygen consumption/hypoxia causes coronary dilation
• Hypoxia induces release of adenosine and other vasodilator substance

14. 2. Nervous Control
• Stimulation of the autonomic nerves affect both directly and indirectly
Control of coronary circulation continue...
sympathetic stimulation
|
release of norepinephrine from sympathetic nerves,
epinephrine & norepinephrine from adrenal medullae
|
increases rate and contractility of heart
|
Increases the rate of metabolism
|
dilating the coronary vessels,
|
blood flow increases approximately
Constriction >
dilatation of coronary
vessel
Direct
effect

15. vagal stimulation
|
release of acetylcholine
| indirect effect
slows the heart and has a slight depressive effect on
heart contractility
|
decrease cardiac oxygen consumption
|
constrict the coronary arteries.
dilate the coronary
arteries
Direct
effect
Control of coronary circulation continue...

16. VENOUS DRAINAGE OF THE
HEART
Coronary sinus
Anterior cardiac veins
Venae Cordis minimae.

17. Cardiac cycle
• Series of pressure changes that take place within the heart.
• These pressure changes result in movement of blood throughout the
cardiac chambers and the body as a whole.
• Wiggers diagram
– A form of graphical representation of various pressure changes over time.
– Published at around 1921.
– The X-axis of the diagram is used to plot time, while the Y-axis contains all of
the following- BP-aortic ventricular atrial, ventricular volume, ECG, Atrial
flow, Heart sound.

18. Cardiac Cycle
• Two distinct phases.
• Systole- Period of ventricle contraction and blood ejection corresponding to period between QRS
and end of T wave in ECG or period between closure of semilunars and opening of AV valves.
Time = 0.3 sec
• Diastole- defined as ventricle relaxation and cardiac filling corresponding to end of T wave and
end of PR interval in ECG or period of time when semilunars are open. Time = 0.5
• Atrial systole= 0.1 sec; atrial diastole =0.7 sec.
• They are subdivided into distinct phases.
• Systole- Isovolumetric contraction: 0.05sec; Early and late ejection: 0.22sec
• Diastole- Isovolumatric relaxation , Inflow, Diastasis, Atrial systole

19. Stages of Cardiac Cycle
1. Isovolumic relaxation – AV valves and
semilunars are closed. S2
2. Inflow
a) Ventricular filling – AV valve are open and
semilunars are closed. Ventricle and atria both
relax together and get filled. Corresponds to T
wave of ECG and end of phase three of action
potential.
b) Ventricular filling with atrial systole- ventricle
expand while atria contract forcing about 20 ml
of volume to end diastolic volume. Seen as P
wave in ECG. End of this phase corresponds to
peak R wave in ECG and phase 0 of action
potential. Diastasis-S3. Atrial systole- S4.

20. Stages of Cardiac Cycle
3. Isovolumetric contraction- AV and
semilunars are closed. Ventricle begin
to contract. Phase 0 of action potential
start here. Begins at peak of R in ECG.
S1.
4. Ejection- AV closed and semilunars
open. Ventricle contract and push
blood through the body.
a) Early/rapid ejection- phase 2. ECG
beginning of T wave.
b) Late ejection- phase 3. Ecg- peak of t wave.

22. Cardiac and Function Curves

23. Cardiac and Function Curves

24. Cardiac and Function Curves

25. Action Potential of Pacemaker

26. Action Potential of Cardiac Myocyte

27. Systemic circulation:
arteries >> arterioles>>capillaris>>venules>>veins
Comprises -80% of total blood volume
Systemic blood pressure decreases as blood travel from aorta to large
vein.
 ↓systolic BP in each portion of systemic circulation >> directly proportional to
resistance to flow in vessel

29. Normal pressure in heart and great vessels
Heart region mmHg mmHg
Right atrium 0-8
Right ventricle systolic pressure :25 Diastolic pressure :4
Pulmonary artery systolic pressure: 25 Diastolic :10
Pulmonary artery occlusion pressure 2-12
Left atrium 8-10
Left ventricle systolic : 120 Diastolic :10
Aorta Systolic: 120 Diastolic : 80

31.  Cardiac output:
 Volume of blood ejected from left ventricle in a minute
 SV*HR = (normal value : 5-7 L/min )
where SV-stroke volume , HR – heart rate
 Stroke volume :
 Amount of blood ejected from left ventricle per heart beat (in each cardiac cycle )
 SV= end diastolic volume –end systolic volume
 70- 90ml
 Ejection fraction :
 described SV as %of diastolic left ventricular volume
 55%-70%

32.  Factors determining cardiac output

33. Venous return is main determinant
 Decreased CO
venous return
 Hemorrhage
 Spinal anesthesia
 PPV
 Increased CO
systemic vascular resistance
 Anemia (decreased viscosity)
 Increased blood volume
 Exercise
 Hyperthyroidism
 AV shunts

34. Methods to measure CO:
1. Fick method
2. Indicator dilution method
3. Thermodilution method
4. Echocardiography
5. Impedance cardiography
6. Pulse control analysis

35.  Fick method:
Cardiac Output = O2 consumption (VO2) / (CaO2-CvO2)
where
VO2: O2 consumption
CaO2: arterial O2 concentration
=(1.34*Hb*SaO2)
CvO2: venous O2 concentration
=(1.34*Hb*SvO2)

36. Cardiac index
 Hemodynamic parameter that relates cardiac output in 1 min to BSA
 Relating heart performance to size of individual
 CI= CO/ BSA = 5 /1.7 = 2.9
 Normal range : 2.4-4.5 L/min/m2
 More accurate indicator of cardiac function than CO

37.  Maintenance of hemodynamic relies on factor affecting MAP ---(SVR, CO)
 Mean arterial pressure(MAP):
= 2/3 (diastolic BP) + 1/3 (systolic BP)
- normal range :60- 90 mmHg

38. Systemic venous resistance(SVR)
 Resistance to blood flow offered by sys. vasculature to left side of heart
 Resistance to flow:
indirectly proportional to radius
directly proportional to length
 ↓vascular luminal diameter --↑resistance --↑SVR
SVR= [(MAP-CVP) ÷ CO]*80
 Normal SVR: 800-1,200 dynes/sec/cm5

39. Pulmonary vascular resistance(PVR)
 Resistance offered to blood flow by pulmonary circulation to rt.side of heart
 Low resistance system
PVR=[(mean PAP – PAOP) ÷ CO] *80
 Normal PVR: < 250 dynes/sec/cm5

40. Pulmonary artery occlusion Pressure (PAOP)
•Also known as Pulmonary capillary wedge pressure/Pulmonary artery wedge
pressure.
•Normal value ranges from 6 to 12 mm hg
•It provides indirect measure of left atrial pressure.
•It is estimation of left ventricular filling pressure for distinction between cardiogenic and
non cardiogenic etiology of pulmonary edema.

41. Measurement
Non invasive methods:
 Transesophageal Echocardiography (TEE)
 Transthoracic Echocardiography (TTE)
Invasive methods:
 Pulmonary Artery Catheterisation (Swan Ganz Catheter)

44. Thank You