abt cardiovascular physiology briefly

1. CardiovasCular
Physiology
CHAIR PERSON :Dr B SRINIVAS RAO Sir
MODERATOR: Dr LAKSHMI NARSAIAH Sir
SPEAKER : Dr ARUN

2. Introduction
• In 1628, Willam Harvey ,first advanced the concept of
circulation with” heart” as generator for circulation.
• Modern concept includes heart as a pump and cellular
aspects of cardiomyocyte and its regulation by neural and
hormonal control.

3. Heart as pump
• To create the “pump” we have to understand the Functional
Anatomy
–Chambers
–Valves
–Intrinsic Conduction System
–Cardiac muscle

4. Anatomy of the Heart
Chambers
• 4 chambers
– 2 Atria
– 2 Ventricles
• 2 systems
– Pulmonary
– Systemic

5. Structure
• Specific architectural order of cardiac
muscles provides basis for heart to
function as pump.
• Ellipsoid shape of LV is result of spiral
bundles of cardiac muscle
• Orientation of muscle bundle is
longitudnal in subepicardium
circufrential in middle and again
longitudnal in subendocardium.
• This orientation allows LV to eject blood
in cork screw type beging from base
and ending at apex. Thus completely
emptying the ventricle.
• Twisted LV function as pulling force
during diastole.

6. Valves
• Function is to prevent backflow
– Atrioventricular Valves
• Prevent backflow to the atria
• Prolapse is prevented by the chordae tendinae
– Tensioned by the papillary muscles
– Semilunar Valves
• Prevent backflow into ventricles

7. Intrinsic Conduction System
• Consists of “pacemaker”
cells and conduction
pathways
• Coordinate the contraction
of the atria and ventricles

8. Functional Anatomy of the Heart
Cardiac Muscle
• Characteristics
– Striated
– Short branched cells
– Uninucleate
– Intercalated discs
– T-tubules larger and
over z-discs

9. Autorhythmic Cells (Pacemaker Cells)
• Characteristics of
Pacemaker Cells
– Smaller than contractile
cells
– Don’t contain many
myofibrils
– No organized sarcomere
structure
• do not contribute to the
contractile force of the heart
normal contractile
myocardial cell
conduction myofibers
SA node cell
AV node cells

10. Autorhythmic Cells (Pacemaker Cells)
• Characteristics of Pacemaker Cells
– Unstable membrane potential
• “bottoms out” at -60mV
• “drifts upward” to -40mV, forming a pacemaker potential
– Myogenic
• The upward “drift” allows the membrane to reach threshold potential (-40mV) by itself
• This is due to
1. Slow leakage of K+
out & faster leakage Na+
in
» Causes slow depolarization
» Occurs through If channels (f=funny) that open at negative membrane potentials and
start closing as membrane approaches threshold potential
2. Ca2+
channels opening as membrane approaches threshold
» At threshold additional Ca2+
ion channels open causing more rapid depolarization
» These deactivate shortly after and
3. Slow K+
channels open as membrane depolarizes causing an
efflux of K+
and a repolarization of membrane

11. Myocardial Physiology
Autorhythmic Cells (Pacemaker Cells)
• Characteristics of Pacemaker Cells

12. NEURAL CONTROL OF HEART
• Altering Activity of Pacemaker Cells
– Sympathetic activity
• NE and E increase If channel activity
– Binds to β1 adrenergic receptors which activate cAMP and
increase If channel open time
– Causes more rapid pacemaker potential and faster rate of action
potentials
Sympathetic Activity Summary:
increased chronotropic effects
↑heart rate
increased dromotropic effects
↑conduction of APs
increased inotropic effects
↑contractility
Sympathetic Activity Summary:
increased chronotropic effects
↑heart rate
increased dromotropic effects
↑conduction of APs
increased inotropic effects
↑contractility

13. Autorhythmic Cells (Pacemaker Cells)
• Altering Activity of Pacemaker Cells
– Parasympathetic activity
• ACh binds to muscarinic receptors M2(distributed more in atria)
– Increases K+
permeability and decreases Ca2+
permeability =
hyperpolarizing the membrane
» Longer time to threshold = slower rate of action potentials
Parasympathetic Activity
Summary:
decreased chronotropic effects
↓heart rate
decreased dromotropic effects
↓ conduction of APs
decreased inotropic effects
↓ contractility
Parasympathetic Activity
Summary:
decreased chronotropic effects
↓heart rate
decreased dromotropic effects
↓ conduction of APs
decreased inotropic effects
↓ contractility

14. Hormonal control on heart
• Angiotensin II – growth & function
• AT1- adult heart ,+ve chrono iono
Cardiac hypertrophy & heart failure
• ATII- anti proliferative ,predominent fetal heart
Ischemia injury upregulation
• ANP , BNP - P-V overload
Chronic heart failure increases - predictor of mortality

15. Conduction system
• The special conductive system of the heart:
• SA node – Keith-Flack´s node (1907) – pacemaker – in the
posterior wall of the right atrium (at the junction of superior
venacava with RA)
• Internodal tracts of: 1. Bachman
2. Wenckebacnh
3. Thorel

16. • AV node – (secondary centre of automatic function)
Conduction in AV node is slow – delay of 0.1 s),
velocity of conduction 20 mm/s.
• Physiological role: It allows time for the atria to empty their contents into
the ventricles before ventricle contraction begins.
• His bundle (v- 4-5 m/s),spread in 0.08-0.1 sec
Right/left bundle branches, Purkinje system
• Very large fibers. This allows quick - immediate transmission of the cardiac
impulse throughout the entire ventricular system.
• Depolarisation starts at left side of interventricular septum and moves
right ---then down the septum to apex.last depolarised are posteriorbasal
portion of heart pul cous.
• Excitation of the myocardium from endocardium to epicardium

17. Conducting system

18. Cardiac muscle
• Special aspects
– Intercalated discs
• Highly convoluted and interdigitated junctions
– Joint adjacent cells with
» Desmosomes & fascia adherens
– Allow for synticial activity
» With gap junctions
– More mitochondria than skeletal muscle
– Less sarcoplasmic reticulum
• Ca2+
also influxes from ECF reducing storage
need
– Larger t-tubules
• Internally branching

19. Action Potential
– The action potential of a contractile cell
• Ca2+
plays a major role again
• Action potential is longer in duration than a “normal” action
potential due to Ca2+
entry
• Phases
4 – resting membrane potential @ -90mV
0 – depolarization
» Due to gap junctions or conduction fiber action
» Voltage gated Na+
channels open… close at 20mV
1 – temporary repolarization
» Open K+
channels allow some K+
to leave the cell
2 – plateau phase
» Voltage gated Ca2+
channels are fully open (started during
initial depolarization)
3 – repolarization
» Ca2+ channels close and K+ permeability increases as
slower activated K+ channels open, causing a quick
repolarization

21. Skeletal Action Potential vs Myocardial Action Potential

22. Myocardial Physiology
Contractile Cells
• Plateau phase prevents summation due to
the elongated refractory period
• No summation capacity = no tetanus
– Which would be fatal

23. Summary of Action Potentials
Skeletal Muscle vs Cardiac Muscle

24. Excitaion Contraction Coupling
• Initiation
– Action potential via pacemaker cells to conduction
fibers
• Excitation-Contraction Coupling
1. Starts with CICR (Ca2+
induced Ca2+
release)
• AP spreads along sarcolemma
• T-tubules contain voltage gated L-type Ca2+
channels which open upon depolarization
• Ca2+
entrance into myocardial cell and opens RyR
(ryanodine receptors) Ca2+
release channels
• Release of Ca2+
from SR causes a Ca2+
“spark”
• Multiple sparks form a Ca2+
signal

25. • Excitation-Contraction Coupling cont…
2. Ca2+
signal (Ca2+
from SR and ECF) binds to troponin to
initiate conformational changes in thin actin filament
3. Myosin head rotate, move the attached actin and
shorten the muscle fibre forming power stroke
4. At the end of power stroke ATP binds to now exposed
site on myosin head and causes detachment from actin
5. ATP is hydrolysed and adp binds to myosin head the
energy produced is used for pi

26. Contraction
– Same as skeletal muscle,
• Length tension relationships exist
– Strongest contraction generated
when stretched between 80 &
100% of maximum (physiological
range)
The filling of chambers
with blood causes stretching

27. • Relaxation
– Ca2+
is transported back into
the SR and
– Ca2+
is transported out of the
cell by a facilitated Na+
/Ca2+
exchanger (NCX)
– As ICF Ca2+
levels drop,
interactions between
myosin/actin are stopped
– Sarcomere lengthens

28. Cardiac Cycle
Coordinating the activity
• Cardiac cycle is the sequence of events as
blood enters the atria, leaves the ventricles
and then starts over
• Synchronizing this is the Intrinsic Electrical
Conduction System
• Influencing the rate (chronotropy &
dromotropy) is done by the sympathetic and
parasympathetic divisions of the ANS

29. Cardiac Cycle
Coordinating the activity
• The electrical system gives rise to electrical changes
(depolarization/repolarization) that is transmitted through
isotonic body fluids and is recordable
– The ECG!
• A recording of electrical activity
• Can be mapped to the cardiac cycle

30. Waves:
•P – atrial depolarization (0.1 – 0.3 mV, 0.1 s)
•QRS – ventricular depolarization (atrial repolarization)
•Q – initial depolarization (His bundle, branches)
•R – activation of major portion of ventricular myocardium
•S - late activation of posterobasal portion of the LV mass and the pulmonary
conus
•T – ventricular repolarization
•U – repolarization of the papillary muscles

31. The duration of the waves, intervals and segments
•P – wave 0.1 s
•PQ – interval 0.16 s
•PQ – segment 0.06 – 0.1 s
•QRS complex 0.05 – 0.1 s
•QT interval 0.2 – 0.4
•QT segment 0.12
•T wave 0.16

33. ECG MONITORING INTRAOPERATIVELY
• 3 lead system is most basic- 3 electrodes Rt arm Lt arm Lt leg
• Its adequate for monitoring Arrythymias but limited use to identify ischemias
• We use modified 3 lead system where electrodes are placed on chest wall which
helps in monitoring of ischemias and improved detection of arrythymias(taller P
waves)
• Modified lead systems
Central subclavicular system- one electrode in Rt clavicular one in v5

34. • Only single lead is used V5 has 75%
sensitivity
• V4 has 61 %
• V4 + V5 has 90%
• V4 + V5 +II has 96% (BEST)

35. Cardiac Cycle
• Duration – 0.8 sec
• Systole = period of contraction atrial - 0.1 sec ventricular 0.3 sec
• Diastole = period of relaxation atrial 0.7 sec ventricular 0.5 sec
• Phases of the cardiac cycle
1. Diastole
• Both atria and ventricles in diastole
• Blood is filling both atria and ventricles due to low pressure conditions
Mechanisms of the filling:
a) residual energy from the left ventricle
b) Negative“ intrathoracic (interpleural) pressure
Ventricular fillling
1)Period of rapid filling (first 1/3 of the diastolic time)
2)Period of slow filling – diastasis (next 1/3)
3) Atrial systole (last 1/3) + 20-30 % of the filling of the ventricles

36. Cardiac Cycle
Phases
2. Atrial Systole ( 0.1 sec)
• Completes ventricular filling
3. Isovolumetric Ventricular Contraction (0.05 sec)
• Increased pressure in the ventricles causes the AV valves to close…
– Creates the first heart sound (lub)
• Atria go back to diastole
• No blood flow as semilunar valves are closed as well
4. Ventricular Ejection
• Intraventricular pressure overcomes aortic pressure and pulmonary
pressure
– Semilunar valves open
– Blood is ejected - Rapid ejection and Reduced Ejection

37. 5. Ventricular Relaxation(Diastole)
Protodiastole
The ventricular pressure falls to a value below that in aorta, closing of
the semilunar valves
– Semilunar valves close = second heart sound (dup)
Isovolumetric relaxation
Pressure still hasn’t dropped enough to open AV valves so volume
remains same (isovolumetric)
Rapid filling Phase
Reduced Filling Phase (Diastasis)

38. Cardiac Cycle
Phases

41. CORONARY CIRCULATION
• 250 ml/ min exercise 1000ml/min
• Rt Coronary Ar – RA, RV, IVS,SA node & Conducting system except lt
bundle.
• Lt coronary Ar– LA, LV, IVS(majority) lt bundle
• 70% Rt, 10% Lt dominance.Remaining both – based on posterior
descending ar supply
• Hypoxia main determinant than neural factors

43. Haemodynamic Calculations
• Cardiac output : per unit time.
• Depends on following factors
- HR
- Contractility : frank starling relationship – EDV
- Preload : VR, EDV, Ventricular compliance, diastolic pause, atrial systole
 Preload / venous return depends on two factors
Rt atrial pressures ( high pressure low return)
Mean Circulatory Filling Pressures (high pressure more return)
• Mean circulatory filling pressure measured by temporary cessation of cardiac
output and equilbration of peripheral pressures

44. • After load – refers to resistance against which heart has to pump
the blood
• Factors affecting after load are
- mechanical obstruction as aortic stenosis
- systemic blood pressure
- pharmocological intervention like
phenylephrine ,ephedrine
increases syst vascular resistance

45. • Cardiac output measured by
CO = SV* HR
SV calculated by Pressure volume Curves
(EDV-ESV)
• Thermodilution method – pulmonary artery catheter
• Fick’s method
(oxygen consumption / arteriovenous o2 difference x 10)
• Echocardiography

46. • Cardiac output = SV x HR 5-7 L/min
• Cardiac Index = CO/BSA 2.4 L/min
• SV = EDV – ESV 70-90 ml (1ml/kg)
• MAP = CO x SVR 60-90 mm Hg
= 2/3 Diastolic pressure + 1/3 Systolic
• SVR =[( MAP –CVP) /CO ] X 80 800-1200 dynes/s/cm

47. Cardiac Reflexes
Baro receptor Reflex :
• Location Internal carotid ar jst abov bifurcation
• Respond to pressure changes
• If MAP is raised stretch in receptors stimulation of CNS and
decreased sympathetic stimulation results in vasodilatation
• Baroreceptors adapt in 1-3 days to sustained raise in BP.
• Halothane inhibit heart rate increase in Baro receptor reflex

48. ChaemoRecptor reflex:
•Located in carotid and aortic bodies
•Abundant blood supply by nutrient arteries
•Respond to changes in arterial blood oxygen concentration by
detecting the pH changes and paO2
•Don’t respond utill BP< 80 mmHg
•Ventillatory response to hypoxemia (pao2<60) is inhibited by
subanesthetic dose of inhalational anesthetics(0.1 MAC)

49. Bezold Jarsich Reflex
• Dec in Lt Ventricular vol activates receptors that cause
paradoxical bradycardia.
• This compensatory bradycardia is to allow filling of
ventricles,but also deteriorates blood pressure.
• Spinal anesthesia and epidural

50. • BainBridge Reflex:
stretching of atria increases heart rate.
• Cushing reflex :
CNS ischemic response towards raised ICP.
when ICP is raised and equals arterial pressure
cushing reflex improves systemic pressure
above ICP
Triad of cushing reflex is Hypertension ,bradycardia and irregular
respirations.

51. Occulo cardiac reflex
•Pressure on globe provokes the signals through ciliary nerves to
opthalmic nerve to gasserian ganglion increased parasympathetic
stimulation results in bradycardia.
•30-90% incidence during surgery
•Anti muscurinic drugs like glycopyrollate or atropine is useful