CardiovasCular Physiology

CHAIR PERSON :Dr B SRINIVAS RAO Sir

MODERATOR: Dr LAKSHMI NARSAIAH Sir SPEAKER : Dr ARUN

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.

Heart as pump

• To create the “pump” we have to understand the Functional Anatomy

–Chambers–Valves–Intrinsic Conduction System–Cardiac muscle

Anatomy of the HeartChambers

• 4 chambers– 2 Atria– 2 Ventricles

• 2 systems– Pulmonary – Systemic

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.

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

Intrinsic Conduction System

• Consists of “pacemaker” cells and conduction pathways

• Coordinate the contraction of the atria and ventricles

Functional Anatomy of the HeartCardiac Muscle

• Characteristics– Striated– Short branched cells– Uninucleate– Intercalated discs– T-tubules larger and

over z-discs

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

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 potential2. 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

Myocardial PhysiologyAutorhythmic Cells (Pacemaker Cells)

• Characteristics of Pacemaker Cells

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

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

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

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

• 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

Conducting system

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

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 @ -90mV0 – 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

Skeletal Action Potential vs Myocardial Action Potential

Myocardial PhysiologyContractile Cells

• Plateau phase prevents summation due to the elongated refractory period

• No summation capacity = no tetanus– Which would be fatal

Summary of Action PotentialsSkeletal Muscle vs Cardiac Muscle

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

• 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

• 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

• 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

Cardiac CycleCoordinating 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

Cardiac CycleCoordinating 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

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

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

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

• Only single lead is used V5 has 75% sensitivity

• V4 has 61 %• V4 + V5 has 90%• V4 + V5 +II has 96% (BEST)

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 cycle1. 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 fillling1)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

Cardiac CyclePhases

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

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 relaxationPressure still hasn’t dropped enough to open AV valves so volume remains same (isovolumetric)

Rapid filling Phase Reduced Filling Phase (Diastasis)

Cardiac CyclePhases

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

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

• 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

• 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

• 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

Cardiac ReflexesBaro 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

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)

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

• 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.

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