Cardiovascular physiology

Dr. Tarun Yadav

Moderator : Dr V. Chandak

Heart

Heart is functionally divided into right and left pumps each consisting of an atrium & a ventricle.

The atria serve as both conduits and priming pumps, whereas the ventricles act as the major pumping chambers.

The right ventricle receives systemic venous (deoxygenated) blood and pumps into the pulmonary circulation

Left ventricle receives pulmonary venous (oxygenated) blood and pumps it into the systemic circulation.

Four valves normally ensure unidirectional flow through each chamber.

specialized striated muscle

self-excitatory nature

Serial low-resistance connections (intercalated disks) between individual myocardial cells.

Electrical activity spreads via specialized conduction pathways.

The normal absence of direct connections between the atria and ventricles except through the atrioventricular (AV) node delays conduction and enables atrial contraction to prime the ventricle.

CARDIAC ACTION POTENTIALS

Myocardial cell membrane is permeable to K+ but is relatively impermeable to Na+.

Na+–K+ATPase concentrates K+ intracellularly in exchange for extrusion of Na+ out.

Intracellular Na+ concentration is kept low, whereas intracellular K+ concentration is kept high.

Relative impermeability to calcium also maintains a high extracellular to cytoplasmic calcium gradient.

Movement of K+ out & down its concentration gradient results in a net loss of positive charges from inside the cell.

An electrical potential is established, with the inside of the cell negative with respect to the extracellular environment.

The resting membrane is the balance between two opposing forces: the movement of K+ down its concentration gradient and the electrical attraction of the negatively charged intracellular space for the positively charged potassium ions.

–80 to –90 mV

When the cell membrane potential becomes less negative and reaches a threshold value, a characteristic action potential (depolarization) develops.

The action potential raises the membrane potential of the myocardial cell to +20 mV.

Spike in cardiac action potentials is followed by a plateau phase that lasts .2–.3 s

Action potential is due to the opening of both fast sodium channels (the spike) and slower calcium channels (the plateau).

Cardiac Cycle

The cardiac cycle is traditionally defined based on events occurring before, during, and after LV contraction. (0.8 sec)

Left ventricular systole is commonly divided into three parts:

isovolumic contraction,

rapid ejection, and

slower ejection.

Isovolumic Contraction

Isovolumic contraction is the interval between closure of the mitral valve and the opening of the aortic valve.

Left ventricular volume remains constant during this period of the cardiac cycle.

The rate of increase of LV pressure reaches its maximum during isovolumic contraction.

Pressure in the aortic root declines to its minimum value immediately before the aortic valve opens.

Rapid EjectionRapid ejection occurs when LV pressure exceeds aortic pressure and the aortic valve opens.

Approximately two thirds of the LV end-diastolic volume is ejected into the aorta during this rapid ejection phase of systole.

Aortic dilation occurs in response to this rapid increase in volume as the kinetic energy of LV contraction is transferred to the systemic arterial circulation as potential energy.

The compliance of the aorta and proximal great vessels determines the amount of potential energy that can be stored and subsequently released to the arterial vasculature during diastole.

The normal LV end-diastolic volume is about 120 mL.

The average ejected stroke volume is 80 mL, and the normal ejection fraction is approximately 67%.

Slow ejection

During the period of slower ejection, aortic pressure may briefly exceed LV pressure. The reversal of the pressure gradient between the aortic root and the LV causes the aortic valve to close, thereby producing the second heart sound (S2)

Diastole is divided into four phases in the LV:

isovolumic relaxation,

early filling,

diastasis, and

atrial systole

Isovolumic relaxation defines the period between aortic valve closure and mitral valve opening during which LV volume remains constant. LV pressure falls precipitously as the myofilaments relax.

Early Filling

When LV pressure falls below left atrial pressure, the mitral valve opens, and blood volume stored in the left atrium rapidly enters the LV driven by the pressure gradient between these chambers.

This early-filling phase of diastole accounts for approximately 70 to 75% of total LV stroke volume available for the subsequent contraction.

Diastasis

After left atrial and LV pressures have equalized, the mitral valve remains open and pulmonary venous return continues to flow through the left atrium into the LV.

This phase of diastole is known as diastasis, during which the left atrium functions as a conduit.

Diastasis accounts for no more than 5% of total LV end-diastolic volume under normal circumstances.

Atrial systole

The final phase of diastole is atrial systole.

Contraction of the left atrium contributes the remaining blood volume (approximately 15 to 20%) used in the subsequent LV systole.

Cardiac output

DEFINATION Cardiac output : vol of blood pumped by heart

per minute. It is measure of ventricular systolic function.

C.O = S V × H R

Stroke volume: vol of blood pumped per contraction

Cardiac index : C I = C O / BSA normal value 2.5 to 4.2 l / min / m2

DETERMINANTS OF C .O

Intrinsic factors

Heart rate

Contractility

Extrinsic factors

Pre load

After load

Heart rate

No of beats per minute

C .O directly proportional to HR

HR is intrinsic function of SA node

HR is modified by autonomic, humoral, local factors

Enhanced vagal activity decrease HR

Enhanced sympathetic activity increase HR

Contractility

Intrinsic ability of myocardium to pump in absence of changes in preload and after load

Factors modifying contractility are exercise, adrenergic stimulation, changes in Ph, temperature, drugs, ischemia anoxia.

Frank starling relationship

Relation between sarcomere length and myocardial force

States that if cardiac muscle is stretched it develops greater contractile tension

Increase in venous return increases contractility and CO

Clinical application is relation between LVEDV and SV

Frank straling relationship

Length

Ten

sion

(= preload)

HOW TO ASSESS CONTRACTILITY ?

Pressure volume loops

Noninvasive like echocardiography, vetriculography

EF = (LVEDV – LVESV)/ LVEDV

NORMAL – 60 ± 6%

PRELOAD

Defined as ventricular load at the end of diastole before contraction has started

In clinical practice PCWP or CVP are used to estimate preload

Determinants of preload

Venous return

Blood volume

Heart rate

Atrial contraction

AFTERLOAD

Defined as systolic load on LV after contraction has began

Aortic compliance is determinant of afterload e.g. AS or chronic hypertension both impede ventricular ejection

Measurement of afterload DONE BY

echocardiography

systolic BP or SVR

AFTERLOAD

Wall stress: Laplace law states that wall stress is product of pressure and radius divided by wall thickness

wall stress= P × R/ 2H

RV load depends on PVR.

CARDIAC WORK

External work( stroke work) is work done to eject blood under pressure. stroke work= SV×P

Internal work is work done to change shape of heart for ejection. Wall stress directly proportional to internal work

Both internal work and external work consume oxygen

Wall motion abnormalities

Valvular dysfunction

Methods to measure CO

Fick principal

Thermodilution

Dye dilution

Ultrasonography

Thoracic bioimpedance

Pressure volume loop

Anatomy and physiology of coronary circulation

Rt coronary artery - arises from anterior aortic sinus - supply RA, RV, inferior wall of LV,

(60% ) SA node, (80%) AV nodePosterior descending artery

- 80% branch of RCA (rt dominant

circulation) - 20% branch of LCA ( lt dominant

circulation) - supplies interventricular septum and

inferior wall

ARTERIAL SUPPLY

Left coronary artery arises from posterior aortic sinus supply LA, LV, most of

interventricular septum Left anterior descending

septum and anterior wallLeft circumflex

lateral wall

Venous drianage

Coronary sinus

great cardiac vein

middle cardiac vein

small cardiac vein

oblique vein

Anterior cardiac vein

Venae cordae minimae

VENOUS DRIANAGE

Determinants of coronary perfusion

Coronary perfusion is intermittent compared to continous in other organs

CPP = Aortic diastolic pressure – LVEDPLV is perfused entirely during diastole

RV is perfused during both systole & diastole

Autoregulation of coronary blood flow

Coronary blood flow = 250 ml/min at rest

Myocardium regulates its blood supply between 50 to 170 mmhg

Metabolic control

Neurohumoral control

Neurohumoral control

When blood pressure decreases

Blood flow decreases

Vascular smooth muscle relaxation

Blood flow increases

Metabolic control

When blood flow decreases

Metabolites accumulate

Vasodilatation occurs

Blood flow increases

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

Myocardial 02 supply & demand

Supply

HR

coronary perfusion pressure

arterial 02 content

coronary vessel diameter

Myocardial 02 supply & demand

Demand

basal requirement

HR

wall tension

contractility

Systemic circulation

Arteries (wind kessel vessels)

Arterioles (resistance vessels)

Capillaries

Veins ( capacitance vessels)

Normal distribution of blood volume

Heart 7%

Pulmonary circulation 9%

Systemic circulation

Arteries 15%

Capillaries 5%

Veins 64%

Autoregulation

Defination

Ability of organ to maintain constant blood flow over wide range of perfusion pressure

Mechanism

metabolic

myogenic

Arterial blood pressure

Mean arterial pressure

MAP = DP + PP/3

Control of arterial blood pressure

Immediate control

Intermediate control

Long term control

Immediate control

Minute to minute control of BP

central sensors

Peripheral baroreceptor( stretch receptors)

aortic

carotid

Chemoreceptor

Intermediate control

After few minutes of sustained decrease in BP

Renin angiotensin aldosteron system

ANP

Altered capillary permiability

Renin angiotensin aldosterone system

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.

Long term control

After hours of sustained change in BP

Sodium and water retension

Cardiac reflexes

Baroreceptor reflex

Chemoreceptor reflex

Bainbridge reflex

Bezold jarish reflex

Valsalva maneuver

Occulocardiac reflex

Baroreceptor reflex↑ BP

↑ BR in carotid sinus & aortic arch

Sinus nerve & Aortic nerve

IX & X nerve

N. solitarius

↑ vagal tone

↓ HR

Chemoreceptor reflex↓pO2 ↑ pCO2 & ↓pH

↑ CR in carotid body & aortic arch

Sinus nerve & Aortic nerve

IX & X nerve

↑ Respiratory centre

↑ ventilatory drive

Bainbridge reflex

Venous engorgement of atria & great veins

Stimulation of stretch receptors

X nerve

CVS center medulla

↓ Vagal tone

↑ HR

Bezold jarish reflex

Ischemia

Receptors in LV

X nerve

Reflex bradycardia, Hypotension & coronary artery dilation

Valsalva maneuver

Forced expiration against closed glottis

↑ Intrathoracic pressure → ↑CVP → ↓ V.R → ↓ CO &BP → sensed by BR → ↑ HR & contractility

When glottis opens

↑ VR → ↑ contractility → ↑ BP →sensed by BR → ↓ HR & BP

Occulocardiac reflex

Pressure on eye

long & short ciliary nvs

ciliary ganglion

gasserion ganglia

↑ PNS → BRADYCARDIA

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