cvs physiology
TRANSCRIPT
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
Thank youwww.anaesthesia.co.in