Anatomy Coronary perfusion Myocardial oxygen balance Electrophysiology Cardiac cycle and PV...
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Transcript of Anatomy Coronary perfusion Myocardial oxygen balance Electrophysiology Cardiac cycle and PV...
CARDIAC PHYSIOLOGYDA REFRESHER 2015
DR J LEMMER
Topics for discussion
Anatomy Coronary perfusion Myocardial oxygen balance Electrophysiology Cardiac cycle and PV loops Cardiac output Intracardiac pressures BP and cardiac reflexes
Anatomy
Coronary perfusion
RCA supplies right heart and septum, inferior wall in 85% of population (right dominant circulation)
LAD supply LV anterior wall and anterior septum
Circumflex supplies lateral wall of LV and inferior wall in 15% of population (left dominant circulation)
Inhalational agents causes coronary vasodilatation
CPP = Aortic DIASTOLIC pressure - LVEDP
Myocardial O2 balance
• Myocardial O2 demand most important determinant of blood flow.
• Hypoxia causes coronary vasodilation• O2 extraction very high (65% vs 25%
extraction in other tissue)• Cannot compensate for reduced blood
flow with increased extraction of O2.• Increased flow needed when O2 demand
increases
Innervation
Parasympathetic innervation primarily in atria and conducting tissue – Ach stimulates M2 receptors - Negative chrono/ino/dromotropic effects.
• Sympathetic innervation more widely distributed – NA from sympathetic stimulates β1 receptors - Positive chrono/ino/dromotropic effects.
• Parasympathetic from vagal nerve (CN X)• Sympathetic from T1-4 via Stellate ganglion
Excitation
Myocardial cell membrane much more permeable to K than Na and Calcium (K leaves the cell much easier than Na and Ca enters it)
Na/K ATPase pumps 2K into cell and 3Na out of cell
Thus the intracellular resting membrane potential becomes negative (-90mV)
When a Threshold potential (-65mV) is reached, an action potential develops (depolarization)
The electrical activity spreads quickly and orderly between the myocardial cells
Excitation: Ventricular action potential
• Different resting potentials in different tissue types in the heart – varying excitability
• Membrane potential determined by permeability to K+, Na+, Ca++
• Intra/extra cellular ion movement controlled by voltage gated channels (fast Na channels, slow K and Ca channels) and ion leak through membranes
• Pacemaker cells constantly leaks sodium and calcium into the cell
• RMP -60mV TP -40mV• Regular spontaneous depolarizations
Excitation: SA node action potential
Conduction
Cardiac pacemaker = conduction tissue with the fastest rate of depolarization
normally SA node 60-100/min AV node junctional areas 40-60/min Purkinje fibres 20-40/min 0.1 sec delay in AV node : slow
conduction gives atria time to empty Fast conduction in Purkinje Fibres to
depolarize the whole endocardium simultaneously
Excitation: Propagation of electrical impulse
Effect of anaesthetic agents
Inhalational agents depresses SA node – junctional rhythm common
Opioids depress AV node and Purkinje fibres
Lignocaine is anti-arythmic but at toxic doses it depresses conduction (bind to Na channels)
Bupivacaine binds strongly to inactivated Na channels – causes bradycardia, VF and arrest
Electrolyte deficiencies and conduction
Hypocalcemia lowers the TP where Na channels open
Can result in repetitive depolarization (tetany)
Hyperkalemia increases RMP to -80mV (increases the excitability) but decreases conduction (bradycardia)
Contraction
• Triggered by influx of Ca++ from extracellular space in response to action potential across membrane.
• Massive intracellular release of Ca++ from cisterns in sarcoplasmic reticulum (Calcium dependent Calcium release).
• Binding of Troponin C on actin conformational change.
• Myosin binding sites exposed• Sequential binding of myosin to actin using ATP
• At end of contraction – ATP dependent reabsorption of Ca++ into SR to reverse the mechanism.
• NB relaxation (diastoly) is energy dependent• Systolic contraction is mainly dependent on
intracellular Ca levels in the myocyte. All inotropes (Adrenalin, Dobutamine, Digoxin, Milrinone etc) act by increasing Ca concentration
All volatiles are Calcium channel blockers (negative inotropic)
Cardiac cycle
Pressure Volume loop
CO = SV x HR
Major factors affecting stroke volume:- Preload- Contractility- Afterload- Wall motion abnormalities- Valvular dysfunction
1. Preload
Muscle length prior to contraction Expressed in terms of volume (LVEDV) Potential energy built up during
distention of ventricle Relationship between this volume and CO
is known as Starling’s law of the heart
Starling curves
PV loop: preload
Diastolic dysfunction
Early compliance = relaxation of the heart, late compliance = stiffness of ventricle
Common in elderly, especially if LVH or IHD
Preload becomes dependent on atrial kick and adequite volume status
2. Contractility
Intrinsic ability of myocardium to pump Rate of myocardial cell shortening Change in ventricular pressure over time during
systole (dP/dt) Dependent on intracellular Ca++ activity Primarily enhanced by β- stimulation Depressed by hypoxia, acidosis, depletion of
catecholamine stores, myocardial infarction and most anaesthetic agents
EF = (EDV-ESV) / EDV Normal EF 60-70%
PV loop: contractility
PV loops: diastolic + systolic dysfunction
3. Afterload
Ventricular wall tension during systole Arterial impedance to ejection (SVR) CO is inversely related to afterload
PV loop: afterload
4. Wall motion abnormalities
The abnormalities may be due to ischemia, scarring, hypertrophy, or altered conduction
When the ventricular cavity does not collapse symmetrically or fully, emptying becomes impaired
5. Valvular dysfunction
Stenosis of the tricuspid or mitral valve reduces stroke volume by decreasing preload
Stenosis of the pulmonary or aortic valve reduces stroke volume by increasing afterload
Valvular regurgitation reduces stroke volume without changes in preload, afterload, or contractility
Cardiac Pressures
Arterial Blood Pressure
MAP= Diastolic BP + Pulse P/3MAP = SVR x CO
Hypotension sensed by central and peripheral receptors- increases sympathetic outflow: systemic vasoconstriction (SVR), elevation in heart rate, and enhanced cardiac contractility (CO)
Cardiac reflexes
Baroreceptor reflex Chemoreceptor reflex Bainbridge reflex Bezold-Jarisch reflex Valsalva maneuver Cushing reflex Oculocardic reflex