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