 Anatomy  Coronary perfusion  Myocardial oxygen balance  Electrophysiology  Cardiac cycle and PV loops  Cardiac output  Intracardiac pressures  BP and cardiac reflexes

Anatomy:ExternalanatomyAnatomy:Externalanatomy

 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 O 2 demand most important determinant of blood flow. Hypoxia causes coronary vasodilation O 2 extraction very high (65% vs 25% extraction in other tissue) Cannot compensate for reduced blood flow with increased extraction of O 2. Increased flow needed when O2 demand increases

 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 β 1 receptors - Positive chrono/ino/dromotropic effects. Parasympathetic from vagal nerve (CN X) Sympathetic from T1-4 via Stellate ganglion

 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

 Cardiac pacemaker = conduction tissue with the fastest rate of depolarization  normally SA node /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

 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

 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)

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)

 Major factors affecting stroke volume: - Preload - Contractility - Afterload - Wall motion abnormalities - Valvular dysfunction

 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

 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

 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%

 Ventricular wall tension during systole  Arterial impedance to ejection (SVR)  CO is inversely related to afterload

 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

 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

MAP= Diastolic BP + Pulse P/3 MAP = 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)

 Baroreceptor reflex  Chemoreceptor reflex  Bainbridge reflex  Bezold-Jarisch reflex  Valsalva maneuver  Cushing reflex  Oculocardic reflex