Ch 14 - Heart physiology and cardiac blood flow

general location of heart in thorax

center but slightly to the left, above the diaphragm, top is by the 2nd rib

pericardium

surrounds the heart, anchors the heart to surrounding structures, protection, reduces friction, volume control

cardiac skeleton

does not conduct electricity

where does blood come from and go to

right atria - receives deoxygenated blood from SVC, IVC, coronary sinus

right ventricle - pushes deoxygenated blood to pulmonary trunk/lungs

left atria - receives oxygenated blood from 4 pulmonary veins

left ventricle - pushes blood through aorta to rest of the body

heart valves

AV (atrioventricular) - stops blood from going from ventricle to atria, 1 on each side (right is tricupsid, left is mitrial)

SL (semilunar) - stops backflow into ventricles from aorta/pulmonary trunk

how is blood flow regulated

valves regulate blood flow, pressure regulates valves, therefore pressure regulates blood flow

opening/closing of AV valves

open when ventricle relaxes/increased pressure in the atria

close when ventricle contracts/atrial pressure is less than ventricular, papillary muscles and chordae tendineae help to keep closed

mitral valve regurgitation

AV valve dysfunction on the left side, weak papillary muscles, some of the blood is going back into the left atria instead of to the ventricle, heart has to work harder

opening/closing SL valves

opens when ventricle contracts/when ventricular pressure is greater than aorta or pulmonary trunk

close when ventricles relax/ventricular pressure is lower than aorta or pulmonary trunk

aortic stenosis

ejection dysfunction, reduced blood outflow, the aortic valve is narrowed and can't close all the way

coronary circulation

coronary vessels supply and drain both sides of the heart, right and left coronary arteries/aorta supply the anterior side, the coronary sinus drains the posterior side, fills during diastole

cardiac muscle cells

contract together, spiral arrangement to squeeze everywhere, intercalated discs/gap junctions/desmosomes all help heart function as one unit (interconnections)

intrinsic innervation to heart

controls the beating of the heart, intrinsic conduction system, sets hr at 100 bpm; the sinoatrial (SA) node generates impulses (sets 100 bpm), the atrioventricular node (AV) is back up if SA fails, AV bundle connects the atria and ventricles, the bundle branches to conduct impulses through the interventricular system, the subendocardial conducting network goes through both ventricles

two types of cardiac cells (electrical)

1st type - pace cell, nodal cell, noncontractile, autorhythmic, slow depolarization, PACE

2nd type - pump cell, non nodal (muscle cells), contractile, fast depolarization, PUMP

intrinsic conduction process

SA node depolarizes, electrical activity spreads rapidly across the atria, slows through AV node, depolarization moves through ventricular conducting system, then spreads upwards from the apex through the ventricles to the base of the heart

two types of action potential

authorhythmic cell - fire spontaneously, very similar to typical AP, never flatlines, Ca enters during depolarization, funny channel (allows Na and K to pass, allows spontaneous depolarization, open in hyperpolarization)

contractile cell - has a plateu phase, competition of K leaving and Ca entering at same time causes plateau

excitation contraction coupling in cardiac muscles

calcium induced calcium release; AP enters from adjacent cell/travels membrane, voltage gated Ca channels open and Ca enters cell, Ca induces Ca release through RyR on SR, local release causes Ca spark, summed sparks create a Ca signal, Ca bind troponin and initiate contraction, relaxation and Ca pump to SR for storage

*electrical activity precedes contraction

refractory period

the refractory period is almost as long as the muscle twitch, allows beating to be efficient b/c 2 contractions can't happen at the same time, no summation in the heart (we want every contraction to be strong)

electrocardiogram (ECG/EKG)

represents summed electrical activity in all cells of the heart recorded from the surface of the body, upward means current flow is towards the positive electrode and downward is towards negative, perpendicular is flat

Einthoven's triangle (ECG)

electrodes attached to both arms and left leg to form a triangle, lead 1 is negative on right arm to positive on left arm, lead 2 is negative on right arm to positive on left leg, lead 3 is negative on left arm to positive on left leg

waves of ECG

P wave - atrial depolarization

P-R segment - conduction through AV node and bundle

QRS complex - ventricular depolarization (atrial repolarization masked during this wave)

T wave - ventricular repolarization

irregular ECG patterns indicate heart problems

problems with internal conduction system

atrial or ventricular fibrillation (irregular contractions), electric shock by AED device may reset the SA node to function normally (which will also reset all of the heart then), implantable defibrillators can be used long term

mechanical events of cardiac cycle

late diastole (both chambers relaxed, ventricles fill passively), atrial systole (atrial contraction forces remaining blood into ventricles), isovolumetric ventricular contraction (contraction when both valves are closed to increase pressure, EDV), ventricular ejection (SL valves open and blood is ejected), isovolumic ventricular relaxation (ventricles relax and pressure falls, atria passively fills with blood, ESV)

EDV and ESV

end diastolic volume (how much ventricles hold after filling with blood), end systolic volume (how much ventricles hold after ejecting blood)

Wiggers diagram

shows electrical activity, pressure changes (lines for left atrial pressure, left ventricular pressure, and aortic pressure), heart sounds, left ventricular volume and heart images; dicrotic notch (aortic slight up before going down, from blood flow into coronary artery after valve closes)

stroke volume

how much blood leaves during contraction, EDV-ESV, avg is 70 mL; influence by preload (degree of stretch before contraction), afterload (pressure/resistance which must be overcome for ventricles to eject blood), contractility

cardiac output

measure of cardiac performance, volume of blood pumped by one ventricle in a given period of time, CO= hr x SV, avg 5 L/min

ways to influence stroke volume

Frank-Starling law of the heart - SV is proportional to EDV, so we want to increase EDV -> increase venous return (skeletal muscle pump, respiratory pump lowers pressure, sympathetic innervation of veins squeezes them), length-tension relationships (degree of stretch is preload, more stretch is greater volume for blood to fill); we want to decrease ESV, increasing would increase afterload, decrease by contracting harder=contractility, increase contractility by increasing positive inotropic agents (NE, Ca)

pumps in cardiovascular system

blood flows down a pressure gradient, goes aorta-arteries-arterioles-capillaries-venules-veins-venae cavae, high pressure when it leaves heart, low when its trying to return to heart

physics of fluid flow

hydrostatic pressure is exerted on walls by fluid, proportional to height of water column, when opened pressure falls with distance as energy is lost b/c of friction, flow requires a pressure change, as radius of tube decreases the resistance to flow increases (so flow decreases), flow = change in pressure/resistance

resistance and fluid flow

flow is inversley proportional to resistance, resistance is proportional to length (resistance increases as length increases, length doesn't change often as adult), resistance is proportional to viscosity (thickness, blood can get thicker from not drinking enough water), resistance is inversely proportional to tube radius to the 4th power (resistance decreases as radius increases, vasoconstriction vs vasodilation