CV Physiology Flashcards
Pericardium
Tough inelastic sheath covering heart (anchors heart) Acts as a constraint to enable ventricular interaction Pericardial fluid (lubrication)
Coronary arteries are on
Surface of heart
This prevents compression during contraction
Right atrium receives from and sends to
Receives from vena cava
Sends to right ventricle
Right ventricle receives from and sends to
Receives from right atrium
Sends to lungs
Left atrium receives from and sends to
Receives from pulmonary veins
Sends to left ventricle
Left ventricle receives from and sends to
Receives from left atrium
Sends to body except for lungs
Vena cava receives from and sends to
Receives from systemic veins
Sends to right atrium
Pulmonary trunk (artery) receives from and sends to
Receives from right ventricle
Sends to lungs
Pulmonary vein receives from and sends to
Receives from veins of the lungs
Sends to left atrium
Aorta receives from and sends to
Receives from left ventricle
Sends to systemic artery
Ventricular torsion
Allows for more efficient ejection
Produces diastolic suction (more efficient filling)
Intercalated disks
Desmosomes = withstands stress
Gap junctions = movement of ions, electrical impulses
2 types of myocardial cells
Autorhythmic cells = generates and spreads action potential, pacemaker cells, conducting cells
Myocardial cells = contractile cells, 99% of cardiac cells, mechanical work of contraction
Each myocardial cell has a distinct action potential
Action potentials are initiated at the pacemakers
Heart muscle electrical excitation
Pacemaker cells
Events = Na+ influx, Ca++ influx, K+ efflux
Pacemaker potential = the slow rise in membrane potential (depolarization) prior to an AP in the SA node
Events in pacemaker potential
Slow depolarization phase of SA node = K+ permeability decrease while Na+ increases (increased leakiness to Na+ = slow influx of Na+) approaches threshold
Near midpoint of slow depolarization = Ca++ (T-type; transient) channels open - voltage sensitive, calcium moves in, don’t stay open long, pacemaker potential continues to rise towards threshold
Threshold is reached = L-type Ca++ channels open, calcium moves in, rapid depolarization and action potential
Repolarization = L-type Ca++ channels close, K+ (rectifier) channels open and K+ moves out of SA node cells
SA node is
Autorhythmic
Self-generated
Events repeat (~70 times/minute)
Other pacemaker regions
AV node (40 beats/min) Purkinje fibres (~20 beats/min) (ectopic beats (extrasystoles)) Both are depolarized by SA node before they depolarize themselves
Action potential of myocardial contractile cells
Depolarization (Na+ moves in)
Plateau ( Ca++ moves in, stays depolarized)
Repolarization (K+ moves out)
Cardiac muscle
Excitation-contraction coupling and relaxation in cardiac muscle
Myocardial contractile cells
Long refractory period in cardiac muscle
Long action potential means long refractory period
Prevents tetanus and allows for relaxation and diastolic filling each beat
Modulation of heart rate by the sympathetic nervous system
Pacemaker cells are more depolarized
Closer to threshold
Will reach threshold faster
Increased heart rate
Modulation of heart rate by the parasympathetic nervous system
Hyperpolarizes pacemaker
Further from threshold
Takes longer to reach threshold
Slower heart rate (normal resting condition)
Skeletal vs. Contractile myocardium vs. Autorhythmic myocardium muscle: membrane potential
Skeletal= stable at -70 mV Contractile = stable at -90 mV Autorhythmic = unstable pacemaker potential, usually starts at -60 mV
Skeletal vs. Contractile myocardium vs. Autorhythmic myocardium muscle: events leading to threshold potential
Skeletal = net Na+ entry through ACh-operated channels Contractile = depolarization enters via gap junctions Autorhythmic = net Na+ entry through ion channels, reinforced by Ca+ entry
Skeletal vs. Contractile myocardium vs. Autorhythmic myocardium muscle: rising phase of action potential
Skeletal = Na+ entry Contractile = Na+ entry Autorhythmic = Ca++ entry
Skeletal vs. Contractile myocardium vs. Autorhythmic myocardium muscle: repolarization phase
Skeletal = rapid, caused by K+ efflux Contractile = extended plateau caused by Ca++ entry, rapid phase caused by K+ efflux Autorhythmic = rapid, caused by K+ efflux
Skeletal vs. Contractile myocardium vs. Autorhythmic myocardium muscle: hyperpolarizatiom
Skeletal = due to excessive K+ efflux at high K+ permeability when K+ channels close, leak of K+ and Na+ restores potential to resting state Contractile = none, resting potential is -90 mV, the equilibrium potential for K+ Autorhythmic = normally none, when repolarization hits -60 mV the ion channels open again and ACh can hyperpolarize the cell
Skeletal vs. Contractile myocardium vs. Autorhythmic myocardium muscle: duration of action potential
Skeletal = short, 1-2 msec Contractile = extended, 200+ msec Autorhythmic = varies, generally 150+ msec
Skeletal vs. Contractile myocardium vs. Autorhythmic myocardium muscle: refractory period
Skeletal = generally brief Contractile = long because resetting of Na+ channel gates delayed until end of action potential Autorhythmic = none
Specialized conduction system of heart
SA node Internodal pathway AV node Bundle of HIS (or Av bundle or bundle branches) Purkinje fibres
Electrocardiogram (ECG)
External recording of electrical events
Waves of ECG can be correlated to specific events
3 types of waves = P-wave, QRS complex, T-wave
P-wave
Atrial depolarization
Initiates atrial contraction
QRS complex
Ventricular depolarization and atrial repolarization
Initiates ventricular contraction
T wave
Ventricular repolarization
Initiates ventricular relaxation
Conduction of impulses
P wave (atrial depolarization) = initiated in SA node, spreads via gap junctions and internodal pathway throughout atria, initiates atrial contraction Impulse moves to AV node = delay of signal (~100 msec), AV nodal delay means ventricles contract after atrial contraction and ventricular filling QRS complex (ventricular depolarization) = impulse moves to bundle of HIS to bundle branches and then to purkinje fibres, initiates ventricular contraction, includes atrial repolarization T wave (ventricular repolarization) = reversed repolarization wave (from apex), initiates ventricular relaxation
Abnormalities in rate
Sinus rhythm = normal (60-120 b/min)
Tachycardia = rapid heart rate of more than 10p b/min (sinus or ventricular)
Bradycardia = slow heart rate (less than 60 b/min), risk of fainting
Abnormalities in rhythm
Arrhythmias = can cause sudden death, fainting, heart failure, dizziness, palpations, or no signs at all
Causes include hypoxia, caffeine, smoking, alcohol, ectopic excitable cells, stress, and damage to conducting path
Examples of arrhythmias
PVCs = premature ventricular contractions (extra beat)
Atrial flutter = extra P waves
Atrial fibrillation = no distinct P waves
Heart block = impulses from SA node don’t reach AV node
Ventricular fibrillation
Causes = arrhythmias, ischemia (heart attack)
No organized pattern of depolarization = no organized contraction, no ejection, leads to death
Cardiac cycle
Electrical events correspond to mechanical events in the heart
Heart wall thickness
Wall thickness correlates to peak pressures Aortic pressure = 120/80 mm Hg Atrial pressure = 3-10 mm Hg RV pressure = 3-35 mm Hg LV pressure = 3-125 mm Hg Systole = contraction Diastole = relaxation
Heart valves
Prevents back-flow of blood
Atrioventricular valves = tricuspid (R) mitral (L)
Aortic
Pulmonary
Pulmonary and aortic valves
Prevent back-flow from aorta and pulmonary artery back into ventricles
Open in systole (contraction)
Atrioventricular valves
Prevent back-flow from ventricles back to atria
Open in diastolic filling
Chordae tendinae anchor AV valves to papillary muscle (prevents eversion of valve)
As heart contracts, papillary muscles contracts (control tension on chordae tendinae)
Valve problems (murmurs)
Stenosis
Insufficiency or regurgitation
Stenosis
Narrowing of heart valve Faulty opening Decreased ejection Heard when valve should be open Whistling
Insufficiency or regurgitation
Faulty closure Backflow Decreased forward ejection Heard when valves should be closed Whirring
4 phases of cardiac cycle
Diastolic filling
Isovolumic contraction
Ejection
Isovolumic relaxation
In the Cardiac cycle the left and right sides…
Contract simultaneously
Right side at lower pressures
Diastolic filling
LAP>LVP
Mitral valve open
LVP
Isovolumic contraction
QRS LV contracts LVP increases Once LVP>LAP mitral valve closes Both valves are closed Pressure still increasing
Ejection
Once LVP>AP aortic valve opens
Blood ejected into aorta
Isovolumic relaxation
T-Wave
Relaxation
LVP decreasing
Once LVP
Stroke volume
Amount of blood pumped in 1 beat
SV = EDV(end-diastolic volume(after filling)) - ESV(end-systolic volume(after ejection))
Average stroke volume = 70mL
Depends on contractility and venous return
Venous return affected by
Skeletal muscle pump
Respiratory pump
Sympathetic innervation
Contractility affected by
Length of muscle fibre
Frank-Starling law of heart
Preload = filling of heart
Greater filling or preload means greater stretch of the myocardium and then a greater force of contraction
Stroke volume increases as EDV increases
Whatever goes in goes out the next beat
Ionotropic effect
The effect of increased sympathetic tone on contractility of heart
Epinephrine and norepinephrine increase both contractility and heart rate
Cardiac output
Amount of blood pumped per minute
CO = stroke volume x heart rate
Average cardiac output = 5L
Ejection fraction
Stroke volume divided by end-diastolic volume
Effects of exercise
Body’s demand for oxygen and blood flow increases (cardiac output must increase by up to 5x)
Body does this by increasing epinephrine (sympathetic tone)
Increases stroke volume (by increasing contractility and venous return)
Increases heart rate
Benefits of exercise
Bigger heart (larger stroke volume, resting heart rate can be lower) Larger coronary artery diameter (increased blood flow) Larger collateral blood vessels (less chance of ischemia)
Heart muscle metabolism
Heart muscle is highly oxidative
Abundant mitochondria and myoglobin
Gets oxygen from coronary circulation
Coronary circulation
During exercise: heart rate increases, filling time (diastole) decreases, heart still gets adequate blood supply due to dilation of coronary arteries via adenosine (vaso-dilator) production by cardiac muscle
Cardiac myopathies
Damage of heart muscle
Myocardial ischemia aka heart attack (inadequate delivery of oxygenated blood to heart tissues)
Fibrosis
Necrosis (death of heart muscle cells)
Actor myocardial infarction aka heart attack (occurs when blood vessel supplying area of heart becomes blocked or ruptured)
Ischemia and infarct
Transient = ischemia
Permanent damage = infarct
Blocked coronary artery = plaque/clots/cholesterol, decreased blood flow and oxygen to heart muscle
Poor muscle function = decreased stroke volume and cardiac output
Treatment = coronary artery bypass graft (CABG), vasodilators, angioplasty, reduce risk factors: exercise, diet, smoking
Arterial hypertension
Causes include = smoking, stress, diet, age/genetics
Increased arterial pressure = LVP must exceed this to open the aortic valve and eject blood
Shorter ejection time = decrease in stroke volume and cardiac output
Heart failure
Compromised heart = valve stenosis , ischemia or infarct, hypertension
Decrease in stroke volume, heart compensates with increasing heart rate = shorter filling time and a decrease in stroke volume, faster fatigue of heart muscle, and decreased contraction
Eventually muscle is so fatigued it barely contracts and there is a decrease in stroke volume, increase in blood volume, and excess blood backs up into lungs (pulmonary edema)
Congestive heart failure
Symptoms = gradual dyspnea and tachypnea, tachycardia, neck vein distension, edema in ankles and lower legs
Right side = congestion of liver and spleen
Left side = congestion of lungs
Pulmonary hypertension
RV pressure > LV pressure
Septum inverts = myocardial compression, decrease in coronary blood flow
Eg) pulmonary stenosis
Cardiac aneurysm
Bulge or ventricular wall = muscle weakness, congenital or from infarct
