cardiovascular physiology Flashcards
ECGs
What does each section of the ECG trace represent?
● P wave = atrial depolarisation
● PR = atrial depolarisation and AV nodal delay
● QRS complex = ventricular depolarisation
● T wave = ventricular repolarisation
What are the typical ECG features of hyperkalaemia?
● Peaked T waves
● P wave flattening and loss of P waves
● Wide or bizarre QRS
● Sinusoidal ECG pattern
● Ventricular arrhythmias
● Asystole
Explain the electrophysiological changes that cause the ST segment changes
seen in a myocardial infarction.
● Abnormally rapid repolarisation from infarcted muscle (accelerated opening of K
channels)
● Decreased resting membrane potential (due to loss of intracellular K)
● Slowed depolarization of affected cells compared to normal cells.
Cardiac Conduction
Describe the normal cardiac conduction pathway
SA node (pacemaker)
● Spreads through the atria via 3 internodal pathways
● AV Node
● Bundle of His
● Right and left bundle branches (anterior and posterior fascicles on the left)
● Purkinje fibres
● Ventricular muscle (left side of septum first, to apex, from endo to epicardial
surfaces)
What are the common mechanisms that cause abnormalities of cardiac
conduction and what are their clinical consequences?
● Abnormal pacemakers
○ Ectopic beats
○ Sinus arrest
○ Atrial or ventricular fibrillation
● Re-entry circuits
○ tachyarrhythmias
● Conduction deficits/blocks
○ Heart blocks
○ Bundle branch blocks
● Prolonged repolarisation
○ Long QTc
● Accessory pathways
○ WPW
● Electrolyte disturbance
What conditions may predispose to increased automaticity?
● IHD
● Scarring, i.e. from a previous repair of a congenital heart defect
● Structural heart disease
● Channelopathies
● Electrolyte imbalances
● Sympathomimetic agents
● Infiltrative cardiac diseases
Describe the action potential of a cardiac pacemaker cell
Prepotential (begins at -60) initially due to K efflux, then completed by Ca influx
through calcium T channels
● Action potential (begins at -40) is due to influx of Ca with L-type calcium
channels
● Repolarisation due to K efflux, no plateau phase
How does sympathetic and parasympathetic stimulation change the prepotential?
sympathetic
● Noradrenaline binds beta 1 receptor and raises cAMP
● This causes increased opening of L type C2+ channels and Ca2+ influx
● This increases the slope of the prepotential and increases the firing rate of the
pacemaker
Parasympathetic
● Ach binds the M2 receptor and decreases cAMP
● resulting in both slowing of Ca channel opening and opening of special
potassium channels (which counter the K efflux decay)
● This leads to a greater fall in prepotential
● Which decreases the slope of the prepotential and the firing rate
Describe the action potential of a ventricular muscle cell
● Resting membrane potential -90mV
● Phase 0 rapid depolarisation due to opening of voltage gated Na channels
● Phase 1 rapid repolarisation from closure of Na channels
● Phase 2 plateau phase - opening of voltage gated Ca2+ channels
● Phase 3 repolarisation after closure of Ca2+ channels
● Phase 4 resting membrane potential set up by Na/K ATPase
Describe the major differences between a ventricular muscle action potential and
a pacemaker cell potential
Ventricular muscle has
● a greater negative resting membrane potential (-90mV)
● Fast depolarisation via Na, versus slower calcium dependent depolarisation in
pacemaker cells
● No prepotential or automaticity in ventricular muscle
● Plateau phase in ventricular but not in pacemaker
Cardiac Cycle
Starting with systole, please describe the pressure and volume changes in the left
ventricle. You might also be asked to draw the pressure/volume loop.
● Start of systole = isovolumetric contraction
○ Mitral valve closes
○ Ventricle contracts and pressure rises sharply without a change in volume
○ When LV pressure > aortic pressure the aortic valve opens
● Ventricular ejection
○ Pressure rises to a plateau and the volume falls during ejection
○ Normal stroke volume is 70-90 mls
● Start of diastole = Isovolumetric relaxation
○ Momentum of ejected blood overcome by arterial pressure and the aortic
valve closes
○ Pressure falls but volume stays the same
○ When ventricular pressure is less than atrial pressure, the mitral valve
opens
● Filling
○ Mitral valve is open and filling occurs
○ End diastolic volume is 130ml
● Atrial systole
○ Final part of ventricular filling prior to systole, small increase in volume
and pressure
Describe how the waveforms of an ECG relate to the cardiac cycle
Atrial systole starts just after the p wave
Ventricular systole starts near the end of the R wave and ends just after the T wave
Please describe (or draw) the jugular venous pressure wave and outline the
origins of the fluctuations in this wave
Up, up, down, up, down
a = atrial systole. Form regurgitation from blood when atria contract.
C = triCuspid bulge back into the atria during isovolumetric contraction
Bit that dips between the a and c occurs when the atria relaxes and blood flows into the
ventricle
X descent = ventricular contraction, downward movement of tricuspid
V = atrial filling and relaxation prior to tricuspid opening
Y = ventricular filling
Cardiac Output
What factors determine cardiac output?
● Cardiac output = stroke volume x HR
● Stroke volume is related to preload (the degree of stretch prior to contraction)
and afterload (resistance to flow) of the heart and the intrinsic contractility of the
myocardial cells
● HR responds to sympathetic or parasympathetic stimulation
What methods can be used to measure cardiac output?
The direct Fick method or the thermal dilution method
● Fick method relies on the Fick principle which states that the amount of
substance taken up by an organ per unit time is equal to the (AV concentration
difference) x blood flow. For the heart, we use oxygen.
● Thermal or indicator dilution method involves injecting the substance into a vein
and doing serial sampling of arterial blood. This is then plotted and extrapolated
to find the circulation time.
● These days we mostly just use ultrasound doppler
Can you draw (or describe) the Frank-Starling curve as it relates to the cardiac
muscle.
● X axis = ventricular end diastolic volume
● Y axis = stroke volume
● Curves arch up and to the right with dashed lines at the ends of the lower lines
where there is high end diastolic volume. These dashed lines indicate portions of
the ventricular function curves where maximum contractility has been exceeded
What factors shift the Frank Starling curve?
Things that shift the curve up and to the left.
● Circulating catecholamines
● Inotropic agents - digitalis, caffeine, adrenergic agents
● Sympathetic stimulation
● Increased myocardial mass
Things that shift the curve down and to the right
● Metabolic changes = acidosis, hypercarbia, hypoxia
● Vagal or parasympathetic stimulation
● Pharmacological depressants such as barbiturates
● Intrinsic depression as in myocardial failure
● Hypothermia
What clinical scenarios can cause a decrease in cardiac output?
● Arrhythmias or heart blocks causing abnormal heart rate
● Reduced preload i.e. from reduced venous return, cardiac tamponade
● Increased afterload
● Reduced contractility from ischaemia, venoms or drugs
Myocardial Oxygen Demand
What factors influence myocardial oxygen consumption?
● Intramyocardial tension which is dependent on pressure (afterload + contractility),
radius (preload) and wall thickness
● The contractile state of the heart
● Heart rate
● Note: pressure load increases oxygen consumption more than volume load
What are the proposed mechanisms involved in autoregulation?
● Myogenic - intrinsic contractile response of smooth muscle to stretch. As
pressure rises, vascular smooth muscles surrounding the vessels contract to
maintain wall tension
● Metabolic - production of vasodilator metabolites by active tissues → vessel
vasodilation → increased flow
● Endothelial products - vasoconstrictors (endothelin, thromboxane A2) and
vasodilators (nitric oxide prostacyclin)
● Circulating neurohumoral substances - vasoconstrictors (adrenaline,
noradrenaline, vasopressin, angiotensin II) and vasodilators (kinins, ANP)
● Neural - sympathetic (alpha -adrenergic receptors, vasoconstriction, beta
adrenergic receptors - vasodilation) and parasympathetic (muscarinic receptors -
vasodilation)
How does decreasing a patient’s heart rate improve symptoms of angina?
Decreasing the HR decreases the O2 demand
At a slower heart rate there is more time for coronary circulation which occurs in diastole
Autoregulation
What is autoregulation of tissue blood flow?
Refers to the capacity of tissues to regulate their own blood flow, which remains
relatively constant despite moderate changes in perfusion pressure. This is achieved by
altering vascular resistance.
What are some local factors that lead to vasodilation?
● Hypoxia
● Hypercarbia
● Increased local temperature
● Hyperkalaemia
● Adenosine
● Lactate
● Prostaglandins
● Histamine
Baroreceptors
What are baroreceptors?
Stretch receptors in the adventitia layer of vessels
