Cardiovascular Physiology Flashcards
What are the components of the cardiac conduction system?
- SA node
- 3 Internodal pathways ( anterior, middle -Wenkebach and posterior - Thorel)
- AV node
- Bundle of His - left bundle branches off at the top, bundle continues as right bundle brance
- Purkinje fibres
Where are the SA node and AV node located?
SA node - Junction of the SVC and the right atrium
AV node - Right posterior portion of the interatrial septum
Where is conduction spread in cardiac tissue the fastest?
The Purkinje system
How long does it take for atrial depolarisation?
0.1 s
What is the speed of conduction in the AV node?
0.05 m/s (slow)
Delay of 0.1s occurs before excitation spreads to the ventricles.
Note: When there is lack of contribution of Na+ current in the depolarisation (ie in pacemaker potential) a marked loss of conduction is oberved
What is the pattern of ventricular depolarisation?
Takes 0.08-0.1s
Left septum > right septum > down to apex > returns along ventricular walls to AV groove > endocardial to epicardial surface
The last part of the heart to be depolarised are the posterobasal portion of the L ventricle, the pulmonary conus and uppermost portion of the septum
Which events in the heart correspond to the waves/intervals seen on the ECG?
P wave - atrial depolarisation
PR interval - Atrioventricular conduction
QRS duration - ventricular depolarisation
QT interval - ventricular action potential
T wave - ventriuclar repolarisation
What are the bipolar leads in an ECG?
WLeads I, II and III
Record the differences in potential between two limbs
- In lead I, an upward deflection is inscribed when the left arm becomes positive relative to the right
- In lead II the electrodes are on the right arm and left leg
- In lead III the elctrodes are on the left arm and left leg
The three bipolar leads roughly form an equilateral triangle that is called Einthoven’s triangle
How do the bipolar leads link to the axial reference system of the heart?
- The positive electrode for lead I is at O<span>0</span>
- The positive electrode for lead II is at 600
- The positive electrode for lead III is at 1200
NORMAL cardiac axis is between -30 to +110
What is a His Bundle electrogram?
Measures the electrical events in the AV node, bundle of His and Purkinje system
- A deflection when AV node is activated
- H spike during transmission through the His bundle
- V defelction during ventricular depolarisation
Can measure 3 intervals:
- the PA interval 27ms- represents condcution time from SA to AV node
- the AH interval 92ms - from A wave to start of H spike, represents AV nodal conduction time
- the HV interval 43ms - start of H spike to the start of QRS deflection represents conduction time in the Bundle of His and Bundle branches
Describe the phenomenon of sinus arrhythmia
During inspiration impulses in the vagi from the stretch receptors in the lungs inhibit the cardio-inhibitory area in the medulla oblongata
The tonic vagal discharge decreases and the heart rate rises
What causes 3rd degree heart block?
Disease in the AV node (AV nodal block) or in the conducting system below the AV node (infranodal block)
What is the difference between AV nodal and infranodal block
In AV nodal block the remaining nodal tissue becomes the pacemaker - approx 45 BPM
In infranodal block (disease in the bundle of His) the ventricular pacemarker is located more peripherally and the ventricular rate is lower - approx 35 BPM
What is an AVNRT?
AV nodal reentrant tachycardia
A regular SVT (the most common cause of paroxysmal SVT) that results from the formation of a re-entry circuit confined to the AV node and peri-nodal atrial tissue
In order for reentry to occur there must be dual pathways with different conduction velocities (ie fast and slow) and refractory periods.
The most common AVNRT is “slow-fast” AVNRT
- A PAC is conducted via the slow pathway, is conducted retrograde up the fast pathway and circus movement develops
- An echo beat develops when the reentrant activity depolarises the atrium
What is accelerated AV conduction syndrome?
Wolff-Parkinson White
An additional aberrant muscular or nodal tissue connection (Bundle of Kent) exists.
The beat conducts normally down the AV node but spreads to the ventricular end of the aberrant bundle and the impulse is transmitted retrograde to the atrium. Circus movement is established
Short PR interval, prolonged QRS with slurred upstroke, normal interval between start of P and end of QRS (PJ interval)
What are the 3 major abnormalities of membrane polarisation associated with acute MI
ACUTE
- Rapid repolarisation due to accelerated K+ channel opening (normal region negative relative to infarct furing latter part of repolarisation)
- Decreased resting membrane potential due to loss of intracellular K+ (Causes current flow into the infarct during diastole)
- Delayed depolarisation (infarcted region positive relative to healthy tissue during early repolarisation)
LATER
- Dead muscle becomes electrically silent
- Infarcted area is relatively negative compared to normal myocardium and does not contribute to normal positivity of ECG complex
- Q waves appear
- Failure or R wave progression
- Bundle branch blocks
Explain the features seen on an ECG in hyper/hypokalaemia
Moderate hyperkalaemia: K+ >7.0
- Tall peaked T waves due to altered repolarisation
Severe hyperkalaemia: K+ > 8.5
- Paralysis of the atria
- Broad slurred QRS complex
- Tall peaked T waves remain
The resting membrane potential decreases as the extracellular K+ level increases. The fibres eventually become unexcitable and the heart stops in diastole
Hypokalaemia:
- Slight lengthening of the PR interval
- Prominent U waves
- ST segment depression
- Late T wave inversion in precardial leads
What are the major differences between the AP in a pacemaker cell and AP in a ventricular myocyte
- Resting membrane potential -90mv in cardiac myocyte, -60mV in pacemaker cell
- Cardiac myocyte has fast depolarisation via Na+ channels whereas pacemaker cell has slow Ca2+ channel dependant depolarisation
- Cardiac myocyte has no prepotential
- Pacemaker potential does not have a plateau phase
Describe the action potential of a cardiac pacemaker cell
- Prepotential due to “funny current” Ih through HCN channels(permeable to both Na+ and K+)
- When prepotential reaches the activation threshold Ca2+ channels open
- ICa through transient T channels completes the prepotential
- ICa through long-lasting L channels produces the impulse
- There is no sharp, rapid depolarising spike before the plateau
- At the peak of each impulse Ik begins and brings about repolarisation
- Ik then declines and a channel permable to both Na+ and K+ is activated (Ih)
Describe the action potential of a ventricular muscle cell
Resting membrnae potential -90mV
Phase 0 Rapid depolarisation due to opening of voltage Na channels
Phase 1 Rapid repolarisation due to closure of voltage gated Na+ channels
Phase 2 Plateau phase due to opening of voltage gated Ca2+ channels
Phase 3 Repolarisation after closure of Ca2+ channels due to K+ efflux
Phase 4 Return to resting membrane potential
What is the effect of sympathtic (noradrenergic) and vagal (cholinergic) stimulation on the membrane potential?
Ach binds to M2 receptors (Gi protein couple receptor)> decreased cAMP > slowed Ca2+ channel opening + activation of special K+ channels > Membrane hyperpolarisation > slope of the pre-potential is decreased > decreased firing rate
Adrenaline and noradernaline bind to Beta 1 receptors >increased cAMP > facilitates opening opening of Ca L channels > increased ICa > increased firing rate
Describe the cardiac cycle
- Atrial systole (phase 1)
- Contraction of the atria propels some blood into the ventricles
- There is some regurgitation of blood into the veins
- Ventricular systole
- The AV valves close (S1)
- Isovolumetric ventricular contraction (phase 2): Ventricle contracts and intraventricular pressure rises sharply
- When pressure in ventricles exceed the pressure in the aorta and PA, the aortic and pulmonary valves open
- the AV valves bulge into the atria causing a small but sharp rise in atrial pressure
- Ventricular ejection (phase 3) occurs when the aortic and pulmonary valves open
- Intraventriuclar pressure rises to a maxiumum and then declines
- The amount of blood ejected is 70-90mL (50mL of blood remains in each ventricle at the end of systole and the EF is about 65%)
- Early diastole
- Protodiastole - Ventricular pressure drop rapidly
- Momentum of ejected blood is overcome and the aortic and pulmonary valves close (S2)
- Pressure drops rapidly but the volume stays the same (isovolumetric ventricular relaxation (phase 4))
- Isovolumetric ventricular relaxation ends when ventricular pressure falls below atrial pressure and the AV vlaves open permitting the ventricules to fill.
- Late diastole
- When ventricular pressure falls below atrial pressure, the AV valves open
- Ventricular filling (phase 5) occurs
- 70% of ventricular filling occurs passively during diastole
- End diastolic volume is 130 mL
Describe a normal pressure-volume loop of the left ventricle
- During diastole the ventricle fills and pressure increases from d to a
- Pressure then rises sharply during isovolumetric ventricular contraction from a to b
- Volume then falls during ventricular ejection from b to c
- At c the aortic valve closes and pressure falls during isovolumetric relaxation from c to d
