Electrical Activity of the Heart Flashcards
Discuss pathways and relative speed with which cardiac action potentials are conducted throughout the heart
Explain why there are diff in conducting velocities
Action potential conduction velocities:
Determined by:
1. size of cells
2. Number of gap junctions between cells
In order of speed:
1. Purkinje (4m/s)
2. Bundle of His and branches (2m/s)
3. Ventricular and atrial muscle (0.5m/s)
4. Nodal cells (0.05m/s)
Describe different leads used to record and ECG and how they are configured
Einthoven’s Triangle
- 3 polar leads w/ heart at the centre of equilateral triangle (vertices at arms and legs)
I = Vleftarm - Vrightarm
II = Vleftleg - Vrightarm
III = Vleftleg - Vleftarm
II = I + III
Explain the ECG waveform
why does it is appear different on different leads?
Basis for ECG
–> AP does not occur at same time in every region of the heart (some are polarized and others are not –> cration of dipole)
–> dipole moment describes mag and direction of dipole
- mag changes based on charge and tissue
Resting:
- negative membrane potential
Atrial Depolarization:
1. SA node depolarizes (invisible b/c mass is small)
2. Atria depolarization spreads outwards (P wave)
3. Depolarization reaches AV node (invisible b/c mass is small)
- slow conduction velocity = flat line
4. Bundle of HIS depolarize quickly (only left bundle is coupled w/ inter ventricular septum –> depolarization moves left to right)
Ventricular Depolarization:
1. Q-wave:
- polarity of depolarizaiton wave on lead II is reversed (downward deflection)
2. R-wave
- dipole moment passes from endocardium to epicardium (large positive deflection)
- atria repolarize during this time (electric activity mased by ventricular depolarization)
3. S-wave
- depolarization wave moves up the ventricular walls from apex towards AV septum
- reversed current flow relative to lead II (downard deflection)
Repolarization
1. Flat line
- atria repolarize and ventricles are completely depolarized –> no net current flow
2. T-wave
- ventricles repolarize from epi to endocardium (positive deflection)
Explain how the funny current affects rate of depolarization of the pacemaker cells and how neural and hormonal input change the heart rate
Funny current:
–> responsible for lack of resting membrane potential in nodal cells
–> highest density in SA node per square micrometer of membrane
Depolarization:
- SA has fastest rate of depolarization and sets the pace for the heart rate: sinus rhythm
Neurohumoral (neuron and hormone)
- changes rate of depolarization of nodal cells –> changes heart rate
Discuss how voltage-gated Ca2+ channels contribute to cardiac action potentials
Changing force of contraction:
- release more Ca2+ from SR
- SNS stimulation increases amt of Ca2+ stored in SR
- more Ca2+ is released every beat –> more bounded to Tropomyosin C –> increased contraction force - change sensitivity of troponin-C to Ca2+
Discuss cardiac output and its regulation
Cardiac output = Heart rate * stroke volume
Regulation:
HR:
- ANS and hormones
SV:
- Preload: wall tension prior to contraction (diastolic pressure / end diastolic volume)
- Afterload: Wall tension during systole (mean arterial pressure)
- Contractility: max force developed during systole and rate at which it devlops
Analyse pressure volume loop to assess cardiac function
- changes in preload, afterload, stroke volume, and compliance
Increased Contractility
- change in slope –> change in ventricle P/V relationship (elastance) –> change in contractility
- steeper slope = increased contractility
Increased Preload
- increased SV (overall loop gets larger but slope does not change)
Increased Afterload
- decreased SV (smaller area)
In Vivo Sympathetic Activation
- contractility and preload increases
Discuss the key aspects and physiological relevance of different blood vessels:
- pressure, flow rate, diameter
Veins and Venous valves
- low pressure system
- valves prevent backflow
- requries muscular contraction to bring blood back to atrium
Discuss factors that regulate blood pressure
Mean Arterial Pressure (MAP)
- const pressure required to produce same flow (provide adequate perfusion of organs)
Baroreceptors embedded in arterial wall in carotid sinuses and aortic arch
- detects when MAP increases (results in decreases SNS and increases PNS) or when MAP decreases (opp)
SNS causes constriction
- (increased BP)
PNS causes dilation
- (decreased BP)
Local factors override neural and hormonal inputs
1. Metabolism
- (decreased pH, pO2, and increase in pCO2 –> arterioral vasodilation)
2. Flow
- increased rate of blood flow –> increased endothelial shear stress
- response: endothelium produces NO —> relaxes arterial smooth muscle cells and increases arteriolar diameter