Medical Physiology Block 3 Week 4 Flashcards Preview

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Flashcards in Medical Physiology Block 3 Week 4 Deck (25):
1

Describe the conduction pathways for the cardiac action potential, from the primary pacemaker cells to ventricular myocytes

SA node → left and right atria →AV node (presence of fibrous atrioventricular ring prevents the direct spread of impulse from atria to ventricles)→ Bundle of His → Purkinje fibers → ventricular muscle

2

List the cell types in the heart that are intrinsic pacemakers, and their location along the conduction pathway. State which region normally initiates the action potential, and describe how it can entrain the other pacemaker cells.

primary pacemaker = sinoatrial node generates the initial action potential (no true resting potential); secondary pacemaker = atrioventricular node (shape of action potential is similar to SA node with the exception that it operates at lower heart rates); tertiary pacemaker: Purkinje fibers (shape of action potential is similar to atrial and ventricular myocytes (not very reliable and even slower than SA node); the pacemaker with the highest frequency will be the one to trigger an action potential that will propagate throughout the heart

3

Describe how gap junctions allow conduction of the cardiac action potential from cell to cell throughout the heart.

a gap junction permits electrical current to flow between neighboring cells; the current flowing between a cell and its neighbor is proportional to the voltage difference and inversely proportion to electrical resistance (or proportional to the conductance)

4

Draw the shapes of action potentials in different cardiac cell types, with appropriate voltage and time scales

nodal cells have a oscillatory hyperpolarization phase, slow depolarization and repolarization; myocytes (atrial and ventricular) as well as the His-Purkinje system have a depolarization phase, initial repolarization, plateau, repolarization and hyperpolarized state (resting potential)

5

Explain the phases of the cardiac action potential (0 to 4), and how they vary among cell types.

phase 4 nodal cells: outward K current, funny current (activated by hyperpolarization), T type calcium channels; phase 4 non-nodal: potassium current (funny current for Purkinje fibers); phase 0 nodal: L-type Ca current; phase 0 non-nodal: Na current; phase 1 non-nodal: Kv4 transient K current; phase 2 non-nodal: Ca current (some K current); phase 3: K current (different channel types)

6

What current sets the resting potential of ventricular myocytes?

inward rectifier current (Kir2); blocked by intracellular magnesium at depolarized membrane potentials; reversal potential is near equilibrium potential of potassium (small outward potassium current just above (more negative) equilibrium potential of potassium)

7

List the conduction velocity of the action potential in different cell types in the heart. Explain how conduction velocity can vary among cell types.

SA node= 0; myocardial cells = 1 m/s; AV node = slowest (five-fold slower than myocardial cells; allows for ventricle filling); His-Purkinje fibers = 2-4 m/s (fastest)

8

Describe the channel that conducts funny current.

HCN channel (non-selective cation channel; permeable to sodium and potassium); related to voltage-gated potassium channels and nucleotide-gated channels

9

Use the conductance equation to explain how the voltage changes during a cardiac action potential depends on the channels open during each phase.

IK = GK × (VM - EK); parallel batteries model: VM = G’Na ENa + G’K EK

10

Distinguish between the conductance (G) of each channel type, and the ionic current (I) flowing through the channel, during each phase of the cardiac action potential

even though the channel may be open (conductance), the ion may be reaching its equilibrium potential thus lower driving force (effectively decreasing the current flow of that ion)

11

Describe the signaling pathways (from receptor activation to the effects on channel gating) underlying sympathetic and parasympathetic regulation of cardiac action potentials, both in pacemaker cells and in ventricular myocytes

mechanisms to increase heart rate: Beta1 receptor activation (increased calcium current) modulates voltage dependence of calcium channel opening (shifts voltage dependence to more negative voltages; PKA-mediated); Beta1 receptor activation also enhances funny current (shifts voltage dependence so less hyperpolarization is needed to activate the channel; cAMP binding to HCN channel); mechanism to decrease heart rate: Activation of muscarinic receptors opens potassium channels (beta gamma subunits open GIRK (Kir3) channels; inhibit cAMP via alpha subunit)

12

Describe the sequence of depolarization in cardiac tissue.

Atrial depolarization (right to left); Septum depolarizes from left to right (vector moves slightly upwards); Anteroseptal region of myocardium depolarizes towards the apex (vector moves downwards); Depolarization of the ventricular endocardium followed by epicardium; Depolarization of the posterior portion of base of the left ventricle (Purkinje fibers carry electrical signals upwards while signal is still spreading from endocardium to epicardium)

13

What two channels are regulating the ionic gradient in cardiac tissue?

NCX and Na/K pump

14

Describe the configuration and axes of the six limb leads (I, II, III, aVR, aVL, aVF) and the six precordial leads (V1-V6).

limb leads: equilateral triangle between both shoulders and groin (lead I: LA + RA -; lead II: LF + RA -; lead III: LF + LA -); Augmented chest leads compare one limb electrode to the average of the other two; precordial leads: anterior medial (V1) to posterior lateral (V6)

15

Describe, using the two-cell model, how an electrical current is detected as a voltage difference between two leads. It is very important to understand how the direction of the electrical vector relative to the orientation of the lead determines the signal amplitude.

a lead records the fluctuation in voltage difference between positive and negative electrodes; The fluctuations in extracellular voltage recorded by an ECG lead are called waves; Positive deflection if a current moves from cell A to cell B is visualized when the positive electrode is near cell B; QRS complex reflects the voltage difference in the two-cells with depolarization and T wave reflects the voltage difference with repolarization (the impulse reaches cell A earlier therefore positive deflection during depolarization and negative deflection during repolarization)

16

Draw the polar coordinate system of the frontal place (limb) leads.

lead I: 0; lead II: +60; lead III: +120; avR: -150; avL: -30; avF: +90

17

Describe the waves (P, Q, R, S, T) and intervals (PR, QRS, QT) in the electrocardiogram and understand what they represent

P wave: atrial depolarization; Q wave: septal depolarization (upward vector; negative deflection); R wave: apical depolarization; S wave: basal depolarization; intervals: beginning of one wave to the end of another wave

18

Calculate heart rate from a standard electrocardiogram (3 large boxes between R waves)

divide 300 by the number of large boxes between subsequent waves (R waves; unless patient has 2nd or 3rd degree AV block); if there are three large boxes between R waves, then the rate is 100 beats/min

19

Describe the basic approach to determining the cardiac rhythm

intervals compared to ventricular depolarization intervals should be equal except in situations with AV block

20

Describe the concept of net electrical axis and how it is calculated from the standard electrocardiogram

weighted average of the frontal leads (limb); find isoelectric QRS complex (equal positive R depolarization and negative S wave; calculated by area under the curve); remember, the axis of the QRS complex is perpendicular to the lead with a isoelectric QRS complex

21

Describe the pathophysiology of atrio-ventricular (AV) conduction block and how it is manifest on the electrocardiogram

Large interval between atrial depolarization and septal depolarization is a first degree AV block (decreased heart rate);Second degree block: sometimes P wave progresses to septal depolarization and sometimes it doesn't (in some cases the PR interval increases until no QRS complex is generated); Third degree block: disassociation between depolarization of atria and ventricles (high heart rate in atria; low heart rate in ventricle (Purkinje fibers act as pacemaker))

22

Describe the basic mechanism of electrical re-entry and how it may cause cardiac rhythm disturbances.

Normally, once a myocardial cell depolarizes, it is refractory to another impulse; When there is unidirectional block, re-entrant excitation allows retrograde transmission and electrical loop (increases heart rate and may act as a pacemaker)

23

How is re-entry loop broken?

Increasing vagal tone can break these loops and reset the system

24

Describe the basic mechanism of automaticity/triggered-activity and how it may lead to cardiac rhythm disturbances

Prolonged depolarization in the ventricle(due to poor calcium or Kto conductance) can lead to an early; afterdepolarization and can be followed by a run of spontaneous activity (tachycardia); can also occur with calcium overload (and metabolic imbalances) when SR dumps and uptakes calcium spontaneously

25

What is the result of placing the positive and negative electrodes are the wrong arms?

lead I: RA + LA - (opposite deflection); lead II and lead III are flipped