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Cardiac Physiology > ECG and Cardio EP > Flashcards

ECG and Cardio EP Flashcards

1
Q

what are the two functional types of cells in the heart? how do they differ?

A

Working cells: greatest in number, Atrial and ventricular muscle, abundant, organized myofibrils, strong contraction, no pacemaker activity
Specialized cells: SA, AV, HIS, and Purkinje, few in number, few poorly organized myofibrils, weak contraction, pacemaker activity

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2
Q

What percent of mass and cell population do the working and specialized cardiac cells make up in the heart? What other cell types exist?

A

80% mass, 20% cell pop; fibroblasts, epithelia etc

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3
Q

What ionically sets up the resting membrane potential in cardiac cells?

A

very sensitive to changes in K+, K+ is the main permeable molecule at rest, only molecule with concentration gradient from outside to inside, so RMP is close to equal to the K+ permeability

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4
Q

How do cardiac cells differ in their RMP?

A

SA node and AV node have Low RMP (-40 to -60mV); Atrial and ventricular working muscle HIS bundle, bundle branches and purkinje fiber are high RMP -80 to -90; then there exist transition fibers between low and high

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5
Q

What is conductance in terms of cardiac membranes?

A

measure of ease with which an ion crosses the membrane and is inversely related to resistance; g=1/R

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6
Q

How is RMP related to conductance? How is it altered in low RMP cells?

A

g=gNa/gK; large gNa/gK ratio is due to lower gK than a higher gNa

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7
Q

What things can change ionic conductance in the heart?

A

can change a a function of voltage, time, receptor ligands, or extracellular second messengers

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8
Q

Ionic current crossing the cell membrane is determined by what?

A

conductance of ions and the driving force acting on the ions; I=g(Vm-E)

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9
Q

What are the phases and what molecules are moving in what direction in each?

A

0=rapid depolarization phase, Na in; 1: early repolarization, activation of transient outward K+; 2: Plateau, Na inactivation, depolarization induced decrease in K+ (anomalous rectification), slow inward Ca2+; 3: final repolarization, inactivation of Ca2+, delayed increase in outward K+ (delayed rectifier); 4: RMP only K+ permeable

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10
Q

What is going on in nodal action potentials?

A

0: rapid influx of Ca2+; 2: Ca2+ in and decreased K+ out; 3: Just K+ ot; 4: RMP K+ open but less so starts higher, then funny channels cause slow influx of Na (open during repolarization at -60mV)

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11
Q

Explain excitation contraction coupling in the myocardial cell?

A

Ca2+ not uniformly distributed in cells 2mM EC, 0.1microM CP and 150microM in SR; so need influx of Ca2+ in plateau phase for contraction

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12
Q

What receptor/proteins are involved in regulation of contraction and how?

A

Voltage gated (L type) Ca2+ channels in sarcolemma control influx of Ca2+ from extracellular space; and Ryanodine receptor (RyR2) Ca2+ release channels in SR membrane stimulated by Ca2+ entering via L-type

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13
Q

What proteins and how are involved regulation of relaxation of cardiac myocytes?

A

SERCA (sarco-endoplasmic reticulum Ca2+ ATPase) ATP dependent pump pulls Ca2+ from ctoplasm into SR (- reg by PLB or phospholamban); PMCA (plasma membrane Ca2+ ATP-ase) ATP dependent Ca2+ pump pulls Ca2+ from cytoplasm to EC; NCX (Na+/Ca2+ exchanger) extrudes 1 Ca to EC for 3 Na down their gradient; and Na+/K+ ATPase not direct Ca2+ handling but it maintains normal Na gradient needed for NCX

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14
Q

What effect do Beta adrenergic receptors have? How?

A

enhance contraction and relaxation; phosphorylation of L-type channels increases Ca influx which increases RyR and both increase contraction strength; phosphorylation of RyR increases rate of Ca release which increases contraction; Phosphorylation of PLB increases Ca uptake by SERCA which increases rate of relaxation

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15
Q

What is the difference in the AP of a fast response and slow response in cardiac cells?

A

fast characterized by high RMP phase 0 mediated by Na influx via INa (Atrial, His-Purkinje, and Ventricle), slow response have low RMP and phase 0 mediated by Ca influx via L-type channels (Sa and AV node)

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16
Q

What happens to fast response under myocardial ischemia?

A

accumulation of EC K+, decrease RMP, deactivation of Na only Ca available for depolarization (slow response)

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17
Q

What is membrane responsiveness?

A

variation in action potential upstroke velocity as a function of membrane potential; Na channel availability for excitation is dependent on membrane voltage from which AP is initiated

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18
Q

What is the refractory period? Different phases?

A

ERP (effective) no matter how great the stimulus no AP; RRP (relative) get AP with a larger stimulus; Fast response= short RRP; Slow response = Long RRP; long ERP due to prominent plateau phase

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19
Q

What is the cause of the refractory periods and why do they differ in length?

A

channels cant open in inactivated state; Na recovery from inactivation is fast, Ca recovery from inactivated state is slow making the RRP longer in slow response cells

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20
Q

What is automaticity? What channels are responsible? Where are they found in hierarchy order and pace?

A

intrinsic property of cardiac cells where excitation is initiated in absence of external stimuli; pacemaker potential die to If channels leaking sodium into the cell; Primary:SA (70-100bpm), Secondary/Latent: Inferior RA (50-70 bpm), AV (30-50bpm), His-Purkinje (30-40bpm)

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21
Q

What effect does the sympathetic nervous system have on the SA Node? NT? Receptor? Changes effected how?

A

Norepinephrine acts on Beta receptors, increase conductance (g) of ICa and If which increases heart rate (also respond to circulating epinephrine)

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22
Q

What effect does the parasympathetic nervous system have on the SA Node? NT? Receptor? Changes effected how?

A

ACh acts on muscarinic receptor increasing conductance of Ik, decreasing conductance of If and ICa, this decreases AP frequency, also activates specific K+ channel (IK1ACh) to increase K+ conductance

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23
Q

Describe local circuit currents in cardiac cells.

A

flow passively between coupled active and resting cells through connexons which can change degree of opening and even close

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24
Q

Define the source and the sink in the source sink relationship. Provide examples.

A

source: factors generating current, active membrane properties, inward current channels underlieing depolarization (INa, ICa); sink: factors that take up current, passive properties, Rm (membrane resistance) and Ri (internal resistamce, mainly gap junctions)

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25
Q

What happens to conduction velocity when the current source is altered?

A

increase source= increase CV (conduction velocity)

decrease source = decrease CV

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26
Q

How is the magnitude of the source measured? How do we know this?

A

CV is proportional to APA (action potential amplitude); Upstroke Velocity (membrane responsiveness or Vmax) is proportional to CV; Slow response APs have smaller APA and Vmax then fast responses

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27
Q

What is Ri? what is it mostly determined by??

A

internal resistance, resistance of the nexus or Rn

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28
Q

If Rn changes what happenes to CV?

A

increase Rn = decrease electrical coupling of cardiac cells = decrease CV; decrease Rn = increase electrical coupling of cardiac cells = increase CV

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29
Q

What pathological features increase Rn?

A

large increase in resting Ca (Ca overload), Excess intracellular H+/acidosis / decrease pH

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30
Q

What physiological factors decrease Rn?

A

increase intracellular cAMP ->B-adrenergic stimulation

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31
Q

What does Rm determine? How does its change effect CV?

A

how much local current will neutralize internal negativity of recipient resting cell; decrease Rm decreases CV, increase Rm = increase CV

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32
Q

what factors effect Rm?

A

membrane damage (ischemia) -> decrease Rm; activation of K= channels at rest (IK1ACh)

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33
Q

What effect does the sympathetic nervous system have on the AV Node? NT? Changes effected how?

A

NE-> increase gCa-> increase Vmax and APA-> increase CV; speeds up mainly by increasing current source

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34
Q

What effect does the parasympathetic nervous system have on the AV Node? NT? Changes effected how?

A

ACh -> increase gK -> decrease Rm and increase RMP (more negative) -> decrease CV; slows mainly by increasing current sink

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35
Q

what are the conduction time through the conduction system of the heart?

A

SA: 0.05-0.1m/s, Atria: 1 m/s, AV: 0.05-0.1m/s, His & Purkinje: 5m/s, Ventrical: 1m/s

36
Q

What makes up the two poles in the heart and what direction is the dipole?

A

Negative pole= depolarized zone; Positive Pole= polarized or resting tissue; dipole moves from negative to positive

37
Q

What factors affect the magnitude and polarity of a arecorded signal in the EKG?

A

depends on dipole strength, angle between dipole axis and recording lead and distance

38
Q

What elicits a positive deflection in an EKG?

A

a dipole vector moving toward a + recording lead

39
Q

What elicits a negative deflection on an EKG?

A

a dipole vector moving away from a + recording lead

40
Q

What is seen on an EKG if the vector is perpendicular to the lead?

A

no deflection

41
Q

Describe the movement of depolarization in the ventricles.

A

Septum -> Apex -> Base; Enodcardium -> Epicardium (His-Purkinje system is in the endocardium

42
Q

Explain the electrode placement for the standard limb leads.

A

Lead I: LA+ RA-, Lead II: RA- LL+, Lead III LL+ LA-

43
Q

What specifically in the heart causes the pathological Q?

A

lack of cancelation after a myocardial infarction

44
Q

What properties of cardiac cells explain why the T wave is so different looking than the QRS complex?

A

last regions to depolarize repolarize first; epicardial AP are shorter than endocardial APs, repolarization is slower in general and less synchronous, does not follow special conduction path

45
Q

What is the calibrations for time and voltage/

A

1mm = 0.04 sec, 1cm = 0.4 sec; 1mm = 0.1mV, 1cm = 1mV

46
Q

How is the PR interval measured? What is normal?

A

beginning of p wave to onset of QRS; 0.12-0.20 ; indicates time required for impulse to pass from atria to ventricles

47
Q

How long is the QRS normally?

A

0.06-0.10

48
Q

What is the ST segment? what is normal?

A

occurs when both ventricles are in a depolarized state, end of S wav to beginning of T wave,

49
Q

what is the QT interval? What is normal?

A

correlates in time with action potential duration of working ventricular muscle cells, beginning of QRS to end of T wave, normally 0.30-0.40

50
Q

How does QT interval change with Heart rate?

A

varies inversely, decrease HR = increase QT and increase HR = decrease QT

51
Q

what must be done to the QRT interval when taken clinically to make it relevant?

A

account for HR variation; QTc= QT/ square root of HR

52
Q

what is Bradycardia? Tachycardia?

A

B: < 60 bpm, T: > 100 bpm

53
Q

What are the numbers for HR in count off method?

A

300, 150, 100, 75, 60, 50

54
Q

what is sinus arrhythmia?

A

cyclic variation in frequency of P waves linked to respiratory cycle; inspiration = increased rate; expiration = decreased rate, generally benign, decreases with age, likely reflects changes in vagal tone to SA node

55
Q

what changes are seen on an EKG that indicate 1st degree heart block?

A

PR interval constant but prolonged > 0.2 sec (1 big box), each p followed by a QRS; gen. benign and asymptomatic, disease may progress

56
Q

what changes are seen on an EKG that indicate 2nd degree heart block? Different types?

A

Mobitz I or Wenkebach: Normal to PR interval increase each time until dropped QRS, intermittent AV conduction failure; Mobitz II: constant long PR with dropped QRS, more serious, usually conduction blocked in His-Purkinje

57
Q

what changes are seen on an EKG that indicate 3rd degree heart block? Causes? where does ventricular impulse originate?

A

no temporal relationship between p wave and QRST, complete heart block, cased by MI, drug toxicity, degeneration of conduction path with age; Vent. impulse from His-Purkinje so slower frequency, need pacemaker

58
Q

What are PACs? Cause?

A

premature atrial contraction, originate in atria, common in healthy and diseased hearts, likely originate from latent pacemaker fibers in atria outside SA node, usually asymptomatic, may cause palpitations

59
Q

What are PVCs?

A

common in healthy hearts, often asymptomatic and benign, with structural disease may predispose more serious arrhythmias and sudden cardiac death, treat with B blockers, Broad QRS due to slower conduction through working ventricular muscle

60
Q

How can you tell if PVC are unifocal or multifocal?

A

unifocal the extra QRS all oriented that same direction, multi focal extra QRS switch from + to - deflection

61
Q

What are the different types of VT? Symptoms?

A

sustained: lasting longer than 30 sec with severe symptoms (syncope), non-sustained: short self terminating, monomorphic: same size and rate, polymorphic: QRS change continually and rate varies beat to beat; Symptoms: syncope, pulm edema, may progress into V Fib and cardiac arrest

62
Q

How is VT different then atrial tachycardia?

A

atrial tachycardia is characterized by high frequency p waves

63
Q

What is the most likely cause of tachycardia and fibrillation (atrial or ventricular)? What is required?

A

reentry of signal, requires unidirectional block and slow (retrograde conduction)

64
Q

What effects the rate of the tachycardia?

A

the size of the reentry circuit, small circuit = rapid tachycardia

65
Q

what is an example of polymorphic VT? Cause?

A

Torsade de Point (TdP), abnormally delayed ventricular repolarization can allow Ca channels to reactivate at low membrane potentials to elicit early afterdepolarizations (EADS)

66
Q

what factors can delay repolarization leading to TdP?

A

electrolyte disturbances ( hypokalemia or Hypomagnesemia), persistent bradycardia, K+ channel blockers, some antiarrhythmic and non-cardiac drugs, genetic channelopathies with K+ channels (Long QT syndrome)

67
Q

what is flutter? how is the wave characterized in atrial flutter? cause?

A

very rapid, ~300 bpm, saw tooth p-waves (QRS unaffected and much slower, paced with AV node), likely reentry mechanism

68
Q

How is the wave characterized for VF? Cause?

A

bag of worms, extremely rapid, irregular and chaotic electrical activation of ventricles, usually precedes VT, caused by multiple continuously changing reentrant currents, fatal if not defibrillated (cardioverted)

69
Q

How is atrial fibrillation characterized? Cause? Treatment?

A

characterized by undulating baseline and irregular ventricular rate; caused by multiple continuously changing reentrant circuits, promotes blood stasis in atria and increased risk of thrombus formation; TX: restore sinus rhythm (cardioversion, ablation, antiarrhythmic drugs, surgery), control ventricular rate (pacemaker), and anticoagulant therapy

70
Q

What is the triaxial lead system?

A

3 standard leads in Einthoven’s triangle collapsed in so center point is center of heart angles remain the same

71
Q

what is Einthoven’s law?

A

I + III = II; net voltage should obey this

72
Q

What is the normal range for heart axis? What is left axis deviation? Right?

A

-30 to +90; Left is < -30, Right is > +90

73
Q

what can cause left axis deviation?

A

left ventricular hypertrophy, left anterior fascicular block, inferior wall MI

74
Q

what can cause right axis deviation?

A

right ventricular hypertrophy, acute right heart strain (massive pulm. edema), or left posterior fascicular block (rare)

75
Q

what leads make up the hexaxial lead system?

A

3 std. limb leads, aVR= RA+, aVL= LA+, aVF= LL+

76
Q

what is the null method for finding the vector?

A

identify the biphasic wave (or net voltage = 0, isoelectric complex) this is the vector, if slightly positive lead I and aVF completely positive vector slightly less than 90; if slightly negative Lead I and completely positive aVF than vector is slightly greater than 90. Lead I needs to be almost biphasic!

77
Q

What does time is muscle mean?

A

the longer it is ischemic the more cardiac tissue dies, administer oxygen, it wont hurt

78
Q

What are rabbit ears indicative of? and which leads?

A

in V1 and V2 it is right bundle branch block, in V5 and V6 is left bundle branch block

79
Q

How is hypertrophy diagnosed?

A

look at chest leads, deviation in front leads vs rotation in horizontal leads- associated with hypertrophy in that rotation, V1 is best place to look for atrial hypertrophy

80
Q

what indicates ischemia on an EKG?

A

symmetrical inversion of T waves, probably due to delayed repolarization in ischemic tissue

81
Q

What indicates injury on an EKG?

A

ST segment elevation, normally elevated 4 mm in lead most closely relate to infarcted area, ST segment depression, usually seen in opposing leads to infarcted area

82
Q

What indicates necrosis?

A

significant Q wave, 1mm height or width or 1/3 R wave height, disregard aVR when looking for significant Q waves,

83
Q

Where do you look for lateral wall infarctions?

A

pathologic Q in leads I and aVL

84
Q

Where do you look for inferior wall infarctions

A

pathological Q in leads II, III, and aVF

85
Q

Where do you look for anterior wall infarctions?

A

pathologic Q in horizontal chest leads V1-V4

86
Q

where do you look for posterior wall infarctions?

A

anterior leads, V1 and V2; but Q wave is up and ST segment elevation is decreased, Large R in V1 and V2; maybe a Q in V6

87
Q

What are the different names for the chest leads?

A

septal- V1 and V2, anterior- V3-V4, Lateral V5-V6, Posterior- V7-V9, Right sided VR4 and VR5

Cardiac Physiology (6 decks)

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