ECG and Cardio EP Flashcards
what are the two functional types of cells in the heart? how do they differ?
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
What percent of mass and cell population do the working and specialized cardiac cells make up in the heart? What other cell types exist?
80% mass, 20% cell pop; fibroblasts, epithelia etc
What ionically sets up the resting membrane potential in cardiac cells?
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
How do cardiac cells differ in their RMP?
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
What is conductance in terms of cardiac membranes?
measure of ease with which an ion crosses the membrane and is inversely related to resistance; g=1/R
How is RMP related to conductance? How is it altered in low RMP cells?
g=gNa/gK; large gNa/gK ratio is due to lower gK than a higher gNa
What things can change ionic conductance in the heart?
can change a a function of voltage, time, receptor ligands, or extracellular second messengers
Ionic current crossing the cell membrane is determined by what?
conductance of ions and the driving force acting on the ions; I=g(Vm-E)
What are the phases and what molecules are moving in what direction in each?
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
What is going on in nodal action potentials?
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)
Explain excitation contraction coupling in the myocardial cell?
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
What receptor/proteins are involved in regulation of contraction and how?
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
What proteins and how are involved regulation of relaxation of cardiac myocytes?
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
What effect do Beta adrenergic receptors have? How?
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
What is the difference in the AP of a fast response and slow response in cardiac cells?
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)
What happens to fast response under myocardial ischemia?
accumulation of EC K+, decrease RMP, deactivation of Na only Ca available for depolarization (slow response)
What is membrane responsiveness?
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
What is the refractory period? Different phases?
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
What is the cause of the refractory periods and why do they differ in length?
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
What is automaticity? What channels are responsible? Where are they found in hierarchy order and pace?
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)
What effect does the sympathetic nervous system have on the SA Node? NT? Receptor? Changes effected how?
Norepinephrine acts on Beta receptors, increase conductance (g) of ICa and If which increases heart rate (also respond to circulating epinephrine)
What effect does the parasympathetic nervous system have on the SA Node? NT? Receptor? Changes effected how?
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
Describe local circuit currents in cardiac cells.
flow passively between coupled active and resting cells through connexons which can change degree of opening and even close
Define the source and the sink in the source sink relationship. Provide examples.
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)
What happens to conduction velocity when the current source is altered?
increase source= increase CV (conduction velocity)
decrease source = decrease CV
How is the magnitude of the source measured? How do we know this?
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
What is Ri? what is it mostly determined by??
internal resistance, resistance of the nexus or Rn
If Rn changes what happenes to CV?
increase Rn = decrease electrical coupling of cardiac cells = decrease CV; decrease Rn = increase electrical coupling of cardiac cells = increase CV
What pathological features increase Rn?
large increase in resting Ca (Ca overload), Excess intracellular H+/acidosis / decrease pH
What physiological factors decrease Rn?
increase intracellular cAMP ->B-adrenergic stimulation
What does Rm determine? How does its change effect CV?
how much local current will neutralize internal negativity of recipient resting cell; decrease Rm decreases CV, increase Rm = increase CV
what factors effect Rm?
membrane damage (ischemia) -> decrease Rm; activation of K= channels at rest (IK1ACh)
What effect does the sympathetic nervous system have on the AV Node? NT? Changes effected how?
NE-> increase gCa-> increase Vmax and APA-> increase CV; speeds up mainly by increasing current source
What effect does the parasympathetic nervous system have on the AV Node? NT? Changes effected how?
ACh -> increase gK -> decrease Rm and increase RMP (more negative) -> decrease CV; slows mainly by increasing current sink
what are the conduction time through the conduction system of the heart?
SA: 0.05-0.1m/s, Atria: 1 m/s, AV: 0.05-0.1m/s, His & Purkinje: 5m/s, Ventrical: 1m/s
What makes up the two poles in the heart and what direction is the dipole?
Negative pole= depolarized zone; Positive Pole= polarized or resting tissue; dipole moves from negative to positive
What factors affect the magnitude and polarity of a arecorded signal in the EKG?
depends on dipole strength, angle between dipole axis and recording lead and distance
What elicits a positive deflection in an EKG?
a dipole vector moving toward a + recording lead
What elicits a negative deflection on an EKG?
a dipole vector moving away from a + recording lead
What is seen on an EKG if the vector is perpendicular to the lead?
no deflection
Describe the movement of depolarization in the ventricles.
Septum -> Apex -> Base; Enodcardium -> Epicardium (His-Purkinje system is in the endocardium
Explain the electrode placement for the standard limb leads.
Lead I: LA+ RA-, Lead II: RA- LL+, Lead III LL+ LA-
What specifically in the heart causes the pathological Q?
lack of cancelation after a myocardial infarction
What properties of cardiac cells explain why the T wave is so different looking than the QRS complex?
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
What is the calibrations for time and voltage/
1mm = 0.04 sec, 1cm = 0.4 sec; 1mm = 0.1mV, 1cm = 1mV
How is the PR interval measured? What is normal?
beginning of p wave to onset of QRS; 0.12-0.20 ; indicates time required for impulse to pass from atria to ventricles
How long is the QRS normally?
0.06-0.10
What is the ST segment? what is normal?
occurs when both ventricles are in a depolarized state, end of S wav to beginning of T wave,
what is the QT interval? What is normal?
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
How does QT interval change with Heart rate?
varies inversely, decrease HR = increase QT and increase HR = decrease QT
what must be done to the QRT interval when taken clinically to make it relevant?
account for HR variation; QTc= QT/ square root of HR
what is Bradycardia? Tachycardia?
B: < 60 bpm, T: > 100 bpm
What are the numbers for HR in count off method?
300, 150, 100, 75, 60, 50
what is sinus arrhythmia?
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
what changes are seen on an EKG that indicate 1st degree heart block?
PR interval constant but prolonged > 0.2 sec (1 big box), each p followed by a QRS; gen. benign and asymptomatic, disease may progress
what changes are seen on an EKG that indicate 2nd degree heart block? Different types?
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
what changes are seen on an EKG that indicate 3rd degree heart block? Causes? where does ventricular impulse originate?
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
What are PACs? Cause?
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
What are PVCs?
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
How can you tell if PVC are unifocal or multifocal?
unifocal the extra QRS all oriented that same direction, multi focal extra QRS switch from + to - deflection
What are the different types of VT? Symptoms?
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
How is VT different then atrial tachycardia?
atrial tachycardia is characterized by high frequency p waves
What is the most likely cause of tachycardia and fibrillation (atrial or ventricular)? What is required?
reentry of signal, requires unidirectional block and slow (retrograde conduction)
What effects the rate of the tachycardia?
the size of the reentry circuit, small circuit = rapid tachycardia
what is an example of polymorphic VT? Cause?
Torsade de Point (TdP), abnormally delayed ventricular repolarization can allow Ca channels to reactivate at low membrane potentials to elicit early afterdepolarizations (EADS)
what factors can delay repolarization leading to TdP?
electrolyte disturbances ( hypokalemia or Hypomagnesemia), persistent bradycardia, K+ channel blockers, some antiarrhythmic and non-cardiac drugs, genetic channelopathies with K+ channels (Long QT syndrome)
what is flutter? how is the wave characterized in atrial flutter? cause?
very rapid, ~300 bpm, saw tooth p-waves (QRS unaffected and much slower, paced with AV node), likely reentry mechanism
How is the wave characterized for VF? Cause?
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)
How is atrial fibrillation characterized? Cause? Treatment?
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
What is the triaxial lead system?
3 standard leads in Einthoven’s triangle collapsed in so center point is center of heart angles remain the same
what is Einthoven’s law?
I + III = II; net voltage should obey this
What is the normal range for heart axis? What is left axis deviation? Right?
-30 to +90; Left is < -30, Right is > +90
what can cause left axis deviation?
left ventricular hypertrophy, left anterior fascicular block, inferior wall MI
what can cause right axis deviation?
right ventricular hypertrophy, acute right heart strain (massive pulm. edema), or left posterior fascicular block (rare)
what leads make up the hexaxial lead system?
3 std. limb leads, aVR= RA+, aVL= LA+, aVF= LL+
what is the null method for finding the vector?
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!
What does time is muscle mean?
the longer it is ischemic the more cardiac tissue dies, administer oxygen, it wont hurt
What are rabbit ears indicative of? and which leads?
in V1 and V2 it is right bundle branch block, in V5 and V6 is left bundle branch block
How is hypertrophy diagnosed?
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
what indicates ischemia on an EKG?
symmetrical inversion of T waves, probably due to delayed repolarization in ischemic tissue
What indicates injury on an EKG?
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
What indicates necrosis?
significant Q wave, 1mm height or width or 1/3 R wave height, disregard aVR when looking for significant Q waves,
Where do you look for lateral wall infarctions?
pathologic Q in leads I and aVL
Where do you look for inferior wall infarctions
pathological Q in leads II, III, and aVF
Where do you look for anterior wall infarctions?
pathologic Q in horizontal chest leads V1-V4
where do you look for posterior wall infarctions?
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
What are the different names for the chest leads?
septal- V1 and V2, anterior- V3-V4, Lateral V5-V6, Posterior- V7-V9, Right sided VR4 and VR5
