Random.CardioReview Flashcards

(35 cards)

1
Q

Describe the phase of action potentials through heart: Phase 4

A

Resting membrane potential (Na-K pump and K leak)

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2
Q

Describe the phase of action potentials through heart: Phase 0

A

Depolarization d/t rapid Na entry (slow Ca entry)

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3
Q

Describe the phase of action potentials through heart: Phase 1

A

rapid/early repolarization (early & transient K exit)

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4
Q

Describe the phase of action potentials through heart: Phase 2

A

Plateau d/t Ca entry and K exit (electrically balanced)

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5
Q

Describe the phase of action potentials through heart: Phase 3

A

Repolarization d/t K continuing to exit; Ca entry stops

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6
Q

Cardiac glycosides (ie digoxin) blocks Na-P pump and work on which phase of the cardiac action potential?

A

Phase 4
(Na-K pump and K leak channels)

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7
Q

na channel blockers (eg, quinidine, lidocaine) work on what phase of the cardiac action potential?

A

Phase 0
(dpolarization occurs d/t rapid Na entry & slow Ca entry)

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8
Q

The rate of Ca entry is responsible for (slow) depolarization of nodal cells) (phase 2 of cardiac action potential) affects what?

A

heart rate
conduction velocity
contractility

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9
Q

Hyperkalemia causes what to electrocardiograms?

A

decreases repolarization time

–> shortens QT interval & see “tall & tented” T waves on ECG
–> delayed conduction velocity–> prolonged PR interval, prolonged QRS
***absent P waves

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10
Q

What are hallmarks of atrial fibrillation on ECG?

A
  1. no p waves
  2. irregular chaotic rhythm
  3. normal appearance of QRS complexes +/- tachycardia
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11
Q

In an attempt to determine the underlying cause of arrhythmias– what is the acronym for diagnosis?

A

HEADS
H– heart dz–> cardiomyopathies, valvular dz, myocarditis, PE/cardiac neoplasia & any severe heart dz

E– electrolyte imbalance/metabolic dz–> K, Ca, Mg

A– Adrenergic tone/Autonomic imbalance–> stress, anxiety, pain, GI dz

D– Drugs/toxins–> catecholamines, digoxin/cardiac glycosides, antiarrhythmics

S– Surgical disease/ “usual suspects”–> splenic dz (benign or malignant), GDV, any severe systemic dz (pancreatitis, severe anemia, sepsis)

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12
Q

Advanced 2nd degree AV block occurs when?

A

when multiple consecutive “dropped beats” occur
**multiple P waves not followed by QRS

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13
Q

Describe how 3rd degree AV block looks on ECG?

A

-complete dissociation between P waves & QRS
-Pwaves at regular interval (normal/elevated rate)
-irreg QRS complexes
-P-R intervals variable
-WRS complexes normal (junctional) or abnormal (ventricular)

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14
Q

Describe how atrial premature depolarizations (APDs) appear on ECG?

A

-early P waves
–irregular PP and RR interval
-PR interval: normal, dec or prolonged
-Variable P wave configuration

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15
Q

Describe how atrial tachycardia appears on ECG?

A

-rapid, usually regular atrial rate
**most cases AV node is blocked, so normal ventricular rate with rapid atrial rate

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16
Q

Describe how ventricular premature depolarizations appear on ECG?

A

–impulses originating in the ventricle, rather than sinus node
–QRS occurs earlier than normal sinus beat, w/o preceding P wave initiating depolarization
**look different from sinus QRS complexes
–T wave appears abnormal

17
Q

describe how ventricular tachycardia appears on ECG?

A

tachyarrythmia with the triggering impulse originating from the ventricles
– QRS complexes abnoraml
– dissociated from P waves
– T waves are abnormal
–atrial rate (P-wave) is slower than ventricular rate, often buried in QRS complexes
**not conducted across the AV node

18
Q

What are the differences between uniform and polymorphic VT

A

Uniform VT: RR interval is regular

Polymorphic VT: WRS differing configurations, RR interval is irregular

19
Q

Describe features of Torsades de pointes on ECG

A

specific type of wide complex tachycardia
-“twisting around the baseline”
-malignant arrhythmia

20
Q

List causes of advanced 2AVB

A

electrolyte imbalances
digitalis toxicity
AV nodal disease (inflammatory or degnerative)

21
Q

List examples of bradyarrythmias

A

-second degree AV block
-sinus arrythmia
- sinus bradycardia
-Sino-atrial (S-A) block & rest

22
Q

completed 3rd degree AV block is the commonly seen when?

A

foals with uroperitoneum

23
Q

What is definitive treatment of 3AVB?

A

-vagolytic drugs
- atropine or glycopyrrolate
-buscopan
-corticosteroids: dexamethasone
-Sympathomimetic drugs: speed idoventricular ryhtm– isoproterenol

24
Q

What is definitive treatmnet for 3AVB if medical management does not work?

25
What are examples of tachyarrythmias?
supraventricular premature complexes (SVPCs) atrial tachycardia atrial flutter atrial fibrillation ventricular premature complexes idioventricular rythm vetnricular tachycardia
26
Define bradyarrythmias in horses
heart rate less than 24 bpm
27
most bradyarrhythmias are
physiological *8assoc with high vagal tone & abolished with excitment, exercise or vagolytic drugs
28
Define sick sinus syndrome
sinus node dysfunction combined with C/S Sinus node dysfunction: abnormal automaticity and/or conduction within sinus node C/S: lethargy, weakness, exercise intolerance, nonsyncol or syncopal collapse
29
What is the primary electrolyte disturbance associated with supression of normal sinus node function?
hyperkalemia
30
What are drugs that can slow excitability of the SA node?
nondihydropyridine ca channel blockers (diltiazem) and beta-bockers
31
When is 2AVB considered pathologic?
-- more than 2 dropped beats in a row over 24 hours(becomes advanced or high-grade block) -- persists despite excitement or exercise
32
When should complete heart block be considered?
when atrial fibrillation if the ventricular rate is slow and regular
33
define paroxysmal atrial fibrillation
self-terminates in 5 days
34
What is the treatment of choice for quinidine-induced torsades de pointes (wide QRS tachycardia)?
administer MgSO4 (1-2.5 g/450 kg/minute rapidly IV to effect or up to 25 gms/450 ks)
35
what is the most common presenting C/S with atrial fibrillation?
exercise intolerance or poor performance