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Rosen's > Medicine - Cardiac > Flashcards

Medicine - Cardiac Flashcards

1
Q

Differential diagnosis of ST elevation n the adult chest pain patient (14)

A 
Acute MI
LV hypertrophy
Ventricular paced rhythm
Normal variant
Hyperkalemia
PE
Prinzmetal's angina
Acute pericarditis 
LV aneurysm
Benign early repolarization 
Osborn wave of hypthermia
Brugadas' syndrome
Acute cerebral hemorrhage 
Post-electrical cardioversion
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2
Q

ST elevation elevation in V1-V4 as well as aVR.

Which coronary artery?

  • if ST elevation in aVR > V1
  • if ST elevation in aVR < V1
A

Anterior wall STEMI, when aVR is elevated, it is suggestive of L main coronary disease. May also represent multivessel disease, proximal LAD, or less commonly, L circumflex or R coronary occlusion.

  • if aVR > V1, favors L main disease.
  • if aVR < V1, favors proximal LAD
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3
Q

Characteristics of Wellen’s syndrome.

What is this a sign of?

A

STEMI equivalent

Type I: deep, symmetric TWI in anterior precordial leads

Type II: biphasic (initial +, terminal neg) TWI.

Other features: 
Isoelectric or <1mm STE
No precordial Q waves
Preserved R wave progression
EKG pattern present when chest pain FREE
Normal or slightly ↑ cardiac markers

*** sign of critical stenosis of LAD → ↑↑↑ risk of extensive anterior wall MI .

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4
Q

deWinter’s EKG presentation.

What is is a sign of?

A

STEMI equivalent

  • upsloping ST depression (> 1mm at J-point) in precordial leads
  • peaked T waves (V2-V6) with ascending limb commencing below baseline
  • ST elevation (> 0.5mm) in aVR

*** sign of acute proximal LAD occlusion

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5
Q

ST elevation isolated to leads I and aVL.

Where is the lesion?

A

Isolated STE in I and aVL suggestive of occlusion of left circumflex

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6
Q

ST elevation in inferior leads.
Lead III > lead II
+ ST depression in aVL and/or I

Where is the lesion?

A

90% sens and 71% specific for RCA occlusion.

(Right dominant, inferior wall of the heart and AVN served by RCA - 90% of population).

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7
Q

ST elevation in inferior leads
Lead III > lead II
+ ST elevation in V1

What does this suggest?

A

Inferior wall MI, likely RCA if lead III > lead II.

+ V1 = concomitant RV infarct

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8
Q

ST elevation in inferior leads
Lead II > Lead III
aVL may be isoelectric/elevated

Where is the lesion?

A

Likely left dominant - inferior wall of heart and AVN served by L circumflex artery (10% of population)

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9
Q

EKG findings in posterior wall MI?

A

Horizontal ST depression in V1-V3
Tall, broad R waves (>30 ms)
Upright T waves
Dominant R wave (R:S >1) in V2

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10
Q

ST elevation in precordial leads with upward concavity of initial portion/notching at the J point, symmetric concordant T waves

A

Findings of benign early repolarization

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11
Q

How to differentiate between STEMI and ST elevations seen with LV aneurysm?

A

Calculation of ratio of amplitude of T wave to QRS complex > 0.36 in any single lead may suggest STEMI

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12
Q

EKG with:
Wide QRS
Dominant S in V1
Broad, monophasic (or notched) in lateral leads
Loss of normal Q wave in V6
Prolonged R wave peak in lateral leads
ST elevations may be present anteriorly, depressions inferiorly

A

LBBB.

*** ST segment and T waves should be expectedly discordant (opposite direction) to QRS

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13
Q

Sgarbossa criteria: (3)

A
  1. STE > 1mm CONCORDANT with QRS (5 points)
  2. STD >1mm in V1-V3 CONCORDANT with QRS (3 points)
  3. STE >1mm with EXCESSIVE DISCORDANCE (> 25% of preceding S wave) (2 points)

3+ points 90% specific for AMI if pt with LBBB or pacer

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14
Q

Situations to use additional EKG leads? (4)

eg 15-lead EKG with V4R, V8, and V9

A
  1. ST changes (elevation/depression) in V1-V3 alone, in isolated lead or more than one lead
  2. Equivocal STE in inferior (II/III/aVF) or lateral (I/aVL) limb leads, or both
  3. All inferior wall STEMI
  4. Hypotension in setting of ACS
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15
Q

Mechanism of action of aspirin when used in ACS

A

Inhibition of platelet activation and aggregation.

Irreversibly inhibits COX-1 → ↓ thromboxane A2 (promotes platelet aggregation).

Overall anti-inflammatory effects may ↓ progression of atherosclerotic disease as well.

*** 23% reduction in mortality in patients with AMI, 42% when used with fibrinolytic therapy.

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16
Q

Mechanism of action of thienopyridines (ticlopidine-Ticlid, clopidogrel-Plavix, prasugrel-Effient, ticagrelor-Brilinta) in ACS and indications for use.

A

MOA: P2Y12 receptor inhibitors

Inhibit transformation of PSY12 receptor into its high-affinity ligand-binding state → irreversible inhibition of platelet aggregation for the duration of life of the platelet.

Ticlopidine: max effect 8-11 days of use, Clopidogrel has rapid onset of action (esp with loading dose).
Ticagrelor does not require hepatic activation and is rapidly absorbed, with peak concentration in 2.5h.

Indications:

  • Should receive loading dose of clopidogrel/ticagrelor prior to PCI.
  • High-risk ACS presentation + ASA allergy
  • ACS patients with medical management and/or delayed time to PCI
  • STEMI patient managed medically

*** Need to weigh risks of bleeding, esp in patients who MAY require urgent CABG.

17
Q

Mechanism of action of heparins and indications for use in ACS

A

Heparins (unfractionated and LMWH) - bind antithrombin, increasing it’s activity.

Activated antithrombin → inactivation of thrombin → ↓ thrombus formation.

Unfractionated heparin should be administered early in patients with the following ACS features:

  • recurrent or persistent chest pain
  • acute MI
  • positive serum markers
  • dynamic EKG

Only high-risk unstable angina (eg recurrent/continued pain, new ischemic EKG changes) should be considered for heparin therapy

18
Q 
Class I Antiarrhythmics:
MOA? 
IA: Example?
IB: Example?
IC: Example?
A

Class I: major effect on fast Na channels → Membrane stabilization

IA: Slow conduction through atria, AVN, his-purkinje system. Suppress conduction in accessory pathways. E.g. Procainamide 20-30mg/min until dysrhythmia is terminated

IB: slow conduction and depolarization + SHORTEN repolarization. Little effect on accessory pathways. E.g. Lidocaine suppresses SA and AVN functioning. 2nd ine in Vtach.

IC: Profoundly slow depolarization and conduction. PRODYSRHYTHMIC. Flecanide and propafenone are approved for oral use only. ** Caution in pts with ischemic or structural heart disease.

19
Q

Class II Antiarrhythmics:
MOA?
Examples? (2)

A

Class II: β-blockers - suppress SA node automaticity and ↓ conduction through AVN. Well-suited to control ventricular rate in patients with atrial tachydysrhythmias and can be used to terminate AVNRT and to prevent ventricular dysrhythmias.

β-1 = cardioselective
- Esmolol - rapid onset, short elimination (min)

β-2 = not cardio selective - act in the heart as well as airway, peripheral vasculature

20
Q

Class III Antiarrhythmics:
MOA?
Examples? (4)

A

Class III: prolong refractory period primarily by blocking K-channels with variable effects on QTc.

Amiodarone - ventricular and SVT, preferred for acute ventricular tachycardia. Also has similar class effects to IA, II, and IV agents.

Ibutilide - induction of a slow inward Na current → prolonged refractory period. Approved for cardioversion of Afib and Aflutter. Risk of QT prolongation and polymorphic VT

Sotalol: β-blocker with type III properties. Suppresses SVT and VT. Watch for QTc prolongation.

Dofetilide: approved for chemical cardioversion and maintenance of sinus rhythm in AFib/flutter

21
Q

Class IV antiarrhythmics:
MOA?
Examples?

A

Class IV: Calcium channel blockers - slow conduction in AVN and suppress SA node to lesser degree. Associated with peripheral vasodilation.

Diltiazem
Verapamil

22
Q

Digoxin/Digitalis
- MOA?

  • Side effects?
A

Inhibits ATP-dependent Na-K exchange pump → ↑ intracellular Na and ↓ intracellular K → → ↑ intracellular Ca

Slows AVN conduction by lengthening of the refractory period.

↑ intracellular Ca → positive inotropic effect

Prodysrhythmia: enhanced automaticity and triggered activity, particularly at high therapeutic or toxic doses

23
Q

Adenosine

- MOA?

A

Best choice for termination of regular, non-atrial, narrow-complex tachycardia, notably junctional re-entry.

Causes abrupt slowing of AVN conduction in anterograde and retrograde pathways.

24
Q

Indications for pacemaker placement? (3)

A
  1. Symptomatic heart block
  2. Symptomatic sinus bradycardia
  3. Afib with symptomatic bradycardia (slow ventricular response rate) in absence of medications that affect AV conduction .
25
Q

Indication for biventricular pacing?

A

aka cardiac resynchronization therapy

Indicated for systolic heart failure with LVEF <35% + LBBB

CHF + LBBB → LV septum contracts before LV wall → ineffective pumping.

Bi-V pacing → both ventricles contract simultaneously, improving EF

** Not shown to be beneficial in HF with narrow QRS (no LBBB)

26
Q

Indications for ICD placement?

A
  1. Cardiac arrest resulting form VF/VT not caused by transient or reversible event.
  2. Spontaneous, sustained VT
  3. Syncope of undetermined origin with clinically relevant, hemodynamically significant sustained VT/VF induced at electrophysiologic study when drug therapy is ineffective, not tolerated, or not preferred
  4. Nonsustained VT + CAD, prior MI, LV dysfunction, and inducible VF/VT at electrophysiologic study that is not suppressible by class I antiarrhythmic.
27
Q

Patient presenting with near-syncope, orthostatic dizziness, fatigue, exercise intolerance, weakness, lethargy, chest fullness, cough, uncomfortable pulsations in neck/abdomen, RUQ pain. H/o recent pacemaker placement.

Diagnosis?
Cause?
Treatment?

A

“Pacemaker syndrome”

Caused by loss of AV synchrony and by the presence of ventriculoatrial conduction.

VVI pacing: ventricle is stimulated and depolarized → ventricular systole.

+ intact SA node function → atrial depolarization by sinus impluse → atrial contraction when tricuspid and mitral valves are closed → contractile assynchrony → ↑ jugular venous pressure and pulmonary venous pressure → sx of CHF

Tx: replacing VVI PM with dual chamber (DDI) PM. If this happens with DDI pacer, need to optimize timing of atrial and ventricular pacing.

28
Q

Causes of pacemaker malfunction (4)

A
  1. Failure to capture: no PM spikes, or spikes not followed by atrial/ventricular contracture – 2/2 lead disconnection/break/displacement, exit block, battery depletion
  2. Undersensing: Lead displacement, inadequate endocardial contact, low voltage intracardiac waves, lead fracture
  3. Oversensing: sensing extracardiac signals/myopotentials, T-wave sensing
  4. Inappropriate PM rate: battery depletion, ventriculoatrial conduction with PM-mediated tachycardia, 1:1 response to atrial dysrhythmias
29
Q

EKG showing wide QRS complexes

Pacemaker spikes precede some QRS complexes.

What type of pacing?

A

VVI - ventricular sensed, ventricular paced, inhibited sensing response

Set rate, ventricular lead set to fire if time between beats exceeds set rate.

Ventricular leads only, no atrial sensing or atrial beats.

If there is an intrinsic ventricular beat, the PM will sense and wait until next appropriately timed beat.

30
Q

EKG showing two PM spikes preceding each QRS complex.

QRS displays LBBB pattern.

What type of pacing?

A

DDD pacing - dual (atrial+ventricular) sensing, dual pacing, dual inhibited.

Set rate; impulse causes atrial depolarization, followed by ventricular depolarization. LBBB morphology because PM lead is initiated in apex of the right ventricle.

31
Q

Metabolic disturbances seen with acute CHF

A

Lactic acidosis + hypoxemia + ↓ pulmonary compliance → tachypnea → concomitant respiratory alkalosis

↑ severity → respiratory acidosis

32
Q

Mechanism of NIPPV in patients with acute CHF

A

↑ functional residual capacity → ↑ PaO2 (Ventilation/Perfusion)

↓ work of breathing → ↓ adrenergic outflow → ↓ HR and ↓ BP → relieves ischemia

↑ intrathoracic pressure → ↓ afterload → ↑ cardiac index (CI) → O2 delivery

33
Q

Treatment in acute CHF with normal/elevated BP (wet and warm) (3)

A
  1. Supplemental oxygenation to maintain SpO2 > 90% (NC, face mask, NIPPV, intubation)
  2. Vasodilator agents: Nitro SL 0.4mg q5min, IV gtt starting 5-10 µg/min, rapidly titrate up +/- Morphine IV 2-5mg boluses
  3. Loop diuretics: Furosemide 0.5-1mg/kg IV OR Bumetanide 0.5-2mg IV
34
Q

Treatment in acute CHF with low BP (wet and cold)

A

Etiology of low BP is either hypovolemia or cardiogenic shock.

  1. Fluid challenge; 250mL bolus over 5-10min. If resp status does not deteriorate, repeat aliquots may be administered. This could restore BP and systemic perfusion without need for pressors.
  2. If in shock, pt requires vasopressors, however they may ↑ afterload → ↓ CO and ↑ myocardial O2 demand.

NE is pressor of choice:
α-vasoconstrictor effect → ↑ BP and ↑ coronary perfusion
modest β-effect → inotropy and the least overall ↑ in HR and contractility, limiting myocardial O2 demand.

35
Q

Stages of pericarditis (3)

A
  1. Diffuse ST segment elevation with reciprocal ST segment depression + PR depression. ST segments are concave upward, and do not follow single coronary artery distribution.
  2. ST and PR segments normalize. Deep, symmetrical T wave inversion
  3. Reverts to normal, although TWI may become permanent.
36
Q

Acute pericarditis treatment

A
  1. NSAIDs - Ibuprofen has best side effect profile. If ineffective after 1 week, different class should be tried.
  2. Colchicine should be added to ↓ risk of recurrent pericarditis. Treatment of choice for recurrent pericarditis, where steroid therapy has shown mixed results.
37
Q

Uremic pericarditis treatment

A
  1. Intensive dialysis.
  2. Systemic steroids in patients who don’t respond to dialysis

*** NSAIDs are ineffective and often are contraindicated.

*** Uremic pericarditis is associated with occult infection, and evaluation should include search for infectious causes.

*** Uremic pericarditis is one of the most common causes of cardiac tamponade.

38
Q

Minimum amount of pericardial fluid required to produce cardiomegaly on CXR?

A

200-250mL

Rosen's (25 decks)

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