Medicine - Cardiac Flashcards
(38 cards)
Differential diagnosis of ST elevation n the adult chest pain patient (14)
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
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
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
Characteristics of Wellen’s syndrome.
What is this a sign of?
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 .
deWinter’s EKG presentation.
What is is a sign of?
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
ST elevation isolated to leads I and aVL.
Where is the lesion?
Isolated STE in I and aVL suggestive of occlusion of left circumflex
ST elevation in inferior leads.
Lead III > lead II
+ ST depression in aVL and/or I
Where is the lesion?
90% sens and 71% specific for RCA occlusion.
(Right dominant, inferior wall of the heart and AVN served by RCA - 90% of population).
ST elevation in inferior leads
Lead III > lead II
+ ST elevation in V1
What does this suggest?
Inferior wall MI, likely RCA if lead III > lead II.
+ V1 = concomitant RV infarct
ST elevation in inferior leads
Lead II > Lead III
aVL may be isoelectric/elevated
Where is the lesion?
Likely left dominant - inferior wall of heart and AVN served by L circumflex artery (10% of population)
EKG findings in posterior wall MI?
Horizontal ST depression in V1-V3
Tall, broad R waves (>30 ms)
Upright T waves
Dominant R wave (R:S >1) in V2
ST elevation in precordial leads with upward concavity of initial portion/notching at the J point, symmetric concordant T waves
Findings of benign early repolarization
How to differentiate between STEMI and ST elevations seen with LV aneurysm?
Calculation of ratio of amplitude of T wave to QRS complex > 0.36 in any single lead may suggest STEMI
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
LBBB.
*** ST segment and T waves should be expectedly discordant (opposite direction) to QRS
Sgarbossa criteria: (3)
- STE > 1mm CONCORDANT with QRS (5 points)
- STD >1mm in V1-V3 CONCORDANT with QRS (3 points)
- STE >1mm with EXCESSIVE DISCORDANCE (> 25% of preceding S wave) (2 points)
3+ points 90% specific for AMI if pt with LBBB or pacer
Situations to use additional EKG leads? (4)
eg 15-lead EKG with V4R, V8, and V9
- ST changes (elevation/depression) in V1-V3 alone, in isolated lead or more than one lead
- Equivocal STE in inferior (II/III/aVF) or lateral (I/aVL) limb leads, or both
- All inferior wall STEMI
- Hypotension in setting of ACS
Mechanism of action of aspirin when used in ACS
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.
Mechanism of action of thienopyridines (ticlopidine-Ticlid, clopidogrel-Plavix, prasugrel-Effient, ticagrelor-Brilinta) in ACS and indications for use.
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.
Mechanism of action of heparins and indications for use in ACS
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
Class I Antiarrhythmics: MOA? IA: Example? IB: Example? IC: Example?
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.
Class II Antiarrhythmics:
MOA?
Examples? (2)
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
Class III Antiarrhythmics:
MOA?
Examples? (4)
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
Class IV antiarrhythmics:
MOA?
Examples?
Class IV: Calcium channel blockers - slow conduction in AVN and suppress SA node to lesser degree. Associated with peripheral vasodilation.
Diltiazem
Verapamil
Digoxin/Digitalis
- MOA?
- Side effects?
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
Adenosine
- MOA?
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.
Indications for pacemaker placement? (3)
- Symptomatic heart block
- Symptomatic sinus bradycardia
- Afib with symptomatic bradycardia (slow ventricular response rate) in absence of medications that affect AV conduction .
