PANCE Prep- Cardiology COPY Flashcards
In the bradycardia algorithm, if there is a pulse and the pt is unstable (Hypotension, AMS, refractory CP, acute HF, or symptomatic, what do you do?
- Give Atropine (1st line)
- if atropine not effective:
- Epi infusion
- Dopamin infusion
- -Transcutaneous pacing
*there are 3 exceptions to symptomatic/unstable bradycardia
What are the only 2 shockable rhythms using defibrillation (unsynchronized cardioversion)
- Ventricular fibrillation
2. Pulseless VT
In the tachycardia algorithm, what do you do if a person has a pulse but is unstable?
- Unstable tachyarrhythmia
1. Synchronized cardioversion
- if regular, narrow QRS complex, may consider Adenosine
Describe what you check for in the tachycardia algorithm and what you do?
- Check pulse
- if yes, Stable or unstable?
- if unstable–> synchronized cardioversion - if stable, is there a wide QRS 0.12 sec or more?
- If yes (Wide QRS complex tachycardia)–> antiarrhythmic med: amiodarone, lidocaine or procainamide
- If no (narrow QRS complex tachycardia-> vagal maneuvers, adenosine**, BB or CCB
What are the 3 important exceptions to stable tachyarrhythmia rule?
- atrial flutter: BB or CCB 1st line (skip adenosine)
- afib: BB or CCB 1st line (skip adenosine even though Aflutter is often regular and narrow QRS)
- Wolff-Parkinson-White: Procainamide preferred** or amiodarone- avoid use of AV nodal blockers
What med do you usue if you have a regular and narrow QRS tachyarrhythmia?
adenosine
What meds should you avoid in WPW and why?
AV nodal blockers (ABCD)
- Adenosine
- BB
- CCB
- Digoxin
*AV nodal blockade may cause preferential conduction through the fast (preexcitation) pathway–> worsening of the tachyarrhythmia
Describe interpreting an EKG
- Determine rhythm (R-R regular?)
- Rate: (300-150-100-75-60-50) or #r waves in 6 second strip x10
- QRS axis deviation?
- P for every QRS
- PR interval?
- QRS interval?
- LBBB or RBBB?
- RVH or LVH?
- Pathological Q waves: >1 box in depth or height or prolonged QT?
- ST depression or elevation: >1mm
Describe the normal intervals
PR:
QRS:
QT:
Small box:
Big box:
PR: 3-5 small boxes (0.12-0.2sec)
QRS: <3 small boxes (<0.12 sec)
QT: 7.5-11 small boxes (0.3-0.44 sec)
Small box:
Big box:
Describe the sympathetic NS control of the heart
Hormones Epi and NE cause
- increased excitability
- increased force of contraction
- increased SA node discharge rate (increase HR)
*Epi and dobutamine are sympathomimetics (stimulate the SNS)
Describe the parasympathetic NS control of the heart
Hormone acetylcholine (regulated by the vagus nerve) causes:
- decreased excitability
- decreased force of contraction
- decreased SA node discharge rate (decrease HR)
- Vagal stimulation or vagal maneuvers slow down the HR
- Conversely, anticholinergic drugs increase the HR
How do you determine LBBB or RBBB
LBBB:
- Wide QRS >0.12sec
- Broad, slurred/bunny ears bumps R in V5,6
- Deep S wave in V1
- ST elevation in V1-V3
RBBB:
- Wide QRS >0.12sec
- RsR’ in V1, V2
- Wide S wave in V6
Describe the leads involved and artery involved for the area of infarction:
Anterior wall
V1-V4 (V3,4*)–Q waves/ ST elevation
LAD artery or LCA
Describe the leads involved and artery involved for the area of infarction:
Septal
V1 and V2– Q waves/ ST elevation
Proximal LAD
Describe the leads involved and artery involved for the area of infarction:
Lateral wall
I, aVL, V5, V6– Q waves/ ST elevation
Left circumflex artery
Describe the leads involved and artery involved for the area of infarction:
inferior
II, III, aVF– Q waves/ ST elevation
RCA
Describe the leads involved and artery involved for the area of infarction:
Posterior Wall
V1-V2 ST Depression**
RCA or LCX
What is a normal QRS axis
- 30 to +90 degrees
* look at leads I and aVF
Causes of Left axis deviations
- LBBB
- LVH
3 Inferior MI - Elevated diaphragm
- L anterior hemiblock
- WPW
Causes of right axis deviations
- RVH
- Lateral MI
- COPD
- Left posterior hemiblock
in NSR, P waves are positive/upright in leads:___ and neg in leads: ___
Positive P: I, II, aVF
Negative P: aVR
Pathologic causes of bradycardia and what is the 1st line tx
- BB
- CCB
- Digoxin
- carotid massage
- SA node ischemia
- Gram Neg. sepsis
- hypothyroidism
*Anticholinergic Atropine is 1st line (bc excess vagal stimulation is the MC cause of bradycardia)
Heart rate typically ___ during inspiration
Increases in inspiration
decreases in expiration
What is sick sinus syndrome
Brady-tachy syndrome
- Combination of sinus arrest w/ alternating pparoxysms of atrial tachyarrhythmias and bradyarrhythmias
- commonly caused by SA node disease and corrective cardiac surgery
Management of Sick Sinus Syndrome
- Permanent pacemaker if symptomatic (dual chamber pacing usually preferred over ventricular pacing).
- *if brady alternating with ventricular tachycardia–> permanent pacemaker w/ automatic implantable cardioverter-defibrillator (AICD)
___ is the most helpful in determining the presence of AV conduction blocks
PR interval
Describe 1st, 2nd type 1 and 2, and 3rd degree AV blocks
1st: Fixed, prolonged PRI (>0.2sec) and QRS followed by every P
2nd Type I (Wenckebach): Progressive PRI lengthening then DROPPED QRS
2nd Type II (Mobitz II): Fixed prolonged PRI then DROPPED QRS
3rd: AV dissociation: P waves NOT related to QRS, all P waves NOT followed by QRS = decreased Cardiac output
What is the management of 1st, 2nd type 1 and 2, and 3rd degree AV blocks
1st: none, observe (may progress)
2nd type I (Wenckebach):
- Symptomatic: ATROPINE, epi +/- pacemaker
- Asymptomatic: observe +/- cardiac consult
2nd type II: ATROPINE OR TEMP. PACING, (progression to 3rd degree is common so PPM is definitive tx)
3rd:
- Acute/symptomatic: temporary pacing–> PPM
- Definitive tx: PPM
Describe the appearance of Aflutter and rate
- “saw tooth” waves
2. Rate: 250-350bpm (no P waves but is usually REGULAR)
Management of Atrial flutter
- Stable: Vagal, BB, or CCB
- Unstable: Direct current synchronized cardioversion
- Definitive tx: Radiofrequency ablation
*Anticoagulation use is similar to afib
___ is the most common chronic arrhythmia
atrial fibrillation
*most patients are asymptomatic
Why are people with atrial fibrillation at increase risk for stroke?
The ineffective quivering of the atria may cause thrombi (clots) to form, which can embolize and cause ischemic strokes
7 Etiologies of Afib and gender/race prevalence
- Cardiac disease
- Ischemia
- pulmonary disease
- infection
- cardiomyopathy
- electrolyte/hormone imbalance (hypothyroidism)
- Idiopathic- age, genetics, hemodynamic stress, meds, alcohol
Men> women, white>black
Describe the 4 different types of Afib
- Paroxysmal: self terminating w/in 7 days (usually <24hrs) +/- recurrent
- Persistent: fails to self terminate, lasts >7 days (requires termination via medical or electrical)
- Permanent: persistent AF >1yr (refractory to cardioversion or cardioversion never tried)
- Lone: paroxysmal, persistent or permanent w/o evidence of heart disease
Management of Stable AFib
- Rate control (usually preferred as initial management of symptomatic AF over rhythm control)
- BB: Metoprolol (cautious use in those w/ reactive airway dz**)
- CCB: Diltiazem*, verapamil (non-dihydropyridines)
- Digoxin: +/- use in elderly, **Preferred for rate control in pts w/ hypotension or CHF (not generally used in active patients) - Rhythm control
- Direct current synchronized cardioversion (DCC):
- Pharmacologic: Ibutilide, Flecainide, Sotalol, Amiodarone
- Radiofrequency ablation: PPM, cath-based ablation or surgical MAZE procedure
Direct current (synchronized) cardioversion (DCC) can be done for AFib if:
- AF present >48 hrs OR
- After 3-4 weeks of anticoagulation and a transesophageal echocardiogram (TEE) shows no atrial thrombi OR
- Start IV heparin, cardiovert w/in 24 hrs and anticoagulation for 4 weeks
Management of unstable Afib
Direct current synchronized cardioversion (DCC)
All patients with non-valvular Afib should undergo what two things:
- assessment of the risk of embolization via CHAD2DS2-VASc or CHADS2
* shown to reduce embolic risk by 70% - Determination benefits vs risks of anticoagulation via clinical judgment and discussion w/ patient
Describe the CHA2DS2-VASc Scoring Criteria for afib
- CHF: 1
- HTN: 1
- Age 75 or older: 2
- DM: 1
- S: Stroke, TIA, thrombus hx: 2
- V: Vascular dz (prior MI, aortic plaque, PAD): 1
- A: Age 65-74: 1
- S: Sex: female: 1
-2 or more= moderate to high risk= chronic oral anticoag. recommended
-1= low risk= consider risks/benefits
0= very low risk= no anticoag. needed
Describe the CHADS2 Scoring Criteria for afib
- C: CHF: 1
- H: HTN: 1
- A: Age: 75 or older: 1
- D: DM: 1
- S: Stroke, TIA, thrombus hx: 2
- 2 or more= high risk: Warfarin
- 1= moderate risk: warfarin or ASA
- 0= low risk: non or ASA
Describe types of anticoagulant agents
- Non-vitamin K antagonist oral anticoagulants (NOAC): usually now preferred over warfarin in most cases due to similar or lower rates of major bleedig and less DDI and less drug monitoring
- Dabigatran: direct thrombin inhibitor
- Rivaroxaban, Apixaban, Edoxaban: factor Xa inhibitors - Warfarin
- Dual Antiplatelet therapy: ASA + clopidogrel (anticoagulant monotherapy is superior to dual antiplatelet therapy)
What are Factor Xa inhibitors?
What are direct thrombin inhibitors?
Describe their MOA
Factor Xa inhibitors: Rivaroxaban (Xarelto), Apixiban (Eliquis), Edoxaban (Savaysa)–> selectively binds to antithrombin III)
Direct thrombin inhibitors: Dabigatran (Pradaxa)–> binds and inhibits thrombin
What are three contraindications to NOAC? (non-vitamin K antagonist oral anticoagulants)
- Severe chronic kidney disease
- HIV pts on potease inhibitor-based therapy
- on CP450 inducing antiepileptic meds such as carbamazepine, phenytoin
What are common causes of prolonged QT syndrome and common clinical manifestations
congenital or acquired
- Macrolides
- TCA
- electrolyte abnormalities
- recurrent syncope,
- Ventricular arrythymias
- sudden cardiac death
Management of Prolonged QT Syndrome
- DC offending drug and correct electrolyte abnormalities
2. AICD if definitive tx for congenital or recurrent ventricular arrhythmias
What describe rate, rhythm, and EKG appearance for (p)SVT?
- HR >100
- Regular rhythm with narrow QRS
- P waves hard to discern due to rapid rate
Describe the 2 main types of pSVT
- AVNRT: AV nodal reentry tachycardia: 2 pathways both within the AV node (slow and fast) **MC TYPE
- AVRT: AV Reciprocating tachycardia: 1 pathway within the AV node and a second accessory pathway OUTSIDE the AV node ex. WPW and LGL
Describe the conduction patterns that result in Narrow complex tachycardia and wide complex tachycardia
Narrow complex tachy: Orthodromic (95%): Impulse goes down the normal AV node pathway first and returns via the accessory pathway in circles, perpetuating the rhythm
Wide complex tachy: Antidromic (5%): Impulse goes down the accessory pathway first and returns to the atria via the normal pathway (mimics VT)
Management of Stable Narrow Complex SVT vs Stable Wide complex SVT
Narrow Complex SVT:
- Vagal maneuvers (vagus nerve stimulation releases acetylcholine = decrease HR)
- Adenosine 1st line medical tx for SVT (terminates 90% of narrow complex SVT) **may cause bronchospasm for those w/ asthma/COPD
- AV nodal blockers: BB or CCB
Wide Complex SVT:
1. Antiarrhythmics: ex. Amiodarone or Procainamide if WPW
Tx of unstable SVT (wide or narrow complex) and what is the definitive tx of SVT
- direct current synchronized cardioversion
Definitive: Radiofrequency ablation
What rhythm?
- HR <100 and
- 3 or more P wave morphologies
Wandering atrial pacemaker: multiple ectopic atrial foci generated impulses that are conducted to the ventricles
What rhythm?
- HR >100 and
- 3 or more p wave morphologies
Multifocal atrial tachycardia
*same as WAP but HR is >100
Multifocal Atrial Tachycardia (MAT) is commonly associated with ___ and is difficult to tx but usually use: ___
Severe COPD
Tx: CCB (Verapamil) or BB if LV fxn presereved
What 3 EKG findings are associated w/ WPW and what is WPW
- Delta wave (slurred QRS upstroke)
- Wide QRS (>0.12sec)
- Short PRI
*accessory pathway (bundle of Kent) pre-excites the ventricles–> a type of of AVRT
Management of
- Stable WPW
- Unstable WPW
- Definitive management
- Vagal maneuver
- Antiarrhythmics ex. Class IA: Procainamide preferred***, amiodarone, flecainide
- Avoid the use of AV nodal blockers (ABCD) in WPW**
Unstable: direct current synchronized cardioversion
Definitive: radiofrequency ablation
What rhythm?
- Short PRI
- Normal QRS complex
Lown-Ganong-Levine Syndrome (LGL)
*type of AVRT leading to a short PRI) but the accessory pathway (bundle of james) connects to the bundle of HIS so the QRS is narrow in LGL (unlike the wide QRS in WPW)
What Rhythm?
- Regular rhythm
- P waves inverted (negative) if present in leads where they are normally positive (I, II, aVF) or are not seen
- Classical associated w a narrow QRS
AV junctional dysrhythmias
*AV node/junction becomes the dominant pacemaker of the heart
MC rhythm seen w/ digitalis toxicity
AV junctional dysrhythmia
What are the 3 types of AV junctional dysrhythmias
- Junctional rhythm: HR 40-60,
- Accelerated Junctional: HR 60-100
- Junctional tachycardia: HR >100
- Wide, bizarre QRS occurring earlier than expected.
- The T wave is in the opposite direction of the QRS usually
- Associated w a compensatory pause
PVC
*no tx usually needed
Ventricular tachycardia is considered:
3 or more consecutive PVCs at a rate >100bpm
-Sustained VT= lasting 30 or more seconds
___ is a common predisposing condition for VT
Prolonged QT interval
Torsades De Pointes is most commonly due to ___
hypomagnesemia, hypokalemia
Management of the following VTs:
- Stable sustained VT
- Unstable VT w/ a pulse
- Pulseless VT
- Torsades de pointes:
- Stable sustained VT: Antiarrhythmics (amiodarone, lidocaine)
- Unstable VT w/ a pulse: Synchronized cardioversion
- Pulseless VT: defibrillation (unsynchronized cardioversion) + CPR (tx as VF)
- Torsades de pointes: IV magnesium
Management of VF
Unsynchronized cardioversion (defibrillation) + CPR
Management of PEA (pulseless electrical activity) or asystole
- CPR
- Epi
- Checks for “shockable” rhythms every 2 min
Causes of increased jugular pressure Increased JVP + \_\_\_\_ = \_\_\_\_ 1. + Crackles/rales 2. + Normal pulmonary exam 3. + decreased breath sounds
- Crackles/rales: CHF
- Normal pulmonary exam: Pericardial (tamponade or constrictive pericarditis)
- decreased breath sounds: Tension pneumothorax
7 Causes of ST Elevation
- Acute MI
- LVH
- LBBB
- Acute pericarditis
- Early repolarization abnormalities
- Coronary vasospasm/Prinzmetal angina/cocaine
- Brugada syndrome
EKG findings with pericarditis
- Diffuse concave ST elevation in precordial leads (V1-V6)
- PR depression in same leads w/ ST elevation
- in aVR: ST depression and PR elevation
3 EKG signs of LVH w/ LV strain
- ST elevation in right precordial leads (V1-V3)
- Increase voltage
- Asymmetric ST depressions and T wave inversions in the lateral leads (I, aVL, V5, V6)
Describe Brugada Syndrome EKG patterns
- RBBB (often incomplete) in V1-V3
- ST elevation V1-V3 (often downsloping)
- T wave inversion in V1 and V2
- +/- S wave in lateral leads (I, aVL, V5, V6)