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KChan Saves the World > KC Cardiac > Flashcards

KC Cardiac Flashcards

1
Q

Define AMI

A

Acute myocardial infarction in the setting of an abonormal troponin (>99th percentile upper reference limit) PLUS one fo the following:

-symptoms of MI
-EKG abnormalities including ischemia or new q waves
-Imaging loss of myocardium or regional wall motion abnormality with ischemic cause
-angiography evidence of thrombus

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2
Q

List the classifications of angina

A
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3
Q

What is Prinzmetal angina? How do we manage it?

A

Coronary artery vasospasm at rest
Has minimal fixed coronary artery lesions
Often relieved with nitroglycerin
ECG may show STEMI pattern, should resolve with sympoms
Can treat with CCB, nitrates or a statin

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4
Q

Describe the 5 types of myocardial infarction

A

Type 5 also has new Q waves or LBBB, angio evidnce of new graft or native coronary occlusion, imaging loss fo myocardium

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5
Q

5 classic and 5 non classic risk factors for AMI

A

Classic - tobacco, HTN, DM, dyslipedemia, hsitory of AMI < 50 years

Non-classic - early menopause, cocaine, RA, HIV, SLE, antiphospholipid

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6
Q

What are complications of AMI?

A

Bradycardia - sinus, AV block (inferior)
Tachycardia - artial or venticular (anterior)
Cardiogenic shock - think big infarct, frail patient

Mechanical complications
LV rupture - first 24 hours to 5 days, sudden death
Septum or pap muscle rupture - 3-5 days, new systolic murmur and flash pulmonary edema

Stroke (LV anneursym, a fib that embolizes)

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7
Q

Besides ST elevation, describe ECG findings suggesting ischemia

A

Can be normal early
Hyperacute T waves
T wave inversions
STD
Q waves

STEMI equivelents: LBBB with scarbossa crtieria, DeWinter, Wellens, depression in V1, V2, elevation in aVR

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8
Q

What are the Smith-modified Sgarbossa criteria?

A

Concordant ST elevation >1mm in leads with a positive QRS
Concordant ST depression >1mm in V1-V3
Disconcordant ST elevations >5mm
- Revised criteria: significantly if ST elevation is >25% of the S wave

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9
Q

Patient is diagnosed with a STEMI and the cath lab is being prepared. What medications would you give?

A

ASA 162-325mg chewed
Plavix 600mg <75, 300mg >75 years
Heparin 60mg/kg bolus (up to 4000U)

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10
Q

What are the doses of plavix for:
1) PCI
2) Fibrinolysis
3) NSTEMI

A
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11
Q

What are 3 options for anti-platelet in ACS?

A

ASA 324mg chewable
Plavix either 300 or 600mg
Ticagrelor 180mg

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12
Q

What are two mechanisms of ASA? How well does it work with and without thrombolytics?

A

Irreversibly acetylates platelet cyclooxygenase (removes activity of platelet for 8-10 days)
Stop production of thromboxane A2 (encourages aggregation)

Without 23% reduction in mortality
With 42% reduction in mortality

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13
Q

What are mechanisms of Ticagrelor and Plavix? What is a difference

A

Both PSY12 inhibitors
Stop P2Y receptor from transforming into high affinity state - binds irreversibly for life of platelet

Plavix - Inhibits ADP platelet aggregator factor
Ticag: is reversible, does not need hepatic metabolism

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14
Q

Describe the antithrombins used in ACS and their indications

A

Unfractionated heparin: 60u/kg bolus (max 4000) used if going to PCI or kidney injury, reversible with protamine, risk of HITT
LMWH (Dalteparin, enoxaparin): 30mg IV bolus for dalteparin, enoxaparin 0.5mg/kg IV, use if delayed or no PCI, not great in in kidney injury, protamine partially effective
Fondaparinux: 2.5mg sub cut, use if delayed or no PCI. Factor 10a inhibitor, cannot give in kidney injury
Bivalirudin Direct thrombin inhibitor - used in STEMI is cant have UFH (allergy, HIT). No antidote very short half life

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15
Q

Describe the use of PCI vs. thrombolysis

A

Thrombolysis: presentation <3 hours, no PCI facility available, FMI to balloon time expected to be >120 mins (ex. Transfer), STEMI only

PCI: presentation >3 hours, contraindications for thrombolysis, cardiogenic shock, unsure of diagnosis

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16
Q

What are four options for thrombolysis and their doses?

A

tissue type plasma activator t-PA, 100mg total infusion over 90 minutes
Two recombinant t-PAs (TNK or retelplase), 30-50mg based on body weight
OG streptokinase (don’t use anymore)

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17
Q

Which thrombolytic do we give and why?

A

TNK
Longer half life so you can bolus it
14x more fibrin specific
80 times more resistant plasminogen activator
>4 hour presentation mortality benefit fewer non ICH bleeds

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18
Q

Describe the goal times for 1) FMC to ECG 2) FMC to balloon in a PCI centre 3) FMC to balloon in a non PCI centre 4) FMC to thrombolysis

A

1) <10 mins 2) <90 mins 3) <120 mins 4) <30 mins

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19
Q

Describe the ECG findings of a left main occlusion

A

Widespread horizontal ST depression, most prominent in leads I, II and V4-6
ST elevation in aVR ≥ 1mm
ST elevation in aVR ≥ V1

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20
Q

Differentiate between early and late post MI pericarditis? What are 2 drugs contraindicated in post MI percarditis?

A

Post MI - NSAIDs and steroids? CONFIRM THIS

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21
Q

What is the earliest finding of ischemia on ECG

A

Peaked T waves —> which will later progress into STE in typical STEMI

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22
Q

Outline the HEART score componets and scoring. What does it tell you?

A

HEART score predicts your short term risk of MACE defined as AMI, need for PCI or CABG, and death within 6 weeks of the ED visit.

Low – 1.7%, Moderate – 12-17%, High 50-65%

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23
Q

*What is the definition of STEMI (5 things)

A

New ST segment elevation in 2+ contiguous
leads >1mm in all leads other than V2-V3

For V2-V3:

≥2mm in Men >40years

≥2.5mm in Men <40 years

≥1.5mm in Women

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24
Q

*Ddx STE (6)

A

ST elevation mnemonic ELEVATIONS - electrolyte (hyper K, hypercalcemia), LBBB/paced, early repol, ventricular hypertrophy, Aneurysmal LV, thrombotic occlusion (MI), inflammation (pericarditis), Osborn (hypothermia), neurogenic, sudden death (Brugada)

plus three more P’s - Post cardioversion, PE, Prinzmental

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25
Q

*What are 6 causes of MI with normal coronaries?

A

Iatrogenic (aortic or coronary manipulation)
Trauma

Aortic dissection
Cocaine or other sympathomimetic abuse
Vasospasm

Sepsis
Tachydysrhythmia

Pregnancy
Thyrotoxicosis
Severe anemia
Hypoxia
Takotsubo

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26
Q

*What 3 treatments for ACS that have proven reduction in mortality? Please also list their mechanism of action.

A

ASA (antiplatelet)
Ticagrelor (antiplatelet)
reperfusion strategy such as PCI or fibrinolysis for STEMI (unless they were only referring to NSTEACS)

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27
Q

*What are 5 reasons to refer a patient to emergent PCI despite no STEMI?

A

1/ De winter
2/ AVR elevation with diffuse STD
3/ Wellens
4/ Posterior MI
5/ LBBB or paced meeting Sgarbossa criteria
6/ Post cardiac arrest

High risk NSTEMI
HD
Electrical instability - lethal arrythmia
Intractable ischemic pain

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28
Q

*What are the 3 acute mechanical complications of MI?

A

Papillary muscle rupture/regurgitation
Free wall rupture
Septal rupture
LV aneurysm

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29
Q

*The patient is found to have infarct pericarditis; what is the treatment?

A

Tylenol: IF remain symptomatic:
High dose ASA

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30
Q

*What are 5 risk factors for atypical MI presentation?

A

Female
Elderly
Non-white ethnicity
Diabetes
Dementia
No prior hx of MI
No FH of coronary disease

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31
Q

*Territory/artery involved in STEMI inferior leads

How can you tell which is which?

A

Inferior, RCA or LCx

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32
Q

*4 physiologic mechanisms why this patient would be hypotensive (inferior MI)?

A
  • decreased RV contractility causing increasing right sided pressures, and decreased preload to right
  • decreased preload to left
  • RV dilation shifting septum decreases LV filling and therefore output

Brady from AV block
RV failure
Wall rupture
Septum rupture
Ischemic VSD

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33
Q

*2 reasons why – for patient going for PCI — ticagrelor better than Plavix? What are 2 reasons why you might not?

A

PLATO Trial
1. Improved vascular mortality (MI or CVA)
2. Reduction in all cause mortality

Higher rates of non-procedure related bleeding (Increase in ICH)
More recent data suggests no difference in MACE at 1 year

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34
Q

*3 risk factors for spontaneous coronary artery dissection (“SCAD”)?

A
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35
Q

*Where is the lesion: De-winter’s wave

A

LAD

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36
Q

*Where is the lesion: Bradycardia (rate 50) + TWI in aVL

A

RCA

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37
Q

*Where is the lesion: Infero-lat depression + AVR & V1 STE

A

Left main

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38
Q

*Where is the lesion: Anterior V1-V4 STE + inferior depression

A

Proximal LAD

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39
Q

*What 4 findings of BER on ECG? What is one example where you do want to be a little more wary?

A
  1. ST elevation –> Concave up
  2. Notching at the J point
  3. Symmetrically large T waves concordant
  4. Diffuse elevation
  5. No reciprocal changes
  6. Temporal stability (Constant) –> no dynamic changes

Exception is if only in limb leads - rare! Think about STEMI

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40
Q

*What are 2 findings for LV aneurysm on ECG.

A
  1. ST elevation, usually V1-V6, I, avL
  2. Q waves often “well formed” - indicate previous MI
  3. No reciprocal changes
  4. T:QRS amplitude > 0.36 - STEMI
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41
Q

*What are 4 clinical findings or findings on ancillary testing for takotsubo’s cardiomyopathy. What is 1 clinical item on history?

A

Tachycardia, hypotensive
STE
Trop elevation
Ballooning of the left ventricular apex is seen on ventriculography or echocardiography.
Clean cath

Recent intense emotional stress

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42
Q

*List three features on ECG that help to identify acute MI in a paced patient

A

Modified Sgarbossa

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43
Q

*5 causes of LBBB? What is Lenegere disease?

A

Also known as idiopathic fibrosis of the conducting system, or acquired complete heart block
Complete and permanent atrioventricular block is often the consequence of lesions involving both bundle branches, and not of a lesion in the common bundle

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44
Q

*Recognize Wellens type A and B - how to manage? (3) Where is the lesion? What are your options for management?

A

STEMI equivalent
Type B - deep symmetrical T wave inversion (75%)
Type A - biphasic T wave changes in the anterior precordial leads (25%)
Other features <1mm STE and no precordial q waves

Proximal LAD lesion that can preceed STEMI

Stable and no CP - DAPT, fonda and cardio (cath wont take but let them know
Unstable, onging pain, on nitro infusion - DAPT + heparin +cath

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45
Q

*What are 5 absolute contraindications for thrombolysis in STEMI? 5 relative?

A

Absolute is 1-2-3, One head bleed ever, spine surgery 2 months, head trauma 3 months, ischemic stroke 3 months and aortic dissection

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46
Q

What are EKG criteria for successful fibrinolysis?

A

Reduction > 50% of STE within 1 hour
Significant relief of pain

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47
Q

*5 causes or precipitants of afib

A

Hypertensive heart disease
Cardiomyopathy
Ischemic heart disease
Valvular disease (especially mitral)
Congestive heart failure
Pericarditis
Hyperthyroidism
Sick sinus syndrome
Myocardial contusion
Acute ethanol intoxication (holiday heart syndrome)
Idiopathic
Cardiac surgery
Catecholamine excess
Pulmonary embolism
Accessory pathway (Wolff-Parkinson-White) syndrome

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48
Q

*Best choice for medical cardioversion

A

Procainamide - 1A
It slows down conduction in everything except for the SA node, including accessory pathways
Use it WPW

Flecanide (supported UTD), propafenone

1C - Flecainide can be used for some SVT and VT
Requires a lot of caution, variable half life, narrow therapeutic index – why it isn’t first line and first dose needs to be observed
Also be careful if someone has structural or ischemic heart disease (why young people get pill in pocket)

Profoundly slow depolarization to the point they can make new arrythmias way worse then 1A

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49
Q

*4 reasons not to cardiovert due to increased risk of stroke

A
  1. Valvular AF (any duration), or
  2. NVAF Duration <12 hours and recent stroke/TIA, or
  3. NVAF Duration 12-48 hours and CHADS2
    ≥2, or
  4. NVAF Duration >48 hours
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50
Q

*According to 2016 CCS guidelines: 5 reasons to start someone on oral anticoagulation (answer now with 2018)

A

2018 indications afib plus:
1. Any CHADS2 RF needs OAC
2. Valvular AF
3. Cardioversion plus (OAC 4 weeks)
i. Hemodynamically unstable acute AF, or
ii. NVAF Duration <12 hours and no recent stroke/TIA, or
iii. NVAF Duration 12-48 hours and CHADS2<2

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51
Q

*List 5 completely irregular/chaotic heart rhythms

A
  • Atrial fibrillation
  • Atrial tachycardia or flutter with varying conduction
  • Multifocal atrial tachycardia
  • Multiple extrasystoles
  • Wandering pacemaker (usually atrial)
  • Parasystole
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52
Q

*List 4 clinical findings that hint at cardiac instability from arrhythmia

A
  • HD unstable
  • Chest pain
  • Dyspnea
  • aLOC
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53
Q

*List 6 patient related factors to take into account when deciding to rate or rhythm control a patient

A
  • Stable or unstable
  • Onset of symptoms (new-onset or newly recurrent, with duration < 48 h)
  • Anti-coagulation status
  • Valvular disease
  • Hypokalemia (increases risk of ventricular fibrillation)
  • Digitalis toxicity (increases risk of ventricular fibrillation)
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54
Q

*List 4 medications that can be used for rhythm control

A
  • Procainamide
  • Amiodarone
  • Ibutilide
  • Propafenone
  • Flecainide
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55
Q

*List the 7 components of the CHADS2-VASc score

A
  • Congestive heart failure
  • Hypertension
  • Age >= 75 years
  • Diabetes mellitus
  • Any previous stroke, transient ischemic attack, embolism
  • Gender–female
  • Age, 65-74
  • Vascular disease (history of MI, PAD, or aortic atherosclerosis)
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56
Q

*What score is “moderate risk” and requires anticoagulation?

A

Scores of 2 or higher, anticoagulation is recommended

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57
Q

*Explain pre-excitation in terms of cardiac conduction?

A

Accessory pathway offers an alternate route for the atrial impulses, so they can bypass the AV node, flow through the fast accessory pathway, causing early excitation of the ventricles which shows up as a slightly wider, slightly early QRS complex (for instance, the delta wave in WPW)

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58
Q

*3 ECG findings of WPW

A
  1. Short PR
  2. Delta wave
  3. Wider QRS
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59
Q

*Recognize Brugada type I and II

A

EKG

Remember Brugada sign is type 1 only that is potentially diagnostic
1 - Coved ST segment elevation >2mm in >1 of V1-V3 followed by a negative T wave.
2 - Brugada Type 2 has >2mm of saddleback shaped ST elevation.
3 - Either but with less than 2mm of elevation

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60
Q

*2 most common dysrhythmias in people with WPW?

A

Orthodromic AV reentrant tachycardia
Afib

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61
Q

*AFib with wide complex given – what’s the most acceptable medication to use?

A

Procainamide (or cardioversion)

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62
Q

*Which two medications are contraindicated in WPW with afib?

A

ABCD
1. Adenosine
2. Beta blockers
3. CCB
4. Dig

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63
Q

*Explain why above medications are dangerous in this case.

A

Treatment with AV nodal blocking drugs e.g. adenosine, calcium-channel blockers, beta-blockers may increase conduction via the accessory pathway with a resultant increase in ventricular rate and possible degeneration into VT or VF

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64
Q

*3 reasons to use warfarin over NOAC for a fib

A
  • Valvular AF (includes mechanical mitral valve and mitral stenosis)
  • Cost
  • Patient preference
  • Renal insufficiency? Low body weight?
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65
Q

*What are 7 classes of causes (besides metabolic) that would cause this rhythm disturbance (complete heart block)?

A
  • Increased vagal tone
  • Progressive cardiac conduction system disease (i.e. fibrosis, sclerosis, calcification)
  • Ischemic heart disease/myocardial infarction
  • Infiltrative cardiomyopathy (e.g. secondary to sarcoidosis, amyloidosis, malignancy)
  • Non-ischemic cardiomyopathy (e.g. post-infectious, such as Chagas disease)
  • Drugs (e.g. beta-blockers, calcium channel blockers, digoxin, anti- arrhythmic)
  • Cardiac surgery (e.g. post valvular surgery)
  • Transcatheter aortic valve implantation
  • Catheter ablation of arrhythmias
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66
Q

*List 4 etiologies of torsades

A

Non-Drugs:
- Congenital long QT and other congenital syndromes
- Electrolyte abnormalities: hypokalemia, hypomagnesemia, hypocalcemia
- Diet-related: starvation, low protein
- Severe bradycardia or AV block
- Hypothyroidism
- Contrast injection
- Cerebrovascular accident
- Myocardial ischemia
Drugs:
- Class IA anti-dysrhythmic (e.g. procainamide)
- Class IC anti-dysrhythmic (e.g. propafenone)
- Butyophenones (e.g. haloperidol)
- TCA
- Antibiotic (e.g. macrolides)
- Organophosphates
- Anti-histamine
- Anti fungal

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67
Q

*3 Treatment for torsades

A

Pulseless: Defibrillation Unstable: Cardioversion Stable:
- Cease QT prolonging medications
- Empirical IV magnesium sulfate (2 g over 10-20 minutes and then infusion at 1-4 g/hr)
- Correct underlying metabolic disturbances (i.e. hypokalemia, hypocalcemia)
- Overdrive pacing (ie chemical or medical with isoproterenol) target rate of 90 100 beats/min higher occasionally

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68
Q

*Treatment for VT

A

Stable: Amiodarone or procainamide
Unstable: Cardioversion at 100J
**Remember, if unsure if SVT with aberrancy vs VT, treat as VT.

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69
Q

*What are the components of the CHADS-Vasc score?

A

CHADS2:
CHF
HTN
Age >75
Diabetes
Stroke or TIA previously (2)
CHA2DS2VASC:
CHF
HTN
Age >65,>75 (2)
Diabetes
Stroke or TIA, previously (2)
Vasc HX (MI, PAD)
Sex (F = 1)

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70
Q

*How to estimate stroke risk in 1 year with CHADS scores?

A

Rule of thumb is to double whatever the score is.

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71
Q

*List 3 electrolyte disturbances that cause long QT.

A
  • Hypomagnesemia
  • Hypokalemia
  • Hypocalcemia
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72
Q

*Name 2 congenital causes of torsades

A

Jervell and Lange-Nielsen syndrome (deafness, autosomal recessive)
Romano-Ward syndrome (normal hearing, autosomal dominant)
Sporadic (normal hearing, no familial tendency)
Mitral valve prolapse

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73
Q

Describe the phases of an action potential

A

Depolarization via Na influx
Plateau phase with stabilization of calcium
Repolarization with K efflux
Refractory period and restoration of ion balance by Na/K ATP pumps

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74
Q

List 4 classes of cardiovascular drugs, list examples of each and briefly describe their mechanism of action

A

Some Block Potassium Channels
Class I: sodium channel blockers ex. Procainamide, lidocaine. Block sodium channels effectively increasing refractoriness
Class 2: beta blockers ex. Metoprolol. Depresses the SA node, slows AV node conduction
Class 3: potassium channel blockers ex. amiodarone, sotalol. Prolongs actions potential and refractory periods (prolongs Qtc)
Class 4: calcium channel blockers ex. verapamil. Slows conduction in the AV node

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75
Q

Describe the subtypes of Class I sodium channel blockers

A

“Quarter pounder, lettuce pickles, fries please”
1A: quinidine, procainamide
1B: lidocaine, phenytoin
1C: flecainide, propafenone

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76
Q

Which sodium channel blockers are generally used for supraventricular vs. ventricular tachycardias

A

Class IA and 1C and generally better for supraventricular tachycardias as they prolong repolarization, and 1B for ventricular tachycardias as it shortens repolarization

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77
Q

Which sodium channel blockers also block potassium channels

A

Class 1A and 1C

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78
Q

List 2 side effects of procainamide

A

Qt prolongation, hypotension

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79
Q

List 10 sodium channel blockers

A

Quinidine, procainamide, lidocaine, phenytoin, flecainide, propafenone
antimalarials (chloroquine), local anesthetics, diphenhydramine, cocaine, propranolol, carbamazepine

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80
Q

Describe the difference between beta 1 and beta 2 receptors

A

B1: mainly myocardium, increases inotropy + chronotropy, activates cAMP
B2: bronchial and visceral smooth muscle, increases bronchodilation and vasodilation

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81
Q

Which beta blockers are cardio selective? Why is this important?

A

A-M cardio selective block B1 ex. Atenolol, metoprolol
N-Z nonspecific B1 and B2 (can cause bronchospasm in asthmatics) ex. Nadolol

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82
Q

Which beta blockers have mixed alpha and beta activity

A

Olol - pure beta blocker
Vowel -lol alpha and beta blocker ex. labetalol

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83
Q

What is a first degree heart block

A

PR interval >200ms, no treatment necessary

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84
Q

What is a second degree heart block Type 1

A

Type 1 (Wenckebach): progressive prolongation of the PR intervention while the P-P interval remains constant. Ends in a non conducted p wave. Due to a conduction block at the AV node. No treat if asymptomatic

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85
Q

What is a second degree heart block Type 2

A

Type 2 (Mobitz): intermittent non conducted P waves without progressive prolongation of the PR interval. Due to a conduction block below the AV node. More likely to be associated with hemodynamic instability; may need pacing

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86
Q

What is a third degree heart block

A

None of the P waves are conducted to the ventricles. May be an junctional or escape ventricular rhythm.

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87
Q

How is afib diagnosed on ECG

A

absence of discernible P waves and an irregular rhythm

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88
Q

List 5 causes for afib

A

HTN, CAD, cardiomyopathy, valvular heart disease, hyperthyroidism, cardiac contusion, CHF, pericarditis, PE

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89
Q

List indications for cardioversion of AF

A

Hemodynamically unstable acute AF
NVAF duration <12 hours and no recent stroke/TIA
NVAF 12-48 hours and CHADS2 <2

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90
Q

What is the definition of valvular AF

A

mechanical valve, rheumatic mitral stenosis, or more than moderate mitral stenosis

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91
Q

List 3 drugs that can be used for rate control in AF

A

Metoprolol
Diltiazem
Digoxin

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92
Q

List 3 drugs that can be used in rhythm control in AF

A

Amiodarone
Procainamide
Flecainide

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93
Q

Briefly describe the landmark studies in rate vs. rhythm control for chronic management of AF

A

AFFIRM and RACE show that embolic events occur with equal frequency
AFFIRM: Trend towards decrease mortality with rate control, but no difference in terms of death or rate of stoke
RACE: Similar findings to AFFIRM; trend towards lower mortality with rate control but no divergence in cardiovascular mortality. Trend towards non fatal endpoints in rhythm control (ex. heart failure VTE) thought to be S/E of the anti arrhythmia drugs

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94
Q

As per the CCS, which patients with AF should receive OAC

A
  1. Age >65
  2. Any CHADS - CHF, HTN, diabetes, prior stroke or TIA

CAD or PAD should get antiplatelet therapy ex. ASA

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95
Q

What is the risk of cardioversion in a patient with AF

A

No anticoagulation - 30 day incidence of 2.39%, with a background rate of 0.5% if no cardioversion is performed
Anticoagulation - 0.27%

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96
Q

Describe ECG findings of aflutter

A

Regular rhythm with P waves of a single morphology in a sawtooth pattern; atrial rate varies depending on the block type

97
Q

Describe the following ECG (AVNT)

A

AVNRT - functional re-entry pathways within the AV node
ECG shows a regular tachycardia with no visible P waves (hidden in QRS) or P waves after the QRS comples

98
Q

What is the difference between orthodromic and antidromic conduction

A

Orthodromic: Anterograde (down) through the AV node, retrograde (up) through the accessory pathway. QRS is narrow and rate is constrained by the refractory period of the AV node. Indistinguishable from ANVRT. Treated with adenosine and vagal maneuvers
Antidromic: anterograde (down) through the accessory pathway, retrograde (up) through the AV node. QRS is wide and rate can be quite rapid; clinically more unstable. Avoid AV blocker agents as this can cause the rhythm to degenerate into VT due to rapid conduction down the accessory pathway. Cardioversion is the treatment of choice, otherwise use procainamide

99
Q

List 3 rhythms in each of the following: narrow and regular, narrow and irregular, wide and regular, wide and irregular

A

See photo

100
Q

What is the recommended energy level for cardioversion

A

Up to 200 J (can consider lower doses if narrow and regular ex. Aflutter)

101
Q

What is the dose of adenosine

A

6mg then 12 mg

102
Q

Describe the Brugada criteria for diagnosing VT

A

VT if any of the following is present:
1. Absence of RS complex in all precordial leads
2. RS interval >100
3. AV dissociation
4. Morphology criteria

103
Q

List clinical, physical examination, and ECG findings that can help determine VT from SVT with aberrancy

A

Table 69.5

104
Q

What is the pathology in this ECG (Brugada)

A

Brugada: RBBB + ST elevation
Type 1: Coved ST elevation >2mm in V1-V3 followed by a negative T wave
Type 2: Saddleback ST elevation
Type 3: Type 1 or Type 2 but less than 2mm of elevation

105
Q

Mention 2 factors slow the rate of SA node and 3 factors that increase it ? (One factor should be a post surgical group of patients)

A

** Factors the slow the SA node :
1- Hypothermia
2- Parasympathetic stimulation
** Factors that increase the SA node rate :
1- Hyperthermia
2- Sympathetic stimulation
3- Loss of parasympathetic (Heart transplant patients)

106
Q

List 10 adverse effects of amiodarone

A

Acute: hypotension, bradycardia, decreased contractility
Long term: corneal deposits, photosensitivity, Gi intolerance, hyperthyroidism, heart failure, pulmonary toxicity

107
Q

List 5 causes of sinus bradycardia

A

1)Normal healthy adult
(2)Sleep
(3)Hypothermia
(4)Diminished sympathetic stimulation (drug related- BB, CCB & Digoxin)
(5)Excessive parasympathetic tone
(6)Early inferior MI
(7)Carotid sinus hypersensitivity (tight shirt collar)
(8) Hypothyroidism
(9) Hypoxia
(10) High ICP

108
Q

List 5 diseases associated with WPW

A

My Heart is Extremely Tired
M: Mitral valve prolapse
H: HCM
I: idiopathic
E: Ebstein anomaly
T: TGA + Tricuspid atresia

EEMMTT

109
Q

*5 considerations in ACLS management of patients with LVAD

A

Treatment of dysrhythmias is same as usual
Don’t CPR in cardiac arrest. Intubate, give IVF, assess LVAD, if machine has hand pump use that. If no response still, CPR.
These patients have no pulse; avoid CPR if perfusion is good

110
Q

*4 ways to assess circulation in patient with LVAD

A
  • Need doppler and BP cuff for MAP
  • Arterial line
  • Auscultate for hum
  • POCUS: check RV (small? fill it. big? PE/STEMI/pHTN). IF RV and LV big - pump thrombosis
111
Q

*ECG showed a pacing spike for A and V…. V always pacing, A sometimes not paced and would intrinsically fire independently ……. What is the issue on the ECG

A

Undersensing? Or failure to capture

112
Q

*4 causes of failure to capture

A

Changes in endocardium:
Fibrosis, hypertrophy, CMP
RVH infarct
Device issues:
Lead #
Displacement
Battery (if failure to capture)

113
Q

*Develops Afib with RVR 160 BPM– what does PM/ICD do

A

Inhibited

114
Q

*Develops VT at 180 what does PM/ICD do?

A

ICD fire

115
Q

*Explain VVI – ie what each letter means

A

V - Chamber paced, V = ventricle
V - Chamber sensed, V = ventricle
I - Sensing response, I = inhibited

116
Q

*If have single lead pacer, which chamber is the lead in?

A

Apex RV

117
Q

*What does ECG look like if have VVI pacer?

A
  • Pacing spike precedes QRS complex
  • Right ventricle pacing lead placement results in QRS morphology similar to LBBB
  • ST segments and T waves should be discordant with the QRS complex
118
Q

*What happens when put magnet on PPM

A

Closure of red switch, turning off sensing function, thus converting the pacemaker to fixed-rate pacing

119
Q

*What happens when put magnet on ICD

A

Temporary ICD deactivation

120
Q

*2 locations of pads on chest when have PPM

A

• Anteroposterior configuration
• If the sternal defibrillation pad is placed adjacent to the sternum,
• it is at a safe distance (>10 cm) from the pulse generator

121
Q

*Pacemaker. It’s a DDD. What does each D stand for.

A

Dual

122
Q

*If lead of PM is in right ventricle, what is ECG pattern.

A

LBBB

123
Q

*If PM lead migrates through septum (into LV), what is ECG pattern.

A

RBBB

124
Q

*What is the pathophysiology of pacemaker mediated tachycardia?

A

PMT is a re-entry tachycardia in which the pacemaker forms the antegrade pathway with retrograde conduction occurring via the AV node. Ventricular beat triggers retrograde atrial depolarization that is sensed by the pacemaker and triggers another beat; creates an endless loop tachycardia. Only occurs in dual chamber pacemakers. Managed by putting a magnet over the pacemaker

125
Q

*What are 2 treatment for infected PM pocket?

A

Ceftri/Vanco and removal of device if BCx positive

126
Q

*What is exit block?

A

Failure of an adequate stimulus to depolarize the paced chamber (i.e. increased stimulation threshold at electrode site)
Leads to failure to capture

127
Q

*What are two causes of exit block?

A
  • Changes in endocardium in contact with pacing system (e.g. ischemia or infarction)
  • Systemic hyperkalemia
  • Use of class III anti-arrhythmic (e.g. amiodarone)
128
Q

*Patient presents with an ICD and shocks. List three causes of the shocks.

A
  • Increased frequency of VF or VT (consider ischemia, electrolyte disorder or drug effect)
  • Displacement or break in ventricular lead
  • Recurrent nonsustained VT
  • Sensing and shock of supraventricular tachyarrhythmias
  • Oversensing of T waves
  • Sensing non-cardiac signals
129
Q

*Elderly female with recent pacemaker insertion, returning with dyspnea while supine, sets 94% on 3L. CXR provided: large heart, left pleural effusion. What pacemaker insertion complication most likely occurred in this patient

A

Myocardial perforation

130
Q

*What 2 CXR findings are associated with myocardial perforation of PM lead?

A

• Extra-myocardial lead positioning
• Extracardiac complications
Pleural
Pericardial effusion
Pneumothorax

131
Q

*What are 3 physical exam findings (other than vital signs) associated with tamponade (say from PM lead myocardial perforation)

A
  • Distended neck veins/Elevated jugular venous pressure
  • Muffled heart sounds
  • Pulsus paradoxus
132
Q

Explain DDD pacemaker settings

A

Dual paced - atrium and ventricle
Dual sensed - atrium and ventricle
Dual response - triggered and inhibited
The pacemaker waits for an endogenous atrial depolarization. If none is sensed, an atrial spike is delivered. The pacemaker then waits for an endogenous ventricular depolarization, in response to either the atrial pacing spike or endogenous atrial depolarization, should this have occurred. If there is no endogenous ventricular depolarization, a ventricular pacing spike is delivered.

133
Q

What are the indications for a pacemaker

A

Third degree AV block or Type II second degree with:
- Bifasicular or trifasicular block
- Symptomatic bradycardia
- Documented periods of systole lasting >3 seconds with an escape rhythm <40bpm
- Catheter ablation of the AV node
- Block triggered by exercise

134
Q

What are the indications for an ICD

A

VF or VT that is spontaneous, or results in cardiac arrest or syncope
Non sustained VT with CAD, MI, reduced EF

135
Q

List 5 complications of pacemaker insertion. What is pacemaker syndrome?

A

Infection
Thrombophlebitis
Bleeding
Pneumothorax w insertion
Pacemaker syndrome: new or worsening symptoms such as syncope, CHF, exercise intolerance, pulsations. Due to the loss of AV synchrony. Can be managed by switching to a dual chamber pacemaker or lowering the pacing rate
Pacemaker malfunction

136
Q

List 3 causes of tachycardia in a patient with a pacemaker

A

Appropriate pacemaker response
Atrial arrhythmia
Pacemaker-mediated tachycardia
Sensory induced tachycardia (undersensing)
Inappropriate rate

137
Q

List 2 causes of bradycardia in a patient with a pacemaker

A

Failure to capture (lead broken, exit block, battery depleted, medical issues - electrolytes, drugs, MI)
Failure to pace (ex. Oversensing, lead broken, crosstalk)
Inappropriate rate

138
Q

What is sensor induced tachycardia

A

Pacemaker senses distracting stimuli and interprets this as triggered activity, causing an in appropriately fast pacemaker rate

139
Q

List 3 modifications to ACLS for someone with a pacemaker

A

Place pads of paddles at least 10cm below the pulse generator. Defibrillation can occur at the normal shock
Should obtain a chest x ray after to ensure that the wires were not displaced
The pacemaker may not resume after defibrillation; this is due to global myocardial ischemia and increased pacing threshold; may need to be transcutaneously paced

140
Q

List 5 reasons why an ICD may fire

A

Shocks may be inappropriate delivered due to false sensing, double counting, broken lead, component failure
Shocks may also be appropriate if there is increase in VT or VF episodes(ischemia, electrolyte, drug effects), cardiac arrest

141
Q

List one complication unique to biventricular pacing

A

coronary sinus dissection or coronary sinus perforation
Becuase that is where the LV lead goes through

142
Q

How does an LVAD work

A

Supports cardiac output via a mechanical pump that draws blood from an inflow canola of the L ventricle and pumps it into the ascending aorta via an outflow cannula

143
Q

*Chronic Heart Failure stem. Patient is hypertensive and hypoxic and has pedal edema. What are 3 immediate management steps?

A

Nitroglycerin
Bipap/oxygen
Lasix

144
Q

*Patient becomes hypotensive (CHFe). What three interventions or treatments do you initiate immediately?

A

Norepinephrine
Careful crystalloid bolus
Inotrope (dobutamine)
Stop nitro.

145
Q

*What are 5 precipitants of chronic heart failure?

A

Coronary artery disease, angina, diabetes, heart valve disease, and high blood pressure

146
Q

*What are the 5 medication classes used to treat heart failure?

A

ACEi
Beta-blocker
Cardiac glycosides (dig)
Diuretics
Nitrates
Statins

147
Q

*List 6 findings on clinical exam for pulmonary edema

A

i. Rales
ii. Wheezing or rhonchi
iii. ­ JVP
iv. S3 gallop
v. Hypoxemia
vi. Hypertension (or hypotension)
vii. Cool/clammy with delayed cap refill
viii. Diaphoresis

148
Q

*List 6 CXR findings of pulmonary edema

A

i. Enlarged cardiac silhouette
ii. Peribronchial cuffing
iii. Fluid in fissures
iv. Pleural effusions
v. Vascular redistribution
vi. Bat wing appearance
vii. Kerley B lines

149
Q

*List 5 precipitants of acute heart failure

A

Pump problems: ischemic heart disease, cardiomyopathy(amyloid infiltration, hemochromatosis, inherited), myocarditis, valvular heart disease, dysrhythmias
Pressure overload ex. sodium or volume excess, AS or HTN, cor pulmonale, pharmacologic complications, outflow track obstruction ex. HOCM
Volume overload (ex. AI, thyrotoxicosis, pregnancy) leads to dilatation and eccentric remodeling
Increased oxygen demands ex. Sepsis, COPD and respiratory problems, anemia

150
Q

*Explain the NYHA classification

A

Class 1 - asymptomatic on ordinary physical activity
Class 2 - symptomatic on ordinary physical activity
Class 3 - symptomatic on less than ordinary physical activity
Class 4 - symptomatic at rest

151
Q

Draw the frank Starling curve

A

see photo

152
Q

How does one calculate cardiac output

A

Heart rate x stroke volume

153
Q

What three factors influence stroke volume

A

Contractility, preload, and afterload

154
Q

List 4 therapies that can be used to reduce preload

A

LMNOP - Lasix, morphine, nitrates, oxygen, positive pressure ventilation

155
Q

List 6 causes of non cardiogenic pulmonary edema

A

WATER BATHS
Water (submersion/drowning)
Aspiration
Toxins (opiates, ASA)
Embolism (fat or PE) and eclampsia
Re-expansion
Bleeding (CNS) - neurogenic pulmonary edema
ARDS
TRALI
HAPE
WATER BATHS
Water (submersion/drowning)
Aspiration
Toxins (opiates, ASA)
Embolism (fat or PE) and eclampsia
Re-expansion
Bleeding (CNS) - neurogenic pulmonary edema
ARDS
TRALI
HAPE
Strangulation

156
Q

What are the 6 physiological steps (in order) that tamponade develops

A

(1) fluid filling the pericardium
(2) fluid accumulating faster than the rate of the pericardium’s stretch
(3) fluid accumulation that exceeds the body’s ability to increase blood volume to support right ventricle filling pressure
(4) Increased pericardial pressure,
(5) decreased ventricle compliance and decreased flow of blood into the heart
(6) decreased stroke volume that leads to decreased cardiac output.

157
Q

*What are the 3 MOST COMMON causes of tamponade?

A

The most common causes of pericardial effusion are viral or idiopathic pericarditis, malignancy, uremia, trauma, and radiation therapy. Drug reactions and autoimmune diseases are less common.

158
Q

*What are the 3 EKG findings of tamponade?

A

Electrical alternans
Small QRS voltage
Tachycardia

159
Q

*What are 4 physical exam findings of tamponade? In addition to tachycardia or tachypnea.

A

Hypotension
Elevated JVP
Muffled heart sounds
Pulsus paradoxus

160
Q

*You are about to do a pericardiocentesis; the patient is on O2 and they have an IV. All the appropriate people are there and the monitor is on. What is the ONE thing you can do right now to manage the patient as you are performing a pericardiocentesis?

A

Volume expansion

161
Q

*Aside from STE, what are 5 ECG changes you might see in pericarditis

A
  • ST segment depression (aVR +/- V1)
  • PR segment elevation (aVR +/- V1)
  • PR segment depression
  • Flattened T waves
  • Deep, symmetrical T wave inversion
162
Q

*3 treatments for pericarditis

A
  • NSAIDs
  • colchicine
  • steroids
163
Q

List 10 causes of pericarditis

A

Idiopathic
Infectious: post-viral, coxsackie virus, S. pneumonia, S. aureus, tuberculosis, beta hemolytic strep with rheumatic fever
Auto-immune/inflammatory: Rheumatoid arthritis, sarcoidosis, lupus, scleroderma, malignancy
Post-MI (early, or late Dressler’s syndrome), post cardiac surgery, post injury (trauma), post radiation)
Metabolic: uremia, myxedema
Vascular: dissecting aneurysm, tumor

164
Q

List 3 clinical signs of pericarditis

A

Friction rub, chest pain (pleuritic, improved with leaning forward), ECG changes, pericardial effusion

165
Q

Describe the ECG changes in pericarditis

A

Stage 1 widespread ST elevation PR depression
Stage 2 T waves flat normalization weeks 1-3
Stage 3 T wave inversions weeks 3+
Stage 4 return to normalization

Downslopping TP - spodick sign

166
Q

List treatments for pericarditis

A

NSAID (Indomethacin, Ibuprofen, ASA if post MI) + Colchicine 0.5mg PO BID for 3 months (contraindicated if liver disease, AKI; mainly used to present recurrence)

167
Q

List 5 causes of myocarditis

A

Coxasackie, influenza, parainfluenza, HIV, lyme, rheumatic fever, chagas (most common worldwide), trichinosis, diphtheria, hepatitis, parvovirus, rubella
Non infectious etiologies: cocaine, drug reaction esp. chemotherapy

168
Q

List 5 causes of pericardial effusion

A

Malignancy, pericarditis, uremia, hemorrhage, trauma, lymphatic obstruction, hypoalbuminemia, TSH, medication related, infectious

169
Q

What is pulses paradoxus

A

> 10mmHg decrease in SBP with inspiration
Inflate a BP cuff, listen, slowly deflate, listen for the first few sounds and then listen for more consistent sounds; this difference is the pulses paradoxus

170
Q

Describe the steps for a pericardiocentesis

A

Position the patient elevated at 30 degrees. May also be done supine or in left lateral decubitus for small volumes
Identify the point of maximal effusion with ultrasound. Measure distance from skin surface to the effusion border
Chose needs trajectory: left parasternal, left sub xiphoid (towards the shoulder)
Sterile prep, including sterile U/S
Local anesthetic
Insert the needle, aspiration during insertion

171
Q

List 5 causes of pneumopericardium

A

bronchial carcinoma, infection, trauma, foreign body, ingestion of caustic substances, invasive procedures, spontaneous increase in intra alveolar pressure (ex. Asthma, valsalva)

172
Q

List 2 primary and 2 secondary causes of cardiomyopathy

A

Primary: hypertrophic, AVRC, dilated (genetic)
Secondary: amyloid, sarcoid, scleroderma, peripartum, infectious/myocarditis, Takotsubo

173
Q

What is the ECG definition of hypertrophy

A

LVH criteria:
- Most common: S wave depth in V1 + tallest R wave in V5, V6 >35
- R wave in aVL > 11 mm
Other criteria:
- Limb leads
- Lead I (R wave) + lead III (S wave) > 25 mm
- aVL (R wave) > 11 mm
- aVF (R wave) > 20 mm
- aVR (S wave) > 14 mm
- Precordial Leads
- V4, V5, or V6 (R wave) > 26 mm
- V5 or V6 (R wave) + V1 (S wave) > 35 mm
- Highest voltage precordial R wave + highest precordial S wave > 45 mm

174
Q

What are the ECG findings of ARVC

A

Epsilon, t wave inversion V1-V3, wide QRS, prolonged S wave upstroke

175
Q

Name 4 POCUS findings of tamponade

A

Pericardial effusion, RV diastolic collapse, RA systolic collapse, plethoric IVC

176
Q

*What are the major and minor criteria for IE?

A

Major Criteria
Positive blood cultures (of typical pathogens) from at least two separate cultures
Evidence of endocardial involvement by echocardiography
Minor Criteria
Predisposition—predisposing heart condition or intravenous drug use
Fever—temperature > 38° C (100.4° F)
Vascular phenomena—arterial emboli, septic pulmonary infarcts, mycotic aneurysm, conjunctival hemorrhages, or Janeway lesions
Immunologic phenomena—Osler’s nodes, Roth’s spots, and rheumatoid factor
Microbiologic evidence—single positive blood culture (except for coagulase-negative Staphylococcus or an organism that does not cause endocarditis)
Echocardiographic findings—consistent with endocarditis but do not meet major criteria

177
Q

*What medications would you use to treat IE?

A

A combination of 15 mg/kg of vancomycin and 2 g of ceftriaxone is a reasonable empirical antibiotic choice in someone with undifferentiated sepsis and suspected endocarditis.

178
Q

*What are 2 bacteria other than SA in IE?

A

Staphylococcus aureus
Viridians group streptococci
Enterococci
Coagulase-negative staphylococci
Streptococcus bovis
HACEK
Fungi

179
Q

*4 echo findings of IE

A

• Endocardial vegetation
• Paravalvular abscess
• New partial dehiscence of prosthetic valve
• New valvular regurgitation

180
Q

*What two diagnostic test would you order immediately for suspected IE?

A

Blood cultures and echo

181
Q

*What are the Duke criteria for IE?

A

Definite Endocarditis
Endocarditis is considered definitely present if any one of the following combinations of clinical findings is present:

• Two major clinical criteria
• One major and any three minor clinical criteria
• Five minor clinical criteria

182
Q

*What is the number 1 bacteria of concern in IE?

A

Mortality is more than 40% in patients with prosthetic valve IE due to Staphylococcus aureus

183
Q

*In general terms describe the indications for prophylaxis for endocarditis?

A

Prosthetic heart valve
History of endocarditis
Unrepaired cyanotic congenital heart disease, including palliative shunts and conduits
Completely repaired congenital heart defects with prosthesis during the first 6 mo after the procedure
Repaired congenital heart disease with residual defect at or adjacent to the site of the prosthetic device
Cardiac valvulopathy in a transplanted heart

184
Q

List 5 risk factors for infective endocarditis

A

Prosthetic valve, IVDU, rheumatic heart disease, bicuspid aortic valve, calcified aortic valve, mitral valve prolapse

185
Q

What are the HACEK organisms

A

HACEK (Haemophilus,Aggregatobacter actinomycetemcomitans,Cardiobacterium,Eikenella, andKingella),Bartonellaspecies, orCoxiella burnetii) in patients with negative blood cultures

186
Q

List indications for prophylaxis for patients with endocarditis. What antibiotic should be used?

A

Prosthetic cardiac valve, previous IE, congenital heart disease, cardiac translation with cardiac valvulopathy

Congenital heart disease: un-repaired cyanotic CHD, completely repaired congenital heart defects win the first 6 most, repaired CHD with a residual defect or leak

Amoxicillin 2g PO 30-60 mins prior or Keflex 600mg PO if indicated

187
Q

What is rheumatic fever

A

Delayed immune reaction to a group A strep infection

188
Q

What is the Jones criteria

A

Acute rheumatic fever is diagnosed when there is a documented prior strep infection and 1) two major or 2) one major and two minor

Major: JONES - joint migratory polyarthritis, O carditis, nodules, erythema marginatum, sydenham chorea
Minor: fever, arthralgia, elevated ESR or CRP

189
Q

Which valve only has two leaflets

A

Mitral

190
Q

Which murmurs are diastolic and which are systolic

A

Diastolic: mitral stenosis, aortic regur/insufficiency, tricuspid stenosis
Systolic: aortic stenosis, mitral regurg, mitral valve prolapse

191
Q

What is the clinical presentation of mitral stenosis

A

Exertional dyspnea, pulmonary congestion, afib, reduced cardiac output

Occurs because the stenosis presents filling of the LV, leading to elevated LA pressures. Associated with rheumatic fever. Often need aggressive rate control so the heart fills better. Keep them slow and full.

192
Q

What is the clinical presentation of aortic regurg

A

Reduced forward flow from the left ventricle; widened pulse pressure with diastolic <50
Needs HR to be increased to shorten diastole, and afterload to be reduced

193
Q

List three causes of aortic stenosis

A

Atherosclerosis, bicuspid aortic valve, rheumatic heart fever

194
Q

List signs of aortic stenosis (other than a murmur)

A

Pulse parvus and tarvus (weak and away), loss of S2, brachial radial delay

195
Q

List 2 acute and 2 chronic causes of mitral regurg

A

Acute: chordae tendinae rupture, pap muscle dysfunction (ex. From STEMI)
Chronic: loss of elastic with age, dilated cardiomyopathy (enlarges the mitral annular ring), connective tissue disorder, rheumatic heart disease

196
Q

What is the clinical presentation of acute mitral regurg

A

Sudden fulminant pulmonary edema. Needs afterload to be reduced.

197
Q

*Cardiac obstructive causes of syncope

A

Mitral, aortic, or pulmonic stenosis
Hypertrophic cardiomyopathy
Atrial myxoma
Pulmonary embolism
Pulmonary hypertension
Cardiac tamponade
Congenital heart disease

198
Q

*In the following patients with syncope: give the most likely diagnosis and one diagnostic test:

i) Young female with vaginal bleeding
ii) Old guy with sudden back pain
iii) Woman with headache
iv) Old guy with flank pain

A

i) Young female with vaginal bleeding – BHCG
ii) Old guy with sudden back pain – CTA
iii) Woman with headache- CTA
iv) Old guy with flank pain - CTA

199
Q

*5 causes of syncope and the EKG finding associated

A
  • Long QT syndrome: Prolonged QT segment
  • Short QT syndrome: Short QT segment
  • WPW: Delta wave, short PR segment (<120 msec), prolonged QRS segment (>110 msec)
  • Brugada’s syndrome: Coved (Type 1) or saddleback ST segment (Type 2) elevation in V1-3 >2 mm, if less <2mm ST elevation, Type 3 (coved or saddleback morphology)
  • Hypertrophic cardiomyopathy: Left ventricular hypertrophy, prominent (i.e. “dagger like”) Q waves in inferolateral leads, diffuse T wave inversions
  • Pulmonary embolism: RV strain pattern
  • Arrhythmogenic right ventricular cardiomyopathy/Arrhythmogenic right ventricular dysplasia: Epsilon wave, T wave inversions and prolonged S wave upstroke in V1 3
200
Q

*Name 5 life-threatening non-cardiogenic causes of syncope

A
  • Thoracic aortic dissection
  • Abdominal aortic aneurysm
  • Massive pulmonary embolism/Air embolism (e.g. hypoxia)
  • Toxic-metabolic derangements (e.g. hypoglycemia, CO)
  • Severe hypovolemia/Hemorrhage (e.g. anemia, ruptured ectopic, GI bleed)
  • Sepsis
  • Thoracic outlet syndrome/Subclavian steal
201
Q

*What are the parameters of the San Francisco Syncope Rule

A
  • CHF history
  • Hematocrit < 30%
  • EKG abnormal
  • SOB symptoms
  • SBP < 90 at triage
202
Q

*78M with syncope, back to baseline, no PMHx given, VS normal: 7 conditions on Ddx

A

i. Orthostatic hypotension
ii. Dysrhythmia
iii. Micturition syncope
iv. GIB
v. AAA/retroperitoneal hemorrhage
vi. Medication related (beta-blockers)
vii. Seizure
viii. Valvular heart disease (AS)
ix. Hypoglycemia
x. MI
xi. PE

203
Q

*5 diagnoses that maybe be seen with an abnormal EKG that could point to a cardiac cause for syncope in above patient (78M healthy back to baseline)

A

i. WPW
ii. Brugada
iii. HOCM
iv. Prolonged QT
v. MI
vi. PE

204
Q

List 4 medications with a mortality benefit in heart failure

A

ACEI or ARB or ARNI ex. entreso, Beta blocker, mineralocorticoid receptor antagonist ex. Spironolactone, SGLT inhibitor ex. Dapagliflozin
Nitrates and diuretics alone are for decongestion and symptom relief; not for mortality

205
Q

Other than ST elevation, list 5 ECG findings of ischemia

A

new Q waves, dynamic ST changes, ST elevation relative to small QRS, reciprocal changes

206
Q

Summarize the DoReMi trial for cardiogenic shock

A

Population: Age >18, admitted to CICU with cardiogenic shock, SCAI criteria
Intervention: Milrinone
Control: Dobutamine
Outcome: composite outcome - in hospital mortality, resuscitated cardiac arrest, receipt of cardiac transplant, non fatal MI, TIA/stroke, RRT. Secondary outcomes include CICU stay >7 days, presence of AKI, non invasive + mechanical ventilation

Double blinded RCT, stratified by affected ventricle.

Bottom line: no difference in primary outcome

207
Q

What are 4 factors that determine prognosis in ACS?

A

Extent of infarct
Time to intervention
Prescence of revascularlization
Residual LV fucntion

208
Q

What is stable angina?

A

Transient episode of chest pain due to myocardial ischemia
It is predictable, reproducible
Can be provoked by physical or psychological stress
Resolves on its own or with nitro

209
Q

What is unstable angina?

A

Angina that is:
New onset (CCS 2 or higher within last 2 months)
Occuring at rest or with minimal exertion (longer than 20 minutes, within 1 week of presentation)
Worsening from previous stable pain in frequency or duration
Easier to provoke (increase in CCS by 1 in last 2 months)
Harder to resolve with effective medications

210
Q

How much of a coronary artery needs to be stenosed to have angina?

What is the underlying difference between unstable angina and AMI?

A

Rest - 95%
Exertion - 60%
Or increased demand with little to no stenosis

unstable vs AMI are both caused by plaque rupture, one has collaterals and one does not. Only 20% are ever totally occlusive

211
Q

Outline the Killip classification system

A

Used to tell how much CHF is associated with an MI
- Class I : No clinical signs of heart failure
- Class II : crackles on the bases , S3 gallop and raised JVP
- Class III : acute pulmonary oedema
- Class IV : Cardiogenic shock

212
Q

Contrast Typical and Atypical agina

A
213
Q

What is pseudo-normalization of a T wave?

A

T wave inversion that becomes normal during acute ischemia can be a sign of ACS and pending STEMI

214
Q

Where are T waves usually upright? Where are they usually inverted?

A

Normal up in L sided leads
(I,II, V3 to V6) and inverted in R sided leads (aVR, V1-V2)

215
Q

Outline reciprocal changes with STEMI

A

Poster STE —> Anterior depressions
Anterior STE —> Inferior depressions
Inferior STE —> Lateral depressions
Lateral STE —> Septal or inferior ! depression
Septal STE —> Posterior depression

216
Q

What are q waves? When are they considered pathologic?

A

Pathological changes indicates irreversible myocardial necrosis. It usually occur within hours from MI but typical within 8 -12 hours.
Negative deflection before QRS , and it is pathological when it is deeper > 2 mm and wider > 1 mm.

217
Q

Outline EKG changes for Inferior MI

A
218
Q

Outline EKG changes for Anterior MI

A
219
Q

Outline EKG changes for Lateral MI. Why are they super tricky?

A

Often seen with other infarctions because lateral wall is variably serviced by LAD, L circ ect
EKG changes not necessarily right next to each other

220
Q

Outline EKG changes for posterior MI. What are two important caveats to this diagnosis?

A

caveats - more subtle changes (farther away, RV thinner) and really just for diagnostic accurancy doesnt necessarily change outcomes

What findings in leads V1-V3 are suggestive of acute posterior MI?
(1) horizontal ST segment depression
(2) an upright T wave
(3) tall wide R wave
(4) (4) R wave amplitude–to–S wave amplitude ratio greater than 1

221
Q

Outline changes with a septal MI

A
222
Q

Outline EKG changes with a RV infarct? What are 3 clinical findings to go along with this? How do you manage it?

A

Elevated JVP
Hypotension (worse with nitrates) BUT
No pericardial effusion (symptoms are also consistent with tamponade)
Volume load and avoid vasodilators

223
Q

When do you do a 15 lead? What does it show you?

A

See lead V7-V9 for posterior MI or
See Rv electrodes (V1R to V6R)

ST segement changes in V1-V3 (depression and elevation)
Equivocal findings in inferior or lateral limbs leads
All inferior STEMI (assess RV)
All hypotensive STEMI (assess RV)

224
Q

What is a DeWinter T wave?

A

STEMI Equivalent
J point depression with ST depression into a prominent T wave in precordial leads with elevation in aVR

LAD lesion

225
Q

Differentiate paced vs LBBB rhythms

A
226
Q

When are trops detectable? What is duration of elevation? What makes it “acute” myocardial injury?

A

2-3 hours after event
Can grow and be elevated for over a week
If you have a risk AND a fall

227
Q

5 cardiac and 5 non cardiac causes of tropenemia?

A
228
Q

4 options for diagnosing clinically sifgnificant CAD if trop and EKG are normal?

A

Exercise stress test
ECHO +/- stress
Myocardial scintigraphy (MIBI)
Coronary CTA

229
Q

Who do you stress test? What are the absolute contraindications to stress test? Is it definitive?

A

Low risk patients with a resolution of symptoms at least 8-12 hours from symptoms onset - if negative with EKG and trop 98% NPV

Not defintive - can have confounders like electrolytes, flase positive like HOCM

230
Q

What is the HEART pathway? Why was it designed?

A

Don’t want to hang your hat on a single trop, so this one uses another trop at 3 hours
Works by calculating your initial score, splitting people into two groups, and then again with the second trop
Benefit is it has higher sensitivity and NPV than HEART alone

231
Q

Summarize the pathophysiology of ACS in 5 steps

A

(1) endothelial damage through plaque disruption, irregular luminal lesions, and shear injury
(2) platelet aggregation
(3) thrombus formation causing partial or total lumen occlusion
(4) coronary artery vasospasm
(5) reperfusion injury caused by oxygen free radicals, calcium, and neutrophils.

232
Q

What are 2 complications of cardiac reperfusion?

A

prolonged ventricular dysfunction (myocardial stunning)
Reperfusion dysrhythmias

233
Q

Compare classic vs atypical angina

A
234
Q

What are 4 advantages of a EMS EKG?

A

1- Early detection of STEMI
2- Ability to select destination based on availability of PCI
3- Improve hospital based preparation
4- Improve the hospital initiation of PCI/Thrombolysis protocols

235
Q

What are two mechanisms of action of nitro? What are 5 contraindications?

A

It increases venous capitance (vessels relax and blood just pools) which decreases preload and myocardial O2 demand
Also dilates coronary arteries directly which can improve blood flow to myocardium

Hypotension (systolic less than 90)
Inferior or RV infarct (pre-load dependant)
Cyanide toxicity
MetHb
Use of Viagra

236
Q

5 meds to give post MI

A

BB, ACE-I, statin (also can give before elective/ emergent PCI to decrease peri-procedural AMI apparently)

237
Q

What is the actual dose of ASA for intubated and non-intubated patients?

A

pending

238
Q

Someone with a pacemaker chugging along at 180 vtach what happens? Duel chamber

A

Over drive pacing if not work
Defibrillate low voltage
Defibrillate high dose up to 6 times

239
Q

What are the clinical Brugada criteria?

A

Documented ventricular fibrillation (VF) or polymorphic ventricular tachycardia (VT).
Family history of sudden cardiac death at <45 years old .
Coved-type ECGs in family members.
Inducibility of VT with programmed electrical stimulation .
Syncope.
Nocturnal agonal respiration.

Think family member had it (died before 45), famimly member has it , you dide (VT or Vfib), died with electrical stimulation
Looked like you died (syncope or agonal respirations)

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