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CCFP(EM) Omar > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Features suggesting instability in cases of dysrrhythmia:

A

ALOC<div>SOB/respiratory distress</div><div>Syncope</div><div>Chest pain (ACS)</div><div>Hypotension</div>

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2
Q

<div>Anti Arrhythmic Medications Classification:</div>

A

“<div><b>Some Block Potassium Channels</b></div> <div>I: Sodium Channel blockers(membrane stab)</div> <div>II: BB (…lols)</div> <div>III: Potassium Channel blockers (Action potential widening)</div> <div>IV: Calcium Channel blockers</div> <div>_____________________________________</div> <div>IA: (Double Quarter Pounder)</div> <div> Disopyramide, Quinidine, <b>Procainamide</b></div> <div></div> <div></div> <div>IB: (Lettuce, Tomato, Mayo)</div> <div> <b>Lidocaine</b>, Tocainamide, Mexiletine</div> <div> Pure Na blockers, only effective inventricular arrhythmias</div> <div></div> <div>IC: (More, Fries, Please)</div> <div> Moricizine, <b>Flecainide</b>, Propafenone</div> <div> <i>Avoid in HF and IHD</i></div> <div></div> <div>III: (A Big Dog Is Scary)</div> <div> <b>Amioradrone</b>, Bretylium, Dofetilide, Ibutilide, <b>Sotalol</b></div> <div></div> <div>IV: (Very Nice Drugs)</div> <div> Verapamil, nifedipine, diltiazem</div>”

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3
Q

Other Na channels blocker drugs

A

TCA<div>Citalopram<br></br><div>Carbamazepine</div><div>Neuroleptics</div><div>Antihistamines</div><div>Cocaine</div><div>Shellfish toxins</div><div><br></br></div></div>

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4
Q

Sick sinus syndrome

A

Sinus brady<div>Sinus arrest</div><div>SA exit block</div><div>Tachy-brady syndrome</div>

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5
Q

SSS is suspected in:

A

Elderly pt with syncope + ECG demonstrate sinus impulse abnormalities

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6
Q

Long term Mx of SSS

A

Permanent pacemaker placement + Rx for A. fib

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7
Q

<div>What are three ECG presentations of sick sinus syndrome?</div>

A

<div>Think about it in any elderly patient with syncope! </div>

<div>● Tachy-brady syndrome </div>

<div>● A. fib with episodes of incomplete sinus block </div>

<div>● Complete sinus block</div>

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8
Q

SINUS ARREST WITH SA EXIT BLOCK

A

● Missing P waves on ECG <br></br>● Sinus block = no impulse conducted from the SA node <br></br>● Sinus arrest = no impulse generated <br></br>● Can be benign (vagal tone) or pathologic

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9
Q

Sinus exit block

A

Complete absence of PQRST comples<div>Completely missed beat</div>

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10
Q

ECG features of rt vent STEMI

A

STE in V1<div>STE III > II</div><div>STE V1>V2</div><div>STE V1 + ST dep V2 (highly specific)</div><div>STE rt sided leads (V3R-V6R)</div>

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11
Q

What is the worst type of STEMI

A

Anterior due to large surface area involved

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12
Q

Features of a significant (pathologic) Q-wave

A

> = 4 ms (0.04 mm)<div>1/3 ht of R wave</div>

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13
Q

Factors favors BER on ECG

A

Features of STE:<div> Concave upwards</div><div> Precordial leads only</div><div> Elevated J-point</div><div>Non-specific for coronary anatomy</div><div>NO receprocal STD</div><div>No dynamic changes with time</div><div>No Q-wave</div>

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14
Q

Features predict MI in ECG

A

STE features:<div> Horizontal</div><div> Convex upwards</div><div>Specific for coronary anatomy</div><div>Presence of receprocal STD</div><div>Dynamic changes with time</div><div>Early features: Hyperacute T-Wave</div><div>Late features: Q-Wave</div>

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15
Q

What STEMI causes heart block

A

Anterior (Mobitz 2 propagating to 3rd degree)<div>Inferior (3rd degree)</div>

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16
Q

Anterior STEMI may cause:

A

Tachydysrrhythmia<div>2nd or 3rd degree heart block</div><div>LV aneurysm</div>

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17
Q

Drugs cause long QT

A

Macrolides (Azithromycin)<div>Fluroquinolones (cipro, levo, moxi)</div><div>Phenothiazines (prochlorperazine, chlorpromazine)</div><div>5HT3 antagonists (ondanosteron)</div>

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18
Q

Rx of unstable TDP

A

Immediate unsynchronized defibrillation<div>Mg sulfate iv</div>

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19
Q

Ind of PCI in MI

A

CHF with hypotension<div>Symp > 12 hrs</div><div>High risk of bleeding</div><div>Recent brain bleed</div><div>Triple vessel dis (? do CABG)</div><div>If can be reached within 90 min</div>

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20
Q

Other causes of STE (STEMI mimics)

A

“LV aneurysm<div>Pericarditis<br></br>Myocarditis</div><div>BER</div><div>Prinzmetal’s angina</div><div>LVH<br></br>WPW<br></br>HOCM</div><div><br></br></div><div>HyperK</div><div>LBBB</div><div>Hypothermia (Osbourne wave)</div><div>Brugada syndrome</div><div>Vent paced rhythm</div><div>Raised IC pressure</div><div>Takotsubo CMP</div>”

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21
Q

What are the components of prehospital management of AMI

A

Activation of the EMS system <br></br>BLS care (for cardiac arrests) <br></br>ACLS care: <br></br> ○ 12 lead ECG - to rule in/out STEMI <br></br> ○ Administration of chewable ASA 160-325 mg PO <br></br> ○ Administration of SL nitroglycerin <br></br> ○ Possibly administration of oxygen if Sp02 <94%

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22
Q

Risk factors for atypical presentation of ACS:

A

● Women <br></br>● Elderly (Especially > 85 years) <br></br> ○ Dyspnea, fatigue, confusion, syncope <br></br>● Diabetics <br></br>● Non-Caucasian <br></br>● No prior hx of MI <br></br>● Dementia

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23
Q

Describe the ECG characteristics of Left Main Occlusion

A

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

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24
Q

ECG Features of Pericarditis

A

Diffuse STE (except aVR=STD)<div>PR seg depression (I, II, aVF, V6) = insensitive</div><div>PR seg elevation in aVR</div>

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25
Q

LBBB

A

QRS duration of > 120 ms <br></br>Dominant S wave in V1 <br></br>Broad monophasic R wave in lateral leads (I, aVL, V5-V6) <br></br>Absence of Q waves in lateral leads (I, V5-V6; small Q waves are still <br></br>allowed in aVL) <br></br>Prolonged R wave peak time > 60ms in left precordial leads (V5-6)

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26
Q

RBBB

A

Broad QRS > 120 ms <br></br>RSR’ pattern in V1-3 (‘M-shaped’ QRS complex) <br></br>Wide, slurred S wave in the lateral leads (I, aVL, V5-6)

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27
Q

STEMI equivalants

A

Wellens type A & B<div>Shark T</div><div>De Winter ST-T</div><div>Sgarbossa</div><div>Isolated post STEMI</div><div>LVH</div><div>Hyperacute T-wave</div><div><br></br></div>

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28
Q

DDX of high Tropinin

A

● Acute coronary ischemia <br></br> ○ ACS <br></br> ○ Cocaine <br></br> ○ Variant angina <br></br> ○ Coronary embolism/vasculitis <br></br>● Comorbidities causing myocardial injury <br></br> ○ Renal failure, sepsis, ARDS, stroke, SAH <br></br>● Systemic shock states <br></br> ○ Distributive shock states (sepsis, CO poisoning, burns) <br></br> ○ Cardiogenic shock states (myocarditis / myocardial contusion / cardiomyopathy)

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29
Q

Advantages of ACEI in ACS

A

Reduce CV mortality<div>Reduces recurrence of MI</div><div>Reduces CHF</div>

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30
Q

Indications of rescue PCI

A
  1. Persistent chest pain <br></br>2. Persistent ST elevation <br></br>3. Cardiogenic shock <br></br>4. Post-reperfusion ischemia <br></br>5. Ventricular dysrhythmias
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31
Q

When to get a 15 lead ECG?

A

(1) ST segment changes (depression or elevation) in leads V1 to V3, either in an isolated lead or in more than one; <br></br>(2) Equivocal ST segment elevation in the inferior (II, III, aVF) or lateral (I, aVL) limb leads or both; <br></br>(3) All inferior STEMI; and <br></br>(4) Hypotension in the setting of ACS

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32
Q

<div><b><i>List 10 possible causes for ST segment elevation</i></b></div>

A

<div>E = EBR (early benign repolarization)</div>

<div>L = LBBB</div>

<div>E = Electrolytes (Hyper K+)</div>

<div>V = Ventricular hypertrophy</div>

<div>A = Aneurysm</div>

<div>T = Treatment</div>

<div>I = Ischemia</div>

<div>O = Osborne</div>

<div>N = Normal variant/neurological</div>

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33
Q

<div><b><i>List five possible findings of aortic dissection on chest x-ray</i></b></div>

A

<div>Widened mediastinum</div>

<div>Depression of L mainstem bronchus</div>

<div>NG tube displacement</div>

<div>L pleural effusion/apical cap</div>

<div>Calcium sign – displaced intimal calcification</div>

<div>AP window opacification</div>

<div>Double density or localized bulge along aorta</div>

<div>Disparity in calibre between ascending and descending aorta</div>

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34
Q

<div><b><i>List three possible presenting symptoms of aortic dissection</i></b></div>

A

<div>Chest pain </div>

<div>Stroke</div>

<div>Heart failure</div>

<div>Syncope</div>

<div>Buttock and leg pain</div>

<div>Back and flank pain</div>

<div>Abdominal pain</div>

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35
Q

QRS too wide

A

BBB<div>Ventricular complexes</div><div>Paced rhythm</div><div>LVH</div><div>Electrolytes imbalance (hyperK, HypoCa)</div><div>Delta wave (WWW)</div>

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36
Q

LBBB causes

A

Conduction system dis<div>MI</div><div>CMP</div><div>LVH</div><div>Myocarditis</div>

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37
Q

<div>List 6 historical predictors of acute HF and 6 clinical features of acute HF</div>

A

<div>● Hx </div>

<div>○ Past history of HF </div>

<div>○ PND </div>

<div>○ SOBOE </div>

<div>○ Orthopnea </div>

<div>○ Nocturia </div>

<div>○ Hx of any type of heart disease </div>

<div></div>

<div>● Px </div>

<div>○ Hypertension </div>

<div>○ Diaphoretic </div>

<div>○ Pulmonary crackles </div>

<div>○ Pulmonary wheezes (cardiac asthma - due to peribronchial edema) - which may respond to bronchodilator therapy!! </div>

<div>○ JVD </div>

<div>○ Edema </div>

<div>○ S3</div>

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38
Q

<div>List 5 CXR and 5 ECG findings of HF</div>

A

<div>❏ Pleural effusions </div>

<div>❏ Cardiomegaly (enlargement of the cardiac silhouette) </div>

<div>❏ Kerley B lines (horizontal lines in the periphery of the lower posterior lung fields) </div>

<div>❏ Upper lobe pulmonary venous congestion (bat wing appearance) </div>

<div>❏ Interstitial oedema.</div>

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39
Q

ECG Findings in acute CHF

A

LVH<div>LAE</div><div>RAE</div><div>RV Strain: ST depression and T wave inversion in the leads corresponding to the right ventricle, i.e The right precordial leads: V1-3, often extending out to V4. The inferior leads: II, III, aVF, often most pronounced in lead III as this is the most rightward-facing lead<br></br></div><div>Fascicular blocks and bundle branch blocks<br></br></div>

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40
Q

Goals of Rx of CHF

A

Reduce cardiac workload by decreaseing preload and afterload<div>Control excessive salt and water retention</div><div>Improve contractility</div>

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41
Q

How to improve contractility

A

Stop bad drugs<div>Optimize Ca ions</div><div>Oxygen</div><div>Decrease excessive catecholamines/acidosis</div>

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42
Q

Rx of CHF + Adequate perfusion

A

POND<div>Positioning</div><div>O2</div><div>NIPPV</div><div>Nitrates</div><div>Diuretics</div><div><br></br></div>

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43
Q

Rx of CHF with inadequate perfusion

A

POND<div>(Avoid nitrates)</div><div>Vasopressors/Inotrops</div>

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44
Q

List 10 treatment options for chronic HF

A
  1. Cardiovascular exercise and strength training / conditioning program <br></br>2. Obesity reduction <br></br>3. Healthy diet <br></br>4. Beta-blockers <br></br>5. ACE Inhibitors <br></br>6. ARBs <br></br>7. Diuretics <br></br>8. Spironolactone <br></br>9. Digoxin <br></br>10. Cardiac resynchro therapy (biventricular pacemaker) <br></br><br></br>These medications have been shown to reduce five-year mortality
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45
Q

Classical ECG of cardiac temponade

A

Low voltage QRS<div>Electrical alternans</div><div>Tacycardia</div>

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46
Q

What does the first letter of the pacemaker code indicate?

A

The first letter indicates the chamber that is paced (A – atrium, V – ventricle, D – dual, 0 – none).

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47
Q

“<span>Question:</span>What infectious etiology is associated with complete heart block?”

A

Lyme disease.

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48
Q

What is the definition of a fusion beat?

A

A supraventricular and a ventricular impulse coincide to produce a hybrid complex called a fusion beat. Indicates 2 foci of pacemaker cells firing spontaneously.

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49
Q

Supraventricular tachycardia that does not convert with adenosine can often be confused with what rhythm?

A

Atrial flutter with a 2:1 block.

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50
Q

Features of unstable cardiac patient

A

Altered mental status<div>Chest pain</div><div>SOB</div><div>Diaphoresis</div><div>Dizziness</div><div>Syncope</div>

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51
Q

In what scenario is it impossible to distinguish a Mobitz type I from type II AV block?

A

If the conduction ratio is 2:1.

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52
Q

Congenital causes of cardiac syncope

A

<ul> <li>Short PR,</li> <li>long QT syndrome,</li> <li>hypertrophic cardiomyopathy,</li> <li>arrhythmogenic right ventricular dysplasia</li> <li>Brugada syndrome</li> </ul>

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53
Q

Name three ECG clues that are highly specific for VT?

A

Very wide QRS (>160)<div>Fusion beats</div><div>Capture beats</div>

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54
Q

Which of the following AV nodal blocks is most commonly associated with an acute inferior wall myocardial infarction?

A

Mobitz type 1

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55
Q

What are the Conduction Abnormalities of Inferior MI

A

Sinus brady<div>First degree AV Block</div><div>Mobitz 1(Wenckebach)</div><div>Third degree AV Block</div>

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56
Q

What are the Conduction abn in Anterior MI

A

First degree AVB<div>Mobitz 2 AVB</div><div>Third degree AVB</div>

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57
Q

Anatomically, where is the block located in Mobitz II?

A

The block is below the level of the AV node, generally in the His-Purkinje system.

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58
Q

Causes of MAT

A

COPD<div>CHF<br></br><div>Hypoxia</div><div>Pulm htn</div></div>

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59
Q

<div><div>What is the most common dysrhythmia associated with Wolff-Parkinson-White syndrome?</div></div>

A

Narrow complex atrioventricular reentry tachycardia (can be treated as PSVT)

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60
Q

Risk factors for DVT in ambulatory pt

A

“<img></img>”

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61
Q

DVT must be treated in:

A

Unprovoked DVT<div>Hx of DVT or PE</div><div>Clot close to proximal veins</div><div>Extensive thrombosis in multiple veins</div><div>Active cancer</div>

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62
Q

What is phlegmasia cerulea dolens?

A

Painful blue leg syndrome caused by extensive iliofemoral occlusion from a venous clot causes vascular congestion and venous ischemia.

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63
Q

Gold standard imaging for DVT

A

Venography

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64
Q

What type of cardiac surgery is often complicated by complete heart block?

A

AVR

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65
Q

Why should electrical cardioversion be performed using the synchronized setting in AVNRT?

A

<div><div>Unsynchronized cardioversion (defibrillation) risks an R on T phenomenon where the electricity is delivered during cardiac repolarization, leading to torsades de pointes or ventricular fibrillation.</div></div>

<div></div>

<div><br></br></div>

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66
Q

Which medications should be avoided in patients with Wolff-Parkinson-White syndrome who develop a wide complex tachydysrhythmia requiring treatment?

A

Adenosine,<div>amiodarone,</div><div>beta-blockers, and</div><div>calcium channel blockers.</div>

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67
Q

What are the six causes of high-output heart failure?

A

Hyperthyroidism,<div>wet beriberi,</div><div>arteriovenous fistula,</div><div>Paget disease,</div><div>severe anemia, and</div><div>pregnancy</div>

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68
Q

ECG features of raised ICP

A

Widespread giant T-wave inversion<br></br>QT prolongation<br></br>Bradycardia<br></br><br></br>Others:<br></br>STE/depression<br></br>U wave

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69
Q

VasospasticAngina (PrinzmetalAngina)

A

<ul><li>Patientwith a history ofHTN,<strong>smoking</strong>,DM, obesity, or<strong>cocaine</strong>use</li><li>Complaining of squeezing, pressure-like chest discomfort<strong>at rest</strong></li><li>ECGwill show<strong>transient ST-segment elevations and cardiac enzymes will be normal</strong></li><li>Diagnosis is made by cardiac stress test</li><li>Most commonly caused by<strong>coronary artery spasm</strong></li><li>Treatment is<strong>calcium channel blockers and nitrates</strong></li><li><strong>BB are contraindicated due to unopposed alpha stimulation</strong></li></ul>

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70
Q

What is the most common physical finding in patients with infective endocarditis?

A

Heart Murmur

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71
Q

Which gram-negative organisms which are difficult to culture can cause endocarditis?

A

HACEK group (<i>Haemophilus, Actinobacillus, Cardiobacterium, Eikenella,</i>and<i>Kingella</i>).

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72
Q

<div>Causes of Acute Pericarditis:</div>

A

<ul> <li>Infectious – mainly viral (e.g. coxsackie virus).</li> <li>Immunological – SLE, rheumatic fever</li> <li>Uremia</li> <li>Post-myocardial infarction / Dressler’s syndrome</li> <li>Trauma</li> <li>Following cardiac surgery (post pericardiotomy syndrome)</li> <li>Paraneoplastic syndromes</li> <li>Drug-induced (e.g. isoniazid, cyclosporin)</li> <li>Post-radiotherapy</li></ul>

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73
Q

What are the most common complications of AAA repair?

A

Graft infection,<div>aortoenteric fistula</div><div>anastomotic aneurysm.</div>

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74
Q

Causes of acute cor pulmonale

A

PE<div>ARDS</div><div><br></br></div><div>Both resulted in RV dilation rather than RV hypertrophy (which occurs in chronic cor pulmonale)</div>

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75
Q

Causes of chronic cor pulmonale

A

COPD<div>PE</div><div>Pulm fibrosis</div><div>OSA</div><div>M. gravis</div><div>Poliomyelitis</div><div>Sarcoidosis</div>

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76
Q

Dx of infective endocarditis by Duke Criteria

A

Either of<div>2 majors</div><div>1 major and 3 minors</div><div>5 minors</div>

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77
Q

Modified Duke Criteria for IE

A

“BE FEVIR<div><br></br></div><div><u><b>Majors:</b></u></div><div>Blood culture positive</div><div>Endocardial involvement (echo +ve for IE like new vegitation/abscess OR new valve regurgitation)</div><div><br></br></div><div><b><u>Minors:</u></b></div><div>Fever > 38</div><div>Immunological phen (GN, Osler nodes, Roth spots)</div><div>Vascular phen (major arterial emboli, septic pulm infarction, Janeway lesions)</div><div>Echo minor criteria eliminated</div><div>Risk factors (IVDU, prosthetic valve, long tubes)</div>”

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78
Q

What is the most common X-ray finding in acute aortic dissection?

A

Mediastinal widening

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79
Q

Takotsubo

A

<ul><li>Patient will be a woman</li><li>With a history of arecent increase in stress</li><li>Complaining of chest pain and other symptoms of STEMI</li><li>Echo will show<strong>apical ballooning</strong></li><li>Diagnosis is made by:<ul><li>1) ST-segment elevation</li><li>2) transient regional wall motion abnormalities of apex and mid ventricle</li><li>3) the absence of coronary artery disease</li><li>4) the absence of other causes of left ventricular dysfunction such as pheochromocytoma or myocarditis</li></ul></li><li>Treatment is supportive care</li></ul>

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80
Q

What is the most common complication of mitral stenosis?

A

Atrial fibrillation.

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81
Q

What is the most common congenital cause of tricuspid regurgitation?

A

Ebstein’s anomaly.

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82
Q

Why does COPD cause right ventricular failure?

A

Via hypoxic vasoconstriction causing increased right ventricular afterload.

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83
Q

What primary disease process is associated with sterile vegetation endocarditis on both sides of the involved valve?

A

SLE

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84
Q

What physical exam findings are specific to high output heart failure?

A

Bounding pulse with a quick upstroke and a wide pulse pressure.

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85
Q

Drugs showed mortality benefit after STEMI

A

ASA<div>ACEI</div><div>BB</div>

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86
Q

What clinical findings represent right ventricular infarction in the setting of an inferior MI?

A

Jugular venous distension<div>hypotension</div>

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87
Q

Viruses responsible for myocarditis

A

Entero<div>Parvovirus B19</div><div>Herpes virus 6</div>

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88
Q

What is the most common cause of myocarditis worldwide?

A

Chagas disease caused by the protozoan<i>Trypanosoma cruzi.</i>

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89
Q

ECG findings of RVH

A

Tall R wave and small S wave in V1

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90
Q

ECG findings in Emphysema

A

Tall P wave in (II, III, aVF)<div>Rt axis deviation</div><div>PR and ST depression in (II, III, aVF)</div><div>Decrease R-wave progression in chest leads</div><div>Low QRS voltage</div>

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91
Q

“<h2><span>Coronary artery bypass graft: indications</span></h2>”

A

“<div><b>DUST</b>:<a>[1]</a>p.31</div><div><b>D</b>epressed ventricular function</div><div><b>U</b>nstable angina</div><div><b>S</b>tenosis of the left main stem</div><div><b>T</b>riple vessel disease</div>”

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92
Q

<h2>Exercise ramp ECG: contraindications</h2>

A

“<div><b>RAMP</b>:<a>[1]</a>p.31</div><div><b>R</b>ecent MI</div><div><b>A</b>ortic stenosis</div><div><b>M</b>I in the last 7 days</div><div><b>P</b>ulmonary hypertension</div>”

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93
Q

<h2>Heart blocks</h2>

A

“<div>If the<b>R</b>is far from<b>P</b>, then you have a<b>First Degree</b>.</div><div>Longer, longer, longer, drop! Then you have a<b>Wenkebach</b>.</div><div>if some<b>P’</b>s don’t get through, then you have<b>Mobitz II</b>.</div><div>If<b>P’</b>s and<b>Q’</b>s don’t agree, then you have a<b>Third Degree</b></div>”

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94
Q

<h2>ST elevation causes in ECG</h2>

A

“<div><b>ELEVATION:</b><a>[1]</a>p.34</div><div><b>E</b>lectrolytes</div><div><b>L</b>BBB</div><div><b>E</b>arly repolarization</div><div><b>V</b>entricular hypertrophy</div><div><b>A</b>neurysm</div><div><b>T</b>reatment (e.g. pericardiocentesis)</div><div><b>I</b>njury (AMI, contusion)</div><div><b>O</b>sborne waves (hypothermia)</div><div><b>N</b>on-occlusive vasospasm</div>”

95
Q

What is the most common cause of heart failure with reduced ejection fraction?

A

Ischemic cardiomyopathy.

96
Q

How does mitral stenosis result in hoarseness?

A

Left atrial enlargement can cause compression of the recurrent laryngeal nerve resulting in hoarseness.

97
Q

Which of the following is the most predictive risk factor for cardiac ischemia?

A

Past medical history of coronary artery disease

98
Q

Above what blood pressure is antihypertensive therapy required prior to giving thrombolytics in acute ischemic stroke?

A

> 185/110 mm Hg.

99
Q

What diagnostic test can help identify right coronary artery vs. left circumflex artery involvement in an acute inferior wall myocardial infarction?

A

Right-sided electrocardiogram with a focus on V4R. An upright T wave in lead V4R indicates involvement of the distal right coronary artery, and ST segment elevation indicates a proximal right coronary artery lesion.

100
Q

What are signs of right ventricular hypertrophy on ECG?

A

Right axis deviation,<div>dominant R wave in V1,</div><div>dominant S wave in V5 or V6,</div><div>QRS < 120 ms.</div>

101
Q

Pulsus paradoxus

A

Cardiac temponade<div>Constrictive pericarditis</div><div>PE</div><div>COPD</div><div>Asthma<br></br></div>

102
Q

What musculoskeletal findings can be associated with mitral valve prolapse?

A

Scoliosis and pectus excavatum.

103
Q

What three classes of medications are used for most patients with STEMI and NSTEMI?

A

Antiplatelet agents, antithrombins, and nitrates.

104
Q

What dysrhythmia is most commonly associated with tricuspid regurgitation?

A

Atrial fibrillation (80% of patients with tricuspid regurgitation).

105
Q

What other anomalies are ass w coarctation of aorta?

A

IC aneurysm<div>Turner syndrome</div>

106
Q

<div>What are the five cyanotic congenital heart defects?</div>

A

<div>Transposition of the great arteries, </div>

<div>tetralogy of Fallot, </div>

<div>tricuspid atresia, </div>

<div>truncus arteriosus, and </div>

<div>total anomalous pulmonary venous return.</div>

107
Q

What is the mechanism by which warfarin can cause a hypercoagulable state early in treatment?

A

Rapid depletion of protein C and protein S

108
Q

Although rare, what is the most common bacterial cause of myocarditis?

A

Acute rheumatic fever caused by group A β-hemolytic streptococci.

109
Q

Which of the following disorders is the most common delayed valvular complication of<em>streptococcal</em>pharyngitis?

A

Mitral stenosis

110
Q

What is the most common nontraumatic cause of cardiac tamponade?

A

Metastatic malignancy.

111
Q

Risk factors for AAA

A

smoking history,<div>male sex,</div><div>history of peripheral vascular disease,</div><div>Caucasian race,</div><div>family history of AAA</div>

112
Q

What are the most common pacemaker settings used?

A

VVI (ventricular paced, ventricular sensed, inhibited sensing output pulse response).<div><br></br></div><div>DDD (dual chamber pace/sense/inh response)</div>

113
Q

What are the two most common post-acute myocardial infarction dysrythmias?

A

Premature ventricular contractions and sinus bradycardia

114
Q

What is the genetic association with hypertrophic cardiomyopathy?

A

<div><div>It is an autosomal dominant disease.</div></div>

<div></div>

<div><br></br></div>

115
Q

In an anterior wall STEMI, what decreases the rate of aneurysm development?

A

Time to revascularization

116
Q

What is the most common cause of aortic stenosis in people < 65 years old?

A

Congenital bicuspid valve.

117
Q

What is the treatment for patients with arrhythmogenic right ventricular cardiomyopathy?

A

Antiarrhythmic medication and an implantable cardiac defibrillator.

118
Q

“<span>Name 7 features on history that would be worrisome for a life-threatening cause of his syncope</span>”

A

-Exertional<br></br>-No prodrome<br></br>-Palpitations<br></br>-Chest pain<br></br>-Occurs after loud noise/fright<br></br>-Prolonged LOC<br></br>-Sudden onset of HA prior to syncope<br></br>-Post-ictal/incontinence/seizure-like activities<br></br>-Recurrent episodes<br></br>-Head trauma<br></br>-PMHx – DM (hypoglycemia), marfan’s, medications, etc<br></br>-FHx of SCD/CM/arrhythmia

119
Q

“<span>What was the likely cause of syncope in HOCM?</span>”

A

Dynamic LVOT obstruction decreases cardiac output and results in syncope, ventricular dysrhythmias, complete heart block

120
Q

“<span>Name one treatment option of HOCM?</span>”

A

beta blockers,<div>myomectomy,</div><div>pacemaker (for right ventricular pacing),</div><div>ICD</div>

121
Q

“<span>Name 4 initial interventions you should order now in ACS</span>”

A

“<span>-IV access</span><br></br><span>-02 via NRB</span><br></br><span>-Cardiac monitor</span><br></br><span>-Move to high acuity bed</span><br></br><span>-Administer ASA 160-320mg to chew</span><br></br><span>-Analgesia</span>”

122
Q

“<span>List six further investigations you would order in ACS</span>”

A

“<span>-CBC: WBC, Hgb</span><br></br><span>-Troponin, CK</span><br></br><span>-Glucose</span><br></br><span>-INR</span><br></br><span>-PTT</span><br></br><span>-Creatinine</span><br></br><span>-Lipase</span><br></br><span>-BNP</span><br></br><span>-D. dimer</span><br></br><span>-Portable CXR</span>”

123
Q

“<span>What are the ECG criteria for thrombolysis in AMI?</span>”

A

“-ST elevation greater than 1mm in 2 contiguous leads (>2mm in anterior leads)<br></br>-New or presumed new LBBB (would probably still get you the mark on the exam)<br></br>-LBBB with sgarbossa’s criteria (more up to date and likely acceptable on exam now)<div><br></br>–all with a history of 30 mins of chest pain consistent with ischemia</div>”

124
Q

“<span>What are five absolute contraindications to thrombolytic therapy in AMI? (5 Marks)</span>”

A

“<span>-Any prior ICH</span><br></br><span>-Known structural cerebral lesion (AVM)</span><br></br><span>-Known malignant intracranial neoplasm</span><br></br><span>-Ischemic stroke >3 hours or < 3 months</span><br></br><span>-Spinal/intracranial surgery in past 2 months</span><br></br><span>-Severe uncontrolled hypertension</span><br></br><span>-Suspected aortic dissection</span><br></br><span>-Active bleeding or bleeding diathesis (excluding menses)</span><br></br><span>-Significant closed head trauma or facial trauma within 3 months</span>”

125
Q

“<span>Name 4 findings on physical examination that would support Dx of aortic dissection:</span>”

A

“<span>-Neurologic deficits</span><br></br><span>-Variation in arm BPs (>20mmHg)</span><br></br><span>-Variation in radial pulses</span><br></br><span>-HTN</span><br></br><span>-New aortic regurgitation murmur (decrescendo diastolic murmur)</span><br></br><span>-Signs of pericardial effusion/tamponade (muffled heart sounds, pulsus paradoxus, JVD, hypotension)</span><br></br><span>-Shock</span>”

126
Q

What are the criteria for thrombolyzing a STEMI?

A

• Ischemic chest discomfort at least 20 minutes in duration but <12 hours since symptom onset AND <br></br>• New ST elevation ≥ 1mm at the J-point in two contiguous leads (except V2-V3) <br></br> • Men >40: ST elevation > 2mm in V2-V3 <br></br> • Men < 40: ST elevation > 2.5 mm in V2-V3 <br></br> • Women ST elevation > 1.5mm in V2-V3<div>. New LBBB or New Sgarbossa criteria for old LBBB</div>

127
Q

Absolute CI of thrombolytic Rx in STEMI

A

CNS:<div> Any prior ICH</div><div> Prior ischemic stroke <= 3 months (exception ischemic stroke within 3 hours)</div><div> Known malignant intracranial neoplasm (primary or metastatic)</div><div> Known cerebral vascular lesion (AVM)</div><div> IC or intraspinal surgery <= 2 months</div><div> Significant closed head injury or facial injury <= 3 months</div><div><br></br></div><div>CVS:</div><div> Suspected aortic dissection</div> Active bleeding or bleeding diathesis (excluding menses)<div> Severe uncontrolled high BP at time of administration</div><div><br></br></div><div>For streptokinase, prior treatment within the previous 6 months<br></br></div>

128
Q

Relative CI of thrombolytic Rx in STEMI

A

CNS:<div> Ischemic stroke > 3 months</div><div> Dementia</div><div><br></br></div><div>CVS:</div><div> SBP>180 or DBP > 110</div><div> Traumatic or prolonged CPR (>10 minutes)</div><div> Infective endocarditis</div><div> Recent (2-4 wks) internal bleeding</div><div> Current use of oral anticoagulant therapy</div><div><br></br></div><div>Procedures:</div><div> Major surgery <= 3 wks</div><div> Puncture of noncompressible blood vessel <= 2 wks</div><div><br></br></div><div>Women:</div><div> Pregnancy</div><div> OCP</div><div><br></br></div><div>GIT:</div><div> Hx of PUD</div><div> Advanced liver disease</div><div> </div>

129
Q

Whar are the causes of STE?

A

<b>Cardiac:</b><div> <i>Dysrrhythmia:</i></div><div> LBBB</div><div> WPW</div><div> Brugada</div><div> BER</div><div> Vent paced rhythm</div><div> Post DC</div><div><br></br></div><div> <i>Vascular:</i></div><div> ACS</div><div> Coronary a. vassospasm</div><div> Aortic dissection</div><div><br></br></div><div> <i>Myocardium:</i></div><div> Myocarditis</div><div> HOCM</div><div> LVH</div><div> LV aneurysm</div><div><br></br></div><div> <i>Pericardium:</i></div><div> Pericarditis</div><div><br></br></div><div><b>SAH and Raised ICP</b></div><div><b>HyperK</b></div><div><b>Hypothermia</b></div>

130
Q

What are the complications post AMI?

A

• Brady/tachyarrhythmias <br></br>• Cardiogenic shock <br></br>• Angina <br></br>• Reinfarction/Infarct Extension <br></br>• CHF <br></br>• Ventricular Septal Rupture <br></br>• Papillary Muscle Rupture (Mitral regurge days 3-5) <br></br>• Left Ventricular Free Wall Rupture <br></br>• Pericarditis (infarct pericarditis, dresslers – delayed 2-10weeks) <br></br>• Left Ventricular Aneurysm (late) <br></br>• LV thrombus (embolic stroke) (late)

131
Q

<div>Medications that causes syncope:</div>

A

<ol> <li>Cardiac medications: CCB, BB, diuretics, digitalis</li> <li>QT prolongers leads to TDP</li> <li>Recreational drugs</li> <li>antidepressants</li></ol>

132
Q

<div>What are 5 ECG findings to look for in the syncopal patient?</div>

A

<div>1. Dysrhythmias </div>

<div>2. Pre-excitation </div>

<div>3. Shortened PR </div>

<div>4. Prolonged QTc </div>

<div>5. ST Elevation (regional and diffuse) </div>

<div>6. Brugada pattern (RBBB in association with ST elevation in V1-V3) </div>

<div>7. Right ventricular strain pattern </div>

<div>8. Electrical alternans</div>

133
Q

List 6 important questions to ask on history of aortic dissection

A

Characteristic of pain <br></br>Onset of pain <br></br>Pattern of pain <br></br>History of same <br></br>Drug/medications <br></br>Associated symptoms – vomit, diaphoresis, syncope, palpitations <br></br>Past medical history <br></br><br></br> <br></br><br></br>Initial investigations: ECG, trop, CXR, bedside echo

134
Q

Name 6 possible findings of aortic dissection on CXR

A

• Wide mediastinum ≧ 6- 8 cm <br></br>• Abnormal aortic contour <br></br>• Left pleural effusion <br></br>• Displacement of NG/trachea to right <br></br>• Displacement of intimal calcification (double calcium sign) <br></br>• Cardiomegaly <br></br>• Upwards displacement of right mainstem <br></br>• Depression of left mainstem bronchi <br></br>• Apical cap

135
Q

Name 5 risk factors for aortic dissection

A

• HTN <br></br>• History of cardiac surgery <br></br>• Bicuspid aortic valve <br></br>• Cocaine use <br></br>• Connective tissue disorders (e.g. Marfans) <br></br>• Family history <br></br>• Pregnancy (T3/peripartum/postpartum) <br></br>• Trauma

136
Q

Name five complications of aortic dissection

A

• Dissection can propagate: <br></br>• Cardiac tamponade <br></br>• Aortic insufficiency <br></br>• RCA (inferior STEMI) <br></br>• CHF <br></br>• Hemorrhage shock <br></br>• Focal neuro deficits (cerebral ischemia/stroke) <br></br>• Spinal cord infarcts <br></br>• Pleural hemorrhage <br></br>• Mesenteric ischemia <br></br>• Aortoenteric fistula <br></br>• Renal failure <br></br>• Lower limb ischemia, pulse deficits <br></br>• HEENT: mass effect- stridor, SOB, horner syndrome, hoarseness, SVC <br></br>syndrome

137
Q

5 tests you would order or perform in patients with suspected pericarditis and why?

A

• TTE (or bedside cardiac ultrasound)- pericardial effusion <br></br>• ECG<br></br>• CXR (pleural effusions, cardiac silhouette, CHF) <br></br>• Bloodwork <br></br> • ESR/CRP – inflammatory markers <br></br> • CBC <br></br> • Trop – concurrent myocardial involvement <br></br> • Urea/Cr <br></br>• Physical exam – pericardial friction rub

138
Q

Name 5 poor prognostic indicators of pericarditis

A

<b>Major</b>: <br></br>• Fever > 38 C <br></br>• Subacute onset <br></br>• Large pericardial effusion <br></br>• Cardiac tamponade <br></br>• Lack of response to aspirin or NSAIDs after >1 week of therapy <br></br><br></br><b>Minor</b> <br></br>• Myopericarditis <br></br>• Immunosuppression <br></br>• Trauma <br></br>• Oral Anticoagulant therapy

139
Q

HEART Score

A

“<img></img>”

140
Q

DDX of acute respiratory distress

A

-Pulmonary embolism<br></br>-AECOPD/asthma<br></br>-Acute decompensated congestive heart failure<br></br>-Anaphylaxis<br></br>-Foreign body aspiration<br></br>-Valve pathology (e.g. acute aortic regurge)<br></br>-Pneumothorax

141
Q

“What are the precipitants of<span>Acute decompensated heart failure?</span>”

A

“<b>"”HEART FAILED””</b><div>H – Hypertension,</div><div> Heart anatomy (valvular, myocarditis, effusion, cardiomyopathy)<br></br>E – endocrinopathies<br></br>A – anemia<br></br>R – rheumatic disorders<br></br>T – toxins (cocaine, ETOH, chemo)<br></br>F – failure to take medications<br></br>A - arrhythmia<br></br>I – infection, infarction, ischemia<br></br>L – lung pathology (COPD, PE, pneumonia)<br></br>E – electrolyte abnormality<br></br>D – diet, diaper (pregnancy)<br></br></div>”

142
Q

“<span>Name four lifestyle modifications you can recommend to this patient to prevent them from returning AECHF</span>”

A

“<span>-Limit alcohol consumption</span><br></br><span>-Low salt diet</span><br></br><span>-Limit fluid intake</span><br></br><span>-Weight reduction</span><br></br><span>-Quit smoking</span><br></br><span>-Compliance with medications</span><br></br><span>-Exercise (supervised) – cardiac rehab</span>”

143
Q

“<span>Name three contraindications to using nitroglycerin.</span>”

A

-Recent use of PDE5 inhibitors (e.g. Viagra)<br></br>-Hypotension<br></br>-Severe aortic stenosis<br></br>-Inferior myocardial infarction with RV involvement

144
Q

Drugs to avoid use in severe aortic stenosis

A

-Nitrates<br></br>-Calcium channel blockers<br></br>-Hydralazine

145
Q

“<span>Name three causes of regular wide complex tachycardia</span>”

A

-<b>Ventricular tachycardia</b><br></br>-Polymorphic VT (torsades)<br></br>-<b>SVT with aberrancy</b><br></br>-<b>A. flutter with aberrancy</b>

146
Q

“<span>Name three causes of irregular narrow complex tachycardia</span>”

A

-Atrial fibrillation<br></br>-MAT (multifocal atrial tachycardia)<br></br>-Atrial flutter with variable conduction

147
Q

“Name precipitants for<span>irregular narrow complex tachycardia</span>”

A

“<b>"”PIRATES””</b><div>P - PE, pulmonary disease, post op<br></br>I - Ischemic heart disease, idiopathic, infectious<br></br>R – Rheumatic valvular disease/ any valvular disease<br></br>A – Anemia, alcohol, age<br></br>T – Thyroid, toxins<br></br>E – Elevated blood pressure, electrolytes<br></br>S – Sleep apnea, sepsis<br></br></div>”

148
Q

“<span>Name two drug classes that can be used in the management of AF</span>”

A

-Rate control: Beta-Blockers, Calcium Channel-blockers, cardiac glycosides (digoxin)<br></br>-Rhythm control: Class Ia (procainamide) - sodium channel blocker<br></br> Class III (amiodarone) – potassium channel blocker

149
Q

CI of DOAC

A

-Mechanical heart valve<br></br>-Severe renal failure<br></br>-Pregnancy<br></br>-Severe liver disease

150
Q

“<span>Define hypertensive emergency versus hypertensive urgency</span>”

A

-Emergency – Elevated BP associated with target organ dysfunction<br></br><br></br>-Urgency – Clinical presentation associated with severe elevations in BP (generally >180/110) without, but at risk for progressive target organ dysfunction

151
Q

“<span>Name 5 clinical syndromes/conditions that would define a patient’s hypertension as a hypertensive emergency</span>”

A

-Aortic Dissection<br></br>-Acute Pulmonary Edema/ Heart Failure<br></br>-ACS<br></br>-ARF<br></br>-Severe pre-eclampsia<br></br>-Hypertensive encephalopathy<br></br>-SAH<br></br>-ICH/SAH<br></br>-Ischemic stroke<br></br>-Sympathetic Crisis<br></br>-MAHA

152
Q

“<span>Name 5 investigations that should be ordered in all patients where hypertensive emergency is a consideration</span>”

A

“-CBC<br></br>-Electrolytes<br></br>-Creatinine<br></br>-Urea<br></br>-Glucose<br></br>-Troponin<br></br>-Urinalysis<br></br>-ECG<br></br>-CXR<br></br>(Note: CT head is not accepted as not ALL patients require this, ONLY if they have symptoms of HTN encephalopathy)”

153
Q

Meds for Hypertensive emergency Rx:

A

CCB: Nicardipine<div>BB: Labetolol</div><div> Esmolol</div><div>Nitrates: Nitroprusside</div>

154
Q

“<span>What is your goal of treatment of HTN emergency?</span>”

A

Reduce BP by 20 % acutely<div>Resolution of symptoms</div>

155
Q

“<span>Name three genetic conditions that may result in a younger patient having an implantable cardioverter-defibrillator (ICD) placed?</span>”

A

-Brugada syndrome<br></br>-Long QTc syndrome<br></br>-Hypertrophic cardiomyopathy<br></br>-Familial dilated cardiomyopathy<br></br>-Arrhythmogenic right ventricular dysplasia (ARVD)

156
Q

“<div><div><div><div>While in the emergency department his ICD fires twice. You review the rhythm strip leading to the firing of the ICD (see below). What is your next step in management? (1 point)</div></div></div></div><div><div><img></img></div></div>”

A

“<span>-Apply magnet (1 point)</span><br></br><span>-Consult cardiology for device interrogation (0.5 points)</span>”

157
Q

“<div><div><div><div>Now assume this rhythm strip below was seen and that the ICD fired three more times. What are two medications that can be used in the management of this patient? (2 points)</div></div></div></div><div><div><img></img></div></div>”

A

“-Amiodarone<br></br>-Procainamide<br></br>-Lidocaine<br></br>-Metoprolol, propranolol, esmolol (beta-blockers)<br></br><br></br>Clinical Pearl: remember to reverse any precipitants (ischemia, heart failure, electrolyte abnormality, hyperthyroidism), despite none having been specifically mentioned in this case”

158
Q

“<div><div><div>A 72 year old male presents with shortness of breath. You order a chest X-ray to assess for pneumonia.</div></div></div><div><div><div><div><div><div>Q1. Interpret the CXR below (1 point)The patient is stable. Given your findings, what is your next step in management. (1 point)</div></div></div></div><div><div><img></img></div></div></div></div>”

A

-Lead dislodgement. (Cannot see ICD atrial electrode, coiling around ICD), no pneumonia.<br></br>-Discuss with cardiology for replacement

159
Q

“<span>Aside from medications or overdoses name five causes of bradycardia</span>”

A

-Ischemia<br></br>-Hyperkalemia<br></br>-Hypothermia<br></br>-Hypothyroidism<br></br>-Structural heart disease<br></br>-Infiltrative (amyloid, hemochromatosis, sarcoid),<br></br>-Autoimmune<br></br>-Lyme disease/infectious/myocarditis

160
Q

“<span>Name four classes of drugs that may of caused symptomatic bradycardia or complete heart block</span>”

A

-Beta- Blockers<br></br>-Calcium-channel blockers<br></br>-Digoxin (digitalis glycosides)<br></br>-Organophosphates (any cholinergic medication e.g. physostigmine)<br></br>-Alpha-agonist (clonidine)<br></br>-Class III anti-arrhythmics (e.g. amiodarone)<br></br>-Class I anti-arrhythmics (e.g. procainamide)<div><br></br></div><div>Also:</div><div>Opiates</div><div>Chloralhydrate</div><div>ETOH</div><div>Benzos</div>

161
Q

High risk conditions for aortic dissection

A

Marfan synd<div>FHx of aortic disease</div><div>Known aortic valve dis</div><div>Recent aortic manipulation</div><div>Known thoracic aortic aneurysm</div>

162
Q

O/E suggestiv of aortic aneurysm

A

Evidence of perfusion deficit:<div> <i>pulse deficit,</i></div><div><i> SBP differential,</i></div><div><i> focal neuro deficit</i><div>New aortic insufficiency mumur</div><div>Hypotension/shock<br></br>Marfanoid Features</div></div>

163
Q

<p>What antiarhythmic agent is used for TDP</p>

A

Lidocain

164
Q

Predisposing factors for Brugada syndrome

A

<ul> <li>Fever</li> <li>Ischemia</li> <li>Drugs</li> <li>HypoK</li> <li>Hypothermia</li> </ul>

165
Q

Predisposing factors for Brugada syndrome

A

<ul> <li>Fever</li> <li>Ischemia</li> <li>Drugs</li> <li>HypoK</li> <li>Hypothermia</li> </ul>

166
Q

Factors predispose to Brugada

A

<ul> <li>Fever</li> <li>Ischemia</li> <li>Drugs</li> <li>HypoK</li> <li>Hypothermia</li> </ul>

167
Q

Drugs to avoid in WPW

A

BB<div>CCB</div><div>Adenosine</div>

168
Q

DDx of Cardiac Syncope

A

WPW<div>Brugada</div><div>Long/short QT syndrome</div><div>HOCM</div><div>PE</div><div>ARVD</div><div>Trifasicular block</div><div>Tachy/brady dysrhythmia (syndrome)</div>

169
Q

What are the general etiology of arrhythmia

A

Re-entry pathway<div>Afterdepolarization</div><div>Automaticity</div>

170
Q

Name findings to help differentiate VT versus SVT with aberrancy

A

<p><strong>Clinically:</strong><br></br>• Clinical: age > 35, cardiac history/risk factors, family history SCD <br></br>• No response to vagal maneuvers <br></br>• No prior ECG with BBB or WPW with similar morphology <br></br>• Cannon A waves</p>

<div></div>

<div><strong>ECG Findings:</strong><br></br>• Absence of typical RBBB or LBBB pattern <br></br>• Extreme axis deviation (northwest axis - QRS is positive in aVR and negative in I + aVF) <div>• QRS duration (very broad > 160msec) <br></br>• AV dissociation (P and QRS at different rates) <br></br>• Positive or Negative Concordance – V1-V6 all same direction <br></br>• Fusion beats <br></br>• Capture beats <br></br>• Brugada Sign <br></br>• Josephen Sign <br></br>• RSR’ complexes with taller Left rabbit ear</div> </div>

171
Q

Name six causes of atrial fibrillation

A

• P-pulmonary embolism, pulm disease, post-op <br></br>• I-Ischemic heart disease, idiopathic, infectious <br></br>• R- rheumatic valvular disease/valvular heart disease <br></br>• A- anemia, alcohol, age <br></br>• T – thyroid, toxins <br></br>• E – elevated BP, electrolytes <br></br>• S- Sleep apnea, sepsis, surgery

172
Q

Name 4 investigations you work consider/order in new onset atrial <br></br>fibrillation.

A

• CBC <br></br>• Electrolytes <br></br>• TSH <br></br>• Cr <br></br>• Coag profile <br></br>• Echo as outpatient

173
Q

How would you decide between rate control versus rhythm control?

A

“<img></img>”

174
Q

Special circumstances to consider Early Rhythm Control of A.Fib

A

Highly symptomatic<div>Multiple recurrences</div><div>Extreme QOL impairment</div><div>Arrhythmia-induced CMP</div>

175
Q

How do you decide who gets anticoagulated?

A

<b>CHADS2 Score:</b><div><br></br></div><div>Congestive heart failure</div><div>Hypertension (>140/90)</div><div>Age >= 65</div><div>DM</div><div>Hxof stroke or TIA</div>

176
Q

What are the four risk factors for bleeding in patients on anti-<br></br>coagulation?

A

HAS BLED<div><br></br></div><div>Hypertension (>160)</div><div>Abnormal liver or kidney function</div><div>Stroke Hx</div><div>Bleeding (Hx or predisposition)</div><div>Labile INR</div><div>Elderly (>65)</div><div>Drugs/Alcoho; (antoplatelets, NSAIDS)</div><div><br></br></div>

177
Q

Name five causes of bradyarrhythmias

A

• Medications (BB, CCB, dig) <br></br>• Ischemia <br></br>• Hyperkalemia <br></br>• Lyme disease/myocarditis <br></br>• Structural heart disease <br></br>• Hypothermia <br></br>• Hypothyroidism (cushing) <br></br>• Autoimmune (lupus) <br></br>• Infiltrative (amyloid, hemochromatosis, sarcoid)

178
Q

What are five management steps you can consider in symptomatic <br></br>bradyarrhythmias?

A

• Atropine <br></br>• Transcutaneous pacemaker <br></br>• Transvenous pacemaker <br></br>• Isoproterenol <br></br>• Pressors: epinephrine, dopamine <br></br>• If overdose – follow treatment for BB/CCB overdose <br></br>• Treat reversible conditions (e.g. hyperkalemia)

179
Q

When is atropine ineffective?

A

• Atropine is ineffective for blocks occurring below the AV node. E.g. <br></br>Second degree Mobitz II, Complete heart block with wide QRS <br></br>• Also, ineffective in cardiac transplant patients

180
Q

List three differences in clinical findings between embolic and <br></br>thrombotic peripheral artery disease/limb ischemia

A

“<img></img>”

181
Q

List three possible metabolic complications after revascularization

A

• Metabolic acidosis <br></br>• Hyperkalemia <br></br>• Myoglobinuria

182
Q

Clinical manifestations of end organ damage HTN emergency

A

“<img></img>”

183
Q

HTN + associated diseases Rx:

A

“<img></img>”

184
Q

Name 6 causes of secondary hypertension

A

• Cushings <br></br>• Pheochromocytomata <br></br>• Hyperthyroidism <br></br>• Obstructive sleep apnea <br></br>• Polycystic kidney disease <br></br>• Renal artery stenosis <br></br>• Nephritic/nephrotic syndrome <br></br>• Toxins – sympathomimetric use/ Chronic ETOH use <br></br>• Coarctation of the aorta

185
Q

Name four causes of non-cardiogenic pulmonary edema

A

• Pancreatitis <br></br>• Sepsis <br></br>• DIC <br></br>• ARDS <br></br>• Burns <br></br>• Drowning <br></br>• Fat embolism/amniotic fluid embolism <br></br>• Re-expansion <br></br>• High altitude pulmonary edema<div>COVID</div>

186
Q

Treatment of Acute Heart Failure

A

“<img></img>”

187
Q

Criteria for D/C from ED after Rx of CHF

A

“<img></img>”

188
Q

Types of Shock

A

“<img></img>”

189
Q

<strong>Cath Lab Activation:</strong>

A

“<ul> <li><span>1st Diagonal Branch of the Left Anterior Descending Artery Occlusion</span><br></br> <ul> <li><span><em>STE in aVL and V2</em></span></li> <li><span><em>Upright T-waves in aVL and V2</em></span></li> <li><span><em>ST-Depression and inverted T waves in Inferior Leads (III and aVF)</em></span></li> </ul> </li> <li><span>de Winter’s T Waves</span></li> <li><span>Left Main Coronary Artery Occlusion</span> <ul> <li><em><span>STE in lead aVR<strong>AND/OR</strong></span></em></li> <li><em><span>Widespread ST-Depression</span></em></li> </ul> </li> <li><span>Posterior STEMI</span></li> </ul>”

190
Q

ECG changes in electrolytes disturbances

A

“<p><img></img></p>”

191
Q

ECG suggestive of temponade

A

Low voltage QRS<div>Tachycardia</div><div>Electrical alternance</div>

192
Q

Echo findings in Temponade

A

RV diastolic collapse<div>RA systolic collapse</div><div>IVC dilation</div><div>Sonographic alternance</div><div><br></br></div><div>With evidence of fluid around the heart</div>

193
Q

“<h2><span><strong>ECG Pearls for Syncope</strong></span></h2>”

A

<ul><li><b>short PR:</b>WPW</li><li><b>long PR</b>: AV conduction block</li><li><b>narrow, deep QRS:</b>HCM</li><li><b>wide QRS + Epsilon waves:</b>arrhythmogenic RV hypertrophy wide QRS: Vtach,WPW, BBB</li><li><b>QT interval:</b>long QT syndrome, (also short QT)</li><li><b>Also, look for Brugada, ACS, myocarditis, and PE changes on ECG</b><br></br></li></ul>

194
Q

<b>Long QT Causes</b>

A

<div><b>Congenital Long QT</b></div>

<ul><li>inherited, often with deafness; syncope can be triggered by sudden loud noises or startling events, or spontaneously.</li></ul>

<div><b>Acquired Causes:</b><b>(& examples)</b></div>

<ul><li>Antiarrhythmics (amiodarone, sotolol)</li><li>Antibiotics (macrolides)</li><li>Antidepressants (TCAs, citalopram)</li><li>Antipsychotics (haldol, seroquel)</li><li>Antihistamines (loratidine, benadryl)</li><li>**Numerous other medications, as well as low K+, Ca+, and Mg+ (due to alcohol abuse, diuretics, malnutrition), myocarditis, hypothermia, methadone, and carbon monoxide, can lengthen the QT segment.**</li></ul>

195
Q

“<b><span>What are the indications for admission in patients with Syncope?</span></b>”

A

<ol><li>history of CHF,</li><li>history of ventricular arrhythmias,</li><li>associated symptoms of ACS,</li><li>exam evidence of significant CHF,</li><li>exam evidence of significant valvular disease,</li><li>abnormal ECG (ischemia, arrhythmia, BBB, prolonged QTc)</li></ol>

196
Q

<b>Syncope Discharge Instructions</b>

A

<ul><li>For vasovagal: avoid known triggers, such as alcohol and warm environments, and maintain adequate hydration, food and sleep.</li><li>To reduce injury: once syncope prodrome starts, lie down, and avoid driving or high risk activities.</li></ul>

197
Q

“<span>Name 7 features on history that would be worrisome for a life-threatening cause of his syncope:</span>”

A

-Exertional<br></br>-No prodrome<br></br>-Palpitations<br></br>-Chest pain<br></br>-Occurs after loud noise/fright<br></br>-Prolonged LOC<br></br>-Sudden onset of HA prior to syncope<br></br>-Post-ictal/incontinence/seizure-like activities<br></br>-Recurrent episodes<br></br>-Head trauma<br></br>-PMHx – DM (hypoglycemia), marfan’s, medications, etc<br></br>-FHx of SCD/CM/arrhythmia

198
Q

“Syncope<br></br><img></img>”

A

-WPW – short PR, delta/slurred upstroke<br></br>-Treatment is ablation

199
Q

“Syncope<br></br><img></img>”

A

-Brugada (cardiac sodium channel gene mutation). This is type I Brugada – coved ST elevation in V1-V3<br></br>-Causes VT/VF to induce syncope<br></br>-Treatment is an ICD

200
Q

“Syncope<br></br><img></img>”

A

-Long QT Syndrome (Na/K ion channel abnormality - congenital in this case, but could be due to meds/lytes etc)<br></br>-Causes torsades/VT/VF. Can be triggered by loud noise, strong emotion, exercise etc<br></br>-Tx – Beta blockers typically for asymptomatic patients, ICD after syncope, arrhythmia

201
Q

“Syncope<br></br><img></img>”

A

-Hypertrophic Cardiomyopathy. LVH, deep needle-like Q waves, anterior T-wave inversion<br></br>-Dynamic LVOT obstruction decreases cardiac output and results in syncope, ventricular dysrhythmias, complete heart block<br></br>-Tx – beta blockers, myomectomy, pacemaker (for right ventricular pacing), ICD

202
Q

Cardiac CP, what are the initial Rx?

A

High acuity bed<br></br>iv access<br></br>Monitor<br></br>O2 NRB<br></br>ASA 160-320 mg<br></br>Analgesia

203
Q

Absolute CI of Thrombolysis

A

-Any prior ICH<br></br>-Known structural cerebral lesion (AVM)<br></br>-Known malignant intracranial neoplasm<br></br>-Ischemic stroke >3 hours or < 3 months<br></br>-Spinal/intracranial surgery in past 2 months<br></br>-Severe uncontrolled hypertension<br></br>-Suspected aortic dissection<br></br>-Active bleeding or bleeding diathesis (excluding menses)<br></br>-Significant closed head trauma or facial trauma within 3 months

204
Q

“<span>Name 4 findings on physical examination that would support Dx of Aortic dissection:</span>”

A

-Neurologic deficits<br></br>-Variation in arm BPs (>20mmHg)<br></br>-Variation in radial pulses<br></br>-HTN<br></br>-New aortic regurgitation murmur (decrescendo diastolic murmur)<br></br>-Signs of pericardial effusion/tamponade (muffled heart sounds, pulsus paradoxus, JVD, hypotension)<br></br>-Shock

205
Q

Emergency BP reduction medicine in acute aortic dissection

A

Esmolol<br></br>Labetolol<br></br>Verapamil<br></br>Nicardipine<br></br>Nitroprusside

206
Q

“<span>Name five precipitants that can lead to this acute decompensated HF</span>”

A

<b>HEART FAILED</b><br></br>H – Hypertension, heart anatomy (valvular, myocarditis, effusion, cardiomyopathy)<br></br>E – endocrinopathies<br></br>A – anemia<br></br>R – rheumatic disorders<br></br>T – toxins (cocaine, ETOH, chemo)<br></br>F – failure to take medications<br></br>A - arrhythmia<br></br>I – infection, infarction, ischemia<br></br>L – lung pathology (COPD, PE, pneumonia)<br></br>E – electrolyte abnormality<br></br>D – diet, diaper (pregnancy)

207
Q

“<span>Name four findings on CXR that suggest Acute decompensated HF</span>”

A

-Pleural effusions<br></br>-Kerley B lines<br></br>-Cardiomegaly<br></br>-Vascular cephalization<br></br>-Interstitial edema

208
Q

“<span>Name four lifestyle modifications you can recommend to this patient to prevent them from returning with acute decompensated HF</span>”

A

-Limit alcohol consumption<br></br>-Low salt diet<br></br>-Limit fluid intake<br></br>-Weight reduction<br></br>-Quit smoking<br></br>-Compliance with medications<br></br>-Exercise (supervised) – cardiac rehab

209
Q

“<span>Name three contraindications to using nitroglycerin</span>”

A

-Recent use of PDE5 inhibitors (e.g. Viagra)<br></br>-Hypotension<br></br>-Severe aortic stenosis<br></br>-Inferior myocardial infarction with RV involvement

210
Q

“<span>Name three causes of regular wide complex tachycardia?</span>”

A

-Ventricular tachycardia<br></br>-Polymorphic VT (torsades)<br></br>-SVT with aberrancy<br></br>-Aflutter with aberrancy

211
Q

“<span>Name three causes of irregular narrow complex tachycardia?</span>”

A

-Atrial fibrillation<br></br>-MAT (multifocal atrial tachycardia)<br></br>-Atrial flutter with variable conduction

212
Q

“<img></img><br></br><span>Name five precipitants that could cause the above ECG rhythm</span>”

A

P - PE, pulmonary disease, post op<br></br>I - Ischemic heart disease, idiopathic, infectious<br></br>R – Rheumatic valvular disease/ any valvular disease<br></br>A – Anemia, alcohol, age<br></br>T – Thyroid, toxins<br></br>E – Elevated blood pressure, electrolytes<br></br>S – Sleep apnea, sepsis

213
Q

“<span>What are two general management steps for this patient with acute AF?</span>”

A

Rate or rhythm control<br></br>Decision/discussion on anticoagulation

214
Q

Criteria for anticoagulation in AF

A

<b>CHADS2-65 or CHADS-VASC criteria</b><br></br>–Congestive heart failure<br></br>–Hypertension<br></br>–Age > 65, >75<br></br>–Diabetes<br></br>–Stroke/TIA/VTE<br></br>–Sex:Male<br></br>–Vascular disease<br></br><br></br>-Absence of high bleeding risk criteria (HAS BLED)

215
Q

“<span>Define hypertensive emergency versus hypertensive urgency:</span>”

A

-<b>Emergency </b>– Elevated BP associated with target organ dysfunction<br></br><br></br>-<b>Urgency </b>– Clinical presentation associated with severe elevations in BP (generally >180/110) without, but at risk for progressive target organ dysfunction

216
Q

“<span>Name 5 clinical syndromes/conditions that would define a patient’s hypertension as a hypertensive emergency:</span>”

A

“-Aortic Dissection<br></br>-Acute Pulmonary Edema/ Heart Failure<br></br>-ACS<br></br>-ARF<br></br>-Severe pre-eclampsia<br></br>-Hypertensive encephalopathy<br></br>-SAH<br></br>Ischemic stroke<span><br></br></span>”

217
Q

“<span>Name 5 investigations that should be ordered in all patients where hypertensive emergency is a consideration?</span>”

A

-CBC<br></br>-Electrolytes<br></br>-Creatinine<br></br>-Urea<br></br>-Glucose<br></br>-Troponin<br></br>-Urinalysis<br></br>-ECG<br></br>-CXR<br></br>(Note: CT head is not accepted as not ALL patients require this, ONLY if they have symptoms of HTN encephalopathy)

218
Q

“<span>Name three reasons an ICD may fire incorrectly</span>”

A

-Supraventricular tachyarrhythmias<br></br>-Electromagnetic interference<br></br>-Hardware failure (lead placement/lead fracture)<br></br>-T wave or atrial oversensing (thinking this is actual a QRS complex)

219
Q

“<span>Third degree AV block,</span><span>Name four classes of drugs that may of caused</span>”

A

-Beta- Blockers<br></br>-Calcium-channel blockers<br></br>-Digoxin (digitalis glycosides)<br></br>-Organophosphates (any cholinergic medication e.g. physostigmine)<br></br>-Alpha-agonist (clonidine)<br></br>-Class III anti-arrhythmics (e.g. amiodarone)<br></br>-Class I anti-arrhythmics (e.g. procainamide)

220
Q

Non-traumatic, non-cardiac causes of pericardial effusion:

A

Idiopathic<br></br>Infectious (viral, bacterial, fungal, parasitic, infective endocarditis)<br></br>Autoimmune (SLE, RA, Scleroderma, Sjogren’s, vasculitis, etc)<br></br>Dissecting aortic aneurysm<br></br>Malignant effusion (mets, primary or paraneoplastic)<br></br>Post-radiation<br></br>Metabolic (hypothyroidism, uremia)<br></br>Medication induced (rare: anticoagulants, thrombolytics, doxorubicin, etc)

221
Q

Mechanical causes for PEA

A

Thrombosis (PE, MI)<br></br>Tension pneumoTx<br></br>Temponade

222
Q

“NSTEMI,<span>Name three indications for more urgent transfer to a tertiary center</span>”

A

Refractory chest pain<br></br>Hemodynamic instability<br></br>Recurrent chest pain with dynamic ECG changes<br></br>Cardiac arrhythmias<br></br>Concurrent heart failure

223
Q

Indications for 15 leads ECG:

A

All inferior STEMI<br></br>Any STE or STD in V1-V3<br></br>Equivocal STE in inf or lat leads<br></br>Hypotension in the setting of ACS

224
Q

<p>List the CHDs that require a patent ductus and why?</p>

A

<p><strong><em>To preserve flow from aorta to pulmonic circulation</em></strong></p>

<ul> <li>Pulmonic atresia</li> <li>Tricuspid atresia</li> <li>Tetralogy of fallot</li> <li>Hypoplastic right heart syndrome</li> </ul>

<p><strong><em>To preserve flow from pulmonic circulation to aorta</em></strong></p>

<ul> <li>Severe coarctation of the aorta</li> <li>Severe aortic stenosis</li> <li>Hypoplastic left heart syndrome</li> </ul>

225
Q

<p>What is the pharmacologic management to keep the ductus patent?</p>

A

<ul> <li>Prostaglandin E1 0.1μg/kg/min</li> </ul>

<p>–Note side effect is apnea and decrease BP, therefore intubate and give boluses, dobutamine prn</p>

226
Q

ECG patterns of PE

A

Tachycardia<br></br>Symmetrical T wave inversion in V1-V4<br></br>S1Q3T3<br></br>RBBB<br></br>RAD

227
Q

PERC Rule

A

“HAD CLOTS<br></br>If all no the pretest probability < 2 %=D/C home<br></br><img></img>”

228
Q

What is ECG findings are suggestive of ventricular tachycardia

A

Wide QRS<br></br>Rate > 100<br></br>Regular rhythm<br></br>Extreme RAD<br></br>

229
Q

What are the causes of vent tachycardia<br></br>

A

IHD<br></br>CMP<br></br>Mitral prolapse<br></br>Toxins (digoxin, procainamide, sympatho)

230
Q

<div><b><u>Induced Hypothermia</u></b></div>

A

<ul> <li>Inclusion Criteria:</li> <ul> <li>Post cardiac arrest</li> <li>ROSC<30 minutes</li> <li>Induction time < 6 hrs fromROSC</li> <li>Comatose</li> <li>MAP >65 mm Hg</li> </ul> <li>Best location for temperature probe: esophagus</li> <li>Target temperature: 32–36°C</li></ul>

231
Q

Narrow complex PEA is considered to be secondary to mechanical pathology including

A

<div>· cardiac tamponade, </div>

<div>· tension pneumothorax, </div>

<div>· pulmonary embolism, or </div>

<div>· hypovolemia</div>

232
Q

<div>Wide complex PEA is considered to be the result of a metabolic abnormality: with a differential diagnosis of</div>

A

<div>· hyperkalemia, </div>

<div>· severe acidosis, </div>

<div>· myocardial infarction, and<br></br>sodium channel blocker overdose</div>

233
Q

HAS-BLED

A

“<img></img>”

CCFP(EM) Omar (27 decks)

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