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Emergency Medicine > Cardiology/Cardiovascular Sx/CCU > Flashcards

Cardiology/Cardiovascular Sx/CCU Flashcards

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Royal College: Emergency Medicine flashcards
1
Q

What are causes of increased Troponin?

A 
ACS
Myocarditis
Pericarditis
PE
Severe Sepsis
Renal failure
cardiomyopathy
Cirrhosis, hypertensive crisis, connective tissues disease, cardiac contusion, cardioversion, electrical injury
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2
Q

When does Troponin rise and peak?

A

Should rise within 3-12 hours and peak at 24 hours

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3
Q

Is troponin elevation in CRF patients correlated with creatinine clearance

A

No

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4
Q

What is the purpose of the TIMI risk score?

A

It is for risk stratification of composite end point of death, MI or need for urgent revascularization within 14 days.

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5
Q

What are some indications for PCI? (aside from STEMI)

A
  1. Cardiogenic shock (proven by shock trial)
  2. Contraindication to lytic
  3. Failure of thrombolytic (ongoing pain/ecg changes)
  4. Large anterior MIs (debatable if not in shock)
  5. Post lytic (within 24-48 hours should get cath)
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6
Q

Which interventions for ACS have a mortality benefit?

A
  1. ASA (NNT 43, NNH 167)
  2. BB
  3. Ace-i (decreases remodeling)
  4. PCI
    (Nitro and CCBs do not decr mortality)
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7
Q

What are contraindications for BB?

A 
Bradycardia
Hypotension
AV Blocks
Bronchospasm:COPD/asthma
Acute HF
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8
Q

What are 7 complications of Acute MI

A

Mechanical

  1. LV aneurysm
  2. VSD
  3. Acute MR from papillary m. rupture
  4. Free wall/ventricular wall rupture, acute tamponade

Electrical

  1. Arrythmias - tachy
  2. Bradycardia/Heart blocks
  3. Reperfusion arrythmias

Hemodynamic

  1. Acute CHF
  2. Cardiogenic shock
  3. VTE
  4. Post MI pericarditis (Dresslers syndrome)
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9
Q

What is the treatment for pericarditis?

what about after an MI?

A

Naproxen 600 mg BID for week (add PPI)
Colchicine 0.6mg BID (can cause diarrhea)

Post MI - ASA 3-4 weeks

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10
Q

Whats the pathophysiology of myocarditis?

A

Viruses gets into myocardium, immune system attacks viruses, creates antigens and there is some crossreactivity with myosin and beta receptors – ends up attacking own heart - causing inflammation in myocardial tissue.

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11
Q

How does digoxin work?

A

1) Blocks Na/K ATPase
- This increases intra-cellular Na
- The Na/Ca anti-porter then is not as active and more calcium accumulates in the cell
- This leads to incr inotropy and contractility

2) increases vagal tone which results in decr conduction thru SA and AV nodes

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12
Q

Why doesn’t digoxin not work for Afib in younger patients?

A

The younger patient’s sympathetic system can overdrive the drugs effect on increasing the vagal tone. In elderly the sympathetic system is not as ‘robust’ and therefore is more likely to work

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13
Q

DDX VT (4)

A
  1. ACS
  2. Scarring (old infarct)
  3. Electrolytes (K, Ca, Mg)
  4. Hypoxia
  5. AbN tissues (myocarditis, rheumatic fever, HCM, ARVD)
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14
Q

What are the hemodynamic goals in a patient with aortic dissection?

A

100/60 rule

Use Labetalol to achieve HR

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15
Q

What clinical risk factors increase the likelihood that a WCT on ecg is VT?

A
  1. Age > 35 (positive predictive value of 85%)
  2. Structural heart disease
  3. Ischaemic heart disease
  4. Previous MI
  5. Congestive heart failure
  6. Cardiomyopathy
  7. Family history of sudden cardiac death (suggesting conditions such as HOCM, congenital long QT syndrome, Brugada syndrome or arrhythmogenic right ventricular dysplasia that are associated with episodes of VT)
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16
Q

What are the Class I anti-dysrhymics? (A,B,C)

A 
Class IA
Double Quarter pounder 
Disopyramide
Quinidine
Procainamide
Class IB
Mayo, Lettuce, tomato, Pickles
Mexilitine
Lidocaine
Tocainamide
Phenytoin

Class IC
Fries Please
Flecanide
Propafenone

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17
Q

What are the broad mechanism of Class I anti-dysrhythmics?

A

Fast Na+ Channel Blockade
“Membrane Stabilizing”

Procainamide
Lidocaine
Flecainide
Phenytoin

18
Q

What are the broad mechanism of Class II anti-dysrhythmics?

A

BB
Depress SA and AVN activity

Metoprolol
Esmolol

19
Q

What are the broad mechanism of Class III anti-dysrhythmics?

A

K+ Channel Blockade
Prolong refractory period and repolarization
‘Anti-fibrillatory’ effect

Sotalol
Amiodarone*
Ibutilide
Bretylium**
Dronedarone
20
Q

What are the broad mechanism of Class IV anti-dysrhythmics?

A

CCBs
Slow AVN conduction

Diltiazem
Verapimil

21
Q

What are the common AVN blocking agents? (6)

A 
Adenosine
Amiodarone
BB
CCB
Clonidine
Digoxin
22
Q

What are 5 causes of new AVB?

A
  1. Fibrosis/sclerosis
  2. Ischemia
  3. Drugs (Amiodarone, adenosine, BB, CCB, Clonidine, Digoxin)
  4. Connective tissues disorders
  5. Metabolic (hyperK)
  6. Myocarditis
  7. Cardiomyopathy
  8. Malignancies
  9. Hypothyroid
23
Q

What are the 4 stages of ecg changes in pericarditis?

A

Note only 50% patients will follow this pattern

Stage 1 - Sinus Tachy, Diffuse STE, PR dep,
PR elevation aVR, STD aVR

Stage 2 - Normalization of STE, PR depression starting to normalize. Biphasic inversion of T waves

Stage 3 - Global TWI and PR depression resolved. (weeks 3-6) but variable

Stage 4 - Normalization of egg (TWI). T waves however can
remain inverted in some patients.

24
Q

What are 7 causes of pericarditis?

A 
Post MI (Dresslers syndrome)
Endocrine (Myexedema, Addison's)
Radiation induced
Infectious (#1), inflammatory, infiltrative
Collagen Vascular Disease
Amyloidosis, Anticoagulation, Autoimmune
Renal failure (uremia)
Drugs (5 P's: penicillin, phenytoin, procainamide, pressure (hydralazine), Pulmonary (INH)
Idiopathic
Trauma
ITP
Secondary Tumors (mets spread)

OR

Infectious

  • Viral
  • bacterial
  • Fungal
  • Parasite
  • Rickettsia

Post Injury

  • Trauma
  • Surgery
  • MI (Dresslers)
  • Radiation

Metabolic

  • Uremia
  • Medications

Systemic Diseases

  • Rheumatoid arthritis
  • SLE
  • Sarcoidosis
  • Dermatomyositis
  • Amyloidosis

Tumors
Aortic Dissection

25
Q

What are the infectious causes of pericarditis?

A

Infections

  • Viruses (Echovirus, coxsakievirus A and B, Mumps, EBV, CMV, HIV, Parvo B19
  • Bacterial (life threatening - less common) Pneumococcus, meningococcus, gonococcus, hemophilus, chamydia, TB
  • Fungal: candida, histoplasmosis
  • Parasitic: Echinococcus, Toxoplasma
  • Rickettsia
26
Q

Which causes of pericarditis do not typically give classic ecg changes?

A

Rheumatologic
Hypothyroid
Hypothermic

27
Q

What is the treatment for pericarditis?

A
  • NSAID (ibuprofen 300-800 mg PO q6-8h, or Naproxen 500 mg BID or 750 once a day ER) x 3-4 weeks
  • Post MI: ASA 3-4 weeks
  • Cholchicine 0.6 mg BID x 3 months (decr duration by 72 hours and recurrence)
  • Dialysis if uremic
  • prednisone (ONLY In SLE, rheumatologic causes, autoimmune, uremic, failed NSAIDs etc).
  • if TnT >400 admit (myocarditis)
28
Q

Why is colchicine added to pericarditis treatment?

Is prednisone an option?

A
  • Reduces symptoms at 72 hours and reduces recurrence at 18 months (COPE trial 2005)
  • Cochrane review NNT=4 to reduce recurrence
  • Prednisone actually increases recurrence and is only indicated in rheumatologic causes or if they are NSAID intolerant.
  • incr recurrence in viral causes: thought is that steroid suppresses the immune system allowing viral proliferation
29
Q

What are 4 complications of pericarditis?

A
  1. Recurrence
  2. Pericardial effusion
  3. Cardiac Tamponade
  4. Myocarditis
30
Q

In addition to hx/pe what other things aid in the diagnosis of myocarditis?

A
  1. Endomyocardial bx
  2. Echo: assess ventricular fxn
  3. Antimoyosin scinitigraphy - binds to damaged myocytes
  4. cMRI
    Lake Louise criteria (2008) developed to diagnose myocarditis on cMRI
31
Q

What are 4 etiologies of myocaridtis?

A
  1. Viral (most common: Enterovirus - coxsakie B, Adenovirus, HCV, ParvoB19)
  2. Toxins (cocaine, anthracyclines(chemoRx))
  3. Inflammatory (Churg-strauss, IBD, Wegener’s)
  4. Hypersensitivity (sulfonamides, diuretics, cephalosporins, steroids)
  5. Post partum (rare)
  6. HIV
  7. Chagas Disease
  8. Rheumatic fever (very rare - ccu case presentation)
  • Chagas Disease (most common world wide for myocarditis)
  • is a parasite, insects are vector
32
Q

What are risk factors for spontaneous coronary artery dissection?

A
  1. Pregnancy – hormonal and hemodynamic changes are suspected of playing a role. Pregnancy is only a risk factor for AoD if pt has Marfans.
  2. Hormonal therapy – related to IVF treatments and menopause
  3. Connective tissue disorders – such as Ehlers-Danlos Type IV (Vascular Type) and Marfan Syndrome are thought to affect artery walls resulting in greater susceptibility to dissection
  4. Fibromuscular dysplasia (FMD) – a condition which causes arteries to narrow (carotids and renal a. most commonly effective)
  5. Extreme physical activity
  6. Cocaine abuse – artery spasms are thought to cause dissection
33
Q

Why does pain from pericarditis commonly refer to the trapezius?

A

The pericardium is close by the phrenic nerve.

34
Q

Whats the difference between a post MI pericarditis and Dresslers syndrome?

A
  • Post MI will occur 3-4 days after MI
  • Dresslers syndrome is autoimmune mediated and will occur 3-4 weeks afterwards. More associated with cardiac surgery (CABG) can occur with PCI (less)
35
Q

what 3 features can distinguish STEMI vs. Pericarditis?

A
  1. Look for reciprocal changes (no STD)
  2. Morphology - smiley face with pericarditis. Concave or horizontal STE in STEMI
  3. STE III>II highly specific for MI

If none of these are there, look for PR depression

36
Q

What are 4 causes of peripheral edema?

A
  1. Increased hydrostatic pressure
  2. Decreased oncotic pressure
  3. Increased vascular permeability
  4. Lymphatic obstruction
37
Q

What are 8 causes of unequal BP on the upper extremity?

A

Congential

  1. Coarctation
  2. Supra valvular aortic stenosis
  3. Patent ductus arteriosus
  4. Anomalous subclavian artery

Acquired HD

  1. Aortic dissection
  2. Arterial thrombosis/aneurysm
  3. Takayasus aortitis
  4. Subclavian steal
  5. Pseudosononthoma elastic
38
Q

What are the causes of infective endocarditis?

A 
Staph aureus
Viridans group strep
Enterococci
Coagulase negative staph
Strep bovis
Fungi
HACEK organisms ( hemophilus, actinobacillus, cardio bacterium, Eikenella, kingella)
39
Q

What are 5 risk factors for AoDissection?

A
  1. Marfans, Ehler Danlos - connective tissue d/o
  2. Family hx aortic disease
  3. Known aortic valve disease (bicuspid aortic valve)
  4. Recent Aortic sx
  5. Known thoracic aortic aneurysm
40
Q

What are 3 Major complications of aortic surgeries

A
  1. Aortoenteric fistulas
  2. Endo leak
  3. Graft infection

Emergency Medicine (39 decks)

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