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EMED Unit 1 > 4 CV and Pulmonary Emergencies > Flashcards

4 CV and Pulmonary Emergencies Flashcards

1
Q

CP DDx - things that will kill you

A 
ACS
Aortic dissection
PE
Tension pneumothorax
Pericardial tamponade
Mediastinitis
Esophageal rupture
Perforated ulcer
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2
Q

Less critical DDx for chest pain

A 
Anxiety
GERD
Esophageal spasm
PNA/pleurisy
Costochondritis
Rib fracture/contusion
Herpes zoster
Pericarditis/myocarditis
Cholecystitis 
Pancreatitis
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3
Q

Important associated symptom to ask about with CP patients

A

Sense of “impending doom”

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4
Q

Dx tests to run for CP

A 
ECG
CXR
Pulse ox
Labs: CBC, CMP, D-dimer (maybe), lipids, BNP, cardiac enzymes
Echo
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5
Q

Classic presentation for angina

A

Pressure, heaviness, tightness, fullness, or squeezing in the center or left of the chest precipiatated by exertion and relieved by rest

Can radiate to shoulder, arms, neck, or jaw

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6
Q

Angina is indicative os some type of _______ happening in the coronaries

A

Ischemic event

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7
Q

Anginal equivalents are atypical presentations common in women, elderly, or diabetic patients

A 
SOB
N/V
Diaphoresis
Fatigue
Dizziness/lightheadedness
Weakness
Palpitations
Syncope
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8
Q

Coronary Artery Disease (CAD) can be subdivided into…

A

Stable Angina (Sx transient, stable, and resolve with rest)

Acute Coronary Syndrome
• Unstable angina (inc severity/freq/duration OR occurs at rest)
• NSTEMI (non-occlusive thrombus —> ischemia with elevated cardiac enzymes)
• STEMI (occlusive thrombus, transmural infarction)

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9
Q

Increasing severity/frequency/duration of anginal symptoms or symptoms occurring at rest

A

Unstable angina

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10
Q

Myocardial infarction caused by a non-occlusive thrombus

A

NSTEMI

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11
Q

Occlusive thrombus and transmural infarction

A

STEMI

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12
Q

CAD risk factors

A 
Male
Age >55
DM
HLD
HTN
Fam Hx of CAD
Tobacco use
Obesity
Hx of MI, CVA/TIA, PAD
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13
Q

What is the main risk calculator for CAD?

A

HEART score

How suspicious is the Hx for ACS (0-2 pt)
ECG changes (0-2 pt)
Age (0-2 pt)
# of Risk factors (0-2 pt)
Initial Troponin value (0-2)

Score of 0-3 send home
Score of 4-6 admit for observation
Score of 7-10 early invasive strategies

Also, TIMI score

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14
Q

What Dx tests do you do FIRST for CAD?

A

12-lead ECG** Always always always
• resting ECG may be normal
• Look for ST-T wave changes

Cardiac enzymes
• Initial troponin, then trend
• Can’t r/o MI on a single test (esp if <4-6h since Sx onset)

Stress testing (if admitted but not STEMI - only if you’re unsure and the patient is stable)

Coronary angiography

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15
Q

_______ is a sensitive and specific determinant of myocardial injury (though it can’t distinguish the etiology of the injury)

A

hs-cTn (high-sensitivity Troponin)

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16
Q

Acutely elevated hs-cTn of _________ (or lower elevations with an associated 2-hour delta of _______) are indicative of an acute process causing myocardial injury

A

> 100ng/L

Or 2h Delta of >10ng/L

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17
Q

Chronic elevations hs-cTn, particularly those w/o a changing pattern, are indicative of…

A

A more chronic process of myocardial injury

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18
Q

Advantages of high sensitivity troponin

A

Rapid r/o or rule in for MI

ID more patients experiencing ACS

Emphasizes the Delta Troponin

Gender specific reference ranges

Reported in whole numbers

Specifies normal, INT, and abnormal ranges

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19
Q

Disadvantages of high sensitivity troponin

A

A significant % of patients with (-) values with the old assay will be elevated now

More elevated values in patients without ACS (false positives)

Changes in management patterns

New documentation needs

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20
Q

For regular troponin, we trend the value every _____

A

Q6 hours (for a total of 3 values)

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21
Q

What are the different options for stress testing?

A

Stress echo (exercise vs pharmacological)

Radionucleotide myocardial perfusion imaging - can visualize areas of hypoperfusion

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22
Q

Which type of stress test is preferred?

A

Exercise - IF they are able to exercise

If not - dobutamine

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23
Q

During a stress test, what should you monitor?

A

BP, ECG changes, echo changes

Test is stopped if pt develops CP, SOB, ST changes, or has decreased BP or ventricular arrhythmias

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24
Q

Medical management for stable angina

A

Nitrates (SL nitro PRN for CP) - can take q5 min but no more than 3 doses within 15 min

Beta blockers

+/- CCB

Anti-platelet meds (Aspirin, Plavix, or combo)

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25
Q

What is Prinzmetal Angina?

A

AKA: Variant angina or vasospastic angina

Episode of Angina 5-15 min, usually at rest and often between midnight and early morning

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26
Q

What tests do you run for Prinzmetal Angina?

A

EKG: ST elevation (only during anginal episodes)

Serial cardiac enzymes needed to r/o MI

Holter monitor

Coronary angiography (diagnostic***)

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27
Q

Treatments for Prinzmetal angina

A

Nitrates and CCB

Don’t need a stent or antiplatelets b/c no thrombus)

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28
Q

What drug do you need to ask about BEFORE giving a patient nitroglycerin

A

VIAGRA

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29
Q

Initial management of a STEMI

A 
ABCs
Cardiac monitoring (telemetry)
IV access
SL Nitro
Aspirin 325mg chewed

+/- beta blocker, unfractionated heparin

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30
Q

What was the old go-to treatment for STEMI?

A

MONA - Morphine Oxygen Nitro Aspirin

BUT, morphine inhibits antiplatelet absorption and increases mortality in STEMI patients

O2 use (when NOT assoc with hypoxia) suggested to increase early myocardial injury and increase infarct size

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31
Q

_________ is important to help improve outcomes in STEMIs

A

Door to PCI time

PCI = Percutaneous Coronary Intervention

If PCI not readily available within 120 min, consider fibrinolytics

If extensive disease, consider CABG

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32
Q

When should you consider fibrinolytics for STEMI?

A

If PCI not readily available within 120 min

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33
Q

Gold standard for diagnosing CAD

A

Coronary angiography

Catheter threaded through femoral vessels into heart to assess lumen of vessels

Dye injected and patency of vessels is seen via fluoroscopy

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34
Q

What are the two PCI interventions?

A

Angioplasty

Stunting

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35
Q

What factors need to be considered for Coronary Artery Bypass Grafts (CABG)?

A

Number of vessels that are occluded (multi-vessel disease)
Large area of potentially ischemic myocardium
Anatomic complexity of lesions
Likelihood to have successful revascularization w/ PCI
Co-morbidities

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36
Q

Contraindications to PCI in cases of NSTEMI/UA

A

Renal failure
Sepsis
Unstable patient

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37
Q

Most cases of NSTEMI/UA can be managed…

A

Medically with heparin continuous infusion and aspirin

NO thrombolytics

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38
Q

What are the contraindications to nitro

A

Hypotension
RV infarction/inferior MI
Recent use of PDE5 inhibitors

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39
Q

What are Peri-infarction emergencies

A

Episodes that occur in the post-MI period

Peri-infarction pericarditis (PIP)
Acute mitral regurgitation
Dressler’s syndrome
Hemorrhage/bleeding
Arrhythmias (esp. bradycardia)
Rupture of LV free wall or intraventricular septum
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40
Q

Peri-infarction pericarditis usually occurs ______

A

Soon after MI (first 2-3 days)

Is transient

PE: pericardial rub

Echo: pericardial inflammation +.- effusion

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41
Q

How do you treat a peri-infarction pericarditis (PIP)

A

Supportive - generally self-limited

Usually just Tylenol - AVOID NSAIDs (b/c they are usually already anticoagulated)

ASA +/- colchicine

42
Q

Other non-MI causes of acute pericarditis

A 
Infectious
Radiation
POST-CARDIAC INJURY SYNDROME
Drugs/toxins
Metabolic
Malignancy
Collagen vascular disease
Immune-related
Idiopathic
43
Q

How does Cardiac tamponade present?

A

CP, tachypnea, dyspnea

PE: sinus tachycardia, HYPOTENSION, JVD, pericardial rub, MUFFLED HEART SOUNDS, pulses paradoxes

ECG: sinus tachycardia, low voltage (electrical alternans)

CXR: enlarged cardiac silhouette

Echo: effusion with tamponade

44
Q

What is Beck’s triad

A

HYPOtension

JVD

Muffled heart sounds

(= cardiac tamponade)

45
Q

Treatment of cardiac tamponade

A

Drainage of pericardial effusion

Percutaneous (pericardiocentesis) or surgical

Subsequent monitoring:
• Continuous telemetry
• Frequent vital signs x 24-48 hours
• Repeat echo prior to discharge

46
Q

Causes of acute mitral regurgitation

A

Ischemia to papillary muscle
LV dilation or true aneurysm
Papillary muscle or chordal rupture (usually 2-7 days after infarct)

47
Q

How will acute mitral regurgitation present?

A

Hypotension and NEW MURMUR

Dx: TTE (or TEE if inconclusive TTE)

48
Q

Treatment of acute mitral regurgitation

A

Emergent surgery - can become very unstable quickly

49
Q

What is Dressler’s Syndrome

A

Post-cardiac injury syndrome (PCIS)

Develops weeks to months post-MI (unlike PIP, which is days) or cardiac surgery, trauma, or PE

Presents with pleuritic CP, fever, malaise

PE: pericardial friction rub

Labs: leukocytosis, elevated ESR

CXR: pleural and/or pericardial effusion or pulmonary infiltrates

50
Q

Treatment for Dressler syndrome

A

NSAIDs

Corticosteroids or colchicine if refractory

51
Q

Extra-CV manifestations of endocarditis?

A

Jane way lesions
Older nodes
Splinter hemorrhages
Roth spots

52
Q

Presentation of endocarditis

A

Fever, chills, cough, dyspnea, ortho Pena, fatigue

PE: palatial, conjunctival, or subungual petechiae, splinter hemorrhages, Osler nodes, janeway lesions, Roth spots, pallor, splenomegaly, HEART MURMUR

53
Q

What labs do you draw for suspected endocarditis?

A

Blood cultures x 3 before abx

Leukocytosis with elevated ESR can be seen on CBC

Echo will show VEGETATION ON VALVES (get TEE)

54
Q

Risk factors for Endocarditis

A 
Artificial heart valves
Congenital heart defects
Hx of endocarditis
Damaged heart valves
IVDU
Poor dentition/dental infection
55
Q

Treatment for endocarditis

A

Abx (usually prolonged, ~6 weeks)

Vancomycin + Rocephin until C&S returns

If condition does not resolve with abx, surgery may be necessary in up to 50% of cases

56
Q

How does heart failure present?

A

Dyspnea, fatigue, diaphoresis, early satiety, cough, orthopnea, PND, edema

PE: tachycardia, tachypnea, rales, JVD, S3/S4, LE edema, ascites

ECG: +/- arrhythmias, ischemia, heart block

57
Q

What labs do you need to do for HF?

A

CBC, CMP, TSH, Cardiac enzymes, BNP

CXR —> cardiomegaly, cephalization, Kerley B lines +/- pulmonary edema

Echo: look at EF, valves, pericardium, wall motion abnormalities

58
Q

How do you treat HF?

A

IV access, control airway (O2), telemetry

1st line med: Furosemide

Sodium and fluid restriction

Strict I&O, daily weights

+/- Inotrope

Chronic HF meds once stable - BB, ACE, Diuretics, +/- digoxin

59
Q

What med should be avoided in acute, unstable, uncompensated heart failure?

A

Beta blockers!

60
Q

Definition of hypertensive urgency?

A

SBP ≥ 180, DBP ≥120

NO end-organ damage

61
Q

What is the definition of hypertension emergency

A

SBP≥180, DBP≥120

Associated with acute end-organ damage (CV, Opto, Cardiac, Renal)

62
Q

95% of cases of elevated BP are…

A

Primary (essential) HTN

Includes new diagnosis of HTN and non-adherence of medications

63
Q

Examples of secondary causes of HTN (only5% of cases)

A 
Sleep apnea
Renal artery stenosis
Pheo
Coarctation of the aorta
Pseudotumor cerebri
Chronic steroid therapy
Cushing’s syndrome
Thyroid/parathyroid disease
Primary hyperaldosteronism
Pregnancy
64
Q

How to workup a hypertensive episode

A

BP measured in both arms

Assess for end-organ compromise
• Neuro check
• Opto check
• CV check (JVP, crackles, murmur, asymmetrical pulses
• Renal

ECG

Labs (UA, UDS, CBC, CMP, card enzymes, TSH, urine metanephrines)

Imaging: +/- CXR, head CT, CTA chest and abdomen

65
Q

Treatment for HTN urgency

A

Rest

Established HTN patients:
• Inc dose of current meds
• Add additional med
• Adherence to sodium restriction

New occurrence of HTN
• BP reduction over several hours

66
Q

How to treat hypertensive emergency

A

Should be hospitalized (usually in the ICU)

Workup secondary HTN causes

Treat end-organ damage - not absolute BP

Reduction of BP ONLY by 20-25% within 1 hour (NOT TOO QUICK)

Good first choice agent is IV labetalol (short half life) or continuous infusion like Nicardipine

Once BP stable with IV therapy, transition to oral therapy

67
Q

___ % of aortic aneurysms are thoracic and ___% are abdominal

A

10% thoracic, 90% abdominal

68
Q

Most common presenting feature of a thoracic aortic aneurysm

A

“Tearing” chest pain

Substernal, back or neck pain +/- dyspnea, stridor, cough, Sx of SVC syndrome

69
Q

Most common presentation of an abdominal aortic aneurysm

A

Pulsating abdominal mass +/- abdominal/back pain

If rupture - also assoc with hypotension/hemodynamics instability

70
Q

Thoracic aortic aneurysm risk is determined by…

A

Size of aneurysm

Often found incidentally on CXR/CT and asymptomatic

Usually managed medically

71
Q

Medical management of Thoracic aortic aneurysms

A

Aggressive BP and HR control (keep SBP <120, HR<60-80)

Beta blockers for symptoms

Serial imaging (CT, MRA at 6 months)

72
Q

Surgical management of Thoracic Aortic Aneurysms

A

Can be open vs endovascular

Considered if symptomatic, rapid expansion (growth >0.5cm in 6 months) or if size >5cm

73
Q

Abdominal aortic aneurysms are typically asymptomatic if…

A

<5.5cm - observation and U/S every 6 months to year

74
Q

Complications of a AAA

A

Rupture (high morbidity and mortality

Aneurysm thrombosis

Thromboembolism —> acute limb ischemia

75
Q

When do you do surgical management of a AAA?

A

Asymptomatic AAA ≥5cm

Rapidly expanding AAA (growth >0.5cm in 6 months)

Associated with peripheral arterial aneurysm or PAD

76
Q

Emergent condition in which the inner layer of the aorta tears, blood then surges through the tear, causing the rest of the layers to dissect

A

Aortic dissection

If the blood filled channel ruptures through the outside aortic wall, it’s often fatal

77
Q

Sx of aortic dissection

A

Thoracic - “ripping” or “tearing” chest pain radiating to the back

Abdominal: severe back, abdominal, or flank pain + hypotension and shock

Both: signs of hemodynamics compromise

78
Q

Risk factors for aortic dissection

A 
Uncontrolled HTN
Atherosclerosis
Pre-existing aortic aneurysm
Bicuspid aortic valve
Aortic coarctation
Connective tissue disease (Marfan)
Cocaine use
Pregnancy 
Male gender, advanced age
79
Q

What is a Type A aortic dissection

A

Acute ascending thoracic dissection - CARDIAC SURGICAL EMERGENCY

80
Q

What is a Type B aortic dissection

A

Descending thoracic aortic dissection - managed medically if hemodynamically stable and w/o end-organ complications

81
Q

How to distinguish between Type A and Type B aortic dissections quickly

A

CT angiography - initial screening study in hemodynamically stable patient

Multiplanar TEE if hemodynamically UNstable

82
Q

Initial management of aortic dissection

A

If unstable or airway compromise:
• Intubate
• Bedside TEE
• Emergent vascular surgery consult

Otherwise:
• Admit to ICU, consult vascular surgery
• Pain control (morphine)
• BP control (SBP 100-120, HR<60) IV beta blocker (esmolol)
• CT
83
Q

What are the Six P’s of acute limb ischemia

A 
Pain 
Pulselessness
Pallor
Paresthesias
Paralysis
Poikilothermia
84
Q

How do you assess neuro in cases of acute limb ischemia?

A

Assess sensation

Assess strength

Pulses
• Doppler for PT, DP
• Ankle-bronchial index (<0.4 indicates significant ischemia)

85
Q

What imaging should you do for acute limb ischemia?

A

CTA, MRA

Performed in patients with viable limbs (anticoagulation prior and monitor progression)

Threatened limbs require immediate surgical revascularization (intraoperative arteriography)

86
Q

Initial management of acute limb ischemia

A

Anticoagulation, close monitoring, surgery as soon as the exam worsens

Consult vascular surgery ASAP

87
Q

Acute, sudden onset of intestinal hypoperfusion

A

Acute mesenteric ischemia

Can be due to acute embolic occlusion (esp elderly patient with a fib) or severe abd pain out of proportion to PE) or Mesenteric thrombosis (may be chronic - with PAD)

88
Q

Chronic post-prandial pain, food aversion, weight loss +/- hematochezia

A

Mesenteric thrombosis

Typically with known PAD

89
Q

What imaging do you do for acute mesenteric ischemia?

A

CT Angiography is test of choice

KUB may be useful to ID related complications (but doesn’t Dx ischemia)

90
Q

Treatment for acute mesenteric ischemia

A

Systemic anticoagulation and pain management

+/- angioplasty with stent

+/- exploratory laparotomy if peritoneal signs

91
Q

Risk factors for DVT

A 
Recent surgery
Prolonged bed rest
Oral contraceptives
Hormone replacement therapy
Factor V Leiden, hypercoagulable states
Recent trip
Malignancy
92
Q

What is Virchow’s triad?

A

Risk factors for DVT

Endothelial damage
Hypercoagulability
Stasis

93
Q

Test of choice for DVT

A

Duplex ultrasound

94
Q

Treatment for DVT

A

Anticoagulation (Lovenox or Heparin bridge to warfarin, possible NOACs)

Prevention in bedridden patients

Prevention in perioperative patients and travelers

95
Q

Presentation of Pulmonary Embolism

A

Pleuritic CP, dyspnea, cough, hemoptysis, syncope

PE: tachypnea, TACHYCARDIA, HYPOXIA, +/- unilateral extremity edema

96
Q

What is the rare ECG pattern they talk about for PE?

A

S1Q3T3

But usually you’ll just see sinus tachycardia

97
Q

Buzzwords for PE CXR findings

A

Hampton’s hump

Westermark sign

98
Q

Gold standard for diagnosing PE

A

Pulmonary angiography (CTA)

Can also do V/Q scan if CTA contraindicated

LE Doppler U/S to evaluate for concurrent DVT

99
Q

What is the name of the criteria used to asses for risk of PE?

A

Well’s criteria

100
Q

How do you treat PE?

A

Supplemental O2
IV access
Cardiac monitoring
ANTICOAGULATION

Consider also: thrombolytics, IVC filter, embolectomy if very severe

EMED Unit 1 (5 decks)

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