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Emergency Medicine EOR > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

What is acute bacterial endocarditis?

A

infection of normal valves with a virulent organism (S. aureus)

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2
Q

What is subacute bacterial endocarditis?

A

indolent infection of abnormal valves with less virulent organism (S. viridans)
-Duke’s criteria, staph aureus in acute and IV drug users, and strep viridans in subacute

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3
Q

What is Duke’s criteria?

A

Major
-blood cultures: S. aureus, S. viridans, S. bovis or other typical species x 2, 12 hours apart
-drug users: staphylococcus, non - drug users: streptococcus
-echocardiogram: vegetations are seen (tricuspid-IV drug users, mitral non-drug users)
-new regurgitant murmur
Minor
-risk factor, fever 100.5, vascular phenomena (splinter hemorrhages, Janeway lesions: painless, palms and soles), immunologic phenomena (Osler node: raised painful tender; Roth spots: exudative lesions on the retina)

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4
Q

What are the classic signs of infective endocarditis?

A
  • Osler’s nodes - tender “ouchy” nodules
  • Janeway lesions - painless macules
  • Roth spots on the retina
  • Splinter hemorrhages on the nail bed
  • Clubbing
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5
Q

What is the tx for endocarditis?

A
  • empiric treatment: IV vancomycin or ampicillin/sulbactam PLUS aminoglycoside
  • prosthetic valve: Add rifampin
  • high-risk patients prophylaxis for procedures: Amoxicillin
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6
Q

What is angina?

A

chest pain or discomfort, heaviness, pressure, squeezing, tightness that is increased with exertion or emotion

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7
Q

What is stable angina?

A

predictable, relieved by rest and/or nitroglycerine

  • stress test demonstrates reversible wall motion abnormalities/ST depression > 1 mm
  • angiography provided a definitive diagnosis
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8
Q

What is the tx of stable angina?

A
  • beta-blockers and nitroglycerin

- severe:angioplasty and bypass

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9
Q

What is unstable angina?

A

previously stable and predictable symptoms of angina that are now more frequent, increasing or present at rest

  • chronic angina - increasing in frequency, duration, or intensity of pain
  • new-onset angina - severe and worsening
  • angina at rest
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10
Q

What is the tx for unstable angina?

A
  • admit to the unit with continuous cardiac monitoring, establish IV access, O2
  • pain control with NTG and morphine
  • ASA, clopidogrel, beta-blockers (first line), LMWH
  • replace electrolytes
  • if the patient responds to medical therapy - stress test to determine if catheterization/revascularization necessary
  • reduce risk factors: stop smoking, weight loss, treat DM/HTN
  • heparin
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11
Q

What is prinzmetal variant angina?

A

Coronary artery vasospasms causing transient ST-segment elevations, not associated with clot

  • look for a history of smoking (#1 risk factor) or cocaine abuse
  • EKG may show inverted U waves, ST-segment or T-wave abnormalities
  • preservation of exercise capacity
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12
Q

What is the tx of prinzmetal variant angina?

A
  • stress testing with myocardial perfusion imaging or coronary angiography
  • pharmacotherapy SL, topical, or IV nitrates (initial)
  • antiplatelet, thrombolytics, statins, BB
  • once diagnosis made - CCB and long-acting nitrates used for long-term prophylaxis (amlodipine)
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13
Q

What is the presentation of arrhythmias?

A
  • a condition in which the heart beats with an irregular or abnormal rhythm
  • they can come from the atria or from the ventricles
  • when they are seen it is imperative to figure out why they are having the arrhythmia and how to treat it
  • commonly complain of chest pain or shortness of breath
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14
Q

What is atrial arrhythmias?

A

premature atrial contractions (these are extra beats from the atria)

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15
Q

What is atrial fibrillation?

A

an irregular heart rate that at a high rate may cause palpitations, fatigue, and shortness of breath
-It occurs when the upper atrial chambers of the heartbeat out of rhythm and there are multiple atria foci

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16
Q

What is atrial flutter?

A

an atria with a single foci having multiple P waves before a QRS is produced unlike atrial fibrillation where the P waves are much more chaotic

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17
Q

What is paroxysmal supra ventricular tachycardia?

A

(PVST) regular, fast (160 to 220 beats per minute) heart rate that begins and ends suddenly and originates in atria

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18
Q

What is accessory pathway tachycardias?

A

an accessory pathway is an additional electrical conduction pathway between two parts of the heart most common is WPW

  • the impulse from the SA node takes an accessory pathway to the AV node and can result in tachycardia
  • shorten PR interval
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19
Q

What is AV nodal reentrant tachycardia?

A

most common type of supra ventricular tachycardia

  • occur because of a reentrant circuit (accessory pathway) located in or near the AV node that causes the heart to beat prematurely
  • heart rates 100-250 bpm regular rhythm late P waves - may be hidden within the QRS
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20
Q

What is premature ventricular contractions?

A

(PVCs) (these are extra beats from the ventricles) early wide “bizarre” QRS, no p wave seen

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21
Q

What is ventricular tachycardia (V-tach)?

A

a type wide QRS complex that is a regular, fast heart rate that arises from improper electrical activity in the ventricles of the heart

  • three or more consecutive VPBs, displaying a broad QRS complex tachyarrhythmia
  • the rhythm may arise from the working ventricular myocardium, the distal conduction system, or both
  • most commonly occurs in patients with structural heart disease, can be associated with an increased risk of sudden death
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22
Q

What is ventricular fibrillation (V-fib)?

A

the ventricles merely quiver and do not contract in a coordinated way

  • no blood is pumped from the heart, very lethal ventricular arrhythmia
  • erratic rhythm with no discenable waves (P, QRS, or T waves)
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23
Q

What are the pearls of arrhythmias?

A
  • narrow tachycardia arrhythmias need to be slowed up with entire calcium channel blockers or beta-blockers, adenosine, procainamide, or cardioversion depending on the scenario
  • wide tachycardic arrhythmias from the ventricles treat with cardioversion or antiarrhythmics such as amiodarone
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24
Q

What is cardiac tamponade?

A

a buildup of fluid between the pericardial sac and the heart; constricts the heart
-heart unable to pump normally = blood through through chambers obstructed = cardiac output decreases = hypotension = lower tissue perfusion = heart rate increases

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25
Q

What are the causes of cardiac tamponade?

A
  • acute onset: trauma, myocardial infarction, aortic dissection, pericardial effusion
  • slow onset: cancer, chronic inflammation, uremic pericarditis, hypothyroidism, connective tissue disease
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26
Q

What are the 3 D’s of cardiac tamponade?

A

distant heart sounds, distended jugular veins, and decreased arterial pressure = beck’s triad

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27
Q

What is beck’s triad?

A
  • hypotension
  • muffled heart sounds
  • elevated necks veins (JVD)
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28
Q

What is pulses paradoxes?

A

a classic finding (drop 10 mmHg in systolic pressure on inspiration), narrow pulse pressure

  • EKG will show electrical alternans (when consecutive, normally-conducted QRS complexes alternate in height) and low voltage QRS complex
  • Chest x-ray finding - water-bottle heart (heart-shaped like a canteen)
  • treatment: pericardiocentesis
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29
Q

What is the presentation of chest pain?

A
  • most common present with chest pain with shortness of breath, with possible radiation to the neck, jaw, arms, shoulders, and back
  • In the ER the workup of a patient with chest pain can include many different etiologies ranging from the benign to the very dangerous
  • vital signs should be addressed immediately
  • always needed an immediate EKG
  • appropriate history and physical exam
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30
Q

How is chest pain diagnosed?

A

in any acute setting, there are five causes of chest pain that must be considered when assessing a patient

  • pericarditis: chest pain that is relieved by sitting and/or leaning forward
  • ACS:chest pain with shortness of breath, with possible radiation to the neck, jaw, arms, shoulders, and back
  • Pulmonary embolism: dyspnea (most common) and pleuritic chest pain, spiral CT is the best initial test
  • Pneumothorax: ipsilateral chest pain and dyspnea with decreased tactile remits, deviated trachea, hyper resonance, diminished breath sounds
  • thoracic aneurysm/dissection: severe, tearing (ripping, knife-like) chest pain radiating to the back
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31
Q

What is the typical workup for chest pain?

A
  • EKG
  • Troponin I
  • BNP
  • CXR
  • CBC/CMP

can include depending on the situation

  • D-dimer (sensitive not specific)
  • CT chest (pneumothorax, tumor, etc.)
  • CT angiogram of the chest (r/o PE)
  • CT aortogram (thoracic aneurysm)
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32
Q

What are the pearls of chest pain?

A
  • ACS or MI (EKG, troponin)
  • pericarditis (EKG, ESR)
  • CHF (CXR and BNP)
  • pneumothorax (CXR and CT)
  • PE (D-dimer and CTA)
  • thoracic aneurysm (CT aortogram)
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33
Q

What is afib?

A

irregularly irregular rhythm with disorganized and irregular atrial activations and an absence of P waves

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34
Q

What is a-flutter?

A

regular, sawtooth pattern and narrow QRS complex

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35
Q

What is supra ventricular tachycardia?

A

narrow, complex tachycardia, no discernible P waves

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36
Q

What is ventricular tachycardia?

A

three or more consecutive VPBs, displaying a broad QRS complex tachyarrhythmia

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37
Q

What is premature beats?

A
  • PVC: early wide bizarre QRS, no p wave seen
  • PAC: abnormally shaped P wave
  • PJC: narrow QRS complex, no p wave or inverted p wave
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38
Q

What is a bundle branch block?

A
  • left: R and R’ (upward bunny ears) in V4-V6

- right: R and R’ (upward bunny ears) in V1-V3

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39
Q

What is non-ST segment elevation?

A

(NSTEMI, subendocardial MI) is myocardial necrosis (evidence by cardiac markers in the blood; troponin I or troponin T and CK will be elevated) WITHOUT acute ST-segment elevation or Q waves

  • ECG changes such as ST-segment depression, T-wave inversion, or both may be present
  • coronary artery not completely blocked
  • subendocardial infarct
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40
Q

What cardiac markers will be elevated with NSTEMI?

A
  • troponin is most sensitive and specific appears at 2-4 hours, peaks around 12-24 hours and lasts for 7-10 days
  • CK/CK-MB appears at 4-6 hours, peaks at 12-24 hours and returns to normal within 48-72 hours
  • myoglobin (Mb) is used less than the other markers and appears at 1-4 hours, the peak is 12 hours, and returns to baseline levels within 24 hours
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41
Q

What is the tx of a NSTEMI?

A

beta blockers + NTG + aspirin and clopidogrel + heparin + ACEI + statins + reperfusion

  • reperfusion via percutaneous coronary intervention (not thrombolysis)
  • less time-sensitive than in STEMI
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42
Q

What is a ST-segment elevation myocardial infarction?

A 
myocardial necrosis (evidence by cardiac markers in the blood; troponin I or troponin T and CK will be elevated) WITH acute ST-segment elevation or Q waves
-coronary artery completely blocked; full thickness of myocardial wall involved
43
Q

What are the EKG findings of anterior wall infarction?

A

Q waves and ST elevation in leads I, AVL, and V2 to V6

44
Q

What are the EKG findings of inferior wall infarction?

A

Q waves and St elevation in leads II, III, and AVF

45
Q

What are the EKG findings of lateral wall infarction?

A

ST elevation in the lateral leads (I, aVL, V5-6), reciprocal ST depression in the inferior leads (III and aVF)

46
Q

What are the EKG findings of posterior wall infarction?

A

ST depressions in V1 to V3

47
Q

What is the tx for a STEMI?

A

beta blockers + NTG + aspirin and clopidrogrel + heparin + ACEI + statins + reperfusion

  • aspirin and clopidogrel are given at once
  • very time sensitive - immediate (within 90 minutes) coronary angiography and primary PCI
  • thrombolytic therapy within the first 3 hours if PCI not available
48
Q

What are the absolute contraindications for fibrinolytic use in STEMI?

A
  • prior intracranial hemorrhage (ICH)
  • known structural cerebral vascular lesion
  • known malignant intracranial neoplasm
  • Ischemic stroke within 3 months
  • suspected aortic dissection
  • active bleeding or bleeding diathesis (excluding menses)
49
Q

What is stable angina?

A

predictable, relieved by rest and/or nitroglycerine

50
Q

What is unstable angina?

A

previously stable and predictable symptoms of angina that are more frequent, increasing or present at rest

51
Q

What is prinzmetal variant angina?

A

coronary artery vasoapasms causing transient ST-segment elevations, not associated with clot

52
Q

What is the presentation of dyspnea on exertion?

A

dyspnea on exertion in the ER should make you think of two areas = the cardiac and pulmonary systems

53
Q

What are the cardiac system causes of dyspnea on exertion?

A
  • coronary heart disease
  • heart failure
  • myocarditis
  • pericarditis
  • MI
  • ACS
54
Q

What are the pulmonary system causes of dyspnea on exertion?

A
  • asthma
  • COPD
  • pneumonia
  • pulmonary hypertension
  • obesity, kyphosis, scoliosis (restrictive lung disease)
  • Interstitial lung disease
  • drugs (methotrexate, amiodarone) or radiation therapy, cancer
  • psychogenic causes
55
Q

What are the pearls of cardiac caused dyspnea on exertion?

A

in other words, the heart is not pumping blood out to the lungs during exertion causing shortness of breath

56
Q

What are the pearls of pulmonary caused dyspnea on exertion?

A

in other words the lungs are not functioning properly and dyspnea on exertion is because the lungs can’t enchange oxygen

57
Q

What are the pearls of hematology caused dyspnea on exertion?

A

anemia is also another cause of shortness of breath usually a chronic problem and can be easily worked up with routine blood work (CBC)

58
Q

What is the presentation of edema?

A

a swelling, usually of the legs, feet and/or hands due to accumulation of excessive fluid in the tissues outside of the vascular vessels
-diseases of the heart, liver, and kidneys = mainly caused by salt retention, which holds the excess fluid in the body

59
Q

How is edema dx?

A
  • physical exam will show edema specifically starting in the lower extremities due to the gravity
  • as it gets worse can see pitting edema
60
Q

What conditions can edema be seen in?

A
  • CHF
  • kidney disease
  • liver disease
  • chronic venous disease
  • pregnancy
  • drugs
  • travel
61
Q

What is the tx of edema?

A
  • reduce salt intake
  • lasix HCTZ
  • compression stockings
  • body position (elevate legs)
62
Q

What are the pearls of edema?

A
  • in other words, when patients in the ER have edema either the heart is failing as a pump (CHF) or the fluid is backing up such as with kidneys or liver disease
  • always remember medications such as calcium channel blockers and Alpha-1 blockers vasodilator the vessels making the fluid come out and will go down to the feet due to gravity
63
Q

What are the most common causes of heart failure?

A

CAD, HTN, MI, DM - LV remodeling: dilation, thinning, mitral valve, incompetence, RV remodeling

64
Q

What are the characteristics of heart failure?

A
  • exertional dyspnea (SOB), then with rest
  • chronic nonproductive cough, worse in a recumbent position
  • fatigue
  • orothopnea (late), night cough, relieved by sitting up or sleeping with additional pillows
  • paroxysmal nocturnal dyspnea
  • nocturia
65
Q

What are the signs of heart failure?

A
  • Cheyne-Stokes breathing: periodic, cyclic respiration
  • Edema: ankles, pretibial (cardinal)
  • rales (crackles)
  • S4 = diastolic HF (ejection fraction is usually normal
  • S3 = systolic HF (reduced EF) with volume overload - tachycardia, tachypnea (rapid ventricular filling during early diastole is the mechanism responsible for the S3)
  • jugular venous pressure: > 8 cm
  • cold extremities, cyanosis
  • hepatomegly ascites, jaundice, peripheral edema
66
Q

What are the labs for heart failure?

A
  • CBC, CMP, U/A +/- glucose, lipids, TSH (occult hyperthyroidism or hypothyroidism
  • serum BNP: increase with age and renal impairment, low in obese, elevated in HF, differentiates SOB in HF from non cardiac issues
  • 12-lead EKG
  • CXR: Kerley B lines
  • echocardiogram (Best test): diagnose, evaluate, manage, most useful, differentiate HF +/- preserved LV diastolic function
67
Q

What is the New York Heart failure classification?

A
  • Class I (<5%) without any limitation of physical activity
  • Class II (10-15%) patients with slight limitation of physical activity, they are comfortable at rest
  • Class III (20-25%) patients with marked limitation of physical activity they are comfortable at rest
  • Class IV (35-40%) patients who are not only unable to carry on any physical activity without discomfort but who also have symptoms of heart failure or the anginas syndrome even at rest
68
Q

What is the treatment of heart failure?

A

Systolic left heart failure: ACE inhibitor + beta-blocker + loop diuretic

Diastolic heart failure: ACE inhibitor + beta-blocker or CCB (do not use diuretics in stable chronic diastolic failure)

  • Lasix - for diuresis
  • morphine - reduces preload
  • nitrates (NTG) - reduce preload O2
  • ACE inhibitor + diuretic (unless contraindicated)
  • CCB in diastolic HF
  • poor prognosis factors: chronic kidney disease, diabetes, lower LVEF, severe symptoms, old age
  • 5-y mortality: 50%
69
Q

What is hypertensive emergency?

A

BP usually >180/12- WITH impending or progressing end-organ damage

70
Q

What is hypertensive urgency?

A

BP usually> 180/120 WITHOUT signs of end-organ damage

71
Q

What is malignant hypertension?

A

diastolic reading > 140 associated with papilledema and either encephalopathy or nephropathy

72
Q

What is the tx for hypertensive emergencies?

A
  • hpertensive emergency = sodium nitroprusside (drug of choice
  • hypertensive urgency = clonidine (drug of choice)
  • malignant hypertension = hydralazine
73
Q

What is cariogenic shock?

A

common causes: acute MI, heart failure, cardiac tamponade

  • physical exam: hypotension (SBP <90 mmHg), cyanosis, cool extremities, altered mental status, crackles
  • Increase capillary wedge pressure > 15 mm
  • treatment: fluid resuscitation, pressers, (dopamine), and treat the underlying cause
74
Q

What is orthostatic hypotension?

A

drop of > 20 mmHg systolic, 10 mmHg diastolic, 15 BPM increase in pulse 2-5 minutes after a change from supine to standing

  • autonomic dysfunction in DM common cause, medications, tilt table testing if autonomic dysfunction is suspected
  • If associated with heart rate > 15 BPM likely related to low blood volume
75
Q

What is the presentation of orthopnea?

A
  • when patients come to the emergency room and complain of orthopnea there’s usually some type of pulmonary edema
  • there are cardiac and pulmonary causes
76
Q

What are the cardiac causes of orthopnea?

A
  • CHF
  • MI
  • arrhythmias (atrial fibrillation)
77
Q

What are the pulmonary causes of orthopnea?

A
  • COPD and cor pulmonale
  • Pulmonary hypertension
  • Indirect causes such as kidney failure and liver failure (will cause fluid back up into the lungs)
78
Q

How does obesity cause orthopnea?

A

when they lie down the belly fat goes up into the lungs making the space smaller and they complain of SOB
-when they lie supine or stand that fat is away from the lungs due to gravity and the SOB stops

79
Q

How is orthopnea dx?

A
  • CXR
  • BNP (CHF)
  • EKG
  • Troponin I
  • ABG (large A-s O2 gradient)
80
Q

What are the pearls of orthopnea?

A
  • when patients complain of orthopnea fluid is in the pulmonary space either by the heart not pumping or failing as a pump (CHF) or the heart is injured (MI)
  • pulmonary causes mean the lungs are failing to move the blood so the fluid leaks out
  • causes like pulmonary hypertension and COPD (secondary cause of pulmonary hypertension)
  • obesity is due to belly fat in the chest especially when lying down and goes away when gravity pulls the fat down such as standing
81
Q

What are the differential diagnosis of palpitations?

A
  • anxiety
  • electrolyte abnormalities (hypokalemia, hypomagnesemia)
  • hyperthyroidism
  • Ischemic heart disease
  • Ingestion of stimulant drugs (cocaine, amphetamines, caffeine
  • medications (digoxin, beta-blockers, calcium channel antagonists, hydralazine, diuretics, minoxidil)
  • pheochromocytoma
  • hypoglycemia in type 1 DM
  • mitral valve prolapse
  • atrial fibrillation
  • Wolff-Parkinson White (WPW) syndrome
  • sick sinus syndrome
  • paoxysmal supra ventricular tachycardia
82
Q

What is pericardial effusion?

A

same symptoms as acute pericarditis except patient will now have signs of fluid buildup around the heart which include low voltage QRS complexes, electrical alternates, distant heart sounds and an echocardiogram showing a collection of pericardial fluid

83
Q

What are the characteristics of pericardial effusion?

A
  • EKG showing low voltage QRS along with electrical alternates
  • echocardiogram with increased pericardial fluid
  • radiograph: water bottle heart
  • treatment: underlying cause, pericardiocentesis if the effusion is large
  • electrical alternans as seen by changing QRS amplitudes best seen in lead II
84
Q

What is peripheral vascular disease?

A

intermittent claudication, ankle-brachial index (ABI) <0.9

  • lower extremity loss of hair, brittle nails, allow, cyanosis, claudication, hypothermia
  • ulcers are pale to black, well-circumscribed and painful, located laterally and distally
85
Q

How is peripheral vascular disease dx?

A

arteriography is the gold standard for diagnosis

86
Q

What is the tx for peripheral vascular disease?

A
  • definitive treatment: arterial bypass

- medical treatment: antiplatelets, anti lipids, manage risk factors, cilostazol aspirin, and plavix

87
Q

What is syncope?

A

refers to a transient los of consciousnes/postural tone secondary to an acute decrease in cerebral blood flow

88
Q

What are the characteristics of syncope?

A
  • characterized by a rapid recovery of consciousness without resuscitation
  • MC causes: vasovagal, idiopathic
  • red flags: syncope during exertion, multiple recurrence in short time, heart murmur/strucutral heart disease, old age, significant injury during syncope, family hx of unexpected death/exertional/unexplained recurrent syncope
  • usually from insufficient cerebral blood flow/from benign causes
  • less common = cardiac arrhythmia
89
Q

What is vasovagal syncope?

A

(neurocardiogenic) most common cause

90
Q

What is cardiac syncope?

A

arrhythmias (e.g AV block, sick sinus syndrome), obstruction of blood flow (aortic stenosis, hypertrophic cardiomyopathy), massive MI

91
Q

What is orthostatic hypotension?

A

defect in vasomotor reflexes, common in elderly, diabetics, patients taking certain medications (diuretics, vasodilators)

92
Q

What is cerebral vascular disease?

A

a rare cause of syncope

93
Q

What are other noncardiogenic causes of syncope?

A

include metabolic causes (hypoglycemia, hyperventilation), hypovolemia (hemorrhage), hypersensitivity (syncope precipitated by wearing a tight collar or turning the head) mechanical reduction of venous return (valsalva maneuver, postmicturation) and various medications (beta-blockers, nitrates, antiarrhythmic agents)

94
Q

How is syncope dx?

A

ECG, glucose, pulse ox, echo, tilt table, CNS imaging = rare

95
Q

What is the tx of syncope?

A

fix the underlying cause

96
Q

What is aortic stenosis?

A

harsh systolic ejection crescendo-decrescendo murmur at the right upper sternal border (aortic area) with radiation to the neck and apex heard best by leaning forward with expiration

  • maneuver: sitting
  • chestpiece position: aortic (RUSB)
  • chestpiece: diaphragm
97
Q

What is aortic regurgitation (diastolic murmur)?

A

soft, early diastolic blowing murmur along the left sternal border with the patient sitting leaning forward after exhaling

  • maneuver: sitting leaning forward
  • chestpiece position: Erbs-point
  • chestpiece: diaphragm
98
Q

What is mitral stenosis?

A

diastolic low pitched decrescendo rumbling murmur with opening snap heard best at the apex (mitral area) with the patient in the lateral decubitus position

  • maneuver: supine left side down
  • chestpiece position: mitral
  • chestpiece: bell
99
Q

What is mitral regurgitation?

A

holosystolic high-pitched blowing murmur at the apex (mitral area) that radiates to axilla with a split S2

  • maneuver: supine
  • chestpiece position: mitral (apex)
  • chestpiece: diaphragm
100
Q

What is abdominal aortic aneurysm?

A

flank pain, hypotension, pulsatile abdominal mass

  • surgical repair if >5.5 cm or expands >0.6 cm per year
  • monitor annually if >3 cm, monitor every 6 months if >4 cm
  • beta-blockers
101
Q

What is an aortic dissection?

A

sudden onset tearing chest pain, between scapulas, diminished pulses

  • chest radiography: widened mediastinum
  • ascending aorta - surgical emergency
  • descending aorta - medical therapy (beta-blockers) unless complications are present
102
Q

What is arterial embolism/thrombosis?

A
  • caused by a sudden arterial occlusion
  • remember the P’s of arterial emboli: pain, pallor, pulselessness, paresthesia, paralysis, poikilothermia
  • atrial fibrillation and mitral stenosis are common causes of thrombus formation
  • angiography is considered the gold standard for diagnosis
  • acute arterial occlusion: treat with IV heparin, if no limb-threatening then call the vascular surgeon for angioplasty, graft or endarterectomy
103
Q

What is phlebitis/thrombophlebitis?

A
  • etiology: spontaneous or after trauma, or IV/PICC lines
  • presentation: dull pain, erythema, induration of vein, palpable cord
  • venous duplex ultrasound gold standard for diagnosis
  • treatment: symptomatic: NSAIDs, warm compress

Emergency Medicine EOR (12 decks)

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