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Internal Medicine > Cardiology > Flashcards

Cardiology Flashcards

1
Q

3 things that describe typical chest pain:

A
  1. ) Substernal location
  2. ) Worse with exertion
  3. ) Better with rest or nitroglycerin
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2
Q

What causes stable angina?

A

A fixed atherosclerotic lesion that narrows the coronary arteries and an imbalance between oxygen demand and available blood supply.

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3
Q

Does ischemic pain change with body position or breathing?

A

NO

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4
Q

How would you describe the clinical features of stable angina?

A
  1. Substernal chest pain that is gradual in onset and lasts less than 10-15 minutes. Usually described as heaviness, pressure, squeezing, tightness.
  2. Brought on by exertion
  3. relieved with rest or nitro
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5
Q

How do you workup CAD?

A
  1. ) Resting EKG

2. ) Stress Test: either EKG or Echo

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6
Q

What does an EKG in stable angina look like?

A

Usually it is normal

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7
Q

What do you see as ischemia on an EKG stress test?

A

ST segment depression

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8
Q

If a patient has a positive stress test, what is the next best step?

A

They should undergo cardiac catheterization.

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9
Q

What medications can you use to induce a pharmacologic stress test in patients who are unable to exercise?

A

-IV adenosine, dobutamine or dipyramidole

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10
Q

What is the definitive test for CAD?

A

Coronary angiography

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11
Q

What is the medical therapy offered to treat CAD?

A
  • Beta blockers
  • Aspirin
  • Nitrates
  • CCBs
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12
Q

Which specific form of medical therapy has been shown to decrease morbidity by reducing the risk of an MI in patients with CAD?

A

ASPIRIN

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13
Q

MOA of beta-blockers

A

Blocks sympathetic stimulation of the heart thereby reducing HR, BP, and contractility thus cardiac workload.

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14
Q

MOA of nitrates

A

Generalized vasodilation. Reduces preload myocardial oxygen demand.

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15
Q

Side effects of nitrates:

A
  • Headache
  • Orthostatic hypotension
  • Tolerance
  • Syncope
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16
Q

MOA of CCBs

A

Cause coronary vasodilation and afterload reduction, in addition to reducing contractility

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17
Q

Does revascularization reduce the incidence of MI?

A

NO

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18
Q

What are the main indications for CABG

A
  • Three vessel disease with >70% stenosis in each vessel
  • Left main coronary disease with >50% stenosis
  • LV dysfunction
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19
Q

Describe the pathophysiology of Unstable Angina Pectoris

A

Oxygen demand is unchanged but supply is decreased secondary to reduced resting coronary flow.

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20
Q

How do you distinguish between unstable angina and NSTEMi?

A

biomarkers. NSTEMi will have elevations of troponins or CK-MB but unstable angina will not

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21
Q

Medical Management of Unstable Angina/NSTEMI

A
  • ASA
  • Clopidogren
  • Beta-blockers
  • LMWH (Enoxaparin based on Essence Trial)
  • Nitrates
  • O2
  • GPIIb/IIIa inhibitors
  • morphine
  • Electrolyte replacement
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22
Q

Pathophysiology of Variant (Prinzmetal) Angina

A

-Transient coronary vasospasm that is usually accompanied by a fixed atherosclerotic lesion but can also occur in normal coronary arteries.

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23
Q

What is the hallmark finding of Prinzmetal Angina on an EKG?

A

-Transient ST segment elevation (transmural ischemia)

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24
Q

Tx of Prinzmetal Angina?

A

-CCBs and Nitrates (vasodilators)

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25
Q

Definitive testing for diagnosis of Prinzmetal Angina?

A

-Coronary angiography: displays coronary vasospasm when the patient is given IV ergonovine or Ach to provoke vasoconstriction

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26
Q

Explain the pathophysiology of an MI

A

Acute atheromatous plaque rupture into a vessel lumen with thrombus formation on top of the lesion which subsequently causes occlusion of the vessel compromising cardiac blood supply leading to necrosis of the myocardium.

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27
Q

Which populations are more likely to have painless MIs or MIs that do not present with classical symptoms?

A
  • Women
  • diabetics
  • elderly
  • post-op patients
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28
Q

What is sudden cardiac death usually the result of?

A

VFib

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29
Q

What clinical features are seen in a right ventricular infarct, what should you NOT do.

A
  • Inferior EKG changes
  • Hypotension
  • JVD
  • clear lungs
  • Hepatomegaly
  • DO NOT GIVE NITRATES OR DIURETICS this will cause CV collapse as they are now preload dependent.
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30
Q

What are the various EKG markers of infarction?

A
  • Peaked T waves: occur early and may be missed
  • ST elevation: indicates transmural injury
  • Q Waves: evidence of necrosis (old MI)
  • T-wave inversion
  • ST segment depression: subendocardial injury
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31
Q

What is the difference between STEMI and NSTEMI in terms of infarction territory?

A 
STEMI = transmural 
NSTEMI = subendocardial (inner 1/3 of wall)
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32
Q

When does Troponin I and T:

  • Begin to increase
  • Peak
  • Return to normal
A
  • Begins to increase within 3-5 hours
  • Peaks at 24-48 hours
  • Returns to normal in 5-14 days
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33
Q

When does CK-MB:

  • Begin to increase
  • Peak
  • Return to normal
A
  • Begins to increase in 4-8 hours
  • Peaks in 24 hours
  • Returns to normal in 48-72 hours which makes it useful for detecting recurrent infarction
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34
Q

What is the medical therapy for management of an MI?

A
  • Aspirin
  • Beta-blockers
  • ACE inhibitors
  • Statins
  • O2
  • Morphine
  • Nitrates
  • Heparin
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35
Q

What medications have been shown to reduce mortality and should be part of long term maintenance therapy for MI?

A
  • Aspirin
  • Beta blockers
  • ACE inhibitors
  • Statins (reduce the risk of further coronary events but not mortality)
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36
Q

What is the door to balloon time for MI?

A

90 minutes

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37
Q

After receiving a stent what medications should a patient definitely go home on?

A
  • ASA + Clopidogrel for 30 days in pts w/ bare metal stent

- ASA + Clopidogrel for 12 months in pts w/ drug eluting stent

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38
Q

What is the most common cause of in-hospital mortality post-MI?

A

Pump Failure/CHF: may lead to cardiogenic shock.

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39
Q

What is the most common cause of death in the first few days following an MI?

A

Ventricular arrhythmia (VFib or VTach)

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40
Q

Mechanical complications of MI

A
  • Free wall rupture
  • Rupture of IV septum
  • Papillary muscle rupture
  • Ventricular pseudoaneurysm
  • Ventricular aneurysm
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41
Q

When does ventricular free wall rupture present, how does it present and what do you do?

A
  • Usually within the first 2 weeks after MI.
  • leads to hemopericardium and cardiac tamponade
  • Immediate pericardiocentesis, hemodynamic stabilization
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42
Q

How does papillary muscle rupture present, and what do you do about it?

A
  • Presents as acute Mitral Regurgitation

- Emergent surgery w/ afterload reduction with sodium nitroprusside or intra aortic balloon pump

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43
Q

How do you treat acute pericarditis following an MI

A

-ASA. NSAIDs and corticosteroids are contraindicated as they may hinder myocardial scar formation.

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44
Q

What is Dressler Syndrome?

A

“Postmyocardial infarction syndrome”

-Immunologically based syndrome consisting of fever, malaise, pericarditis, leukocytosis, and pleuritis occurring weeks to months after an MI

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45
Q

How do you treat Dressler Syndrome?

A
  • ASA

- Ibuprofen is a second option

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46
Q

Signs of Digoxin Toxicity

A

GI: N/V anorexia
CV: ectopic beats, AV block, AFib
CNS: visual disturbance, disorientation, yellow vision

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47
Q

Medications that have been shown to lower mortality in systolic heart failure

A
  • ACE inhibitors and ARBs
  • Beta-blockers
  • Aldosterone antagonists (spironolactone)
  • Hydralazine + nitrate
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48
Q

Causes of systolic heart failure

A 
Ischemic heart disease 
HTN 
Valvular heart disease 
Myocarditis 
Alcohol abuse
Radiation, hemochromatosis 
Thyroid Disease
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49
Q

Causes of high output heart failure

A
  • Chronic anemia
  • Pregnancy
  • Hyperthyroidism
  • AV Fistulas
  • Wet Beriberi
  • Paget disease of bone
  • MR
  • Aortic Insufficiency
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50
Q

Causes of diastolic heart failure

A
  • HTN leading to myocardial hypertrophy
  • Valvular disease like AS, MS, and AR
  • Restrictive cardiomyopathy (amyloidosis, sarcoidosis, hemochromatosis
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51
Q

Symptoms of left sided heart failure

A
  • Dyspnea
  • Orthopnea
  • Paroxysmal nocturnal dyspnea
  • Nocturnal cough
  • Confusion and memory impairment 2/2 decreased brain perfusion
  • Diaphoresis and cool extremities at rest
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52
Q

Signs of left sided heart failure (cont)

A
  • Displaced PMI
  • S3 ventricular gallop
  • S4 gallop
  • Crackles/rales at lung base
  • Dullness to percussion and decreased tactile fremitus of lower lung fields caused by pleural effusion
  • Increased intensity of pulmonic component of S2 indicating pulmonary HTN
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53
Q

Symptoms of right sided heart failure

A
  • Peripheral pitting edema
  • NOcturia
  • JVD
  • Hepatomegaly
  • Ascites
  • Right ventricular heave
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54
Q

NYHA Class I

A

Symptoms only occur with vigorous activity

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55
Q

NYHA Class II

A

Symptoms occur with prolonged or moderate exertion

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56
Q

NYHA Class III

A

Symptoms occur with usual activities of daily living

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57
Q

NYHA Class IV

A

Symptoms occur at rest.

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58
Q

What tests do you order for a new patient with CHF?

A
  • CXR (r/o COPD, check for cardiomegaly or pulmonary edema)
  • EKG
  • Echo (r/o pericardial effusion, estimate EF)
  • CBC
  • Cardiac Enzymes (r/o MI)
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59
Q

What level of BNP correlates with the presence of decompensated CHF

A

> 150

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60
Q

What levels of NT-pro BNP virtually exclude the diagnosis of HF?

A

<300

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61
Q

Which beta blockers have benefit in HF?

A

Carvedilol, metoprolol, and bisoprolol

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62
Q

What are 3 medications that are contraindicated in patients with CHF?

A
  • Metformin (lactic acidosis)
  • Thiazolidinediones (fluid retention)
  • NSAIDs (may increase risk of CHF exacerbation)
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63
Q

What medications have proven mortality benefit in diastolic dysfunction?

A

NONE

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64
Q

What are premature atrial complexes

A

Early beat arising in the atria, firing on its own

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65
Q

What are some causes of premature atrial complexes?

A

Adrenergic excess, drugs, alcohol, tobacco, electrolyte imbalance, ischemia, and infection

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66
Q

What do premature atrial complexes look like on an EKG?

A

-Early P waves that differ in morphology from normal sinus P waves because they originate in the atria and not the sinus node. QRS complexes are normal because conduction below the atria is normal.

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67
Q

Tx for symptomatic premature atrial contractions?

A

Beta blockers

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68
Q

What is a premature ventricular complex?

A

An early beat that fires on its own from a focus in the ventricle which then spreads to the other ventricle.

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69
Q

Causes of premature ventricular complexes

A

Hypoxia, electrolyte abnormalities, stimulants, caffeine, medications, structural heart disease

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70
Q

What do premature ventricular complexes look like on an EKG?

A
  • Wide QRS: since conduction is not through the normal conduction pathway but rather through the ventricular muscle, it is slower than normal and causes a widened QRS.
  • Wide, bizarre QRS complexes followed by a compensatory pause are seen; a P wave is not usually seen because it is buried within the wide QRS complex.
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71
Q

Define sick sinus syndrome and the associated symptoms.

A

Sinus node dysfunction characterized by a persistent spontaneous sinus bradycardia. Sx include dizziness, confusion, syncope, fatigue, and CHF. May require a pacemaker.

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72
Q

What is a first degree AV block?

A

PR interval is persistently prolonged to >0.20 seconds but a QRS wave follows each P wave

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73
Q

Does first degree AV block require treatment?

A

Usually not.

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74
Q

What is a mobitz type I (Wenckebach) block?

A

It is characterized by progressive prolongation of the PR interval until a . P wave fails to conduct.

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75
Q

Does Mobitz type I usually require treatment?

A

Usually not

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76
Q

What is Mobitz type II block?

A

It is characterized by the sudden failure of a P wave to conduct without a preceding PR interval prolongation. With the failure of the P wave to conduct there is subsequently no QRS that follows.

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77
Q

Where is the site of the block in Type I AV block and Mobitz Type I block?

A

Usually within the AV node.

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78
Q

Where is the site of the block in a Mobitz type II block?

A

Usually within the His-Purkinje system.

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79
Q

Does Mobitz type II require treatment?

A

Yes, implantation with a pacemaker is usually necessary.

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80
Q

What is a third degree AV block?

A

It is the absence of conduction of atrial impulses to the ventricles. There is no relationship between the P waves and the QRS complexes. Characterized by AV dissociation.

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81
Q

Does third degree heart block require treatment?

A

Yes, pacemaker implantation is necessary.

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82
Q

What maintains the ventricular rate in a third degree AV block?

A

There is usually a ventricular pacemaker/escape rhythm that maintains a ventricular rate of 25-40 bpm.

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83
Q

What is the most common type of cardiomyopathy?

A

Dilated cardiomyopathy

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84
Q

List some causes of dilated cardiomyopathy

A
  • Idiopathic
  • CAD
  • Toxic: alcohol, doxorubicin, adriamycin
  • Metabolic: thiamine or selenium deficiency, hypophosphatemia, uremia
  • Infectious: Viral, Chagas, Lyme, HIV
  • Thyroid dz
  • Peripartum cardiomyopathy
  • Collagen Vascular Disease: SLE, Scleroderma
  • Prolonged uncontrolled tachycardia
  • Catecholamine induced: pheochromocytoma, cocaine
  • Familial/genetic
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85
Q

Signs and sx of dilated cardiomyopathy:

A
  • Symptoms of left and right sided CHF
  • S3 and S4
  • Murmurs of mitral or tricuspid insufficiency
  • Cardiomegaly
  • Existing arrhythmia
  • Sudden death
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86
Q

What is AFib

A

Multiple foci in the atria fire continuously in a chaotic pattern causing a totally irregular rapid ventricular rate. Instead of intermittently contracting, the atria quiver continuously. Atrial rate is usually over 400 bpm, but most impulses are blocked at the AV node so ventricular rate ranged between 75 and 175.

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87
Q

Clinical features of AFib

A
  • Fatigue and exertional dyspnea
  • Palpitations, dizziness, angina, or syncope
  • Irregularly irregular pulse
  • Blood stasis secondary to ineffective contraction, leads to formation of intramural thrombi which can embolize to the brain.
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88
Q

What are the 3 main goals in the treatment of AFib/AFlutter?

A
  1. ) Control ventricular rate
  2. ) Restore normal sinus rhythm
  3. ) Assess the need for anticoagulation
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89
Q

Tx of acute AFib in a hemodynamically unstable patient?

A

Immediate electrical cardioversion

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90
Q

Tx of acute AFib in a hemodynamically stable patient

A
  1. ) Rate control: BBs or CCBs
    * *If CHF or LV dysfunction consider digoxin or amiodarone for rate control
  2. ) Cardioversion to sinus rhythm after rate control is achieved
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91
Q

What medications can you use for pharmacologic cardioversion in AFib?

A
  • Parenteral ibutilide
  • Procainamide
  • Flecainide
  • Sotalol
  • Amiodarone
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92
Q

Anticoagulation Guidelines for AFib (long!)

A
  1. ) If AFib is present for >48 hours or unknown period of time, the risk of embolization during cardioversion is 3-5%. Anticoagulate patients for 3 weeks before and 4 weeks after cardioversion. INR of 2-3 is the goal range.
  2. ) To avoid waiting 3 weeks for anticoagulation before cardioversion, obtain a TEE to image the left atrium. If there is no thrombus, start IV heparin and perform cardioversion within 24 hours. Patients still require 4 weeks of anticoagulation after cardioversion.
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93
Q

How do you treat CHRONIC AFib?

A

Rate control with a BB or CCB

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94
Q

Which patients with AFib do not require anticoagulation?

A

If a patient has “lone AFib” that is AFib with the absence of underlying heart disease or other CV risk factors and is under the age of 60, they do not require anticoagulation.

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95
Q

What happens if you give a shock during T wave

A

You cause VFib!

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96
Q

Difference between cardioversion and defibrillation

A
  • Cardioversion is when you give a shock in synchrony with the QRS. The purpose is to terminate certain dysrhythmias like PSVT or VT
  • Defibrillation is delivery of a shock that is not in synchrony with the QRS. The purpose is to convert a dysrhythmia to normal sinus rhythm.
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97
Q

Indications for cardioversion

A
  • AFib
  • AFlutter
  • VT w/o a pulse
  • SVT
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98
Q

Indications for defibrillation

A
  • VFib

- VT w/o a pulse

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99
Q

Pathophysiology of AFlutter

A

One irritable automaticity focus in the atria fires at about 250-350 bpm giving rise to regular atrial contractions. The atrial rate is around 300 bpm. The long refractory period in the AV node allows only one out of every two or three flutter waves to conduct to the ventricles.

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100
Q

Causes of AFlutter

A
  • Heart failure (most common)
  • CAD
  • Rheumatic heart disease
  • COPD
  • ASD
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101
Q

In what type of patients do you normally see multifocal atrial tachycardia?

A

-Patients with severe pulmonary disease (COPD)

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102
Q

What are the EKG findings in MAT?

A

Variable P wave morphology and variable PR and RR intervals. At least THREE different P wave morphologies are required to make an accurate diagnosis.

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103
Q

Treatment of MAT

A
  • Treat the underlying pulmonary disease
  • If no LV dysfunction: CCBs, BBs, digoxin, amiodarone, IV flecainide, IV propafenone
  • If LV dysfunction: digoxin, diltiazem, or amiodarone
  • Electrocardioversion should not be used.
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104
Q

Pathophysiology of Paroxysmal SVT AVNRT

A

There are two pathways, one is fast and the other is slow within the AV node so the reentrant circuit is within the AV node.

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105
Q

What is the most common cause of SVT?

A

AVNRT

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106
Q

What do you see on an EKG in AVNRT?

A

Narrow QRS waves with no discernible P waves. The P waves are buried within the QRS complexes. This is because the circuit is short and conduciton is rapid, so impulses exit to activate the atria and ventricles simultaneously.

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107
Q

What are the two types of SVT?

A

AVNRT and Orthodromic AVRT

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108
Q

What is Orthodromic AV Reentrant Tachycardia?

A

An accessory pathway between the atria and ventricles that conducts retrogradely. It is called a concealed bypass tract. With orthodromic AVRT the accessory pathway is at some distance from the AV node, therefore the reentrant circuit is longer and there is a difference in the timing of the activation of the atria and ventricles.

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109
Q

What do you see on an EKG with orthodromic AV reentrant tachycardia?

A

Narrow QRS complexes with P waves which may or may not be discernible depending on the rate. This is because the accessory pathway is at some distance from the AV node, therefore the reentrant circuit is longer, and there is a difference in the timing of the activation of the atria and ventricles.

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110
Q

Causes of SVT

A
  • Ischemic heart disease
  • Digoxin toxicity: paroxysmal atrial tach w/ 2:1 block is the most common arrhythmia associated with dig toxicity
  • AV node reentry
  • AFlutter with RVR
  • AV reciprocating tachycardia
  • Excessive caffeine or alcohol consumption
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111
Q

Treatment for SVT

A

Maneuvers that stimulate the vagus will delay AV conduction and thus block the reentry mechanisms. You can try valsalva maneuver, carotid sinus massage, breath holding or head immersion in cold water.

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112
Q

Pharmacologic tx for SVT

A
  • IV adenosine
  • IV verapamil
  • IV esmolol
  • Digoxin
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113
Q

MOA of adenosine

A

It works by decreasing SA and AV nodal action.

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114
Q

Prevention of SVT

A
  • Verapamil or beta blockers

- Radiofrequency ablation of either the AV node or the accessory pathway

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115
Q

Side effects of adenosine

A 
Headache 
Flushing 
SOB 
Chest pressure 
Nausea
FEELS LIKE DEATH
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116
Q

What is WPW syndrome?

A

When there is an accessory conduction pathway from the atria to the ventricles through the bundle of Kent which causes premature ventricular excitation because it lacks the delay seen in the AV node.

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117
Q

What is seen on the EKG of WPW?

A
  • Narrow QRS
  • Shortened PR interval
  • Delta wave
118
Q

What are the two mechanisms that can produce paroxysmal tachycardia in WPW syndrome?

A
  1. ) Orthodromic reciprocating tachycardia

2. ) SVT

119
Q

Treatment of WPW

A
  • Radiofrequency ablation of one arm of the reentrant loop.

- Meds: procainamide or quinidine

120
Q

What drugs should be avoided in WPW syndrome?

A

Drugs that work on the AV node: digoxin, verapamil, beta blockers. This is because they may accelerate conduction through the accessory pathway. Type IA or IC antiarrhythmics are a better choice.

121
Q

How do you define VTach?

A

Rapid and repetitive firing of three or more PVCs in a row at a rate between 100-250 bpm.

122
Q

EKG findings of VTach

A
  • Wide and bizarre QRS complexes
  • AV dissociation is present.
  • QRS complexes may be monomorphic or polymorphic
123
Q

Where does VTach originate?

A

Below the bundle of His (widened QRS)

124
Q

What are some causes of VTach?

A
  • CAD with prior MI (most common)
  • Congenital defects
  • Prolonged QT
  • Cardiomyopathies
  • Drug toxicity
  • Active ischemia, hypotension
125
Q

What is sustained VTach?

A

A life threatening arrhythmia that persists in the absence of intervention. It lasts longer than 30 sec and is almost always symptomatic. It is often associated with marked hemodynamic compromise and the development of myocardial ischemia. It can progress to VFib if untreated.

126
Q

What is nonsustained VTach?

A

It is brief, self limited runs of VTach that is usually asymptomatic. However, when CAD and LV dysfunction are present, it is a risk factor for sudden death.

127
Q

Clinical features or symptoms of VTach

A
  • palpitations, dyspnea, light headedness, angina, impaired consciousness
  • Sudden cardiac death
  • May present with cardiogenic shock
  • May be asymptomatic
  • Cannon A waves in the neck
  • S1 that varies in intensity.
128
Q

What are cannon A waves?

A

Associated with VTach. They are secondary to AV dissociation which results in atrial contraction during ventricular contraction

129
Q

Does VTach respond to vagal maneuvers?

A

NO

130
Q

Treatment for hemodynamically stable patients with sustained VTach?

A
  • IV amiodarone
  • IV sotalol
  • IV procainamide
131
Q

Treatment for hemodynamically unstable patients with sustained VTach or patients with severe symptoms?

A
  • DC cardioversion

- Followed by VI amiodarone to maintain sinus rhythm.

132
Q

Treatment of nonsustained VT

A
  • If no underlying heart disease and asymptomatic: do nothing!
  • If underlying heart disease, recent MI, LV dysfunction, or symptomatic–> order electrophysiologic study. May need ICD placement.
  • Pharmacologic therapy is 2nd line tx: Amiodarone has best results
133
Q

What is VFib?

A

-Multiple foci in the ventricles fire rapidly, leading to a chaotic quivering of the ventricles and no cardiac output. Most episodes of VFib begin with VTach!

134
Q

Discuss the recurrence of VFIb.

A
  1. ) If VFib is not associated with an acute MI the recurrence rate is high and these patients require chronic tx with either prophylactic antiarrhythmic (amio) or an implanted automatic defib.
  2. ) If VFib develops within 48 hours of an acute MI, then the long term prognosis is favorable and recurrence rate is low.
135
Q

Causes of VFib

A
  • Ischemic heart disease (most common)
  • Antiarrhythmic drugs (esp those that prolong QT intervals).
  • AFib with RVR in pts w/ WPW syndrome
136
Q

Clinical features of VFib:

A
  • Cannot measure BP, absent heart sounds and pulse
  • Unconscious
  • Untreated leads to sudden cardiac death
137
Q

What is seen on an EKG in VFIb?

A
  • No atrial P waves
  • No identifiable QRS
  • Pretty much can’t miss it
138
Q

Tx of VFIb

A

CPR and immediate defibrillation

139
Q

If CPR + defibrillation doesn’t terminate VFib, what can you do?

A
  • Continue CPR
  • Possibly intubate
  • Administer 1 mg IV bolus of epinephrine then administer every 3-5 minutes.
140
Q

How do you treat refractory VFib

A
  • IV amiodarone followed by shock

- 2nd line: lidocaine, magnesium, procainamide

141
Q

Mode of inheritence of hypertrophic cardiomyopathy?

A

Autosomal dominant

142
Q

Pathophysiology of hypertrophic cardiomyopathy?

A

Diastolic dysfunction due to a stiff hypertrophied ventricle with elevated diastolic filling pressures. Patients may also have dynamic outflow obstruction due to asymmetric hypertrophy of the IV septum.

143
Q

What maneuvers increase the murmur in hypertrophic cardiomyopathy?

A

Valsalva and standing because these decrease the LV size and thus increase the outflow obstruction (decreased preload)

144
Q

What maneuvers decrease the murmur in HOCM?

A

-Squatting
-Lying down
-Straight leg raise
(all the above decrease the outflow obstruction by increasing the preload)
-sustained handgrip (increased systemic resistance leads to decreased gradient across the aortic valve.)

145
Q

What is a bisferious pulse?

A

A rapidly increasing carotid pulse with two upstrokes, associated with HOCM.

146
Q

Tx for HOCM?

A
  • Avoid dehydration
  • Avoid exercise and strenuous activity
  • Symptomatic patients can be treated with BBs or CCBs. Beta blockers work by improving diastolic filling and reducing myocardial contractility and O2 consumption.
  • Myomectomy surgery
147
Q

Pathophysiology of restrictive cardiomyopathy

A

infiltration of the myocardium results in impaired diastolic ventricular filling due to decreased ventricular compliance.

148
Q

List some causes of restrictive cardiomyopathy

A
  • Amyloidosis
  • Sarcoidosis
  • Hemochromatosis
  • Scleroderma
  • Carcinoid syndrome
  • Chemotherapy or radiation induced
  • Idiopathic
149
Q

How do you make the diagnosis of restrictive cardiomyopathy

A
  • Low voltage or conduction abnormalities on EKG
  • Thickened myocardium and increased RA and LA size with normal LV and RV size on echo
  • In amyloidosis myocardium appears brighter and may look sparkly
  • Endomyocardial biopsy is diagnostic
150
Q

Treatment of restrictive cardiomyopathy

A
  • Treat the underlying disorder
  • Amyloidosis: no tx
  • Hemochromatosis: phlebotomy or deferoxamine
  • Sarcoidosis: glucocorticoids
151
Q

Pathophysiology and some causes of myocarditis:

A

-Inflammation of the myocardium caused by viruses (coxsackie, parvo B19, HHV-6), bacteria (Gp. A Strep in RF, Lyme, Mycoplasma), SLE, medications (sulfonamides) or may be idiopathic.

152
Q

What is the classic patient with myocarditis? What lab abnormalities might be present?

A

A young male with elevated cardiac enzymes and elevated ESR.

153
Q

Tx for myocarditis

A

-Supportive; tx the underlying disease if possible

154
Q

What is acute pericarditis?

A

Inflammation of the pericardial sac.

155
Q

What are 2 complications of acute pericarditis?

A
  • Cardiac tamponade

- Pericardial effusion

156
Q

List some causes of pericarditis? (There’s a lot!)

A
  • Idiopathic
  • Infectious (coxsackie, echo, adenovirus, EBV, influenze, HIV, HepA, HepB) TB, Fungal, toxo
  • Acut MI
  • Uremia
  • Collagen vascular disease (SLE, scleroderma, RA, sarcoid)
  • Neoplasm (Hodgkin lymphoma, breast and lung cancer)
  • Drug induced lupus (hydralazine, procainamide)
  • After MI (Dressler)
  • Post-percariotomy syndrome
  • Amyloidosis
  • Radiation
  • Trauma
157
Q

What are the four cardinal manifestations of pericarditis?

A
  • Chest pain
  • Pericardial friction rub
  • EKG changes: diffuse ST elevations, PR depressions
  • Pericardial effusion (w/ or w/o tamponade)
158
Q

What is different about the chest pain associated with pericarditis?

A

It is pleuritic and positional!

It may also radiate to the neck and the ridge of the trapezius.

159
Q

What classically relives and aggravates the pain of pericarditis?

A

Relieved by: sitting up and leaning forward.

Aggravated by: lying supine, coughing, swallowing, and deep inspiration.

160
Q

When is the pericardial friction rub heard best?

A

During expiration with the patient sitting upright.

161
Q

EKG changes associated with pericarditis

A
  • Diffuse ST segment elevation and PR depression

- ST segment returns to normal in about 1 week, T wave may invert and then return to normal.

162
Q

Tx of acute pericarditis

A
  • Most cases are self limited and resolve in 2-6 weeks
  • Treat the underlying cause if known
  • NSAIDs
  • Possibly colchicine (restricted by dose dependent diarrhea)
163
Q

What is constrictive pericarditis?

A

Fibrous scarring of the pericardium leading to rigidity and thickening of the pericardium with obliteration of the pericardial cavity.

164
Q

Describe the pathophysiology of constrictive pericarditis

A

A fibrous rigid pericardium restricts the diastolic filling of the heart. Ventricular filling is therefore unimpeded during early diastole because intracardiac volume has not yet reached the limit defined by the stiff pericardium. When the intracardiac volume reaches the limit set by the noncompliant pericardium, ventricular filling is halted abruptly.

Early diastole: rapid filling
Late diastole: halted filling

165
Q

Causes of constrictive pericarditis

A
  • Idiopathic
  • Uremia
  • Radiation
  • TB
  • Chronic pericardial effusion
  • Tumor invasion
  • Connective tissue disorders
  • prior surgery involving the pericardium
166
Q

Clinical features of constrictive pericarditis

A
  • Patients appear very ill. May have fluid overload with edema, ascites and effusions or have decreased CO with dyspnea, fatigue, cachexia etc.
  • JVD
  • Kussmaul sign: JVD fails to decrease during inspiration
  • Pericardial knock: corresponds to the abrupt cessation of ventricular filling
  • Ascites and dependent edema
167
Q

How do you make the diagnosis of constrictive pericarditis?

A
  • EKG: nonspecific low QRS, T wave flattening, AFib
  • Echo: increased pericardial thickness, atrial enlargement, halted ventricular diastole
  • CT/MRI: pericardial thickening and calcifications
  • Cardiac cath: equal diastolic filling pressures in all chambers, ventricular pressure tracing shows a rapid y descent which is described as a dip and plateau or square root sign
168
Q

Tx of constrictive pericarditis

A
  • Tx the underlying condition
  • Diuretics
  • Surgical pericardiectomy
169
Q

Clinical features of pericardial effusion

A
  • Muffled heart sounds
  • Soft PMI
  • Dullness at left lung base
  • +/- pericardial friction rub
170
Q

What is the imaging test of choice for a pericardial effusion?

A

Echocardiogram. It should be performed in all patients with acute pericarditis to rule out an effusion.

171
Q

What other imaging test should you order for pericardial effusion and what would it show?

A
  • CXR
  • May show prototypical water bottle appearance. It shows enlargement of the cardiac silhouette when >250 mL of fluid has accumulated.
172
Q

EKG changes in pericardial effusion?

A

Low QRS voltage and T wave flattening; electrical alternans suggest massive pericardial effusion or tamponade.

173
Q

When is pericardiocentesis indicated in the tx of pericardial effusion

A

If signs and sx of cardiac tamponade are indicated. Otherwise if it’s small just do a repeat each in 2 weeks.

174
Q

How much fluid is needed to develop rapidly to cause tamponade?

A

200 mL

175
Q

How much fluid is needed to accumulate slowly to cause tamponade?

A

2 L

176
Q

Causes of cardiac tamponade?

A
  • Penetrating trauma
  • Central line placement, pacemaker insertion, pericardiocentesis
  • Idiopathic, neoplastic or uremic pericarditis
  • Post MI w/ free wall rupture
177
Q

Pathophysiology of cardiac tamponade?

A

There is impaired diastolic filling of the heart. Pressures in the LV, RV, LA, and RA, pulmonary artery and pericardium equalize during diastole and ventricular filling is impaired during diastole. This leads to decreased SV and CO.

178
Q

What is Beck’s Triad

A
  • Hypotension
  • Muffled Heart sounds
  • JVD
179
Q

Clinical features of cardiac tamponade

A
  • Elevated JVD
  • Narrow pulse pressure (due to decreased VS)
  • Pulsus paradoxus
  • Distant heart sounds
  • Tachypnea, tachycardia, hypotension, cardiogenic shock
180
Q

What is pulsus paradoxus

A

The pulse gets strong during expiration and weak (>10 mmHg drop) during inspiration

181
Q

What 4 things do you order to make the diagnosis of cardiac tamponade

A
  • EKG
  • Echo
  • CXR
  • Cardiac cath
182
Q

EKG findings in cardiac tamponade?

A

-Electrical alternans: alternate beat variation in the direction of the EKG waveforms due to the pendular swinging of the heart within the pericardial space.

183
Q

Tx of cardiac tamponade in a hemodynamically unstable patient

A
  • Pericardiocentesis

- If this doesn’t work you can try a fluid challenge.

184
Q

How does rheumatic fever cause mitral stenosis?

A

Immune mediated damage to the mitral valve is caused by cross-reactivity between the streptococcal antigen and the valve tissue which leads to scarring and narrowing of the mitral valve orifice.

185
Q

What are two complications of mitral stenosis

A
  • LA enlargement leading to AFib

- Pulmonary HTN and subsequent right heart failure

186
Q

What is one unique symptom of mitral stenosis?

A

Hemoptysis-as the elevated LA pressure ruptures anastomoses of small bronchial veins.

187
Q

Describe the mitral stenosis murmur

A

S2 followed by an open snap followed by a low pitched diastolic rumble. Heard best with the bell of the stethoscope in the left lateral decubitus position. This is all followed by a loud S1!

188
Q

What indicates the severity of the stenosis in mitral stenosis?

A

The length of time between S2 and the opening snap. The closer the opening snap to S2, the worse the stenosis.

189
Q

With Mitral Stenosis what do you see on a CXR?

A

Left atrial enlargement

190
Q

With mitral stenosis what do you seen on an echocardiogram?

A
  • LAE
  • thickened/calcified mitral valve
  • Narrow fish-mouth shaped orifice
  • Signs of RVF in advanced disease
191
Q

Medical treatment of mitral stenosis?

A
  • Diuretics for pulmonary congestion and edema

- BBs to decrease HR and CO

192
Q

Surgical therapy for MS?

A

Percutaneous balloon valvuloplasty or open heart valve replacement

193
Q

Describe the course of aortic stenosis and complications.

A

With long standing aortic stenosis the LV dilates causing progressive LV dysfunction. With severe AS, the LV dilation pulls apart the mitral valve annulus causing MR.

194
Q

What are 3 classic symptoms associated with aortic stenosis?

A
  • Angina
  • Syncope
  • Heart failure
195
Q

What are the signs of aortic stenosis (+ murmur description)

A
  • Harsh crescendo-decrescendo systolic murmur heard in the second right intercostal space with radiation to the carotid arteries.
  • Soft S2
  • S4
  • Pulsus parvus et tardus (delayed and diminished carotid upstrokes)
  • Sustained PMI
  • Precordial thrill
196
Q

Treatment of aortic stenosis?

A

Aortic valve replacement in symptomatic patients.

197
Q

How do you make the diagnosis of AS?

A
  • CXR
  • Echo
  • Cardiac cath
198
Q

Pathophysiology of aortic regurgitation

A

Due to inadequate closure of the aortic valve leaflets. Regurgitant blood flow increases LVEDV. LV dilation and hypertrophy occur in response in order to maintain stroke volume and prevent diastolic pressure from increasing excessively. Over time these compensatory mechanisms fail and there is increased left sided and pulmonary pressures.

199
Q

Causes of aortic regurg

A
  • Infective endocarditis
  • Trauma
  • Aortic dissection
  • Iatrogenic
  • Chronic causes that are primarily valvular: rheumatic fever, bicuspid valve, Marfan syndrome, Ehlers-Danlos, ankylosing spondylitis, SLE
  • Chronic aortic root diseases: syphilitic aortitis, osteogenesis imperfecta, aortic dissection, Behcet syndrome, Reiter syndrome, systemic HTN
200
Q

Important physical exam findings in aortic regurg

A
  • Widened pulse pressure: increased SBP, decreased DBP
  • De Musset Sign: head bobbing
  • Muller sign: Uvula bobs
  • Duroziez sign: pistol shot sound heard over the femoral arteries
  • Diastolic decrescendo murmur heard at LSB
  • Corrigan Pulse (water hammer pulse)
  • Austin Flint Murmur
  • Displaced PMI down and to the left
201
Q

What maneuver increases the murmur in aortic regurg and why?

A

Sustained handgrip–> it increases SVR which causes an increased backflow through the incompetent aortic valve.

202
Q

Tx for aortic regurg if stable and asymptomatic

A
  • Salt restriction
  • Diuretics
  • Vasodilators
  • Digoxin
  • Afterload reduction with ACEis or arterial dilators
  • Restrict strenuous activity
  • Perform echos serially to assess the need for surgery (look at LV size and function, dilated aortic root and reversal of blood flow)
203
Q

Tx of aortic regurg in symptomatic pts

A

Valve replacement

204
Q

Acute causes of mitral regurg

A
  • Endocarditis
  • Papillary muscle rupture
  • Chordae Tendinae rupture
205
Q

Chronic causes of mitral regurg

A
  • Marfan syndrome
  • Mitral valve prolapse
  • Rheumatic fever
  • Cardiomyopathy
206
Q

Describe the murmur of mitral regurg

A

Holosystolic murmur best heard at the apex with radiation to the back or clavicles.

207
Q

What other signs on PE are associated with mitral regurg?

A
  • Diminished S1
  • Widening of S2
  • S3 gallop
  • Laterally displaced PMI
  • Loud, palpable P2
208
Q

Tx of mitral regurg

A
  • Symptomatic: afterload reduction with vasodilators; chronic anticoagulation if the patient has AFib
  • Mitral valve repair or replacement (before LV dysfunction becomes too bad)
209
Q

Causes of tricuspid regurg

A
  • Anything that causes RV dilation!
  • LV failure
  • RV infarction
  • Cor pulmonale
  • Inferior wall I
  • Tricuspid endocarditis (IVDA)
  • Rheumatic heart disease
  • Epstein’s anomaly
  • Carcinoid syndrome
  • SLE
  • myxomatous valve degeneration
210
Q

Describe the murmur of tricuspid regurg

A
  • Blowingi holosystolic murmur heard best at the LLSB intensified with inspiration and reduced during expiration or valsalva
  • Other clinical features: pulsatile liver, signs and sx of RHF, prominent V waves in jugular venous pulse with rapid y descent.
211
Q

What is mitral valve prolapse?

A

MVP is defined as the presence of excessive or redundant mitral leaflet tissue due to myxomatous degeneration of mitral valve leaflets and/or chordae tendinae. The redundant leaflets prolapse toward the LA in systole which results in an auscultative click and murmur.

212
Q

Describe the murmur of mitral valve prolapse

A

-A midsystolic or late systolic click followed by a mid to late systolic murmur that can be described as rumbling. The murmur increases with standing and the valsalva and decreases with squatting.

213
Q

How do you make the diagnosis of rheumatic fever (major and minor)

A
  1. ) two major criteria

2. ) OR one major and two minor criteria

214
Q

What are the major criteria for rheumatic fever

A
  1. ) Migratory polyarthritis
  2. ) Erythema marginatum
  3. ) Cardiac involvement: CHF, pericarditis, valve disease
  4. ) Chorea
  5. ) Subcutaneous nodules
215
Q

What are the minor criteria for rheumatic fever?

A
  1. ) Fever
  2. ) Elevated ESR
  3. ) Polyarthralgias
  4. ) Prior history of rheumatic fever
  5. ) Prolonged PR interval
  6. ) Evidence of preceding strep infection.
216
Q

How do you treat acute rheumatic fever and how do you monitor the progress of treatment?

A
  • Treat acute rheumatic fever with NSAIDs

- CRP is used to measure response to treatment.

217
Q

What is the most common cause of acute endocarditis?

A

Staph aureus

218
Q

What is the most common cause of subacute endocarditis?

A

Less virulent organisms! Like strep viridans or enterococcus.

219
Q

What is the difference in terms of valve damage in acute and subacute endocarditis??

A

Acute endocarditis occurs on a previously normal valve. Subacute endocarditis occurs on a previously damaged valve.

220
Q

list some organisms that cause native valve endocarditis

A
  • Strep Viridans (most common)
  • Staph species
  • Enterococcus
  • HACEK organisms
221
Q

What is the most common cause of early onset endocarditis in prosthetic heart valves?

A

-Staphylococci

222
Q

What is the most common cause of late onset endocarditis in prosthetic heart valves?

A

-Streptococci

223
Q

What is the most common cause of endocarditis in IVDA?

A

-Still staph aureus!

224
Q

What type of echo do you want to get for endocarditis?

A

TEE is better than a TTE!

225
Q

Complications of endocarditis?

A
  • Cardiac failure
  • Myocardial abscess
  • Solid organ damage from showered emboli
  • Glomerulonephritis
226
Q

What are the criteria required for diagnosis of endocarditis?

A
  1. ) Two major criteria
  2. ) One major and three minot
  3. ) Five minor criteria
227
Q

What are the major Duke’s Criteria?

A
  1. ) Sustained bacteremia by an organism known to cause endocarditis
  2. ) Endocardial involvement or new valvular regurgitation
228
Q

What are the minor Duke’s criteria?

A
  1. ) Predisposing condition (valve abnormality, IVDA)
  2. ) Fever
  3. ) Vascular phenomenon (septic or pulmonary emboli, mycotic aneurysm, Janeway lesion)
  4. ) Immune phenomenon (glomerulonephritis, Osler nodes, Roth spots)
  5. ) Positive blood cultures not meeting major criteria
  6. ) Positive echocardiogram not meeting major criteria
229
Q

What are qualifying cardiac conditions that warrant Abx prophylaxis for endocarditis?

A
  • Prosthetic heart valves
  • Hx of infective endocarditis
  • Congenital heart disease (unrepaired cyanotic or repaired with prosthetic material during first 6 months after procedure)
  • Cardiac transplant with valvuloplasty
230
Q

What are qualifying procedures that warrant Abx prophylaxis for endocarditis?

A
  • Dental procedures involving manipulation of gingival mucosa or periapical region of teeth
  • Procedures involving biopsy or incision of respiratory mucosa
  • Procedures involving infected skin or MSK tissue
231
Q

What is marantic endocarditis associated with?

A

Metastatic cancer patients.

232
Q

what is the pathology of marantic endocarditis?

A

Sterile deposition of fibrin and platelets along the closure line of cardiac valve leaflets.

233
Q

What is libman sacks endocarditis?

A

Associated with lupus, typically involves the aortic valves. Associated with the formation of warty vegetations on BOTH SIDES of the valve leaflets. May present with regurgitant murmurs.

234
Q

What are the SIRS criteria?

A
  1. ) Fever >38 C or hypothermia <36C
  2. ) Hyperventilation (>20 bpm, or PaCO2 <32)
  3. ) Tachycardia >90 bpm
  4. ) Leukocytosis (>12,000 cells/hpf or >10% bands)
235
Q

How do you define sepsis?

A

When a suspected source of infection and SIRS is present.

236
Q

How do you define septic shock?

A

When there is hypotension induced by sepsis persisting despite adequate fluid resuscitation

237
Q

What is multiple organ dysfunction syndrome?

A

Altered organ function in an acutely ill patient usually leading to death.

238
Q

Most common type of ASD

A

Ostium Secundum

239
Q

Pathophysiology of ASD

A

Oxygenated blood from the LA passes into the RA increasing the right heart output and thus pulmonary blood flow. This leads to increased work of the right side of the heart. As shunt size increase RA and RV dilation occurs. Pulmonary HTN is a serious sequelae but is rare in ASD.

240
Q

Describe the murmur characteristics of ASD

A
  • Fixed split S2
  • Mid systolic ejection murmur at the pulmonary area secondary to increased pulmonary blood flow.
  • Diastolic flow rumble murmur across the tricuspid valve area secondary to increased blood flow.
241
Q

What is Eisenmenger Syndrome?

A

A late complication of ASD in which the irreversible pulmonary HTN leads to reversal of the shunt, heart failure, and cyanosis.

242
Q

What is the most common congenital heart defect

A

A VSD

243
Q

Describe the murmur of a VSD. What decreases the murmur?

A

A harsh blowing holosystolic murmur with a thrill heard at the 4th left intercostal space. Murmur decreases with Valsalva and handgrip.

244
Q

What is coarctation of the aorta?

A

Narrowing/constriction of the aorta usually at the origin of the left subclavian artery near the ligamentum arteriosum, which leads to obstruction between the proximal and distal aorta and thus to increased left ventricular workload.

245
Q

What are the classic findings of coarctation of the aorta seen on a CXR?

A
  • Notching of the ribs

- Figure 3 appearance of the aorta

246
Q

What is a PDA?

A

Connection between the aorta and pulmonary artery.

247
Q

What keeps the PDA open? What closes it?

A
  • Keeps it open: prostaglandin and low O2 tension

- Closes it: indomethacin

248
Q

Describe the murmur of PDA

A

Continuous machine like murmur at the left second intercostal space (both systolic and diastolic components)

249
Q

What are the abnormalities in Tetralogy of Fallot

A
  • Overriding aorta
  • VSD
  • Pulmonary artery stenosis
  • RVH

These all occur secondary to defects in the development of the infundibular septum.

250
Q

Murmur in TOF?

A

Pulmonary artery stenosis: crescendo decrescendo heart best at the LUSB

251
Q

What is a tet spell?

A

Patients will squat after exertion such as exercise or crying spells in an infant. This maneuver increases the SVR and forces blood to be shunted out the RV to the lungs rather than to the aorta. O2, morphine and BBs can be needed if the patient continues to be cyanotic.

252
Q

CXR in TOF?

A

Boot shaped heart

253
Q

Define HTN emergency

A

SBP >220, DBP >120 with end organ damage.

254
Q

What is HTN urgency?

A

Elevated BP levels alone w/o end organ damage

255
Q

What signifies end organ damage in HTN emergency?

A
  • Eyes: papilledema
  • CNS: AMS, ICH, encephalopathy
  • Kidneys: renal failure, hematuria
  • Heart: MI, CHF w/ pulmonary edema, aortic dissection
  • Lungs: pulmonary edema
256
Q

What is PRES?

A

Caused by hypertensive encephalopathy. It is posterior reversible encaphalopathy syndrome which is a radiographic condition (posterior cerebral white matter edema)which is postulated to be caused by autoregulatory failure of the cerebral vessels as well as endothelial dysfunction.

257
Q

How do you treat hypertensive emergency?

A

-Lower the mean arterial pressure by 25% within 1-2 hours. The goal is not to immediately achieve normal BP but to get the patient out of danger. You can use IV agents like hydralazine, esmolol, nitroprusside, labetalol or nitroglycerin if the patient is severe or has hypertensive encephalpathy. If not severe, oral agents like captopril, clonidine, labetalol, nifedipine or diazoxide can be used.

258
Q

How do you treat hypertensive urgency?

A

-BP should be lowered in 24 hours using ORAL agents.

259
Q

Conditions that predispose to aortic dissection

A
  • HTN
  • Cocaine use
  • Trauma
  • CT disease like Marfans or ED
  • Bicuspid aortic valve
  • Coarctation
  • Third trimester of pregnancy
260
Q

Type A aortic dissection

A
  • Involves the ascending aorta proximal to the subclavian

- Treatment is surgical

261
Q

Type B aortic dissection

A
  • Involving the descending aorta distal to the subclavian

- Treatment is medical

262
Q

What is the immediate medical therapy for aortic dissection?

A
  • IV labetalol

- IV nitroprusside

263
Q

What are the three signs incidcating a ruptured AAA and what do you do about it?

A
  • Hypotension
  • Pulsatile abdominal mass
  • abdominal pain
  • Emergent laparotomy!
264
Q

What are the imaging modalities to diagnose AAA

A
  • Abdominal ultrasound: preferred

- CT scan: only do in hemodynamically stable patients

265
Q

How do you managed unruptured AAA?

A
  • If >5 cm surgical resection with graft placement is recommended.
  • If <5 cm monitor size over time.
266
Q

What is Leriche Syndrome?

A

Atheromatous occlusion of distal aorta just above the bifurcation causing bilateral claudication, impotence, and absent/diminished femoral pulses.

267
Q

3 most common site of cocclusion/stenosis in atherosclerotic disease?

A
  1. ) Superficial femoral artery
  2. ) Popliteal artery
  3. ) Aortoiliac occlusive disease
268
Q

What is a normal ABI

A

0.9-1.3

269
Q

What is ABI >1.3

A

Indicates severe disease and is due to incompressible vessels. Ex: patients with calcified arteries (especially those with DM)

270
Q

What ABI causes claudication?

A

<0.7

271
Q

What ABI is associated with rest pain?

A

<0.4

272
Q

Indications for surgery for PAD?

A

Rest pain, ischemic ulcerations, severe symptoms refractory to conservative treatment

273
Q

Where is the most common site of occlusion due to acute arterial occlusion (remember this is usually caused by embolization!)

A

The common femoral artery

274
Q

What are the 6 P’s of acute arterial occlusion?

A
  • Pain
  • Pallor
  • Polar (cold)
  • Paralysis
  • Paresthesias
  • Pulselessness
275
Q

How do you workup acute arterial occlusion?

A
  • Arteriogram to look for the site of occlusion
  • EKG to look for MI or AFib
  • Echo to look for cardiac source of emboli
276
Q

Tx for acute arterial occlusion?

A
  • Immediate anticoagulation with IV heparin
  • Emergent surgical embolectomy
  • Possible infusion of thrombolytics intra-arterially
277
Q

What is cholesterol embolization syndrome?

A

It is due to showers of cholesterole crystals that originate from a proximal source, often aggravated by a surgical or radiographic intervention or thrombolytic therapy. it presents as small discrete areas of tissue ischemia resulting in black/blue toes, renal insufficiency, and/or abdominal pain or bleeding

278
Q

Tx of cholesterol embolization syndrome

A
  • Supportive, control BP

- DO NOT ANTICOAGULATE

279
Q

What is a mycotic aneurysm

A

An aneurysm that results from damage due to the aortic wall that is secondary to some type of infection.

280
Q

Tx of a mycotic aneurysm

A

IV antibiotics

Surgical excision

281
Q

What is a luetic heart?

A

A complication of syphilitic aortitis. It is an aneurysm of the aortic arch with retrograde extension backwards causing AR and stenosis of aortic branches.

282
Q

Tx of luetic heart

A

IV PCN and cardiac repair

283
Q

What is Virchow’s Triad

A

Venous stasis
Endothelial injury
Hypercoagulable state

284
Q

What studies do you order in the workup of DVT?

A
  • Dopper analysis and U/S
  • Venography
  • Impedance plethysmography
  • D-dimer testing
285
Q

3 Complications of a DVT

A
  1. ) PE
  2. ) Postthrombotic syndrome (chronic venous insufficiency)
  3. ) Phlegmasia cerulea dolens (painful, blue, swollen leg)
286
Q

Indications for placement of an IVC filter

A

Absolute contraindication to anticoagulation or failure of appropriate anticoagulation. Only prevents a PE not a DVT

287
Q

Clinical features of superficial thrombophlebitis

A
  • Pain, tenderness, induration and erythema along the course of the vein
  • A tender cord may be palpated
288
Q

Treatment of localized thrombophlebitis

A

A mild analgesic (NSAIDs), elevation and hot compresses (continue activity)

289
Q

Treatment of suppurative thrombophlebitis

A

Septic phlebitis is usually due to infection of an IV cannula. Redness extends beyond the are of the vein and purulent drainage may be present. Remove the cannula and administer systemic abx.

290
Q

What are 2 conditions that could be confused with superficial thrombophlebitis and how do you distinguish them?

A

-Could be confused with cellulitis or lymphangitis. In these conditions, swelling and erythema are more widespread and there is no palpable indurated vein.

291
Q

When superficial thrombophlebitis occurs in different locations over a short period of time, what should you think of?

A

Migratory superficial thrombophlebitis secondary to occult malignancy, often the pancreas. This is known as Trousseau Syndrome.

Internal Medicine (6 decks)

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