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PANCE Prep Pearls > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

What is dilated cardiomyopathy and some clinical manifestations associated with it?

A

Systolic dysfunction, leading to a dilated, weak heart.

Systolic heart failure symptoms such as dyspnea/fatigue (left-sided) and edema/JVD/hepatomegaly (right-sided)

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2
Q

What is a hallmark physical exam finding of dilated cardiomyopathy?

A

S3 gallop (due to filling of the dilated ventricle)

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3
Q

What is the diagnostic test of choice for determining dilated cardiomyopathy and what will be found?

A

Echocardiogram

Left ventricular dilation, thin ventricular walls, decreased EF

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4
Q

How is dilated cardiomyopathy managed?

A

Standard systolic heart failure treatment:

  • ACE-I
  • Beta blockers
  • Symptom control with diuretics

Implantable cardioverter/defibrillator if EF is less than 35-30%

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5
Q

What are some etiologies of dilated cardiomyopathy?

A
  • Idiopathic (most common)
  • Viral infections (Coxsackievirus B)
  • Alcohol abuse
  • Doxorubicin (anthracycline)
  • Vitamin B1 (thiamine) deficiency
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6
Q

What is stress (Takotsubo) cardiomyopathy?

A

Transient systolic dysfunction of the left ventricle that can imitate MI but is not associated with obstructive CAD or evidence of plaque ruptures.

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7
Q

What are risk factors for stress (Takotsubo) cardiomyopathy?

A

Post-menopausal women exposed to physical or emotional stress

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8
Q

What is the pathophysiology of stress (Takotsubo) cardiomyopathy?

A

Thought to be multi-factorial including catecholamine surge during physical or emotional stress, microvascular dysfunction, and coronary artery spasm

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9
Q

What are clinical manifestations associated with stress (Takotsubo) cardiomyopathy?

A

Substernal chest pain, dyspnea, syncope

***Similar to ACS

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10
Q

In a patient with stress (Takotsubo) cardiomyopathy, what will likely be found on EKG, cardiac enzymes, coronary angiography, and echo?

A

EKG: ST elevations (especially in the anterior leads)

Cardiac enzymes: Often positive

Coronary angiography: Absence of acute plaque rupture or obstructive CAD

Echo: Transient left ventricular systolic dysfunction, especially apical left ventricular ballooning

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11
Q

What is the management for stress (Takotsubo) cardiomyopathy?

A

Initially treated similar to ACS due to similar presentation (aspirin, beta blocker, heparin, coronary angiography to rule out obstructive CAD)

Conservative and supportive care is mainstay of treatment including beta blocker and ACE-I for 3-6 months with serial imaging to assess for improvement.

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12
Q

What is restrictive cardiomyopathy?

A

Diastolic dysfunction in a non-dilated ventricle which impedes ventricular filling (decreased compliance)

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13
Q

What are some etiologies of restrictive cardiomyopathy?

A

Infiltrative disease:

  • Amyloidosis (most common)
  • Sarcoidosis
  • Hemochromatosis
  • Metastatic disease
  • Endomyocardial fibrosis
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14
Q

What clinical manifestations are associated with restrictive cardiomyopathy?

A
  • Right-sided heart failure symptoms (peripheral edema, JVD, hepatomegaly, ascites)
  • Left-sided heart failure symptoms (dyspnea most common)
  • Kussmaul’s sign (increase in JVP with inspiration)
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15
Q

What is the diagnostic test of choice for determining restrictive cardiomyopathy and what will be found?

A

Echocardiogram

Non-dilated ventricles with normal thickness, diastolic dysfunction, marked dilation of both atria

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16
Q

What diagnostic study will provide a definitive diagnosis of restrictive cardiomyopathy?

A

Endomyocardial biopsy (not used often)

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17
Q

What is the management for restrictive cardiomyopathy?

A
  • Treat underlying disorder

- Gentle diuresis for symptoms, vasodilators

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18
Q

What are clinical manifestations associated with hypertrophic cardiomyopathy?

A
  • Dyspnea (most common symptoms)
  • Angina
  • Arrhythmias
  • Sudden cardiac death (especially during times of extreme exertion due to V-fib)
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19
Q

What can be found on physical examination in a patient with hypertrophic cardiomyopathy?

A
  • Harsh systolic murmur best heard at the left sternal border
  • May have loud S4
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20
Q

In a patient with hypertrophic cardiomyopathy, what will cause the associated murmur to increase or decrease in intensity?

A

Increased intensity with valsalva and standing (decreased venous return)

Decreased intensity with squatting, supine, hand grip, leg raise (increased venous return)

***Valsalva and standing will decrease intensity of all other murmurs

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21
Q

What will be seen on echocardiogram in hypertrophic cardiomyopathy?

A

Asymmetric ventricular wall thickness (especially septal)

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22
Q

What will be seen on EKG in hypertrophic cardiomyopathy?

A

Left ventricular hypertrophy

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23
Q

What is the first-line medical management for hypertrophic cardiomyopathy?

A

Beta blockers

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24
Q

What are the management options for hypertrophic cardiomyopathy?

A

Medical: Beta blockers (first-line), CCB (alternative)
Surgical: Myomectomy in young patients refractory to medical therapy

Patient should avoid dehydration, extreme exertion, and exercise. Cautious use of Digoxin, Nitrates, and diuretics

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25
Q

What are some etiologies associated with myocarditis (inflammation of the heart muscle)?

A
  • Infectious: viral most common (especially the enterioviruses - Coxsackievirus B)
  • Autoimmune
  • Medications (Clozapine)
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26
Q

What are clinical manifestations associated with myocarditis?

A
  • Viral prodrome followed by symptoms of systolic dysfunction (dilated cardiomyopathy)
  • Heart failure symptoms (dyspnea, fatigue, S3 gallop)
  • Megacolon
  • Pericarditis (pericardial friction rub)
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27
Q

What is the gold standard diagnostic study for determining myocarditis?

A

Endomyocardial biopsy (infiltration of lymphocytes; reserved for severe or refractory cases)

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28
Q

What will be seen on CXR and echo in myocarditis?

A

CXR: Cardiomegaly

Echo: Ventricular systolic dysfunction

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29
Q

What is the management for myocarditis?

A

Standard systolic heart failure treatment:

  • ACE-I
  • Beta blockers
  • Diuretics
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30
Q

What is the first-line treatment for sinus tachycardia?

What should be considered if the tachycardia is persistent?

A

Treat underlying cause as first-line.

Beta blockers used for persistent tachycardia.

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31
Q

What is the first-line treatment for symptomatic or unstable sinus bradycardia?

What should you consider if this treatment does not work?

A

Atropine is first-line

Epinephrine or transcutaneous pacing if not responsive to atropine

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32
Q

If EKG shows signs of a 1st degree AV block, how does the treatment vary for an asymptomatic patient versus a symptomatic patient?

A

Asymptomatic: Observation, possible cardiology consult

Symptomatic: Atropine is first-line, epinephrine, pacemaker definitive if persistent

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33
Q

If EKG shows signs of a 2nd degree AV block - Type I, how does the treatment vary for an asymptomatic patient versus a symptomatic patient?

A

Asymptomatic: Observation, possible cardiology consult

Symptomatic: Atropine is first-line, epinephrine, possible pacemaker

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34
Q

What is the treatment for a 2nd degree Type II AV block?

A

Atropine or temporary pacing.

Permanent pacemaker is definitive treatment.

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35
Q

What is the management for a 3rd degree AV block?

A

Transcutaneous pacing often followed by permanent pacemaker placement

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36
Q

How does the acute management vary in a stable versus an unstable patient with atrial flutter?

A

Stable: Vagal maneuvers, rate control with beta blockers, or CCB

Unstable: Synchronized cardioversion

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37
Q

What is the definitive management of atrial flutter?

A

Radiofrequency catheter ablation

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38
Q

How does the acute management vary in a stable versus an unstable patient with atrial fibrillation?

A

Stable: Rate control with Beta Blockers or CCB (Digoxin may be used when BB/CCB are contraindicated)

Unstable: Synchronized cardioversion. Anticoagulation must be continued for 4 weeks after cardioversion.

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39
Q

What is the first-line medical management of stable SVT (narrow complex) if vagal maneuvers are not effective?

A

Adenosine

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40
Q

What is the first-line medical management of stable ventricular tachycardia?

A

Anti-arrhythmic (Amiodarone, lidocaine, procainamide)

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41
Q

What is the management for unstable ventricular tachycardia with a pulse?

A

Synchronized cardioversion

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42
Q

What is the management for unstable ventricular tachycardia without a pulse?

A

Defibrillation (unsynchronized cardioversion) + CPR

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43
Q

What is the management for Torsades de pointes?

A

IV magnesium sulfate

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44
Q

What is the management for ventricular fibrillation?

A

Defibrillation (unsynchronized cardioversion) + CPR (initiate ACLS)

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45
Q

What is the management for pulseless electrical rhythm (PEA)?

A

CPR + epinephrine + checks for “shockable” rhythm every 2 minutes

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46
Q

What are some side effects of cardio selective beta blockers?

A

Bradycardia, AV blocks, may mask symptoms of hypoglycemia

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47
Q

When using non-selective beta blockers, what should you be cautious with?

A

Nonselectives may cause bronchospasm in patients with asthma and COPD

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48
Q

If giving adenosine to a patient, what side effects should you warn them about?

A

Chest discomfort, dyspnea, flushing, headache, but note that they are very common and short-lived

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49
Q

What is amiodarone most commonly used for?

A

Stable wide-complex tachycardias

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50
Q

What is the most common adverse effect of IV amiodarone?

A

Hypotension

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51
Q

What are some common adverse effects associated with long-term use of amiodarone?

A

Thyroid disorders, pulmonary fibrosis, increased LFTs

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52
Q

What is the function of the foramen ovale?

A

Shunts blood from the right atrium directly into the left atrium

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53
Q

What is the function of the ductus arteriosus?

A

Shunts blood from the pulmonary artery directly into the aorta, bypassing fetal lungs

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54
Q

What medications are given to keep the ductus arteriosus patent?

A

Prostaglandin analog (Alprostadil)

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55
Q

What is the most common innocent mumur?

What is the pathophysiology behind it?

A

Still murmur

Thought to be due to the vibration of the valve leaflets.

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56
Q

Describe a still murmur.

A

Musical, vibratory, noisy, twanging, low-pitched best heard at the left lower sternal border and apex

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57
Q

What is the most common continuous benign murmur?

A

Cervical venous hum

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58
Q

Describe a cervical venous hum murmur.

A

Soft, low-pitched, continuous murmur best heard in right sternal border and right infraclavicular area.

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59
Q

What will increase and decrease the intensity of a cervical venous hum murmur?

A

Increase: Sitting or upright position with head extended

Decrease: Supine, jugular compression, rotation/flexion of the head, valsalva

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60
Q

Where is a pulmonary ejection murmur best heard?

A

Best heard in mid-systole in second left intercostal space

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61
Q

What may be found on physical exam in a patient with an atrial septal defect?

A
  • Systolic ejection murmur at the pulmonic area (left upper sternal border)
  • Wide, fixed split S2 that does not vary with respirations
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62
Q

What is the best diagnostic study to make the diagnosis of an atrial septal defect?

A

Echocardiogram

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63
Q

What may be seen on EKG in a patient with an atrial septal defect?

A
  • Incomplete RBBB

- Crochetage sign (notching of the peak of the R wave in the inferior leads)

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64
Q

What is the management for an atrial septal defect?

A
  • If small and less than 5 mm, may be observed (most spontaneously close in first year of life)
  • Surgical correction if greater than 1 cm or symptomatic
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65
Q

What is Eisenmenger syndrome?

A

Pulmonary HTN and cyanotic heart disease occuring when a left-to-right shunt switches and becomes a right-to-left shunt (cyanotic). Patients may develop cyanotic lower extremities.

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66
Q

What may be found on physical exam in a patient with a patent ductus arteriosus?

A
  • Continuous machine-like murmur loudest at the pulmonic area
  • Wide pulse pressures (bounding peripheral pulses)
  • Loud S2
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67
Q

What is the first-line medical treatment of a patent ductus arteriosus?

A

NSAIDs (IV indomethacin, ibuprofen)

***NSAIDs inhibit prostaglandin synthesis

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68
Q

What is coarctation of the aorta?

A

Congenital narrowing of the aortic lumen at the distal arch or descending aorta, resulting in HTN in the arteries proximal to the lesion (primary arteries supplying the upper extremities) with relative hypotension in the lower extremities.

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69
Q

What are some conditions associated with coarctation of the aorta?

A
  • Bicuspid aortic valve
  • Turner syndrome
  • Mitral valve defects
  • Patent ductus arteriosus
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70
Q

What are some clinical manifestations that can be associated with coarctation of the aorta?

A
  • Bilateral claudication
  • DOE
  • Syncope
  • Failure to thrive and poor feeding 1-2 weeks after birth in infants
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71
Q

What may be found on physical exam in a patient with coarctation of the aorta?

A

Upper extremity systolic hypertension with lower extremity hypotension and/or diminished or delayed lower extremity pulses

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72
Q

What is the confirmatory diagnostic test for coarctation of the aorta?

A

Echocardiogram (shows narrowing of the aorta)

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73
Q

What will be found on CXR in a patient presenting with coarctation of the aorta?

A
  • Posterior rib notching

- 3 sign

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74
Q

What is the management for coarctation of the aorta?

A
  • Corrective surgery or transcatheter-based intervention
  • Prostaglandin E1 (Alprostadil) preoperatively to stabilize condition by maintaining patent ductus arteriosus, reducing symptoms and improves lower extremity blood flow
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75
Q

Chest x-ray reveals posterior rib notching and “3-sign.” What should be on your differential?

A

Coarctation of the aorta

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76
Q

What is the most common cyanotic congenital heart disease associated with a right-to-left shunt?

A

Tetralogy of Fallot

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77
Q

What are the four components of Tetralogy of Fallot?

A
  • RV outflow obstruction
  • RVH
  • VSD
  • Overriding aorta
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78
Q

What clinical manifestations are associated with Tetralogy of Fallot?

A

Infancy: Cyanosis most common (baby blue syndrome)

Older children: Tet spells (paroxysms of cyanosis) relieved with squatting

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79
Q

What may be found on physical exam in a patient with Tetralogy of Fallot?

A
  • Harsh systolic murmur at left mid to upper sternal border (VSD)
  • Right ventricular heave (RVH)
  • Cyanosis
  • Digital clubbing
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80
Q

What is the diagnostic test of choice to diagnosis Tetralogy of Fallot?

A

Echocardiogram

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81
Q

Chest x-ray reveals a boot-shaped heart. What is your likely diagnosis?

A

Tetralogy of Fallot

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82
Q

What is the management for Tetralogy of Fallot?

A
  • Surgical repair (ideally in first 4-12 months of life)

- Prostaglandin infusion prior to surgery to maintain a patent ductus arteriosus to improve circulation

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83
Q

What clinical manifestations are associated with transposition of the great arteries (TOGA)?

A

Severe cyanosis and tachypnea within the first 30 days of life not affected by exertion or the use of oxygen

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84
Q

What is the gold standard to diagnose transposition of the great arteries (TOGA)?

A

Cardiac cath (rarely used)

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85
Q

How is transposition of the great arteries (TOGA) primarily diagnosed?

A

Echocardiogram

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86
Q

What is the management for transposition of the great arteries (TOGA)?

A

Arterial switch operation

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87
Q

What is the most common type of congenital heart disease in childhood?

A

Ventricular septal defect

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88
Q

What is the most common type of ventricular septal defect?

A

Perimembranous

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89
Q

What may be found on physical exam in a patient with a ventricular septal defect?

A
  • High-pitched harsh holosystolic murmur best heard at the lower left sternal border
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90
Q

What is the management of a ventricular septal defect?

A
  • If small and asymptomatic, observation (most close within 12 months)
  • Patch closure if symptomatic or uncontrolled CHF, growth delay, recurrent respiratory infections. Large shunts repaired by 2 years of age to prevent pulmonary HTN.
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91
Q

List the congenital cyanotic heart disease.

A

The 5 T’s:

  • Truncus arteriosus (1 vessel instead of 2)
  • Transposition of the great arteries
  • Tricuspid atresia (absence of tricuspid valve)
  • Tetralogy of fallot
  • Total anomalous pulmonary venous return (all 4 pulmonary veins connect to superior vena cava instead of left atrium)
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92
Q

What is the pathophysiology associated with pulmonary atresia?

A

Complete obstruction to right ventricular outflow. Blood is unable to flow from the right ventricle into the pulmonary artery and the lungs.

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93
Q

What clinical manifestations are associated with pulmonary atresia?

A
  • Cyanosis

- Single heart sound (due to single semi-lunar valve - aortic valve)

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94
Q

What are some risk factors for CAD?

A
  • Diabetes mellitus (worst risk factor)
  • Smoking (most important modifiable risk factor)
  • Hyperlipidemia
  • Hypertension
  • Men
  • Age > 45 in men or > 55 in women
  • Family hx of CAD
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95
Q

What symptoms are typically associated with angina pectoris (stable angina)?

A
  • Substernal chest pain which is exertional and short in duration and relieved with rest or Nitroglycerin; pain may radiate
  • Dyspnea, nausea, vomiting diaphoresis
  • Dyspnea and epigastric or shoulder pain seen in women, elderly, obese
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96
Q

What is the initial test of choice when diagnosing stable angina?

What classic finding may be found with this test?

A

EKG

ST depression is classic finding

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97
Q

What is the typical outpatient management of stable angina?

A
  • Daily aspirin
  • Beta blocker (or CCB if BB contraindicated)
  • Sublingual nitroglycerin
  • Daily statin
  • Reduction of risk factors through exercise, diet, and smoking cessation
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98
Q

What is the most useful non-invasive test in the diagnosis of CAD?

A

Stress testing

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99
Q

What is the gold standard for diagnosis of CAD?

A

Coronary angiography

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100
Q

What is the purpose of giving beta blockers in stable angina?

A
  • Increase myocardial blood supply by increasing oxygen through prolonging coronary artery filling times
  • Decrease demand
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101
Q

What is the purpose of giving aspirin in stable angina?

A
  • Prevents platelet activation/aggregation (inhibits COX –> decreasing thromboxane A2)
  • Decrease thrombosis risk
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102
Q

What is the purpose of giving nitroglycerin in stable angina?

A
  • Increase myocardial blood supply by increasing blood flow and reducing coronary vasospasm
  • Decrease cardiac demand by decreasing preload and afterload through vasodilation (vasodilation occurs due to stimulation of guanylate cyclase, which increases cGMP)
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103
Q

What are contraindications to giving nitroglycerin for angina?

A
  • SBP < 90 (as nitro can cause hypotension via vasodilation)
  • RV infarction
  • Use of Sildenafil (Viagra) and other PDE-5 inhibitors (combo can lead to severe hypotension)
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104
Q

What are some etiologies of ACS?

A
  • Atherosclerosis (most common cause of MI)

- Coronary artery vasospasm: cocaine-induced, variant (Prinzmetal) angina

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105
Q

What symptoms are typically associated with ACS?

A
  • Chest pain that is severe and new in onset, occurs at rest, lasting > 30 minutes, and not relieved with rest or nitroglycerin; can radiate
  • Dyspnea, nausea, vomiting diaphoresis
  • Dyspnea and epigastric or shoulder pain seen in women, elderly, obese
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106
Q

What is the triad of right ventricular infarction?

A

Increased JVP + clear lungs + Kussmaul sign

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107
Q

What EKG leads will show ST elevations in an anterior wall infarction?

What artery is involved?

A

V1 through V4

Left Anterior Descending (LAD)

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108
Q

What EKG leads will show ST elevations in a lateral wall infarction?

What artery is involved?

A

Leads I, aVL, V5, V6

Left circumflex artery

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109
Q

What EKG leads will show ST elevations in an inferior wall infarction?

What artery is involved?

A

Leads II, III, aVF

Right Coronary Artery (RCA)

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110
Q

What EKG leads are involved with a posterior wall infarction?

A

ST depressions in V1-V2

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111
Q

What is the management for an anterior or lateral wall MI?

A

Initial: Aspirin (chewed), Nitroglycerin, Oxygen (if hypoxic), Morphine (if nitro fails) MONA

Adjunct: Heparin, Beta blockers, Clopidogrel (Plavix)

Long-term management with ACE-I slows progression to heart failure

Reperfusion/Cath lab (PCI) within 90 minutes of ER presentation and within 12 hours of chest pain onset

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112
Q

What medication should be avoided in an inferior or posterior wall MI?

A

Avoid Nitroglycerin and Morphine as right-sided MIs are preload dependent to maintain cardiac output (nitro is pre-load reducing)

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113
Q

What are some contraindications to giving beta blockers in CAD/ACS?

A
  • CHF
  • Bradycardia
  • Hypotension
  • Severe reactive airway disease (severe asthma, COPD)
  • Shock
  • Cocaine-induced MI (causes unopposed alpha mediated vasoconstriction)
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114
Q

What are some adverse effects of nitroglycerin?

A
  • Headache
  • Flushing
  • Hypotension
  • Tachyphylaxis after 24 hours
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115
Q

What are some adverse effects of ACE-I?

A
  • Angioedema
  • Cough
  • Hyperkalemia
  • Renal insufficiency
  • Hyperuricemia
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116
Q

What is the MOA of Alteplase (rTPA)?

A

Dissolves clot by activating tissue plasminogen –> plasmin

***Plasmin is a proteolytic enzyme that degrades fibrin

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117
Q

When is Alteplase (rTPA) used in STEMI treatment?

A

Used if PCI is not an option or unable to get PCI early

118
Q

What is Streptokinase and why is it used?

A

Thrombolytic that binds to plasminogen and activates it into plasmin.

Only used in patients in whom PCI is contraindicated and patient has a high risk of intracerebral hemorrhage

119
Q

What are clinical manifestations associated with Vasospastic (Variant, Prinzmetal) Angina?

A

Chest pain at rest (especially midnight to early morning)

120
Q

What may be seen on EKG in Vasospastic (Variant, Prinzmetal) Angina?

A

Transient ST elevations in affected artery that resolve with symptom resolution (may resolve with CCB or nitroglycerin)

121
Q

What is the first-line management for Vasospastic (Variant, Prinzmetal) Angina?

What is the second-line?

A

1st-line: Calcium channel blockers at night (Diltiazem, Verapamil, Amlodipine, Nicardipine)

2nd-line: Nitroglycerin

122
Q

What medication should be avoided in coronary vasospasm disorders (cocaine-induced and Prinzmetal)? Why?

A

Beta blockers are avoided as they may lead to unopposed vasospasm

***alpha receptors vasoconstrict and beta receptors vasodilate

123
Q

What is the pathophysiology behind a cocaine-induced MI?

A

Coronary artery vasospasm due to cocaine’s activation of the sympathetic nervous system and alpha-1 receptors, leading to vasoconstriction of the coronary arteries

124
Q

What will be seen on an EKG if a patient is suffering from a cocaine-induced MI?

A

Transient ST elevations

125
Q

What is the management of a cocaine-induced MI?

A

Calcium channel blockers and nitroglycerin to reverse the vasospasm.

***Often treated with aspirin, Heparin, and benzos until atherosclerotic disease is ruled out

126
Q

What is the most common cause of heart failure?

A

Coronary artery disease

127
Q

What are the most common causes of left-sided heart failure versus right-sided heart failure?

A

Left sided: CAD and HTN

Right-sided: Left-sided heart failure, pulmonary disease

128
Q

What are common characteristics of systolic heart failure?

***think EF and heart chambers

A
  • Decreased ejection fraction
  • Thin ventricular walls
  • Dilated LV chamber
  • S3 gallop
129
Q

What are common etiologies of systolic heart failure?

A
  • Post myocardial infarction

- Dilated cardiomyopathy

130
Q

What are common characteristics of diastolic heart failure?

***think EF and heart chambers

A
  • Preserved ejection fraction
  • Thick ventricular walls
  • Small LV chamber
  • S4 gallop
131
Q

What are common etiologies of diastolic heart failure?

A
  • HTN
  • LVH
  • Elderly
  • Valvular heart disease
  • Constrictive pericarditis
132
Q

What are clinical manifestations and physical exam findings of left-sided heart failure?

A

Symptoms:

  • Dyspnea (most common)
  • Fatigue
  • Chronic cough (either nonproductive or pink/frothy)
  • **symptoms are due to fluid back up into the lungs (L for lungs and L-sided)

Physical:

  • Rales, rhonchi, tachypnea (due to pulmonary edema/congestion)
  • Cheyne-Stokes breathing (deeper, faster breathing with gradual decrease and periods or apnea/cyanosis)
  • S3 gallop (systolic) or S4 gallop (diastolic)
  • Cool extremities, dusky pale skin
133
Q

What are clinical manifestations and physical exam findings of right-sided heart failure?

A
  • Peripheral edema (fluid backing up in IVC)
  • JVD (fluid backing up in SVC/increased JVP)
  • Hepatojugular reflex (increased JVP with liver palpation)
  • GI and hepatic congestion
134
Q

What is the diagnostic test of choice in the outpatient setting to make the diagnosis of heart failure?

A

Echocardiogram

135
Q

What are the initial tests of choice for suspected congestive (decompensated) heart failure (CHF)?

A

Chest radiograph and BNP

136
Q

What BNP value indicates that CHF is likely?

A

BNP > 100

***Ventricles release BNP during volume overload (CHF) in attempt to reverse the process (causing decreased RAAS, decreased total body fluid volume, increased sodium excretion)

137
Q

What medication is first-line for HFrEF (systolic)?

A

ACE-I (+ diuretic for symptoms)

138
Q

When would a beta blocker be used in heart failure?

A

HFrEF with no or minimal current evidence of fluid retention. Usually added after ACE-I or ARB if additional treatment is needed.

***Discontinue or reduce dose in decompensated CHF

139
Q

When would a hydralazine + nitrate combination be used for heart failure?

A

In African-Americans with NYHA class III to IV HF with LVEF < 40% despite optimal therapy

140
Q

What diuretics are the most effective treatment for symptoms for mild-moderate CHF?

What are some adverse effects of these medications?

A

Loop diuretics such as Furosemide (Lasix), Bumetanide, Torsemide

AE: Hyperglycemia, hyperuricemia (is an acid and competes with uric acid for excretion), hypokalemia, sulfa allergies

141
Q

What are some adverse effects of potassium sparing diuretics such as spironolactone?

A

Hyperkalemia, gynecomastia, metabolic acidosis

142
Q

What are some indications to using a sympathomimetic/positive inotrope such as Digoxin?

A
  • Systolic heart failure (decrease hospitalizations but not mortality)
  • Atrial fibrillation (in patient whom BB and/or CCB are contraindicated such as hypotension or CHF)
143
Q

What can be seen on an EKG if patient is taking Digoxin/digitalis?

A
  • Downsloping of the ST segment

- PVCs common

144
Q

What does digitalis toxicity cause in regards to electrolytes and symptoms?

A
  • Digitalis toxicity directly causes hyperkalemia but hypokalemia prediposese to Digoxin toxicity

Symptoms:

  • GI symptoms (most common)
  • Visual changes (yellow/green color changes)
  • Arrhythmias (bradycardia, A-fib)
145
Q

What is Nesiritide and when is it used?

A

Synthetic BNP used for CHF in the ER or inpatient setting

146
Q

What are some CXR findings consistent with CHF?

A
  • Kerley B lines
  • Butterfly (Batwing) pattern
  • Cardiomegaly
147
Q

Compare the BP readings between elevated BP, stage I HTN, and stage II HTN.

A

Elevated: 120-129 systolic and < 80 diastolic

Stage I HTN: 130-139 systolic or 80-89 diastolic

Stage II HTN: 140 or greater systolic or 90 or greater diastolic

148
Q

How can HTN be diagnosed?

A

Systolic BP of 130 or more and/or diastolic BP 80 or more. The elevations must be at least 2 different readings on at least 2 different visits.

149
Q

What is the most common cause of primary HTN?

Secondary HTN?

A

Primary: Idiopathic

Secondary: Renovascular disease

150
Q

What is included in the initial workup for HTN?

A

12 lead EKG, funduscopy (looking for retinopathy), creatinine, cholesterol, urine albumin to creatinine ratio

151
Q

If a patient is newly diagnosed with HTN, what should the initial management be?

A

Lifestyle management including weight loss, DASH diet, exercise, smoking cessation, salt restriction (2.4 or less g/day), limit alcohol consumption

152
Q

What is the typical blood pressure target in patients with HTN?

A

< 140/90

< 150/90 in adults 60 years or older

153
Q

What four classes of medication are used in initial HTN therapy when lifestyle management has failed?

A
  • Thiazide-type diuretics
  • ACE-I
  • ARB
  • Calcium channel blockers
154
Q

Describe the different MOA between the different classes of calcium channel blockers.

Which class is more commonly used in HTN?

A

Dihydropyridines (Nifedipine, Amlodipine): potent vasodilators with little or no effect on cardiac contractility or conduction

Non-dihydropyridines (Verapamil, Diltiazem): affects cardiac contractility and conduction, potent vasodilator

Dihydropyridines (Nifedipine, Amlodipine) more commonly used in HTN.

155
Q

What are some adverse effects of calcium channel blockers?

When are they contraindicated?

A
  • Vasodilation: headache, dizziness, lightheadedness, flushing, peripheral edema.
  • Constipation with Verapamil.

Contraindicated in CHF (especially non-dihydropyridines), 2nd/3rd degree heart block

156
Q

Define hypertensive urgency.

What are some common clinical manifestations?

What is the management?

A

SBP > 180 and/or DBP > 120 WITHOUT evidence of end organ damage.

Clinical Manifestations: headache (most common), chest pain, dyspnea, focal neuro deficits, nausea, vomiting

Management: Gradual reduction of MAP by no more than 25% over 24-48 hours with oral medications (Clonidine, Captopril, Labetalol, Nicardipine, Furosemide). Treatment goals are BP < 160/100

157
Q

What is the MOA for Clonidine?

What are some adverse effects?

A

MOA: Centrally acting alpha 2 adrenergic agonist

Adverse effects: headache, tachycardia, rebound HTN if discontinued abruptly (mimics pheochromocytoma)

158
Q

Define hypertensive urgency.

What are some common clinical manifestations?

What is the management?

A

SBP > 180 and/or DBP > 120 WITH evidence of end organ damage.

Clinical Manifestations: headache (most common), chest pain, dyspnea, nausea, vomiting, stroke, ACS, aortic dissection, AKI, severe retinopathy

Management: Gradual reduction of MAP by about 10-20% in the first hour and by an additional 5-15% over the next 23 hours.

159
Q

While the main objective during hypertensive urgency/emergency is to gradually lower the BP, what are three exceptions to this?

A
  • Acute phase of an ischemic stroke: BP not lowered unless > 185/110 in patients who are candidates for reperfusion OR > 220/120 for those who are not candidates
  • Acute aortic dissection: SBP rapidly lowered to a goal of 100-120 mmHg within 20 minutes
  • Intracerebral hypertension
160
Q

Define postural hypotension.

Other than labs, what testing is included in the workup for postural hypotension?

What is the management?

A

Hypotension with 2-5 minutes of quiet standing defined by at least 20 mmHg fall in SBP and/or at least 10 mmHg fall in DBP.

Tilt table test: BP reduction at a 60-degree angle.

Management: Conservative initial management of choice includes increasing salt and fluid intake, gradual position changes, discontinuing offending medications. Fludrocortisone is the first-line medical management for persistent symptoms.

161
Q

What are some clinical manifestations associated with hypovolemic shock?

A
  • Loss of volume –> tachycardia, hypotension, vasoconstriction
  • Increased SVR –> pale/cool/dry skin (due to vasoconstriction), slow cap refill > 2 seconds, decreased skin turgor, dry mucus membranes

***Usually does not cause profound respiratory distress

162
Q

What is the management of hypovolemic shock?

A
  1. ACBDE’s
  2. Volume resuscitation with crystalloids (NS or Lactated Ringer’s; often 3-4 liters)
  3. Control source of hemorrhage
  4. Prevention of hypothermia, treat any coagulopathies
163
Q

What is the management for cardiogenic shock?

A
  1. Oxygen, isotonic fluids (use smaller amounts of fluid)
  2. Inotropic support to increase myocardial contractility and cardiac output (Dobutamine, Epinephrine)
  3. Treat underlying cause
164
Q

What are some etiologies of obstructive shock?

A
  • Massive PE: obstruction to pulmonary artery blood flow
  • Pericardial tamponade: blood in pericardial space prevents venous return to heart
  • Tension pneumothorax: positive air pressure causes external pressure on the heart
  • Aortic dissection
165
Q

What is the management for obstructive shock?

A
  • Oxygen, isotonic fluids, inotropic support

- Treat the underlying cause

166
Q

What are the four types of distributive shock and which is the most common?

A
  • Septic shock (most common)
  • Anaphylactic shock
  • Neurogenic shock
  • Endocrine shock
167
Q

What are clinical manifestations associated with sepsis?

A
  • Hypotension with wide pulse pressure
  • Warm, flushed extremities (early phase)
  • Met SIRS criteria (discussed on another notecard)

***Only major type of shock associated with increased cardiac output combined with decreased SVR, leading to fast capillary refill time and flushed, warm extremities

168
Q

What is required to meet SIRS criteria?

A

At least 2 of the 4 following:

  • Temperature: fever > 38C/100.4F or hypothermia
  • Pulse: > 90 bpm
  • Respiratory rate: > 20 or PaCO2 < 32
  • WBC count: > 12,000 or < 4,000
169
Q

Compare the definition of sepsis, severe sepsis, and septic shock.

A
  • Sepsis: SIRS + focus of infection . Often associated with increased lactate ( > 4 mmol/L)
  • Severe Sepsis: SIRS + multi system organ failure
  • Septic shock: Sepsis + refractory hypotension despite fluid administration
170
Q

What is the management for septic shock?

A
  • Broad spectrum IV antibiotics (Zosyn + Ceftriaxone)
  • **choose depending on suspected organism
  • IV fluid resuscitation: isotonic crystalloids
  • Vasopressors if no response to 2-3L of fluids
171
Q

What is the management for anaphylatic shock?

A
  • Epinephrine (1st-lie)
  • Airway management
  • Antihistamines
  • Observe patients for 4-6 hours (some patients have biphasic phenomenon and return of symptoms)
172
Q

What is the pathophysiology behind neurogenic shock?

A

Acute spinal cord injury or regional anesthesia leads to autonomic sympathetic blockade –> unopposed increased vagal tone –> bradycardia and hypotension

173
Q

What are clinical manifestations associated with neurogenic shock?

What is the management?

A

Clinical signs:

  • Warm, dry skin (loss of sympathetic tone)
  • Bradycardia, hypotension
  • Wide pulse pressure

Management:
- Fluids and pressors

174
Q

What is an example of endocrine shock and its associated treatment?

A

Adrenal insufficiency (Addisonian crisis)

Hydrocortisone 100 mg IV

175
Q

What are clinical manifestations associated with hyperlipidemia?

A
  • Most are asymptomatic

- May develop Xanthomas (Achilles tendon) or Xanthelasma (lipid plaques on the eyelids)

176
Q

When should screening for hyperlipidemia be done?

A

Higher risk: initiate screening at age 20-25 for males, 30-35 for females

Lower risk: initiate screening at 35 for males and 45 for females

177
Q

What are the best medications to decrease LDL levels?

What are the best medications to decrease triglyceride levels?

What are the best medications to increase HDL levels?

A

LDL: Statins

Triglycerides: Fibrates

HDL: Niacin

178
Q

What medication is best to use in pregnancy to decrease LDL levels?

A

Bile acid sequestrants (Cholestyramine, Colestipol, Colesevelam)

***Statins are contraindicated in pregnancy

179
Q

What are some adverse effects of statins?

A
  • Muscle damage (myositis, rhabdomyolysis)

- Increased liver function tests, hepatitis

180
Q

What are some adverse effects of Niacin?

A
  • Increased prostaglandins: flushing, warm sensation, pruritis (pre-treatment of 30 minutes with NSAIDs or aspirin to counter flushing)
  • Hyperuricemia
  • Hyperglycemia
  • GI symptoms (take with meals)
181
Q

What are some adverse effects of Fibrates (Fenofibrate, Gemfibrozil)

A
  • Increased gallstones
  • Increased liver function tests
  • Headache, dizziness
182
Q

What are some adverse effects of bile acid sequestrants (Cholestyramine, Colestipol, Colesevelam)?

A
  • Increased triglyceride levels
  • GI
  • May impair absorption of other medications (antibiotics, Digoxin, warfarin, fat-soluble vitamins)
183
Q

What heart valve is most commonly associated with infective endocarditis?

A

Mitral valve

Exception is IV drug use - tricupsid valve is most common in IV drug users

184
Q

What organism is most commonly associated with each type of infective endocarditis (acute bacterial, subacute bacterial, IV drug-related, prosthetic valve)?

A

Acute bacterial endocarditis: S. aureus (affects normal valves)

Subacute bacterial endocarditis: S. viridans (affects damaged valves)
***part of oral flora (associated with poor dentition or dental procedures)

IV drug-related endocarditis: S. aureus (especially MRSA)

Prosthetic valve endocarditis: Staphylococcus epidermis (early, within 60 days of procedure)

185
Q

If patient has presumed endocarditis, but negative blood cultures, what organisms should you suspect?

A

HACEK organisms

186
Q

What are some clinical manifestations of infective endocarditis?

A
  • Persistent fever (most common)
  • New onset murmur or worsening of existing murmur
  • Osler nodes: painful/tender raised violaceous nodules on pads of digits/palms
  • Janeway lesions: painless erythematous macules on palms and soles
  • Splinter hemorrhages: linear reddish-brown lesions under nail beds
  • Roth spots: retinal hemorrhages with central clearing
187
Q

What Modified Duke Criteria must be met for diagnosis of endocarditis?

A

2 major OR 1 major + 3 minor OR 5 minor

188
Q

What is the treatment for infective endocarditis of a native valve?

A

Anti-staphylococcal penicillin (Nafcillin, Oxacillin) + Ceftriaxone or Gentamicin for 4-6 weeks

189
Q

What is the treatment for infective endocarditis of a prosthetic valve?

A

Vancomycin + Gentamicin + Rifampin for 4-6 weeks

190
Q

Which cardiac conditions should be treated with endocarditis prophylaxis prior to certain procedures (dental, respiratory, infected skin/MSK tissue)?

What medication is prescribed for this prophylaxis?

A
  • Prosthetic heart valves
  • Heart repairs using prosthetic material (not including stents)
  • Prior history of endocarditis
  • Congenital heart disease
  • Cardiac valvulopathy in transplanted heart

Prophylaxis:

  • Amoxicillin 2 grams 30-60 minutes before procedure
  • Clindamycin 600 mg if penicillin allergy
191
Q

What is Libman-Sacks Endocarditis?

A

Nonbacterial thrombotic endocarditis due to sterile platelet thrombi deposition on the affected valve which can be seen with malignancy, SLE, rheumatic fever, other inflammatory conditions

192
Q

What are Osler nodes and what condition are they associated with?

A

Painful/tender raised violaceous nodules on pads of digits/palms associated with endocarditis

193
Q

What are Janeway lesions and what condition are they associated with?

A

Painless erythematous macules on palms and soles associated with endocarditis

194
Q

What are the most common causes of acute pericarditis?

A
  • Idiopathic

- Viral (especially Coxsackievirus and Echovirus)

195
Q

What is Dressler syndrome and how is it treated?

A

Post-MI pericarditis + fever + pleural effusion

Treated with Aspirin or Cholchicine (avoid NSAIDs as they can interfere with myocardial scar formation)

196
Q

What are clinical manifestations associated with acute pericarditis?

A
  • Pleuritic chest pain which is worse when supine and improved with sitting foward
  • Pericardial friction rub (best heart when leaning forward)
197
Q

What EKG findings are suggestive of acute pericarditis?

A

Diffuse ST elevations in the precordial leads (V1-V6) with associated PR depressions

198
Q

What is the management for acute pericarditis?

A
  • NSAIDs or aspirin are first-line x 7-14 days

- Colchicine is second-line

199
Q

What are clinical manifestations of pericardial effusion?

A
  • Chest pain, dyspnea, fatigue

- Decreased (muffled) heart sounds due to fluid

200
Q

What is the test of choice for diagnosis of pericardial effusion?

A

Echocardiogram

201
Q

What may be found on EKG in pericardial effusion?

A
  • Electrical alternans

- Low QRS voltage

202
Q

What is the management for pericardial effusion?

A
  • Treat underlying cause

- Large effusions may require pericardiocentesis

203
Q

What is Beck’s triad and what condition is it associated with?

A

Distant (muffled) heart sounds + JVD + hypotension

Associated with cardiac tamponade

204
Q

What clinical manifestations are associated with cardiac tamponade?

A
  • Beck’s triad: distant (muffled) heart sounds + JVD + hypotension
  • Pulsus paradoxus: exaggerated decrease in SBP with inspiration
  • Dyspnea, fatigue, cool extremities
205
Q

What will be seen on echocardiogram, EKG, and chest x-ray in cardiac tamponade?

A

Echo: pericardial effusion + diastolic collapse of cardiac chambers

EKG: Electrical alternans and low voltage QRS (signs of pericardial effusion)

CXR: enlarged cardiac silhouette

206
Q

What is the management for cardiac tamponade?

A

Immediate pericardiocentesis to remove the pressure on the heart

207
Q

What is the pathophysiology behind constrictive pericarditis?

A

Loss of pericardial elasticity due to fibrosis leading to restriction of ventricular diastolic filling

208
Q

What are clinical manifestations of constrictive pericarditis?

A
  • Dyspnea
  • Right-sided heart failure: increased JVD, peripheral edema, increased hepatojugular reflex, Kussmaul’s sign (increase in JVP with inspiration)
  • Pericardial knock: high pitched diastolic sound similar to S3 due to sudden cessation of ventricular filling
209
Q

What will be seen on imaging (echo, CT scan, MRI) in constrictive pericarditis?

A

Pericardial thickening and/or calcification

210
Q

What is the management of constrictive percarditis?

A
  • Diuretics for symptom relief

- Pericardiectomy is definitive management

211
Q

If a murmur is harsh/rumbling in quality, should you think stenosis or regurgitation?

What about a blowing quality?

A

Harsh/Rumble = Stenosis

Blowing = Regurgitation

212
Q

What positions increase venous return and how does this affect certain murmurs?

A

Supine, squatting, leg elevation

Increases intensity of ALL murmurs except for hypertrophic cardiomyopathy

213
Q

What positions decrease venous return and how does this affect certain murmurs?

A

Standing, valsalva maneuver

Decreases the intensity of ALL murmurs except for hypertrophic cardiomyopathy

214
Q

Which murmurs are systolic versus diastolic?

A

Systolic - Aortic stenosis, mitral regurgitation

Diastolic - Aortic regurgitation, mitral stenosis

215
Q

How does inspiration affect murmurs?

A

Increases intensity of all right-sided murmurs as it increases venous return on the right side. Right-sided murmurs best heard with inspiration.

Decreases intensity of all-left sided murmurs.

216
Q

How does expiration affect murmurs?

A

Increases intensity of all left-sided murmurs as it increases venous return on the left side. Left-sided murmurs best heard after maximal expiration.

217
Q

What are some clinical manifestations of aortic stenosis?

A
  • Dyspnea
  • Angina
  • Syncope
  • CHF

***once symptomatic, lifespan dramatically reduced

218
Q

Describe the murmur associated with aortic stenosis including what increases and decreases its intensity.

A

Systolic crescendo-decrescendo murmur best heard at the right upper sternal border, radiating to the carotid artery

Increased intensity with sitting while leaning forward, squatting, supine, and leg raise (increased venous return)

Decreased intensity with valsalva and standing (decreased venous return), handgrip

219
Q

What is the best diagnostic test for aortic stenosis?

What test provides a definitive diagnosis

A

Echocardiogram

Cardiac cath

220
Q

What will be seen on EKG in aortic stenosis?

A

Left ventricular hypertrophy

221
Q

What is both the only effect treatment and the treatment of choice for aortic stenosis?

A

Aortic valve replacement

  • Mechanical: must be placed on long-term anticoagulant
  • Bioprosthetic: used in patients that are not candidates for anticoagulant
222
Q

Prior to surgery, what should be advised for a patient with severe aortic stenosis?

A

Avoid physical exertion, vasodilators (nitrates), and negative inotropes (CCB, beta blockers)

223
Q

Describe the murmur associated with aortic regurgitation including what increases and decreases its intensity.

A

Diastolic blowing descrescendo murmur best heard at the left upper sternal border

Increased intensity with sitting while leaning forward, squatting, supine, and leg raise (increased venous return), handgrip

Decreased intensity with valsalva and standing (decreased venous return), amyl nitrate (decreases afterload, leading to less resistance to blood flow thus less blood being regurgitated)

224
Q

A weak, delayed carotid pulse and narrow pulse pressure is associated with which kind of murmur?

A

Aortic stenosis

225
Q

Bounding pulses with wide pulse pressure is associate with which kind of murmur?

A

Aortic regurgitation

226
Q

What is Hill’s sign?

A

Classic sign of wide pulse pressure in aortic regurgitation in which popliteal artery systolic pressure > brachial artery by 60 mmHg

227
Q

What is Water Hammer pulse?

A

Classic sign of wide pulse pressure in aortic regurgitation in which there is a swift upstroke and rapid fall of radial pulse accentuated with wrist elevation

228
Q

What is Quincke’s pulses

A

Classic sign of wide pulse pressure in aortic regurgitation in which there are visible fingernail bed pulsations with light compression of fingernail bed

229
Q

What diagnostic study provides a definitive diagnosis of aortic regurgitation?

A

Cardiac cath

230
Q

What are management options for aortic regurgitation?

A

Medical management: afterload reduction (ACE-I, ARBs, Nifedipine, Hydralazine)

Surgical management: definitive management

231
Q

What is most always the cause of mitral stenosis?

A

Rheumatic heart disease

***most common onset in 3rd/4th decade, but if rheumatic in origin, symptoms begin in 20-30s

232
Q

How does mitral stenosis lead to CHF?

A

Obstruction of flow from LA to LV –> blood backs up into the left atrium –> increased left atrial pressure/volume overload –> pulmonary HTN –> CHF

233
Q

What are clinical manifestations associated with mitral stenosis?

A
  • Pulmonary symptoms: dyspnea (most common), hemoptysis, cough, pulmonary HTN
  • Atrial fibrillation: secondary to atrial enlargement
  • Right-sided heart failure: due to prolonged pulmonary HTN
  • Mitral facies = ruddy (flushed) cheeks with facial pallor
  • Ortner’s syndrome: recurrent laryngeal nerve palsy due to compression by the dilated left atrium leading to hoarseness
234
Q

Describe the murmur associated with mitral stenosis including what increases and decreases its intensity.

A

Prominent S1 with opening snap. Low-pitched, mid-diastolic rumbling murmur best heard at the apex.

Increased intensity with left lateral decubitus position as well as squatting, supine, and leg raise (increased venous return)

Decreased intensity with valsalva and standing (decreased venous return)

235
Q

What will be found on EKG in mitral stenosis?

A
  • Left atrial enlargement (P wave > 3 mm, biphasic P wave in V1 and V2)
  • Atrial fibrillation
  • Pulmonary HTN (RVH, RAD)
236
Q

What is the management for mitral stenosis?

A
  • Percutaneous balloon valvuloplasty: best treatment for symptomatic MS in younger patients
  • Valve replacement: if valvuloplasty is contraindicated or if unfavorable valve morphology
  • Medical: diuretics and sodium restriction for edema and volume overload. Rate control of A-fib with beta blockers, CCB, or Digoxin.
  • Anticoagulation in patients with A-fib (warfarin)
237
Q

What is the most common cause of mitral regurgitation in the US?

A

Mitral valve prolapse

238
Q

What are some clinical manifestations associated with mitral regurgitation?

A
  • Chronic: heart failure symptoms (dyspnea, fatigue), atrial fibrillation, HTN
  • Acute: pulmonary edema
239
Q

Describe the murmur associated with mitral regurgitation including what increases and decreases its intensity.

A

High-pitched, blowing holosystolic murmur best heard at the apex with radiation to the axilla

Increased intensity with left lateral decubitus position, handgrip, squatting, supine, and leg raise (increased venous return)

Decreased intensity with valsalva and standing (decreased venous return), amyl nitrate (decreases afterload, leading to less resistance to blood flow thus less blood being regurgitated)

240
Q

What is the most useful non-invasive test for diagnosis of mitral murmurs?

A

Echocardiogram

241
Q

What is the management for mitral regurgitation?

A

Medical: symptom control with afterload reducers (ACE-I, ARBs, hydralazine, nitrates) or diuretics

Surgical: repair preferred over replacement (indicated if EF is 60% or less or refractory to medical treatment)

242
Q

What are some etiologies of mitral valve prolapse?

A
  • Myxomatous degeneration of the mitral valve

- Connective tissue disease

243
Q

What are more common clinical manifestations associated with mitral valve prolapse?

A
  • Most are asymptomatic

- Autonomic dysfunction: atypical chest pain, panic attacks, palpitations

244
Q

What physical exam findings are consistent with mitral valve prolapse?

A

Narrow AP diameter, low body weight, hypotension, pectus excavatum

Mid-late systolic ejection click best heard at the apex

  • any maneuver that makes the LV smaller (decreases preload - valsalva, standing) results in an earlier click
  • any maneuver that makes the LV bigger (increases preload - squatting, leg raise, supine) results in delayed click
245
Q

What is the management for mitral valve prolapse?

A
  • Reassurance in most patients

- Beta blockers in those with automatic dysfunction

246
Q

What is Ortner’s syndrome and what condition is it associated with?

A

Recurrent laryngeal nerve palsy due to compression by the dilated left atrium in mitral stenosis, leading to hoarseness.

247
Q

What is the etiology of pulmonic stenosis?

How is the associated murmur described?

What is the treatment?

A

Almost always congenital and a disease of the young

Harsh, mid-systolic ejection crescendo-decrescendo murmur at the left upper sternal border which radiates to the neck and increases with inspiration.

Balloon valvuloplasty is the preferred treatment.

248
Q

What is the etiology of pulmonic regurgitation?

What are symptoms associated with it?

How is the associated murmur described?

What is the treatment?

A

Almost always congenital.

Clinical insignificant, but if symptomatic then will have right-sided heart failure symptoms due to RV volume overload.

Graham-Steell murmur: brief decrescendo early diastolic murmur at the left upper sternal border with full inspiration. Increased intensity with increased venous return (squatting, supine, inspiration).

No treatment needed in most.

249
Q

Describe the Graham-Steell murmur. What condition is it associated with?

A

Brief decrescendo early diastolic murmur at the left upper sternal border with full inspiration.

Associated with pulmonic regurgitation.

250
Q

What is Carvallo’s sign and why is it helpful?

A

Increased murmur intensity with inspiration.

Helps to distinguish tricupsid regurgitation from mitral regurgitation.

251
Q

What are four major risk factors associated with an abdominal aortic aneurysm (AAA)?

What is the most common site of a AAA?

A

Smoking, age > 60 years, Caucasian, male

Infrarenal most common site

252
Q

What are some clinical manifestations associated with an abdominal aortic aneurysm?

A
  • Most patients are asymptomatic and AAA is found incidentally on imaging
  • Symptomatic (unruptured): abdominal, flank, or back pain, abdominal bruit, pulsatile abdominal mass
  • Symptomatic (ruptured): Same as unruptured + hypotension or syncope and flank ecchymosis
253
Q

What imaging is the best initial test to obtain in a symptomatic AAA patient who is hemodynamically stable versus unstable.

What about in an asymptomatic patient with suspected AAA?

A

Stable: CT scan with IV contrast

Unstable: Bedside ultrasound

Asymptomatic: Abdominal ultrasound

254
Q

What are the guidelines for AAA screening?

A

One-time screening via abdominal ultrasound in men 65-75 years of age who ever smoked.

255
Q

What AAA size warrants immediate surgical repair?

A

5.5 cm or greater OR > 0.5 cm expansion in 6 months

256
Q

Where is the most common site for an aortic dissection?

What is the most important risk factor for an aortic dissection?

A

Ascending is most common.

Hypertension

257
Q

What are clinical manifestations associated with an aortic dissection?

A
  • Sudden onset of severe, tearing chest/upper back pain which may radiate between the scapulae
  • Unequal blood pressure in both arms
  • Can be hypertensive or hypotensive
258
Q

What are commonly used first-line imaging modalities in suspected aortic dissection?

A
  • CT angiogram***
  • MR angiogram
  • TEE
259
Q

What types of aortic dissection require surgical versus medical treatment?

What is used in medical treatment?

A

Surgical: Acute proximal/ascending (Stanford A/DeBakey I and II) OR distal with complications

Medical: Descending/distal (Standford B/DeBakey III)
***Nonselective beta blockers (Labetalol) with sodium nitroprusside added if needed. SBP rapidly lowered to 100-120 within 20 minutes.

260
Q

What are clinical manifestations of peripheral artery disease (PAD)?

A
  • Intermittent claudication is most common (lower extremity pain with ambulation)
  • Ischemic rest pain: in advanced disease. Most common at night and relieved with foot dependency.
261
Q

What physical exam findings are consistent with peripheral artery disease?

A
  • Decreased or absent pulses
  • Atrohpic skin changes (thin/shiny skins, hair loss, muscle atrophy, cool limbs)
  • Ulcers (lateral malleolar ulcers)
  • Pale skin on elevation, dependent rubor (dusky red with dependency)
262
Q

What is the MOST USEFUL screening test for peripheral artery disease?

A

Ankle-brachial index (ABI)

***Positive for PAD if ABI is < 0.09. Normal ABI is 1-1.2.

263
Q

What is the gold standard diagnostic test for peripheral artery disease?

A

Arteriography

264
Q

What is the management for peripheral artery disease?

A
  • First-line is supportive: exercise, smoking cessation, reduce risk factor such as HLD
  • Platelet inhibitor: Cilostazol most effect medical therapy (Aspirin, Clopidogrel are other choices)
  • Revascularization: Percutaneous transluminal angioplasty is first-line procedure
265
Q

What is the most common etiology for acute arterial occlusion?

A

Thrombotic occlusion is most common; most common in the superficial femoral or popliteal artery

266
Q

What are clinical manifestations of acute arterial occlusion?

A
  • 6 P’s: paresthesias, pain, pallor, pulselessness, poikilothermia, paralysis
  • Decreased cap refill, cool temperature
267
Q

What does the workup include in acute artieral occlusion?

What does the management include?

A

Bedside arterial doppler to assess for pulses. CT angiography.

Reperfusion is mainstay of treatment - surgical bypass, surgical or catheter based thromboembolectomy.

268
Q

If a young smoker/tobacco user presents with distal extremity ischemia/ischemic ulcers or gangrene of the digits, what should you suspect?

A

Thromboangiitis Obliterans (Buerger’s Disease)

269
Q

What is Thromboangiitis Obliterans (Buerger’s Disease) and major risk factors associated with it?

A

Nonartherosclerotic inflammatory small and medium vessel vasculitis, leading to vasocclusive phenomena

  • Tobacco use
  • Young men 20-45 years of age especially in India, Asia, Middle East
270
Q

What triad is associated with Thromboangiitis Obliterans (Buerger’s Disease)?

A
  • Distal extremity ischemia both upper and lower extremities
  • Raynaud’s phenomenon
  • Superficial migratory thrombophlebitis
271
Q

What testing can be done to determine Thromboangiitis Obliterans (Buerger’s Disease)?

A
  • Abnormal Allen test
  • Aortography: corkscrew collaterals
  • Biopsy: segmental vascular inflammation
272
Q

What is the management for Thromboangiitis Obliterans (Buerger’s Disease)?

A
  • Smoking/tobacco cessation is cornerstone of management
  • Iloprost: prostaglandin analog that may help with critical limb ischemia while smoking cessation is in progress
  • Calcium channel blockers for Raynaud’s phenomenon
273
Q

What is Giant Cell (Temporal) Arteritis and risk factors associated with it?

A

Large and medium vessel granulomatous vasculitis of the extracranial branches of the carotid artery.

Risk factors: Women, > 50 years old

274
Q

What are some symptoms associated with Giant Cell (Temporal) Arteritis?

A
  • Headache (new in onset, localized, temporal area)
  • Jaw claudication with mastication
  • Visual changes
  • May have scalp tenderness, specifically in area of temporal artery
275
Q

How is Giant Cell (Temporal) Arteritis diagnosed?

A
  • Primarily clinical diagnosis, but can have increased ESR

- Temporal biopsy is definitive diagnosis

276
Q

What is the management for Giant Cell (Temporal) Arteritis?

A
  • High-dose corticosteroids once suspected to prevent blindness (blindness is most common complication)
  • Low-dose aspirin
277
Q

What is Trousseau sign?

A

Migratory thrombophlebitis associated with malignancy

278
Q

What is superficial thrombophlebitis common associated with?

What are associated clinical manifestations?

A

IV catheterization, pregnancy, varicose veins

Local phlebitis: tenderness, pain, induration, edema, and erythema along the course of the vein. May feel palpable cord.

279
Q

What testing can be performed for superficial thrombophlebitis?

What is the mainstay treatment?

A
  • Mainly clinical diagnosis
  • Venous duplex ultrasound: noncompressible vein

Supportive care is mainstay of treatment with NSAIDs, extremity elevation, and warm compresses

280
Q

What is Virchow’s triad and what condition is associated with it?

A
  • Intimal damage: trauma, infection, inflammation
  • Stasis: immobilization
  • Hypercoagulability: protein C/S deficiency, Factor V Leiden, oral contraceptive use, malignancy, pregnancy, smoking
281
Q

What are some clinical manifestations associated with a DVT?

A
  • Unilateral lower extremity swelling and edema ( > 3 cm is most specific sign)
  • Calf pain and tenderness
282
Q

How is a DVT diagnosed?

A
  • Venous duplex ultrasound: first-line imaging
  • D-dimer
  • Contrast venography: definitive but rarely used
283
Q

What is the management for a DVT?

A

Anticoagulation: first-line treatment in most patients

  • **at least 3 months of treatment in those with reversible risk factors/not idiopathic
  • **LMWH preferred in pregnancy

IVC filter if recurrent DVT despite treatment, anticoagulation is contraindicated

284
Q

What are varicose veins?

What are associated clinical manifestations?

What is the management?

A

Dilation of superficial veins due to failure of the venous valves in the saphenous veins.

Most are asymptomatic but may have dull ache or pressure that is worse with prolonged standing or sitting with leg dependent. Most patients present for cosmetic issues.

Conservative management with compression stockings, leg elevation, and pain control. Ablation may be performed.

285
Q

What are clinical manifestations associated with chronic venous insufficiency (peripheral venous disease)?

A
  • Leg pain that is worse with leg dependency, standing, prolonged sitting
  • Leg pain that improves with walking, elevation of leg
286
Q

What are physical exam findings consistent with chronic venous insufficiency (peripheral venous disease)?

A
  • Stasis dermatitis: eczematous rash, thickening of skin, brownish/purple hyperpigmentation of the skin
  • Dependent pitting leg edema
  • Medial malleolus ulcers
287
Q

What is the management for chronic venous insufficiency (peripheral venous disease)?

A
  • Conservative is initial management of choice including leg elevation, compression stockings, exercise
  • Ulcer management
288
Q

Are the following symptoms associated with PAD or PVD?

  • Leg pain better with leg dependency and rest
  • Leg pain worse with walking, elevation of leg, cold
  • Dependent rubor and cyanotic leg with elevation
  • Lateral malleolus ulcers with clean margins
A

PAD

289
Q

Are the following symptoms associated with PAD or PVD?

  • Leg pain worse with leg dependency, standing, prolonged sitting
  • Leg pain that improves with walking, elevation of leg
  • Cyanotic leg with dependency
  • Medial malleolus ulcers with uneven margins
A

PVD

290
Q

Are the following symptoms associated with PAD or PVD?

  • Stasis dermatitis on lower extremities: eczematous rash, thickening of skin, brownish discoloration
  • Pulses and temperature normal
  • Prominent edema
A

PVD

291
Q

Are the following symptoms associated with PAD or PVD?

  • Atrophic skin changes: thin/shiny skin, loss of hair, muscle atrophy, pallor, thick nails
  • Livedo reticularis (mottled appearance)
  • Decreased pulses and cool temperature
  • Minimal to no edema
A

PAD

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