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First AId 2CK COPY > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Jugular Venous Distention

A

> 7cm above sternal angle

- suggests right HF, pulmonary HTN, volume overload, tricuspid regurgitation, pericardial disease

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2
Q

Hepatojugular reflex

A
  • fluid overload

- impaired right ventricular compliance

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3
Q

Kussmaul’s sign

A 
- increased JVP with inspiration
suggests:
- right ventricular infarction
- post-op cardiac tamponade
- tricuspid regurgitation
- constrictive pericarditis
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4
Q

Aortic stenosis

A
  • harsh systolic ejection murmur that radiates to carotids
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5
Q

Mitral regurgitation

A
  • holosystolic murmur that radiates to the axilla or carotids
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6
Q

Mitral valve prolapse

A
  • midsystolic or late systolic murmur with a preceding click
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7
Q

Flow murmur

A
  • very common

- doesn’t imply cardiac disease

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8
Q

Aortic regurgitation

A
  • early decrescendo diastolic murmur
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9
Q

Mitral stenosis

A
  • mid to late, low-piched diastolic murmur
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10
Q

S3 gallop

A
  • dilated cardiomyopathy (floppy ventricle)
  • often normal in younger patient and in high output states (e.g. pregnancy)
  • mitral valve disease
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11
Q

S4 gallop

A
  • seen in hypertension
  • diastolic dysfunction (stiff ventricle)
  • aortic stenosis
  • often normal in younger patients and in athletes
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12
Q

Pulmonary edema

A
  • left heart failure (fluid “backs up” into lungs
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13
Q

Peripheral edema

A
  • right heart failure
  • biventricular failure (fluid “backs up” into the periphery)
  • Peripheral Venous Disease
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14
Q

Increased peripheral pulses

A
  • compensated aortic regurgiation
  • coarctation (arms > legs)
  • PDA
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15
Q

Decreased peripheral pulses

A
  • peripheral arterial disease

- Late stage heart failure

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16
Q

Pulsus Paradoxus

A 
- decreased systolic BP with inspiration
seen in:
- pericardial tamponade
- COPD and asthma
- Tension pneumothorax
- Foreign body in airway
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17
Q

Pulsus alternans

A
  • alternating weak and strong pulses
  • cardiac tamponade
  • LV systolic function
  • Poor prognosis
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18
Q

Pulsus parvus et tardus

A
  • Weak and delayed pulse

- Aortic stenosis

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19
Q

CHF

A
  • caused by inability of heart to pump enough blood to maintain fluid and metabolic homeostasis
  • risk factors: CAD, HTN, cardiomyopathy, valvular heart disease
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20
Q

Systolic Dysfunction

A
  • decreased EF (< 50%)
  • increased LV EDV
  • caused by inadequate LV contractility or increased afterload
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21
Q

Management options for A-Fib

A 
"ABCD"
A-anticoagulate
B- beta blockers
C- cardiovert/calcium channel blockers
D- digoxin
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22
Q

Hx and PE: CHF

A
  • exertional dyspnea is earlist and most common symptom
  • can progress to orthopnea, paroxysmal nocturnal dyspnea
  • S3/S4 gallop, JVD, and peripheral edema
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23
Q

Sinus bradycardia: etiology

A
  • normal response to cardiovascular conditioning
  • result form sinus node dysfunction
  • from B-blockers or calcium channel blockers
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24
Q

Sx: sinus bradycardia

A
  • may be asymptomatic

- present w/ lightheadedness, syncope, chest pain, or hypotension

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25
Q

Ecg findings: sinus bradycardia

A
  • sinus rhythm

- ventricular rate < 60 bpm

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26
Q

1st degree AV block: etiology

A
  • can occur in normal individuals

- associated with incr. vagal tone and with B-blocker or CCB use

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27
Q

1st degree AV block: signs/sx

A

asymptomatic

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28
Q

1st degree AV block: ECG findings

A

PR interval > 200msec

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29
Q

Tx: 1st degree AV block

A

None necessary

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30
Q

Etiology: 2nd degree AV block

A
  • Drug effects (digoxin, B-blockers, CCBs)
  • Incr. vagal tone
  • Right coronary ischemia or infarction
  • usually asymptomatic
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31
Q

ECG: 2nd degree AV block (Mobitz I)

A
  • Progressive PR lengthening until a dropped beat occurs;

the PR interval then resets

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32
Q

Tx: 2nd degree AV block (Mobitz I)

A
  • stop offending drug

- atropine as clinically indicated

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33
Q

Etiology: 2nd degree Av block (Mobitz II)

A
  • results from fibrotic disease of conduction system or acute, subacute, or prior MI
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34
Q

Sx: 2nd degree AV block (Mobitz II)

A
  • Occasionally syncope

- Frequent progression to third degree AV block

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35
Q

ECG findings: 2nd degree AV block (Mobitz II)

A

Unexpected dropped beat(s) w/o a change in PR interval

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36
Q

Tx: 2nd degree AV block (Mobitz II)

A

Pacemaker placement

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37
Q

Etiology: 3rd degree AV block (complete)

A
  • no electrical communication btwn the atria and ventricles
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38
Q

Sx: 3rd degree AV block (complete)

A
  • syncope
  • dizziness, acute heart failure
  • hypotension
  • cannon A waves
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39
Q

ECG findings: 3rd degree AV block (complete)

A

No relationship between P waves and QRS complexes

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40
Q

Tx: 3rd degree AV block (complete)

A

Pacemaker placement

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41
Q

Etiology: sick sinus syndrome/tachycardia-bradycardia syndrome

A

Heterogenous disorder that leads to intermittent supraventricular tachy- and bradyarrhythmias

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42
Q

Sx: Sick sinus syndrome/ tachycardia -bradycardia syndrome

A
  • Secondary to tachycardia or bradycardia;

May include syncope, palpitations, dyspnea, chest pain, TIA, and stroke

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43
Q

Tx: sick sinus syndrome/ tachycardia-bradycardia syndrome

A

Pacemaker placement

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44
Q

Etiology: sinus tachycardia

A

normal physiologic response to fear, pain and exercise

- can be secondary to hyperthyroidism, volume contraction, infection or pulmonary embolism

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45
Q

Sx: sinus tachycaria

A
  • palpitations

- SOB

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46
Q

ECG findings: sinus tachycardia

A
  • sinus rhythm

- ventricular rate > 100 bpm

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47
Q

Tx: sinus tachycardia

A
  • treat the underlying cause
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48
Q

Etiology: atrial fibrillation

A 
Acute  AF: "PIRATES"
P-pulmonary disease
I- ischemia
R- rheumatic disease
A - anemia/atrial myxoma
T - thyrotoxicosis
E - ethanol
S - sepsis
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49
Q

Sx: atrial fibrillation

A
  • often asymptomatic
  • may present w/ SOB, chest pain, or palpitations
  • irregularly irregular pulse
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50
Q

ECG findings: atrial fibrillation

A

no discernible P waves with variable and irregular QRS response

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51
Q

Tx: atrial fibrillation

A
  • Estimate risk of stroke using CHADS2 score
  • anticoagulate if score > 48 hrs ( to prevent CVA)
  • rate control (B-blockers, CCBs, digoxin)
  • Initiate cardioversion only if only new onset
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52
Q

Etiology: atrial flutter

A
  • Circular movement of electrical activity around atrium at a rate of approx 300 times per minute
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53
Q

Sx: atrial flutter

A
  • usually asymptomatic, but can present with palpitations, syncope, and lightheadness
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54
Q

ECG findings: atrial flutter

A

Regular rhythm
“sawtooth appearance” of P waves can be seen
- atrial rate is usually 240-32 bpm and the ventricular rate ~ 150 bpm

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55
Q

Tx: atrial flutter

A

anticoagulation,
rate control
cardioversion guidelines

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56
Q

Etiology: multifocal atrial tachycardia

A

multiple atrial pacemakers or reentrant pathways

- COPD and hypoxemia

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57
Q

Sx: multifocal atrial tachycardia

A
  • may be asymptomatic

- at least 3 different P wave morphologies

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58
Q

ECG findings: multifocal atrial tachycardia

A
  • 3 or more unique P wae morphologies

- rate > 100 bpm

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59
Q

Tx: multifocal atrial tachycardia

A
  • treat underlying disorder

- verapamil or B-blockers for rate control and suppression of atrial pacemakers (not very effectors)

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60
Q

Etiology: atrioventricular nordal reentry tachycardia (AVNRT)

A
  • a reentry circuit in the AV node depolarizes the atrium and ventricle simultaneously
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61
Q

Sx: AVNRT

A 
palpitations
SOB
Angina
Syncope
Lightheadedness
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62
Q

ECG findings: AVNRT

A
  • rate 150 - 250 bpm

- P wave is often buried in QRS or shortly after

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63
Q

Tx: AVNRT

A
  • cardiovert if hemodynamically unstable

- carotid massage, Valsalva, or adenosin can stop the arrhythmia

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64
Q

Etiology: atrioventricular reciprocating tachycardia (AVRT)

A
  • an ectopic connection between the atrium and ventricle that causes a reentry circuit
  • seen in WPW
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65
Q

Sx: AVRT

A
  • palpitations
  • SOB
  • angina
  • lightheadedness
  • syncome
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66
Q

Tx: AVRT

A

Cardiovert vs. procainamide
- blockage of AV node (CCBs, adenosines, digoxin)
thru ectopic P waves

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67
Q

Ecg: AVRT

A
  • Retrograde P wave is often seen after a normal QRS

- pre-excitation delta wave is characteristically seen in WPW

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68
Q

Mitral stenosis

A

mid diastolic rumbling murmur heard at apex

- can often lead to LA dilitation

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69
Q

Atrial fibrillation

A
  • irregularly irregular rhythm and loss of P waves
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70
Q

Aortic dissection

A
  • presents with tearing chest pain radiating to back

- may include cardiac tamponade, acute aortic regurgitation stroke, and renal failure

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71
Q

Order of ECG

A
  1. Rate
  2. Rhythm (P wave before QRS complex)
  3. Axis
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72
Q

Normal Axis on ECG

A
  1. Upright QRS on leads I and AVF
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73
Q

Left-axis deviation

A

Upright QRS in lead I and downward QRS

* up to -30 degrees is normal variant

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74
Q

Right axis deviation

A

A downward QRS in lead I and upright QRS lead in AVF (up to +105 degrees is considered nrl variant)

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75
Q

Normal intervals

A

PR interval btwn 120 and 200ms

QRS < 120 msec

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76
Q

AV block

A

PR > 200msec

P with no QRS afterwards

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77
Q

Left bundle branch block

A
  1. QRS > 120msec
    no R wave in V1
    tall R waves in I, V5, V6
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78
Q

Right bundle branch block on ECG

A

QRS duration > 120 msec
RSR’ complex (“rabbit ears”)
qR or R morphology with wide R wave in V1
QRS pater with a wide S wave I, V5, V6

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79
Q

Long QT syndrome on ECG

A

QTc > 440msec

- underdiagnosed congenital disorder that predisposes to ventricular tachyarrhythmias

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80
Q

Ischemia on ECG

A

new inverted T wave
poor R wave progression in precordial leads
ST segment changes (elevation or depression)

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81
Q

Transmural infarct on ECG

A

Significant Q waves > 40msec or more than 1/3 of the QRS amplitude
ST elevations with T wave inversions

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82
Q

Atrial enlargement: right atrial abnormality (P pulmonale)

A

P wave amplitude in lead II is > 2.5 mm

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83
Q

Left atrial enlargement on ECG

A

P wave width in lead II is > 120 msec or
terminal negative deflection in V1 is > 1mm in amplitude and > 40msec in duration
Nothced P waves can be frequently seen in lead II

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84
Q

Signs of LVH on ECG

A
  • amplitude of ( S in V1 )+ (R in V5 or V6 )is > 35mm
    OR:
  • amplitude of R in AVL + S in V3 is > 28mm
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85
Q

Right ventricular hypertrophy

A

right axis deviation and R wave in V1 > 7mm

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86
Q

College age male “passed out” while playing basket ball and had no prodromal symptoms or signs of seixure. His cardiac exam is unremarkable. ECG shows a slurred upstroke of QRS. Next step?

A

Wolf-Parkinson Syndrome

  • advise against vigorous physical activity
  • treat arrhythmias w/ procainadmide
  • refer for electrophysiology study
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87
Q

Systolic dysfunction

A
  • decreased EF (< 50%) and increased LEDV
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88
Q

Etiology of systolic dysfunction

A
  • Inadequate left ventricular contractility or increased afterload
  • headrt compensated for decr. EF and increased preload through hypertrophy and ventricular dilitation
  • eventually compensation fails leading to incr. myocardial work and worsening systolic dysfunction
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89
Q

CHF: Hx

A

Exertional dyspnea is earliest and most common presenting symptom
- progresses to orthopnea, paroxysmal nocturnal dyspnea (PND) and rest dyspnea

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90
Q

CHF: PE

A
  • parasternal lift
  • an elevated and sustained LV impulse
  • S3/S4 gallop
  • Peripheral edema
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91
Q

Man was admitted for CHF exacerbation w/ low EF

Patient now ready for discharge, and his meds include furosemide and metoprolol. Next step in management?

A 
Add ACE inhibitors to current regiment
- ACEis have positive mortality benefit when used with beta blockers in NYHA class II-IV heart failure patients
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92
Q

CHF: Diagnosis

A
  • clinical syndrome
  • CXR: shows cardiomegaly, cephalization of pulm vessels, vascular congesion
  • Echo: decr. EF and ventricular dilitation
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93
Q

Lab values associated w/ CHF

A

BNP > 500 pg/mL

  • increased creatinine
  • decreased sodum
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94
Q

Acute CHF Management

A

LMNOP

  • Lasix
  • Morphine
  • Nitrates
  • Oxygen
  • Position (upright)
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95
Q

Acute treatment of CHF

A
  1. Treat underlying cause (e.g. arrhytmias, MI and drugs)
  2. Diurese aggressively with loop and thiazide diuretics
  3. Give diuretics to patients who can tolerate them
  4. Use LMNOP for pulmonary congestion
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96
Q

NYHA Class I

A

no limitation of activiy

no symptoms w/ normal activity

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97
Q

NYHA Class II

A

Slight limitation of activity

Comfortable at rest or w/ mild exertion

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98
Q

NYHA Class III

A

Marked limitation of activity

Comfortable only at rest

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99
Q

NYHA Class IV

A

Any physical activity brings on discomfort;

symptoms present at rest

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100
Q

Chronic Tx of CHF

A
  • Long term B-blockers and ACEis/ ARBS help prevent remodeling of heart and decrease mortality for NYHA Class II-IV
  • daily ASA and statin if underlying cause of prior MI
  • Chronic diuretics (loops +/- thiazides)
  • low dose spironolactone decr mortality risk in patients
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101
Q

When should you consider ICDs in CHF patient?

A

Patients w/ EF < 35%

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102
Q

Systolic dysfunction: common factors

A 
Pts < 65 y/o
Co-morb: Dilated cardiomyopathy, valvular heart dz
PE: Displaced PMI, S3 gallop
CXR:  Pulmonary congestion, cardiomegaly
ECG/Echo: Q waves, decr (< 40%)
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103
Q

Nonsystolic dysfunction: common characteristics

A

Often > 65 y/o
Co-morb: Restrictive or hypertrophic cardiomyopathy, renal dz, or HTN
PE: Sustained PMI, S4 gallop
CXR: Pulmonary congestion, normal heart size
ECG/Echo: LVH, normal EF (> 55%)

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104
Q

Left-Sided CHF: symptoms

A
  1. Left sided S3/S4 gallop
  2. Bilateral basilar rates
  3. Pleural effusions
  4. Pulmonary edema
  5. Orthopnea, paroxysmal nocturnal dyspnea
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105
Q

Right-Sided CHF: symptoms

A
  1. Right sided S3/S4 gallop
  2. JVD
  3. Hepatojugular reflex
  4. Peripheral edema
  5. Hepatomegaly, ascites
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106
Q

Loop diuretics

A
  • acts on Loop of Henle
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107
Q

Loop diuretics : mechanism of actiion

A
  • decreases Na/K/2CL co-transported
  • decreases urine concentration
  • increases calcium excretion
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108
Q

Loop diuretics: side effects

A
  • Ototoxicity
  • Hypokalemia
  • Hypocalcemia
  • Dehydration
  • Gout
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109
Q

Thiazide diuretics: sites of action

A

Early distal tubule

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110
Q

Thiazide: mechanism of action

A
  • decreases NaCL reabsorption leading to decreased diluting capacity of nephron;
  • decreased Ca excretion
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111
Q

Thiazide: side effects

A 
Hypokalemic metabolic alkalosis
Hyponatremia
HyperGLUC
- hyperglycemia
- hyperlipidemia
- hyperuricemia
- hypercalcemia
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112
Q

K-sparing agents

A

spironolactone
triamterene
amiloride

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113
Q

K-sparing agents: site of action

A

cortical collecting tubule

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114
Q

Spironolactone: MOA

A
  • aldosterone receptor antagonist
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115
Q

Triamterene and Amiloride

A

Block Na channels

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116
Q

K-sparing agents: side effects

A
  • Gynceomastia
  • Hyperkalemia
  • Sexual dysfunction
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117
Q

Carbonic anhydrase inhibitors

A

Acetazolamde

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118
Q

Carbonic anhydrase inhibitors: Site of aCtion

A

Proximal convoluted tubule

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119
Q

Carbonic anhydrase inhibitors: MOA

A

NaHCO3 diuresis decreases total body NaHCO2

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120
Q

Carbonic anhydrate inhibitors: Side effect

A

Hypercholeric metabolic acidosis
Neuropathy
NH3 toxicity
Sulfa allergy

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121
Q

Osmotic agents

A

mannitol

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122
Q

Osmostic agents: site of action

A

proximal tubule

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123
Q

Osmotic agents: MOA

A

Creates increased tubular fluid osmolaity, leading to increased urine flow

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124
Q

Osmotic agents: side effects

A

Pulmonary edema
Dehydration
Contraindicated in anuria and CHF

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125
Q

Nonsystolic dysfunction: Hx and PE

A
  • associated with stable and unstable angina
  • SOB
  • Dyspnea on exertion
  • Arrhythmias
  • Heart failure
  • Sudden failure
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126
Q

Nonsystolic dysfunction: Tx

A

Diuretics (first line therapy)

  • Maintain rate and BP via B-blockers, ACEis, ARBs, or CCBs
  • Digozxin is not useful in patients
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127
Q

S3 gallops

A

signifies rapid ventricular filling in the setting of fluid overload and is associated w/ dilated cardiomyopathy

128
Q

Loop diuretics vs Thiazide

A

Loops LOSE Calcium

Thiazides take it in Ca

129
Q

Common causes of dilated cardiomyopathy

A
  • Ischemia

- Long standing hypertension

130
Q

Drugs associated w/ dilated cardiomyopathy

A

Doxorubicin
AZT
Cocaine

131
Q

Infection associated w dilated cardiomyopathy

A
  • Coxsackievirus
  • HIV
  • Chagas’ disease
  • Parasites
132
Q

Dilated Cardiomyopathy: Hx and PE

A
  • often presents w/ gradual sx of CHF
  • displacement of LV impulse
  • S3/S4 gallop
  • Mitral/tricuspid regurgitation
133
Q

Dilated Cardiomyopathy

A
  • impaired contractility
  • very increased LV- EDV
  • very increased LV - ESV
  • very decreased EF
  • decreased wall thickness
134
Q

Hypertrophic cardiomyopathy

A
  • impaired relaxation
  • decreased LV - EDV
  • very decreased LV - ESV
  • increased or unchanged EF
  • very increased wall thickness
135
Q

Restrictive Cardiomyopathy

A
  • impaired elasticity
  • increased LV - EDV
  • increased LV - ESV
  • decreased or normal EF
  • increased wall thickness
136
Q

Dilated Cardiomyopathy: Diagnosis

A
  1. ECHO
  2. ECG show ST-T changes, low voltage WRS, sinus tachycadia, and ectopy (LBBB is comon)
  3. CXR show enlarged balloon-like heart and pulm congestion
137
Q

Dilated cardiomyopathy: Tx

A

Address underlying etiology

  • treat sx with CHF meds (ACEis/ARBs and B-blockers)
  • AVOID CCBs in heart failure
  • Consider anticoagulation to decr thrombus risk if AF or IV thrombus
  • Consider ICD if < 35%
138
Q

A woman w/ hypertension and prior MI has an exam notable for displaced PMI, S3, nonelevated JVP and bibasilar rale. Next best step in dx?

A

Dilated cardiomyopathy

- next best step is echocardiogram

139
Q

Common HOCM scenario

A

most common cause of sudden death in young, healthy athletes in the United States

140
Q

Hypertrophic Cardiomyopathy

A
  • impaired LV relaxation and filling (nonsystolic dysfunction)
  • involves interventricular septum
  • leading to LV outflow tract obstruction and impaired ejection of blood
141
Q

Hypertrophic cardiomyopathy: Hx and PE

A
  • may be assymptomatic byt present w/ dyspnea, palpitations, angina or sudden cardiac death
  • sustained apical impulse, S4 gallop
  • crescendo-decrendo systolic murmur increases w/ decreases preload
142
Q

Hypertrophic cardiomyopathy: Dx

A

Echocardiogram - show asymmetrical septum and obstruction of blood flow

  • ECG shows LVH
  • CXR reveal left atrial enlargement 2/2 mitral regurgitation
143
Q

Hypertrophic cardiomyopathy: Tx

A

B-blockers are initial therapy for symptomatic relief: CCBs are second line

  • surgical ablation: dual chamer pacing, partial excision or alcohol ablation
  • should avoid intense competition
144
Q

Hypertension

A

systolic BP > 140 mmg Hg and/or diastolic BP > 90 mm Hg based on 2 measurements separated by time

145
Q

Hypertension: Hx and PE

A
  • asymptomatic until complications
  • pts should be evaluated for end-organ damage to brain, eye, heart, and kidneys
  • renal bruits may signify stenosis
146
Q

Ocular signs of hypertension

A

Cotton-wool exudates

Hemorrhage

147
Q

Heart signs of hypertension

A

LVH

148
Q

Renal signs of HTN

A

Proteinuria

Chronic kidney disease

149
Q

Neuro signs of HTN

A
  • Stroke

- Dementia

150
Q

Dx of HTN

A

To assess extent of end-organ damage

  • Obtain UA
  • BUN/CR
  • CBC
  • Electrolytes
151
Q

Tx of HTN

A

After ruling on secondary causes:

  1. Lifestyle modifications
  2. Diuretics, ACEis and B-blockers decrease mortablity in uncomplicated HTN
  3. Periodically test for end-organ damage
152
Q

Tx for Stage 2 HTN (SBP > 160 or DBP > 100)

A

Two drug combo

- thiazide plus ACEi, ARB, B-blocker, or CCB

153
Q

Tx of HTN

A 
ABCD
ACEIs/ARBs
B-blockers
CCBs
Diuretics
154
Q

Causes of 2 hypertension

A 
CHAPS
Cushing's Syndromes
Hyperaldosteronism
Aortic coarctation
Pheochromocytopma
Stenosis of renal arteries
155
Q

Primary Renal Disease

A

-often unilateral renal parenchymal disease

156
Q

Management of primary renal disease

A

treat w/ ACEis which slow progression of disease

157
Q

Renal artery stenosis

A

especially common in patients < 25 and > 50 o age with recent onset hypertension
- include fibromuscular dysplasia (younger patients) and atherosclerosis (older patients)

158
Q

Mgmt renal artery stenosis

A

Diagnose w/ MRA or Renal Artery Dopplyer

  • Treat w/ angioplasty or stenting
  • Consider stenting in undilateral diz
159
Q

Why should ACEis be used in renal artery stenosis?

A

ACEis can accelerate kidney failure by preferential dilation of efferent arteriole

160
Q

OCP use in HTN

A

Common in woman > 35 yo, obse woman and those w. longstanding use

161
Q

Tx of OCP associated HTN

A

Discontinue OCPs - effect may be delayed

162
Q

Pheochromocytoma

A

adrenal gland tumor that secretes epinepherine and norepipnepherine

  • leads to episodic headaches
  • sweating
  • tachycardia
163
Q

Mgmt of pheochromocytoma

A

Diagnose with urinary metanepherine and catecholemine levels or plasma metanepherine
- Surgical removal of tumor after tx with both alpha and beta blockers

164
Q

When removing pheochromocytoma what should be done?

A

Administer both alpha and beta blockers before surgical removal of tumor

165
Q

Conn’s syndrome (hyperaldosteronism)

A

Most often secondary to aldosterone producing adrenal adenoma

166
Q

Conn’s syndrome triad

A
  • Hypertension
  • Unexplained hypokalemia
  • Metabolic alkalosis
167
Q

Conn’s syndrome management

A

Metabolic workup w/ plasma aldosterone and renin level

  • increased aldosterone and decreased renin levels suggest hyperaldosteronism
  • Surgical removal of tumor
168
Q

Cushing’s syndrome

A

due to ACTH producing pituitary tumor OR
ectopic ACTH-secreting tumor
cortisol secretion by adrenal adenoma or carcnoma
also cause by exogenous steroids

169
Q

Tx of Cushing’s syndrome

A

Surgical removal of tumor

Removal of exogenous tumor

170
Q

Hypertensive Crisis

A

clinical presentation of elevated BPs leads to end organ damage

171
Q

Hypertensive Crisis: History and PE

A

present w/ end-organ damage revealed by renal disease, chest pain (ischemia or MI), back pain (aortic dissection) or changes in mental status (hypertensive encepholapty)

172
Q

Hypretensive urgency: Dx

A

Elevated BP with mild to moderate sx (headache, chest pain) w/o end organ damage

173
Q

Hypertensive emergency: Dx

A

Elevated BP with signs or symptoms of impending end-organ damage such as acute kidney injury, intracranial hemorrhage, papilledema or ECG changes suggestive of ischemia

174
Q

Hypertensive urgency: Tx

A

can be treated w/ oral hypertensive with goal of gradually lower BP over 24-48 hrs

175
Q

Hypertensive emergencies: tx

A

Treat w/ IV meds (labetalol, nitroprusside, nicardipine) w/ goal of lowering MAP by no more than 25% over first 2 hrs to prevent cerebral hypoperfusion on coronary insufficiency

176
Q

NSTEMI

A
  • chest pain at rest
  • absence of ST elevation on EKG
  • elevated biomarkers of myocardial injury
  • ST depression on EKG
177
Q

Acute pericarditis diagnosis

A

2 of 3 classic features:

  • pleuritic chest pain
  • friction rub (can be squeaky, scratchy or high pitched)
  • diffuse concordant ST-segment elevation on EKG
178
Q

Management of STEMI

A
  • Percutaneous Angioplasty and stent placement are preferred therapies
179
Q

STEMI

A
  • chest pain at rest
  • elevated cardiac biomarkers
  • ST-segment elevation in inferior leads II, III, aVF
180
Q

Contraindications to thrombolytic therapy

A
  • Prior intracranial hemorrhage
  • Ischemic stroke within 3 months
  • Suspected aortic dissection
  • Active bleeding
181
Q

Ischemic heart disease

A
  • chest pain in relation to exercise and relief with rest of nitroglycerin
182
Q

Right ventricular MI

A
  • hypotension
  • clear lung fields
  • elevated CVP
    • ST segment elevation on right sided EKG
183
Q

Treatment of right ventricular MI

A

Volume expansion (w/ normal saline)

184
Q

First step in management of esophageal noncardiac chest pain

A

Prescribe PPI

185
Q

Third degree block

A
  • complete absence of conduction of atrial impulses to ventricles (no P waves)
  • most common cause of marked bradycardia
186
Q

Lyme carditis

A
  • presence of skin rash (erythema migrans) with known hx of tick bite (presence in endemic regions)
  • caused by Borrelia burgdoferi
  • manifested by acute, high grade AV conduction defects occasionally associated with myocarditis
187
Q

Panic disorder

A
  • recurrent, unexpected panic attacks that feature abrupt onset of numerous somatic symptoms such as palpitations, sweating, tremulousness, dyspnea, chest pain, nausea, dizziness, and numbness
188
Q

Mobitz type I (second degree AV block)

A

progressive prolongation of PR interval until dropped beat occurs

189
Q

Mobitz type II second degree AV block

A

regularly dropped beat (i.e. nonconducted P wave every 2nd or 3rd beat) without progressive prolongation of PR interval

190
Q

Therapy for chronic stable CAD

A

Anti-anginals: B-blockers, CCBs, and nitrates

Vascular protective: aspirin, ACE, and statins

191
Q

B-blockers in tx of chronic stable angina

A

should be titrated to achieve resting heart rate of approximately 55 - 60 /min and approximately 75% of heart rate

192
Q

Sx of pulmonary embolism

A
  • assymetric leg edema
  • elevated CVP
  • tachypnea and tachycardia
193
Q

Best diagnostic test

A

Pulmonary embolism

194
Q

Causes of pericarditis

A 
CARDIAC RIND
Collagen vascular disease
Aortic dissection
Radiation
Drugs
Infections
Acute renal failure
Cardiac (MI)
Rheumatic fever
Injury 
Neoplasms
Dressler's syndrome
195
Q

Pericarditis

A
  • inflammation of the pericardial sac

- can compromise cardiac output via tamponade or constrictive pericarditis

196
Q

Pericarditis: Hx and PE

A
  • may present pleuritic chest pain, dyspnea, cough and fever
  • chest pain tends to worsen in supine position and w/ inspiration
  • exam reveals pericardial rub
  • elevated JVP and pulsus paradoxus
197
Q

Pericarditis: Diagnosis

A

CXR, ECG and echo to r/o MI and pneumonia

  • EKG changes include DIFFUSE ST-SEGMENT ELEVATION AND PR-SEGMENT DEPRESSIONS followed by T-wave inversions
  • pericardial thickening or effusion may be evident
198
Q

20 y/o M presents with an initial BP of 150/85 mm Hg and repeat measurement yields 147/85 mm Hg. Potassium level is 3.2 mg/dl Next step?

A

Hyperaldosteronism workup with serum aldosterone and renin levels is an appropriate next diagnostic step

199
Q

Hypertensive crises are diagnosis on what basis?

A

Basis of end-organ damage, not BP measurement

200
Q

B-blockers

A
  • decrease cardiac contractility and renin release
201
Q

B-blockers: side effects

A

Bronchospasm (in severe active asthma), bradycardia, CHF exacertbation, impotence, fatigue, depression

202
Q

ACE inhibitors (e.g. captopril, enalapril, fosinopril, benzanapril)

A

block aldosterone formation, reducing peripheral resistance and salt/water retention

203
Q

ACE inhibitors: side effects

A

Cough, rashes, leukopenia, hyperkalemia

204
Q

ARBs (e.g. losartan, valsartan, irebsartaN

A

Block aldosterone effect, reducing peripheral resitance and salt/water retention

205
Q

ARBs: side effects

A

Rashes
Leukopenia
Hyperkalemia but no cough

206
Q

Calcium channel blockers

e. g. dihydropyridines – nifedipine, felodipine, amlodipine
(e. g. nondihydropyridines – diltiazem, verapramil)

A

decreased smooth muscle tone and cause vasodilation;

may also decrease cardiac output

207
Q

Calcium channel blockers: side effects

A

Dihydropyridines: headaches, flushing, peripheral edema

Nondihydropyridines: decreased contractility

208
Q

Vasodilators (e.g. hydralazine, minoxidil)

A

decrease peripheral resistance by dilating arteries/arterioles

209
Q

Vasodilators (e.g. hydralazine, minoxidil)

A

Hydralazine: headache, lupus-like syndrome

Minoxidil: orthostasis, hirsuitism

210
Q

Alpha1- adrenergic blockers (e.g. prazosin, terazosin, phenoxybenzamine)

A

cause vasodilation by blocking actions of norepinepherine on vascular smooth tone

211
Q

Alpha 1 adrenergic blockers: side effects

A

Orthostatic hypotension

212
Q

Centrally acting adrenergic agonists (e.g methyldopa, clonidine)

A

inhibit sympathetic nervous system via centrial alpha 2 adrenergic receptors

213
Q

Centrally acting adrenergic agonists

A

somnolence
Orthostatic hypotenson
Impotence
Rebound hypertension

214
Q

Pericarditis: Tx

A
  • address underling cause (e.g steroids for SLE, dialysis for uremia) or sx (ASA for post-MI carditis)
  • pericardial effusions w/o symptoms can be monitored by evidence of tamponade
215
Q

Cardiac tamponade

A

excess fluid in the pericardial sac, leading to compromised ventricular filling and decreased cardiac output
- rate of fluid formation is more important than size

216
Q

Risk factors for cardiac tamponade

A 
Pericarditis
Malignancy
SLE
TB
Trauma (stab wounds medial to left nipple)
217
Q

Cardiac tamponade: Hx and PE

A
  • presents with fatigue, dyspnea, anxiety, tachycardia, and tachypnea that progresses from shock to death
  • Beck’s triad (hypotension, JVD, and muffled heart sounds)
  • narrow pulse pressure, pulsus paradoxus, and Kussmaul’s sign (JVD on inspiration)
218
Q

Cardiac tamponade: diagnosis

A

Echo shows right atrial and right ventricular diastolic collapse

  • CXR shows enlarged, globular, water bottled shaped heart w/ large effusion
  • Electrical alternans on ECG
219
Q

Cardiac tamponade: Tx

A
  • Aggressive volume expansion w/ IV fluids
  • urgent pericardiocentesis (aspirate will be nonclotting blood)
  • decompensation may warrant pericardial window
220
Q

Aortic stenosis: Etiology and Hx

A
  • most often seen in elderly
  • unicuspid/bicuspid valves leads to earlier presentation
  • may be asymptomatic for years
  • once symptomatic progresses from angina –> CHF –> syncope within 5 years
221
Q

Aortic Stenosis: Ex

A

PE: pulsus parvus et tardus (weak, delayed, carotid upstroke) and paradoxically split S2 sound
- systolic murmur radiating to carotids
Dx: Echocardiogram

222
Q

Aortic Stenosis: Tx

A

Aortic valve replacement

223
Q

ACUTE Aortic regurgitaton: Etiology

A

Infective endocarditis
Aortic dissection
Chest trauma

224
Q

CHRONIC Aortic Regurgitaiton: Etiology

A

Valve malformations,
rheumatic fever,
connective tissue disorders

225
Q

ACUTE Aortic Regurgitation: Hx

A

Rapid onset of pulmonary congestion, cardiogenic shock, chest trauma

226
Q

CHRONIC Aortic Regurgitation

A

Slowly progressive onset of dyspnea on eertion, orthopnea, and PND

227
Q

Aortic Regurgitation: PE

A
  • Blowing diastolic murmur at LSB
  • mid-diastolic rumble (Austin Flint Murmur)
  • mid systolic apical murmur
  • Widened pulse pressure causes de Muzzet’s sign, Corrigan’s signs and Duroziez’s sign
228
Q

de Musset’s sign

A
  • associated with aortic regurgitation

- head bob with heartbeat

229
Q

Corrigan’s sign

A
  • associated with aortic regurgitation

- water-hammer pulse

230
Q

Duroziez’s sign

A
  • associated with aortic regurgitation

- femoral bruit

231
Q

Aortic Regurgitation: Dx

A

Echocardiogram

232
Q

Aortic Regurgitation: Tx

A

Vasodilator therapy (dihydropyridines or ACES) for isolated AR until sx become apparent enough for valve replacement

233
Q

Mitral valve stenosis

A
  • most common etiology is rheumatic fever

- symptoms range from dyspnea, orthopnea, and PD to infective endocarditis and arrhythmias

234
Q

Mitral valve stensosis: PE and Dx

A
  • opening snap and mid-diastolic murmur at apex, pulmonary edema
  • diagnosed with echocardiogram
235
Q

Mitral valve stenosis: Tx

A

Antiarrhythmics (B-blockers, digoxin) for symptomatic relief

Mitral valve ballon valvotomy and valve replacement are effective for severe cases

236
Q

Mitral valve regurgitation

A

primary secondarily to rheumatic fever or chordae tendinae rupture after MI
- infective endocarditis

237
Q

Mitral valve regurgitation: HX

A

patients present with dyspnea, orthopnea, ad fatigue

238
Q

Mitral valve regurgitation: PE and Dx

A
  • holosystolic murmur radiating to axilla
  • diagnosed with echo will demonstrate regurgitant flow;
  • angiography can assess severity
239
Q

Mitral valve regurgitation: tx

A

Antiarrhythmics if necessary
(A-fib is common w/ LAE)
- Nitrates and diuretics to decrease preload
- Valve repair or replacement for severe cases

240
Q

Unstable angina

A
  • defined as chest pain with new onset, is accelerated with less exertion, lasts longer
  • signals presence of impending infarction
241
Q

NSTEMI (non ST elevated MI)

A
  • myocardial necrosis marked by elevations in tropnonin I and CKMB without ST elevations on EKG
242
Q

NSTEMI: Dx

A
  • should risk stratified according to TIMI score

- serial cardiac enzyme elevations and KEG

243
Q

Unstable angina: Dx

A

suddent onset chest pain associated with exertion, longer lasting or nonresponsive to meds
- NO elevation in cardiac enzymes on EKG

244
Q

Unstable angina: Tx

A

Clopidogrel
Unfractionated heparin
Enoxaparin

245
Q

NSTEMI

A
  • patients with chest pain refractory to meds, TIMI score > 3, or ST changes > 1mm should be given IV heparin and scheduled for angiography, PCI or CABG
246
Q

ST- Elevations MI

A

defined as ST segment elevations and cardiac enzymes release secondary to prolonged ischemia and necrosis

247
Q

ST- Elevation MI: Hx and PE

A
  • acute onset chest pain with tightness or pressure that radiates to left arm, neck, or jaw
  • associated with diaphoresis, SOB, lightheadness, N/V, and syncope
  • PE may show arrhythmias, hypotension, and new onset CHF
248
Q

Best predictor of STEMI survival

A

LVEF

249
Q

Med Management of MI

A

MONA

  • Morphine
  • Oxygen
  • Nitrates
  • Aspirin
250
Q

STEMI: Dx

A
  • ECG: ST segment elevations or new LBBB
  • Sequence of ECG changes
  • Cardiac enzymes (Troponin and CK-MB)
251
Q

ECG changes after STEMI

A
  1. peaked T waves
  2. ST elevations
  3. Q waves
  4. T wave inversion
  5. ST segment normalization
  6. ST wave normalization
252
Q

Cardiac enzymes after STEMI

A
  • Troponin > CK-MB more sensitive to STEMI

- can take up to 6 hours to rise

253
Q

ST segment elevation in leads II, III, aVF

A
  • signifies INFERIOR MI (involving RCA/PDA)

- get right sided ECG to look for RV infarct

254
Q

ST segment elevation in leads V1 - V4

A
  • signifies ANTERIOR MI (involving (LAD and diagonal branches)
255
Q

ST segment elevation in leads I, aVL, and V5 - V6

A
  • signifies LATERAL MI (involving LCA)
256
Q

ST segment elevation in leads V1 - V2 (anterior leads)

A
  • acute TRANSMURAL INFARCT in POSTERIOR WALL

- obtain ECG leads V7 - V9 to assess for ST segment elevations

257
Q

Ddx chest pain

A
  • MI
  • GERD
  • Esophageal pain
  • MSK disorders (costochrondritis, trauma)
  • Pneumonia
258
Q

Woman is found w/ pulseless electrical activity on HD # 7 suffering lateral wall STEMI. ACLS protocol is initiated. Next best step?

A

LV free wall rupture with acute cardiac tamponade

- emergent pericardiocentesis is next best therapeutic and diagnostic step

259
Q

Main meds for STEMI

A

BC MONA

  • Beta-blockers
  • Clopidogrel
  • Morphine
  • Oxygen
  • Nitrates
  • Aspirin
260
Q

Pt had STEMI but is in heart failure or cardiogenic shock. What medication should not be given?

A

B-blockers are contraindicated give ACEis instead if patient is not hypotensie

261
Q

STEMI: Tx

A
  • BC MONA meds

- Emergent angiography and PCI

262
Q

PT has STEMI but lives 3 hours away from closest hospital with cath lab. Next best step?

A

TPA – if patient doesn’t have contraindications to thrombolysis (hx of hemorrhagic stroke, recent ischemic stroke, severe HF, or cardogenic shock
** must be given within 3 hours of chest pain onset

263
Q

Indications for CABG

A

“ULTD”

  • Unable to perform PCI (diffuse disease)
  • Left main coronary artery disease
  • Triple vessel disease
  • Depressed ventricular function
264
Q

Complications of MI

A
  • Arrhythmia (lethal ones MCC of death post-MI)
  • Dressler’s syndrome
  • LV rupture, papillary muscle rupture, VSD, etc
265
Q

Dressler’s syndrome

A

autoimmune process that occurs 2- 10 wks post MI presents with fever, pericarditis, pleural effusion leukocytosis, and increased ESR

266
Q

Complication of Post MI Day #1

A

Heart failure

267
Q

Complication of post MI day # 2-4

A

Arrhythmia, pericarditis

268
Q

Complication of post MI day # 5 - 10

A

LV wall rupture (acute pericardial tamponade causing electrical alternans, PEA)
Papillary muscle rupture (severe MR)

269
Q

Complications of post MI weeks to months

A

Ventricular aneurysm (CHF, arrhythmia, persistent ST segment elevation, MR, thrombus formation)

270
Q

Dyslipidemia

A
  • total cholesterol > 200
  • LDL > 130 mg/DL
  • Triglycerides > 150 mg/dL
271
Q

Dyslipidemia: Risk factors

A

CAD Risk factors

  • Obesity, DM,
  • Hypothyrodism, Nephrotic syndrome
  • Cushing’s syndrome,
272
Q

Dyslipidemia: Hx and PE

A
  • NO SPECIFIC SIGNS OR SYMPTOMS
  • patients with extremely high triglyceride or LDL levels may have xanothomas (eruptive nodules on skin over tendons)
  • xanthelasmas (yellow fatty deposits in skin around eyes)
  • lipidemia retinals (creamy appearance of retinal vessels)
273
Q

Dyslipidemia: Dx

A
  • conduct fasting lipid profile for pts > 35 yrs in age or > 20 w/ CAD risk factors (repeat q 5 yrs)
  • total serum cholesterol > 200 on 2 different occasions
  • LDL > 130 or HDL < 40 even if total cholesterol is < 200
274
Q

Dyslipidemia:: Tx

A

In patients with no known atherosclerotic disease - 12 week trial of diet and exercise

275
Q

HMG-COA reductase (e.g. atorvastain, simvastatin)

A
  • inhibit rate limiting step in cholesterol synthesis

- decreases LDL and triglycerides

276
Q

HMG-COA reductase side effects

A
  • increase LFTs, myositis, warfarin potentiation
277
Q

Lipoprotein lipase stimulators ./ Fibrates

e.g. gemfibrozil

A
  • increase lipoprotein lipase leading to increasing VLDL and triglyceride catabolism
  • decrease triglycerides and increased HDL
278
Q

Lipoprotein lipase stimulators: side effects

A

GI upset
Cholelithiasis
Myositis
Increased LFTs

279
Q

Cholesterol absorption inhibitors (e.g. Ezetimibe)

A
  • decreased absorption of cholesterol at the small intense brush border
  • decreased LDL
280
Q

Cholesterol absorption inhibitors: side effects

A

Diarrhea
Abdominal pain
Can cause angioedema

281
Q

Niacin (e.g. niaspan)

A
  • decreased fatty acid release from adipose tissue
  • decreased hepatic synthesis of LDL
  • increase HDL
  • decrease LDL
282
Q

Niacin: side effects

A 
Skin flushing (can be prevented with ASA)
Parasthesias
Pruritis
GI upset
Increased LFTs
283
Q

Bile acid resins (cholestyramine, colestipil)

A
  • bind instestinal bile acids
  • leads to decreaed bile acid stones and increased catabolism of LDL from plasma
  • decreased LDL
284
Q

Bile acid resins: side effects constipation

A 
Constipation
GI upset
LFT abnormalities
Myalgias
- can decreae absorption of other drugs from small intestine
285
Q

Aortic dissection

A
  • transverse tear in intima of vessel that reults in blood enterine media creating false lumen
  • SECONDARY TO HYPERTENSION
286
Q

Common sites of aortic dissection

A
  • aortic valve

- distal to left subclavian arter

287
Q

Aortic Dissection: Hx and PE

A
  • sudden tearing/ripping pain in anterior chest
  • typically hypertensive
  • ASYMMETRIC PULSES AND BP MEASUREMENTS
  • Neuro deficits seen if aortic arch or spinal arteries are involved
288
Q

Aortic Dissection: Dx

A

CT angiography
Type A Aortic dissections are proximal to left subclavian artery
Type B Aortic dissections are distal to left subclavian artery

289
Q

Aortic Dissection Tx

A
  • monitor and medically manage BP and HR as necessary

- begin B- blockage before starting vasodilators to prevent reflex tachycardia

290
Q

When aortic dissection a surgical emergency?

A

When aortic disesection involves ascending aortia

Descending aorta dissections can be managed with BP and HR control

291
Q

Deep Vein Thombosis

A
  • clot formation in large veins of extremities or pelvis

- Virchow’s triad (venous stasis, endothelial trauma, or hypercoaguable state)

292
Q

Risk factors for DVT

A 
Venous stasis
- immobilization, bed rest, incompetent valves
Endothelial injury
- surgery, injury to lower extremities
Hypercoagulable states
- malignancy, pregnancy, OCP use
293
Q

DVT: Hx and PE

A
  • presents with unilateral lower extremity pain and swelling

- Homan’s sign (calf tenderness w/ passive foot dorsiflexion)

294
Q

DVT: Dx

A
  • Doppler U/S

- spiral CT or V/Q scan may be used to eval

295
Q

DVT: Tx

A
  • Anticoagulate with IV unfractionated heparin or SQ LMWH followed by PO warfarin for 3-6 months
  • if anticoagulants are contraindicated: IVC filters
296
Q

In low risk patients, what test can be used to rule out PE in low risk patients?

A

Negative D-dimer test

297
Q

Peripheral arterial disease

A
  • restriction of blood supply to extremities by atherosclerosis
  • lower extremities most commonly affect
298
Q

Peripheral arterial disease: Hx and PE

A
  • intermitent claudication (reproducible w/ walking and relieved with rests)
  • progression of disease causes pain at rest
  • dorsal foot ulcers cause poor perfusion
  • painful, cold, numb foot is sign of limb ischemia
299
Q

Aortoiliac disease

A
  • buttock claudication
  • decreased femoral pulses
  • male impotence (Leriche’s syndrome)
300
Q

Femoropopliteal disease

A
  • calf claudication

- decreased pulses below the femoral artery

301
Q

Acute ischemia

A
  • often caused by embolization from the heart
  • commonly occurs at bifurcations distal to the last palpable pulse
  • may be secondary to cholesterol atheroembolism (“blue toe syndrome”)
302
Q

Chronic ischemia

A
  • lack of blood perfusion leads to muscle atrophy

- leads to: pallor, cyanosis, hair loss, and gangrene necrosis

303
Q

Peripheral arterial disease: Dx

A

Ankle-Brachial Index (ABI) to provide evidence of atherosclerosis
- rest pain with ABI < 0.4
- Doppler U/S identifies stenosis and occlusion
(normal doppler readings > 90% brachial)

304
Q

Peripheral arterial disease: Tx

A
  • control underlying conditions (DM, tobacco) and institute gangrene and foot care
  • ASA, Cilostazol, and thromboxane inhibitors may improve symptoms
  • angioplasty and stenting have variable success rate
  • surgery and amputation employed when medical management fails
305
Q

Lymphedema

A
  • disruption of lymphatic circulation that results in peripheral edema and chronic infxn of extremities
  • often complication of lymph node dissection
306
Q

Lymphademia: Hx and PE

A
  • postmatectomy pts present w/ unexplained swelling of upper extremity
  • immigrants presents with progressive lower extremity wswelling with no cardiac abnormalities (e.g. filarisis)
  • children with b/l swelling of extremities
307
Q

Lymphedema: Dx

A

Clinical

- diagnosis of exclusion after ruling out cardiac and metabolic disorders`

308
Q

Lymphedema: Tx

A
  • symptom management (exercise, massage, and pressure garments ) to mobilize and reduce fluid accumulation
  • diuretics are contraindicated
  • maintain vigilance for cellulitis
309
Q

Syncope

A
  • sudden termporary loss of consciousness and postural tone secondary to cerebral hypoperfusion
310
Q

Cardiac etiologies: syncope

A 
Valvular lesions
Arrhythmias
PE
Cardiac tamponade
Aortic dissection
311
Q

Noncardiac etiologies

A

Orthostatic/hypovolemic
Hypotension
Neurologic (TIA, Stroke)
Metabolic abnormalities

312
Q

Syncope: Hx and PE

A
  • triggers, prodromal symptoms and associated
  • cardiac causes associated with brief or absent prodromal sx, hx of exertion, lack of association with changes in position and hx of cardiac disease
313
Q

Syncope: Dx

A

Depends on etiology

  • Arrhythmias (Holter monitors / event recorders)
  • Echocardiograms (structural)
  • Stress tests (ischemia)
  • Tilt table testing (mediated syncope)
314
Q

Syncope: Tx

A

Commonly B-blockers for heart rate control

315
Q

PVC

A

ectopic beart aise from ventricular foci

- associated with hypoxia, electrolyte abnormalities, and hypoerthyroidism

316
Q

PVC: ECG finds

A

Early wide QRS note preceded by P wave

- often followed by compensatory pause

First AId 2CK COPY (22 decks)

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