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Cardiology > Cardiology Diseases > Flashcards

Cardiology Diseases Flashcards

1
Q

Volume Overload HF: Exam/EKG Findings

A

S3, JVD, narrow PP, pulsus alternans, cool extremities, +/- rales, hepatomegaly (HJ reflex)

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2
Q

Volume Overload HF: Labs/Imaging/BP

A

BNP >400, ↓Na AND ↑PCWP, ↑EDP

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3
Q

Volume Overload HF: Pathophysiology

A

Excessive preload → eccentric remodeling → decreased contractility

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4
Q

Volume Overload HF: Etiologies

A

MR, AR, volume overload, L→R shunt, chronic kidney disease

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5
Q

Volume Overload HF: Treatment/Notes

A

Stage A: Diuretics (↓preload), beta blockers (↓HR, ↑filling time), ACEi’s/ARBs, statins, aldosterone antagonists (↓afterload),↓Na, exercise +/- anticoag and diabetes control. Stage B: Add ICD if LV systolic dysfunction. Stage C: Add more! Stage D: death or transplant

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6
Q

Pressure Overload HF: Epi

A

Hypertension

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7
Q

Pressure Overload HF: Symptoms

A

FACES - Fatigue, Altered Activity, Congestion, Edema, SOB. Can get difficulty sleeping (paroxysmal nocturnal dyspnea), cachexia, orthopnea, Valsalva square wave

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8
Q

Pressure Overload HF: Exam/EKG Findings

A

S3, JVD, narrow PP, pulsus alternans, cool extremities, +/- rales, hepatomegaly (HJ reflex)

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9
Q

Pressure Overload HF: Labs/Imaging/BP

A

BNP >400, ↓Na AND ↑BP, ↓SV, ↑PCWP

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10
Q

Pressure Overload HF: Pathophysiology

A

Excessive afterload → concentric hypertrophy → decreased filling

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11
Q

Pressure Overload HF: Etiologies

A

HTN, AS, aortic coarctation

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12
Q

Pressure Overload HF: Treatment/Notes

A

Stage A: Diuretics (↓preload), beta blockers (↓HR, ↑filling time), ACEi’s/ARBs, statins, aldosterone antagonists (↓afterload),↓Na, exercise +/- anticoag and diabetes control. Stage B: Add ICD if LV systolic dysfunction. Stage C: Add more! Stage D: death or transplant

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13
Q

Systolic HF: Epi

A

All ages

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14
Q

Systolic HF: Symptoms

A

FACES - Fatigue, Altered Activity, Congestion, Edema, SOB. Can get difficulty sleeping (paroxysmal nocturnal dyspnea), cachexia, orthopnea, Valsalva square wave

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15
Q

Systolic HF: Exam/EKG Findings

A

S3, JVD, narrow PP, pulsus alternans, cool extremities, +/- rales, hepatomegaly (HJ reflex)

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16
Q

Systolic HF: Labs/Imaging/BP

A

BNP >400, ↓Na AND ↓BP, ↓SV, ↓CO, ↑PCWP, S3

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17
Q

Systolic HF: Cat

A

Heart Failure

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18
Q

Systolic HF: Pathophysiology

A

Decreased contractility ↔ eccentric remodeling

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19
Q

Systolic HF: Etiologies

A

ischemic cardiomyopathy, viral myocarditis, toxins

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20
Q

Systolic HF: Treatment/Notes

A

Stage A: Diuretics (↓preload), beta blockers (↓HR, ↑filling time), ACEi’s/ARBs, statins, aldosterone antagonists (↓afterload),↓Na, exercise +/- anticoag and diabetes control. Stage B: Add ICD if LV systolic dysfunction. Stage C: Add more! Stage D: death or transplant

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21
Q

Diastolic HF: Epi

A

> 60 yo, female

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22
Q

Diastolic HF: Symptoms

A

Same as systolic HF, but EF is preserved

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23
Q

Diastolic HF: Exam/EKG Findings

A

S3, S4,JVD, narrow PP, pulsus alternans, cool extremities, +/- rales, hepatomegaly (HJ reflex)

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24
Q

Diastolic HF: Labs/Imaging/BP

A

BNP >400, ↓Na AND ↓Capacitance, EDPVR shifts up + left, normal EF

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25
Q

Diastolic HF: Cat

A

Heart Failure

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26
Q

Diastolic HF: Pathophysiology

A

Decreased filling ↔ concentric hypertrophy

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27
Q

Diastolic HF: Etiologies

A

HTN, MS, RCM, tamponade, HCM, infiltrative

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28
Q

Diastolic HF: Treatment/Notes

A

Stage A: Diuretics (↓preload), beta blockers (↓HR, ↑filling time), ACEi’s/ARBs, statins, aldosterone antagonists (↓afterload),↓Na, exercise +/- anticoag and diabetes control. Stage B: Add ICD if LV systolic dysfunction. Stage C: Add more! Stage D: death or transplant

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29
Q

Acute Decompensated HF (ADHF): Symptoms

A

FACES, paroxysmal nocturnal dyspnea, cachexia, orthopnea, Valsalva square wave, with worsened dyspnea and fatigue

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30
Q

Acute Decompensated HF (ADHF): Exam/EKG Findings

A

Same as HF, with acute respiratory distress, severe JVD.

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31
Q

Acute Decompensated HF (ADHF): Labs/Imaging/BP

A

BNP >400, ↓Na

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32
Q

Acute Decompensated HF (ADHF): Cat

A

Heart Failure

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33
Q

Acute Decompensated HF (ADHF): Pathophysiology

A

Compensatory mechanisms fail

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34
Q

Acute Decompensated HF (ADHF): Treatment/Notes

A

Based on ACC Stage: Stage A: Diuretics (↓preload), beta blockers (↓HR, ↑filling time), ACEi’s/ARBs (↓afterload), statins, aldosterone antagonists (↓afterload),↓Na, exercise +/- anticoag and DM mgmt
Stage B: Add ICD if LV systolic dysfunction. Stage C: A

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35
Q

High CO HF: Symptoms

A

Same as HF

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36
Q

High CO HF: Exam/EKG Findings

A

Same as HF

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37
Q

High CO HF: Labs/Imaging/BP

A

BNP >400, ↓Na AND High PP

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38
Q

High CO HF: Etiologies

A

Anemia, pregnancy, obesity, etc.

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39
Q

High CO HF: Treatment/Notes

A

Stage A: Diuretics (↓preload), beta blockers (↓HR, ↑filling time), ACEi’s/ARBs, statins, aldosterone antagonists (↓afterload),↓Na, exercise +/- anticoag and diabetes control. Stage B: Add ICD if LV systolic dysfunction. Stage C: Add more! Stage D: death or transplant

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40
Q

Acute Cardiorenal Syndrome: Symptoms

A

Triad: (1) ↓kidney function: dark urine, low urine output. (2) Therapy-resistant HF: JVD, congestion, PE, rales, ↑BNP (3) Worsening kidney function (↑creatinine)

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41
Q

Acute Cardiorenal Syndrome: Exam Findings

A

Salt + water retention, congestion, edema, JVD

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42
Q

Acute Cardiorenal Syndrome: Labs

A

↑Creatinine, BUN (blood urea nitrogen, suggests renal failure)

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43
Q

Acute Cardiorenal Syndrome: Category

A

Heart + Kidney

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44
Q

Acute Cardiorenal Syndrome: Pathophysiology

A

Acute cardiac event → ↓CO, ↓renal perfusion, acute kidney injury → inflammation, kidneys ↑BP via RAAS

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45
Q

Acute Cardiorenal Syndrome: Etiologies

A

MI: ↓CO, vasodilators

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46
Q

Acute Cardiorenal Syndrome: Treatment

What indicates poor prognosis?

A

Tx: reduce or d/c ACEis, ARBs; titrate diuretics down; consider inotropes, aldosterone antagonists, vasodilators, assist devices, heart ± kidney xplant, dialysis
↑creatinine poor prognosis

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47
Q

Chronic Cardiorenal Syndrome: Symptoms

A

Triad: (1) ↓kidney function: dark urine, low urine output. (2) Therapy-resistant HF: JVD, congestion, PE, rales, ↑BNP (3) Worsening kidney function (↑creatinine)

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48
Q

Chronic Cardiorenal Syndrome: Exam

What is effect of ACEi?

A

RAAS-mediated anemia, edema, uremia. ACEi’s cause chronic renal hypoperfusion, sclerosis, fibrosis

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49
Q

Chronic Cardiorenal Syndrome: Labs

A

↑Creatinine, BUN

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50
Q

Chronic Cardiorenal Syndrome: Cat

A

Heart + Kidney

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51
Q

Chronic Cardiorenal Syndrome: Pathophysiology

A

Heart failure (or treatment for it) → ↓CO → ↓renal perfusion → ischemic nephropathy, RAAS kicks in → ↑BP

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52
Q

Chronic Cardiorenal Syndrome: Etiologies

Substances that worsen kidney function

A

Contrast media, ACEi, diuretics, vasodilators, inotropes will worsen kidney function

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53
Q

Chronic Cardiorenal Syndrome: Treatment

A

Tx: reduce or d/c ACEis, ARBs; titrate diuretics down; consider inotropes, aldosterone antagonists, vasodilators, assist devices, heart ± kidney xplant, dialysis; ↑creatinine poor prognosis

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54
Q

Acute Renocardiac Syndrome: Symptoms

A

Dark urine, low urine output, edema

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55
Q

Acute Renocardiac Syndrome: Exam/symtpoms

A

Volume expansion symptoms, dilated cardiomyopathy

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56
Q

Acute Renocardiac Syndrome: Labs

A

↑BP ± uremia

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57
Q

Acute Renocardiac Syndrome: Cat

A

Heart + Kidney

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58
Q

Acute Renocardiac Syndrome: Pathophysiology

A

Acute renal problem → ↓GFR, oliguria → acute cardiac issues: HTN, HF

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59
Q

Acute Renocardiac Syndrome: Etiologies

A

Glomerulo-nephritis, etc.

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60
Q

Acute Renocardiac Syndrome: Comorbidity/treatment

A

Comorbid conditions: smoking, obesity, HTN, dyslipidemia, chronic inflammation
Tx: control BP, add/increase diuretics, treat anemia and Ca++/P+ abnormalities, kidney ± heart xplant, dialysis

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61
Q

Chronic Renocardiac Syndrome: Symptoms

A

CHF, CAD, arrhythmias

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62
Q

Chronic Renocardiac Syndrome: Exam/Symptoms

A

Volume expansion symptoms, dilated cardiomyopathy

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63
Q

Chronic Renocardiac Syndrome: Labs

A

↑BP ± uremia

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64
Q

Chronic Renocardiac Syndrome: Cat

A

Heart + Kidney

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65
Q

Chronic Renocardiac Syndrome: Pathophysiology

A

Chronic kidney disease → volume overload

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66
Q

Chronic Renocardiac Syndrome: Etiologies

A

diabetes, etc.

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67
Q

Chronic Renocardiac Syndrome: Treatment/Comorbidity

A

Comorbid conditions: smoking, obesity, HTN, dyslipidemia, chronic inflammation
Tx: control BP, add/increase diuretics, treat anemia and Ca++/P+ abnormalities, kidney ± heart xplant, dialysis

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68
Q

Secondary Cardiorenal Syndrome: Cat

A

Heart + Kidney

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69
Q

Secondary Cardiorenal Syndrome: Pathophysiology

A

Infiltrative process (e.g. amyloidosis) independently destroys both kidneys + heart

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70
Q

Secondary Cardiorenal Syndrome: Treatment

A

Treat underlying condition

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71
Q

Pulmonary Venous Hypertension (PVH): Symptoms

What happens to the fingers?

A

Pulmonary congestion: cough, dyspnea, fatigue, orthopnea, hemoptysis, paroxysmal nocturnal dyspnea
Systemic congestion from RV failure: edema, ascites, RUQ pain (liver congestion), clubbing, cyanosis

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72
Q

Pulmonary Venous Hypertension (PVH): CXR/cath

A

CXR: ↑pulmonary vasculature in upper lobes → interstitial edema → alveolar edema (“white-out”)
↑LAP + PCWP

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73
Q

Pulmonary Venous Hypertension (PVH): Cat

A

Heart + Lungs

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74
Q

Pulmonary Venous Hypertension (PVH): Pathophysiology by the numbers

A

PAP mean of >25mmHg @ rest or >30 with exercise + PCWP or LVED > 15 → vessels hypertrophy, dilate

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75
Q

Pulmonary Venous Hypertension (PVH): Etiologies

A

↑LA pressure, from any number of left-sided heart pathologies, excess IV fluid, mitral stenosis

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76
Q

Pulmonary Venous Hypertension (PVH): Treatment

A

Diuretics

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77
Q

Dilated Cardiomyopathy: Symptoms

A

SOB, fatigue, ↓ET

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78
Q

Dilated Cardiomyopathy: Exam/EKG Findings

A

S3, left shift of axis, poor precordial R wave propagation, lat.-displaced PMI

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79
Q

Dilated Cardiomyopathy: Imaging/EF

A

↓EF, LV dilation

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80
Q

Dilated Cardiomyopathy: Cat

A

Cardiomyopathies

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81
Q

Dilated Cardiomyopathy: Pathophysiology

A

Systolic dysfunction from weakened ventricular wall

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82
Q

Dilated Cardiomyopathy: Many Etiologies

A

Congenital (glycogen storage disorder), regurgitation, myocarditis (Giant cell, CMV, toxo, Chagas, Rheumatic, Lyme), infiltrative (amyloid, sarcoid, Fe, ↑eos, tumor), toxin (doxo, XRT, EtOH), ASD/VSD

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83
Q

Dilated Cardiomyopathy: Treatment

A

Treat underlying cause + heart failure

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84
Q

Restrictive Cardiomyopathy: Symptoms

A

Orthopnea, PND, R>L sided HF, thromboembolic events

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85
Q

Restrictive Cardiomyopathy: Exam/EKG Findings

A

↑JVP, edema, ascites, refractory to diuretics, low voltage QRS, S4 ± S3

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86
Q

Restrictive Cardiomyopathy: Labs/Imaging

A

Thickened heart wall; Cardiac cath: Ms or Ws (x and y descents) in atria, dip+plateau in ventricles

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87
Q

Restrictive Cardiomyopathy: Cat

A

Cardiomyopathies

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88
Q

Restrictive Cardiomyopathy: Pathophysiology

A

Diastolic dysfunction from junk in ventricular wall

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89
Q

Restrictive Cardiomyopathy: Etiologies

A

Amyloidosis, hemochromatosis, scleroderma, tumor, sarcoid, Pompe’s, chronic ↑eos

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90
Q

Restrictive Cardiomyopathy: Treatment

A

Treat underlying cause + heart failure, anticoagulation

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91
Q

Hypertrophic Cardiomyopathy: Epi

A

1/500; AD, sporadic

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92
Q

Hypertrophic Cardiomyopathy: Symptoms

A

Angina, dyspnea, syncope, chest pain, SOB, fatigue

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93
Q

Hypertrophic Cardiomyopathy: Exam/EKG Findings

A

S4, ↑JVP, prominent v wave, spike-and-dome pulse, maybe mitral regurg, a.fib

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94
Q

Hypertrophic Cardiomyopathy: Labs/Imaging

A

↑BNP, high voltage LV, LV hypertrophy (septum>free wall)

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95
Q

Hypertrophic Cardiomyopathy: Cat

A

Cardiomyopathies

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96
Q

Hypertrophic Cardiomyopathy: Pathophysiology

A

Diastolic dysfunction from thick ventricular wall

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97
Q

Hypertrophic Cardiomyopathy: Etiologies

A

Inherited HCM, “athlete’s heart,” aortic stenosis (L), pulmonary HTN (R)

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98
Q

Hypertrophic Cardiomyopathy: Treatment/Notes

A

↑Risk of sudden cardiac death; Tx: Beta blockers, calcium channel blockers

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99
Q

Sinus Tachycardia

A

> 100bpm but otherwise normal sinus

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100
Q

Sinus Tachycardia: Cat

A

Supraventricular Tachyarrhythmias (SVTs)

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101
Q

Sinus Tachycardia: Pathophysiology

A

pulmonary embolism, fever, anxiety, etc. →↑SA node rate

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102
Q

Sinus Tachycardia: Treatment

A

Treat underlying cause / β blockers

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103
Q

Premature Atrial Contractions (PAC): Symptoms

A

Perceived irregular rhythm

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104
Q

Premature Atrial Contractions (PAC): EKG Findings

A

P waves from another focus (earlier in cycle, diff. morphology)

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105
Q

Premature Atrial Contractions (PAC): Cat

A

Supraventricular Tachyarrhythmias (SVTs)

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106
Q

Premature Atrial Contractions (PAC): Pathophysiology

A

Cardiac tissue injury → automaticity outside nodes

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107
Q

Premature Atrial Contractions (PAC): Treatment

A

Benign; like atrial tachycardia but only once in awhile; β blockers to ↓freq

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108
Q

Paroxysmal SVTs: Cat

A

Supraventricular Tachyarrhythmias (SVTs)

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109
Q

Paroxysmal SVTs: Treatment

Acute v. Chronic

A

Acute Tx: if unstable, cardiovert; if stable, vagal maneuvers / adenosine + β / calcium channel blockers Chronic Tx: avoid triggers, antiarrhythmics / catheter ablation

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110
Q

Atrial Tachycardia : EKG Findings

A

Many different P wave morphologies

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111
Q

Atrial Tachycardia : Cat

A

Supraventricular Tachyarrhythmias (SVTs)

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112
Q

Atrial Tachycardia : Pathophysiology

A

Atrial focus/foci faster than SA node

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113
Q

Atrial Tachycardia : Notes

A

Can be focal or multifocal

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114
Q

AV Nodal Reentrant Tachycardia (AVNRT): EKG Findings

A

P can come after QRS, or be inverted, or hidden within QRS

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115
Q

AV Nodal Reentrant Tachycardia (AVNRT): Cat

A

Supraventricular Tachyarrhythmias (SVTs)

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116
Q

AV Nodal Reentrant Tachycardia (AVNRT): Pathophysiology

A

Altered refractory period in AV node allows impulse to return backwards via AV node

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117
Q

AV Nodal Reentrant Tachycardia (AVNRT): Treatment

A

Ablate slower pathway within AV node

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118
Q

AV Reciprocating Tachycardia (AVRT): EKG Findings

A

Short PR, delta waves (widened QRS)

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119
Q

AV Reciprocating Tachycardia (AVRT): Cat

A

Supraventricular Tachyarrhythmias (SVTs)

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120
Q

AV Reciprocating Tachycardia (AVRT): Pathophysiology

A

Signal goes down normal pathway and back up via accessory pathway (orthodromic) or down accessory and up normal (antidromic)

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121
Q

AV Reciprocating Tachycardia (AVRT): Caused by

A

Can be caused by Wolff-Parkinson-White syndrome (short PR); AV valve rings are usual culprit

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122
Q

Atrial Fibrillation (AF): Epi

A

Most common

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123
Q

Atrial Fibrillation (AF): Exam/EKG Findings

A

Irregularly irregular ventricular rhythm, random baseline, no clear P waves, small fibrillatory waves >300bpm

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124
Q

Atrial Fibrillation (AF): Cat

A

Supraventricular Tachyarrhythmias (SVTs)

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125
Q

Atrial Fibrillation (AF): Pathophysiology

A

Many reentrant circuits in atrium

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126
Q

Atrial Fibrillation (AF): Etiologies

A

HF, coronary or valvular dz, cardio-myopathy, PE, HTN

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127
Q

Atrial Fibrillation (AF): Treatment

A

Anticoagulants (dabigatran; turbulence triggers clot formation), anti-arrhythmics if severe symptoms, BBs/digoxin for rate control, rhythm control if refractory

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128
Q

Atrial Flutter (AFL): EKG Findings

A

“Sawtooth” P waves, ~300bpm in atria

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129
Q

Atrial Flutter (AFL): Cat

A

Supraventricular Tachyarrhythmias (SVTs)

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130
Q

Atrial Flutter (AFL): Pathophysiology

A

Single large reentrant circuit in atrium

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131
Q

Atrial Flutter (AFL): Treatment

A

Anticoagulants (dabigatran; turbulence triggers clot formation), anti-arrhythmics if severe symptoms, BBs/digoxin for rate control, rhythm control if refractory

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132
Q

Premature Ventricular Contractions (PVC): Epi

A

Common

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133
Q

Premature Ventricular Contractions (PVC): Symptoms

A

Asymptomatic, may get dizzy/fatigued

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134
Q

Premature Ventricular Contractions (PVC): EKG Findings

A

Occasional taller, wider QRS, can lead to P wave burial if signal → retrograde to atria

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135
Q

Premature Ventricular Contractions (PVC): Cat

A

Ventricular Tachyarrhythmias

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136
Q

Premature Ventricular Contractions (PVC): Pathophysiology

A

Cardiac tissue injury → automaticity outside nodes

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137
Q

Premature Ventricular Contractions (PVC): Treatment

A

No treatment necessary; BBs if symptomatic

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138
Q

Ventricular Tachycardia (V.Tach): EKG Findings

A

Buried P waves; Non-sustained: >100bpm

Sustained: >100bpm for >30s

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139
Q

Ventricular Tachycardia (V.Tach): Cat

A

Ventricular Tachyarrhythmias

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140
Q

Ventricular Tachycardia (V.Tach): Pathophysiology

A

Reentrant circuit or ↑rate in ventricle

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141
Q

Ventricular Tachycardia (V.Tach): Treatment

A

BBs, amiodarone/sotalol to reduce symptoms, ICD, catheter ablation

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142
Q

Torsades de Pointes: EKG Findings AND Labs

A

Polymorphic, long QT, oscillating amplitude; hypomagnesemia

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143
Q

Torsades de Pointes: Cat

A

Ventricular Tachyarrhythmias

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144
Q

Torsades de Pointes: Pathophysiology

A

Oscillating amplitude of EKG

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145
Q

Torsades de Pointes: Etiologies

A

Long QT syndrome, ischemia, drugs

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146
Q

Torsades de Pointes: Treatment

A

Mg++, K+, isoproterenol or pacemaker @ 100bpm, lidocaine to decrease QT

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147
Q

Ventricular Fibrillation: EKG Findings

A

> 300bpm, chaotic, disorganized ventricular rhythm

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148
Q

Ventricular Fibrillation: Cat

A

Ventricular Tachyarrhythmias

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149
Q

Ventricular Fibrillation: Pathophysiology

A

Multiple reentrant circuits in ventricle

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150
Q

Ventricular Fibrillation: Treatment

A

Life-threatening, defibrillation stat

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151
Q

Sinus Bradycardia: EKG Findings

A

<60 bpm, both otherwise normal sinus

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152
Q

Sinus Bradycardia: Cat

A

Bradyarrhythmias

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153
Q

Sinus Bradycardia: Pathophysiology

A

↓SA rate or heart block

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154
Q

Sinus Bradycardia: Etiologies

A

Acute MI, hypothyroidism, infiltrative, drugs, athletes/teens

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155
Q

1st Degree AV Block: Symptoms

A

Angina, syncope

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156
Q

1st Degree AV Block: EKG Findings

A

PR interval >0.2 sec “long PR syndrome”

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157
Q

1st Degree AV Block: Cat

A

Bradyarrhythmias

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158
Q

1st Degree AV Block: Pathophysiology

A

↓AV conductivity

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159
Q

1st Degree AV Block: Treatment

A

Benign if asymptomatic

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160
Q

2nd Degree AV Block (Mobitz I) (Wenckebach): EKG Findings

A

PR progressively ↑ until QRS dropped

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161
Q

2nd Degree AV Block (Mobitz I) (Wenckebach): Cat

A

Bradyarrhythmias

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162
Q

2nd Degree AV Block (Mobitz I) (Wenckebach): Pathophysiology

A

Progressive PR prolongation

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163
Q

2nd Degree AV Block (Mobitz I) (Wenckebach): Etiologies AND Treatment

A

Drugs that slow conduction, athletes;

Tx: correct if reversible cause, pacemaker if syncope or angina

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164
Q

2nd Degree AV Block (Mobitz II): Symptoms

A

Pre-syncope, syncope

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165
Q

2nd Degree AV Block (Mobitz II): EKG Findings

A

PR stays constant but QRS dropped intermittently

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166
Q

2nd Degree AV Block (Mobitz II): Cat

A

Bradyarrhythmias

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167
Q

2nd Degree AV Block (Mobitz II): Pathophysiology

A

AV node blocks some atrial impulses

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168
Q

2nd Degree AV Block (Mobitz II): Etiologies

Where is the block?

A

Block is below AV node (His-Purkinje)

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169
Q

2nd Degree AV Block (Mobitz II): Treatment/Notes

A

More severe than Mobitz I, worsened by exercise;

Tx: pacemaker for everyone

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170
Q

3rd Degree AV Block: Symptoms

A

Dizziness, syncope, angina, HF

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171
Q

3rd Degree AV Block: EKG Findings

A

P waves dissociated from QRS but otherwise each normal

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172
Q

3rd Degree AV Block: Cat

A

Bradyarrhythmias

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173
Q

3rd Degree AV Block: Pathophysiology

A

No conduction from atria to ventricles at all

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174
Q

3rd Degree AV Block: Treatment/Notes

A

Atrial rate higher than ventricular rate (per natural frequencies);
Tx: pacing

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175
Q

Junctional (Nodal) Escape Rhythm: EKG Findings

A

Widened QRS, no P for awhile, 50-60bpm

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176
Q

Junctional (Nodal) Escape Rhythm: Cat

A

Bradyarrhythmias

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177
Q

Junctional (Nodal) Escape Rhythm: Pathophysiology

A

SA rate slows to the point where AV node takes over

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178
Q

Ventricular Escape Rhythm: EKG Findings

A

Widened QRS, long PR, 30-40bpm

Slower than Nodal escape rhythm

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179
Q

Ventricular Escape Rhythm: Cat

A

Bradyarrhythmias

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180
Q

Ventricular Escape Rhythm: Pathophysiology

A

SA rate slows to the point where ventricular pacemakers take over

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181
Q

Four ways to pancreatitis

A

Secondary hypertriglyceridemia
Familial hypertriglyceridemia IV
lipoprotein lipase deficiency
Apo-II deficiency

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182
Q

Secondary Cholesterolemia: Labs/Imaging/BP

A

↑Plasma cholesterol

↑LDL, the most important atherogenic lipoprotein

Normal TG levels

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183
Q

Secondary Cholesterolemia: Cat

A

Dyslipidemias

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184
Q

Secondary Cholesterolemia: Pathophysiology AND Etiologies

A

↓LDLr activity from diet high in saturated fat/cholesterol, hypothyroidism, biliary obstruction, or drugs; or ↓VLDL synthesis from nephrotic syndrome

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185
Q

Secondary Cholesterolemia: Treatment/Notes

A

↓LDL is primary target: lifestyle change, assess for CVD risk

LDL-lowering drugs
Statins: prevent CHD, reduce all-cause mortality + coronary lesions
Bile acid sequestrants: no reduction in all-cause mortality
Niacin: no reduction in coronary lesions
Fibr

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186
Q

Polygenic Hypercholesterolemia: Epi

A

Common

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187
Q

Polygenic Hypercholesterolemia: Symptoms

A

↑CHD risk

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188
Q

Polygenic Hypercholesterolemia: Exam/EKG Findings

A

↑LDL

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189
Q

Polygenic Hypercholesterolemia: Labs/Imaging/BP

A

↑Plasma cholesterol

↑LDL, the most important atherogenic lipoprotein

Normal TG levels

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190
Q

Polygenic Hypercholesterolemia: Cat

A

Dyslipidemias

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191
Q

Polygenic hypercholesterolemia v. Monogenic

A

Less severe LDL elevation than monogenic, not very strong inheritance

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192
Q

Polygenic Hypercholesterolemia: Treatment/Notes

A

↓LDL is primary target: lifestyle change, assess for CVD risk

LDL-lowering drugs
Statins: prevent CHD, reduce all-cause mortality + coronary lesions
Bile acid sequestrants: no reduction in all-cause mortality
Niacin: no reduction in coronary lesions
Fibr

193
Q

Familial Hypercholesterolemia (IIa): Epi

A

1/500, AD

194
Q

Familial Hypercholesterolemia (IIa): Symptoms AND Exam/EKG Findings

A

↑LDL, coronary heart disease, tendon xanthomas, xanthelasmas (cholesterol in eyelids), corneal arcus (white ring in iris)

Mostly AD with increased severity if homozygote

195
Q

Familial Hypercholesterolemia (IIa): Labs/Imaging/BP

A

↑Plasma cholesterol

↑LDL, the most important atherogenic lipoprotein

Normal TG levels

196
Q

Familial Hypercholesterolemia (IIa): Cat

A

Dyslipidemias

197
Q

Familial Hypercholesterolemia (IIa): Pathophysiology AND Etiologies

Defect?

A

Defect in LDLr → ↑LDL synthesis, ↑↑CHD risk (worse if homozygote (1/million))

198
Q

Familial Hypercholesterolemia (IIa): Treatment/Notes

A

↓LDL is primary target: lifestyle change, assess for CVD risk

LDL-lowering drugs
Statins: prevent CHD, reduce all-cause mortality + coronary lesions
Bile acid sequestrants: no reduction in all-cause mortality
Niacin: no reduction in coronary lesions
Fibr

199
Q

Familial Defective apoB (IIa): Epi

A

1/1000, AD

200
Q

Familial Defective apoB (IIa): Symptoms AND Exam/EKG Findings

A

↑LDL, coronary heart disease, tendon xanthomas, xanthelasmas (cholesterol in eyelids), corneal arcus (white ring in iris)

Mostly AD with increased severity if homozygote

201
Q

Familial Defective apoB (IIa): Labs/Imaging/BP

A

↑Plasma cholesterol

↑LDL, the most important atherogenic lipoprotein

Normal TG levels

202
Q

Familial Defective apoB (IIa): Cat

A

Dyslipidemias

203
Q

Familial Defective apoB (IIa): Pathophysiology AND Etiologies

A

apoB gene defect → defective ligand for LDLr, ↓LDL clearance, 1/4M homozygous

204
Q

Familial Defective apoB (IIa): Treatment/Notes

A

↓LDL is primary target: lifestyle change, assess for CVD risk

LDL-lowering drugs
Statins: prevent CHD, reduce all-cause mortality + coronary lesions
Bile acid sequestrants: no reduction in all-cause mortality
Niacin: no reduction in coronary lesions
Fibr

205
Q

Autosomal Dominant Hypercholesterolemia: Epi

A

<1/2500, AD

206
Q

Autosomal Dominant Hypercholesterolemia: Symptoms AND Exam/EKG Findings

A

↑LDL, coronary heart disease, tendon xanthomas, xanthelasmas (cholesterol in eyelids), corneal arcus (white ring in iris)

Mostly AD with increased severity if homozygote

207
Q

Autosomal Dominant Hypercholesterolemia: Labs/Imaging/BP

A

↑Plasma cholesterol

↑LDL, the most important atherogenic lipoprotein

Normal TG levels

208
Q

Autosomal Dominant Hypercholesterolemia: Cat

A

Dyslipidemias

209
Q

Autosomal Dominant Hypercholesterolemia: Pathophysiology AND Etiologies

Gene?

A

GOF mutation in PCSK9 → ↑LDLr lysosomal degradation

210
Q

Autosomal Dominant Hypercholesterolemia: Treatment/Notes

A

↓LDL is primary target: lifestyle change, assess for CVD risk

LDL-lowering drugs
Statins: prevent CHD, reduce all-cause mortality + coronary lesions
Bile acid sequestrants: no reduction in all-cause mortality
Niacin: no reduction in coronary lesions
Fibr

211
Q

Autosomal Recessive Hypercholesterolemia: Epi

A

1/5M, AR

212
Q

Autosomal Recessive Hypercholesterolemia: Symptoms AND Exam/EKG Findings

A

↑LDL, coronary heart disease, tendon xanthomas, xanthelasmas (cholesterol in eyelids), corneal arcus (white ring in iris)

Mostly AD with increased severity if homozygote

213
Q

Autosomal Recessive Hypercholesterolemia: Labs/Imaging/BP

A

↑Plasma cholesterol

↑LDL, the most important atherogenic lipoprotein

Normal TG levels

214
Q

Autosomal Recessive Hypercholesterolemia: Cat

A

Dyslipidemias

215
Q

Autosomal Recessive Hypercholesterolemia: Pathophysiology AND Etiologies

Gene?

A

Defect in ARH gene (bridges LDLr and clathrin coated pit) → ↓LDL clearance

216
Q

Autosomal Recessive Hypercholesterolemia: Treatment/Notes

A

↓LDL is primary target: lifestyle change, assess for CVD risk

LDL-lowering drugs
Statins: prevent CHD, reduce all-cause mortality + coronary lesions
Bile acid sequestrants: no reduction in all-cause mortality
Niacin: no reduction in coronary lesions
Fibr

217
Q

Familial Combined Hyperlipidemia (IIb): Epi

A

AD, most common

218
Q

Familial Combined Hyperlipidemia (IIb): Symptoms

A

Metabolic syndrome

219
Q

Familial Combined Hyperlipidemia (IIb): Note!

A

May not see ↑LDL + ↑TG in same people

220
Q

Familial Combined Hyperlipidemia (IIb): Labs/Imaging/BP

A

↑LDL and ↑TG

221
Q

Familial Combined Hyperlipidemia (IIb): Cat

A

Dyslipidemias

222
Q

Familial Combined Hyperlipidemia (IIb): Pathophysiology AND Etiologies

Defect?

A

↑apoB hepatic synthesis→↑CHD risk, cause for 30% of hyperlipidemic MI survivors

223
Q

Familial Combined Hyperlipidemia (IIb): Treatment/Notes

A

↓LDL is primary target: lifestyle change, assess for CVD risk

LDL-lowering drugs
Statins: prevent CHD, reduce all-cause mortality + coronary lesions
Bile acid sequestrants: no reduction in all-cause mortality
Niacin: no reduction in coronary lesions
Fibr

224
Q

Type III Hyperlipoproteinemia: Epi

A

AR with ↓penet.

225
Q

Type III Hyperlipoproteinemia: Symptoms AND Exam/EKG Findings

A

Atherosclerosis, palmar + tuboeruptive xanthomas; +↑VLDL in Type V

226
Q

Type III Hyperlipoproteinemia: Labs/Imaging/BP

A

↑LDL and ↑TG

227
Q

Type III Hyperlipoproteinemia: Cat

A

Dyslipidemias

228
Q

Type III Hyperlipoproteinemia: Pathophysiology AND Etiologies

Defect?

A

mutant ApoE impairs binding + clearance of chylomicrons

229
Q

Type III Hyperlipoproteinemia: Treatment/Notes

A

↓LDL is primary target: lifestyle change, assess for CVD risk

LDL-lowering drugs
Statins: prevent CHD, reduce all-cause mortality + coronary lesions
Bile acid sequestrants: no reduction in all-cause mortality
Niacin: no reduction in coronary lesions
Fibr

230
Q

Secondary Hypertriglyceridemia: Symptoms

A

Pancreatitis from ↑pancreatic lipase, eruptive xanthomas, lipemia retinalis

231
Q

Secondary Hypertriglyceridemia: Labs/Imaging/BP

A

↑TG ± ↑VLDL

232
Q

Secondary Hypertriglyceridemia: Cat

A

Dyslipidemias

233
Q

Secondary Hypertriglyceridemia: Pathophysiology AND Etiologies

A

↑TG from obesity/EtOH, T1/2DM, nephrotic syndrome, estrogens, glucocorticoids, protease inhibitors, tretinoin

234
Q

Secondary Hypertriglyceridemia: Treatment/Notes

A

↓LDL is primary target: lifestyle change, assess for CVD risk

LDL-lowering drugs
Statins: prevent CHD, reduce all-cause mortality + coronary lesions
Bile acid sequestrants: no reduction in all-cause mortality
Niacin: no reduction in coronary lesions
Fibr

235
Q

Familial Hypertriglyceridemia (IV): Epi

A

1%, AD, common

236
Q

Familial Hypertriglyceridemia (IV): Symptoms

A

Pancreatitis from ↑pancreatic lipase, eruptive xanthomas, lipemia retinalis

237
Q

Familial Hypertriglyceridemia (IV): Exam/EKG Findings

A

↑VLDL

238
Q

Familial Hypertriglyceridemia (IV): Labs/Imaging/BP

A

↑TG ± ↑VLDL

239
Q

Familial Hypertriglyceridemia (IV): Cat

A

Dyslipidemias

240
Q

Familial Hypertriglyceridemia (IV): Pathophysiology AND Etiologies

Defect?

A

↑hepatic TG synthesis, ↑VLDL, saturates LPL clearance, usually moderate disease

241
Q

Familial Hypertriglyceridemia (IV): Treatment/Notes

A

↓LDL is primary target: lifestyle change, assess for CVD risk

LDL-lowering drugs
Statins: prevent CHD, reduce all-cause mortality + coronary lesions
Bile acid sequestrants: no reduction in all-cause mortality
Niacin: no reduction in coronary lesions
Fibr

242
Q

Lipoprotein Lipase Deficiency (Ia): Epi

A

1/M

243
Q

Lipoprotein Lipase Deficiency (Ia): Symptoms

A

Pancreatitis from ↑pancreatic lipase, eruptive xanthomas, lipemia retinalis

244
Q

Lipoprotein Lipase Deficiency (Ia): Labs/Imaging/BP

A

↑TG ± ↑VLDL

245
Q

Lipoprotein Lipase Deficiency (Ia): Cat

A

Dyslipidemias

246
Q

Lipoprotein Lipase Deficiency (Ia): Pathophysiology AND Treatment

A

Results in early childhood pancreatitis from ↑↑pancreatic lipase Tx: low fat diet, MC TGs

247
Q

Lipoprotein Lipase Deficiency (Ia): Treatment/Notes

A

↓LDL is primary target: lifestyle change, assess for CVD risk

LDL-lowering drugs
Statins: prevent CHD, reduce all-cause mortality + coronary lesions
Bile acid sequestrants: no reduction in all-cause mortality
Niacin: no reduction in coronary lesions
Fibr

248
Q

Apo-II Deficiency (Ib): Symptoms

A

Pancreatitis from ↑pancreatic lipase, eruptive xanthomas, lipemia retinalis

249
Q

Apo-II Deficiency (Ib): Labs/Imaging/BP

A

↑TG ± ↑VLDL

250
Q

Apo-II Deficiency (Ib): Cat

A

Dyslipidemias

251
Q

Apo-II Deficiency (Ib): Pathophysiology, duh

A

ApoCII deficiency

252
Q

Apo-II Deficiency (Ib): Treatment/Notes

A

↓LDL is primary target: lifestyle change, assess for CVD risk

LDL-lowering drugs
Statins: prevent CHD, reduce all-cause mortality + coronary lesions
Bile acid sequestrants: no reduction in all-cause mortality
Niacin: no reduction in coronary lesions
Fibr

253
Q

Aortic Stenosis: Epi

A

70s

254
Q

Aortic Stenosis: Symptoms

A

Angina, syncope/pre-syncope, CHF, dyspnea

255
Q

Aortic Stenosis: Exam/EKG Findings

A

Systolic crescendo-decrescendo murmur @ RUSB, ↓carotid upstroke, S4, ejection murmur, ↓A2, paradoxical S2 split

256
Q

Aortic Stenosis: Cath, Echo

A

Cath: LV > aortic pressure during most of systole
Echo: LVH

257
Q

Aortic Stenosis: Cat

A

Valvular Disorder

258
Q

Aortic Stenosis: Pathophysiology

A

Aortic valve doesn’t open properly → LV hypertrophies because of increased resistance

259
Q

Aortic Stenosis: Etiologies

A

Age-related degeneration, congenital bicuspid aortic valve, rheumatic fever

260
Q

Aortic Stenosis: Treatment/Notes

A

Staging: based on mean gradient, aortic valve area, peak gradient
Pulsus parvus et tardus is buzzword for ↓carotid upstroke
Tx: valve replacement

261
Q

Aortic Regurgitation / Insufficiency: Symptoms

A

Dyspnea, rare angina

262
Q

Aortic Regurgitation / Insufficiency: Exam/BP

A

Early diastolic decrescendo (>) murmur @ LUSB, wide PP, bounding pulses, S3

263
Q

Aortic Regurg Cath and Echo

A

Cath: Aortic diastolic pressure plummets, LV diastolic pressure may shoot up
Echo: Dilated LV

264
Q

Aortic Regurgitation / Insufficiency: Cat

A

Valvular Disorder

265
Q

Aortic Regurgitation / Insufficiency: Pathophysiology

A

Aortic valve leaks → LV dilates because of backflow

266
Q

Aortic Regurgitation / Insufficiency: Etiologies

A

Marfan’s, Ehlers-Danlos, syphilis

267
Q

Aortic Regurgitation / Insufficiency: Treatment/Notes

A

Staging: regurgitant volume, regurgitant fraction, and effective regurgitant orifice
Tx: valve replacement

268
Q

Mitral Stenosis: Symptoms

A

Dyspnea, hemoptysis, fatigue, ↓ET, edema, a.fib

269
Q

Mitral Stenosis: Exam

A

Low-pitched mid-diastolic rumble @ apex ± opening snap, ↑S1

270
Q

Mitral Stenosis: Cath Echo

A

Cath: LA pressure > LV pressure at times
Echo: Dilated LA

271
Q

Mitral Stenosis: Cat

A

Valvular Disorder

272
Q

Mitral Stenosis: Pathophysiology

A

Mitral valve doesn’t open properly → LA dilates from ↑resistance; can→a.fib

273
Q

Mitral Stenosis: Etiologies

A

Rheumatic fever

274
Q

Mitral Stenosis: Treatment/Notes

A

Staging: mean gradient, mitral valve area, PA systolic pressure
Tx: diuretics, rate/rhythm control, anticoag, valvuloplasty, replace valve

275
Q

Mitral Regurgitation / Insufficiency: Symptoms

A

Acute: pulmonary congestion; Chronic: fatigue, etc.

276
Q

Mitral Regurgitation / Insufficiency: Exam

A

High-pitched holosystolic murmur @ apex (worse with clenched fists), S3

277
Q

Mitral Regurgitation / Insufficiency: Cat

A

Valvular Disorder

278
Q

Mitral Regurgitation / Insufficiency: Pathophysiology

A

LV and LA dilate from excess blood volume, can → a.fib (stretched electrical fibers in LA)

279
Q

Mitral Regurgitation / Insufficiency: Etiologies

A

MVP, endocarditis, ischemic heart disease, rheumatic fever

280
Q

Mitral Regurgitation / Insufficiency: Treatment/Notes

A

Staging: same as AR
Tx: diuretics, afterload reduction, valve repair/replacement

281
Q

Pulmonic Stenosis: Exam

A

Systolic @ LUSB

282
Q

Pulmonic Stenosis: Cat

A

Valvular Disorder

283
Q

Pulmonic Stenosis: Pathophysiology

A

RV hypertrophies

284
Q

Pulmonic Stenosis: Treatment/Notes

A

Not very clinically significant (rare), treat with valve repair or replacement

285
Q

Pulmonic Regurgitation: Exam

A

Diastolic @ LUSB

286
Q

Pulmonic Regurgitation: Cat

A

Valvular Disorder

287
Q

Pulmonic Regurgitation: Pathophysiology

A

RV dilates

288
Q

Pulmonic Regurgitation: Treatment/Notes

A

Not very clinically significant (rare), treat with valve repair or replacement

289
Q

Tricuspid Stenosis: Exam

A

Diastolic @ LLSB

290
Q

Tricuspid Stenosis: Sign!

A

JVD

291
Q

Tricuspid Stenosis: Cat

A

Valvular Disorder

292
Q

Tricuspid Stenosis: Pathophysiology

A

RA dilates

293
Q

Tricuspid Stenosis: Treatment/Notes

A

Not very clinically significant (rare), treat with valve repair or replacement

294
Q

Tricuspid Regurgitation: Exam

A

Systolic @ LLSB

295
Q

Tricuspid Regurgitation: Sign!

A

JVD

296
Q

Tricuspid Regurgitation: Cat

A

Valvular Disorder

297
Q

Tricuspid Regurgitation: Pathophysiology

A

RA, RV dilate

298
Q

Tricuspid Regurgitation: Treatment/Notes

A

Not very clinically significant (rare), treat with valve repair or replacement

299
Q

Stable Angina: Symptoms

A

↓ET, chest pain / SOB on exertion

300
Q

Stable Angina: Cat

A

Coronary Artery Dzs

301
Q

Stable Angina: Pathophysiology AND Etiologies

A

Mild atherosclerosis → ischemia on exertion

302
Q

Stable Angina: Ddx

A

DDx: Prinzmetal’s (variant) angina, coronary vasospasm

303
Q

Unstable Angina / Non-ST Segment Elevation Myocardial Infarction (UA/NSTEMI): Epi

A

Age >65, prior CAD, DM, angina, FHx, HTN, smoking

304
Q

Unstable Angina / Non-ST Segment Elevation Myocardial Infarction (UA/NSTEMI): Symptoms

A 
Chest pain (angina) / SOB even while at rest, diaphoresis, dyspnea, N/V, palpitations, may be asymptomatic
NSTEMI usually 30
Angina pain = retrosternal pressure/pain ± rad to neck, jaw, arms, ↑with exertion
305
Q

Unstable Angina / Non-ST Segment Elevation Myocardial Infarction (UA/NSTEMI): Exam/EKG Findings

Pulse, Lungs, BP

A

Dyskinetic apical impulse, rales, S4, mitral regurg (papillary muscle dysfunction), ↑BP, HR

306
Q

Unstable Angina / Non-ST Segment Elevation Myocardial Infarction (UA/NSTEMI): Labs

EF v. STEMI?

A

+Troponins in NSTEMI
-Troponins in UA

Usually lower EF than STEMI at time of presentation

307
Q

Unstable Angina / Non-ST Segment Elevation Myocardial Infarction (UA/NSTEMI): Cat

A

Coronary Artery Dzs

308
Q

Unstable Angina / Non-ST Segment Elevation Myocardial Infarction (UA/NSTEMI): Pathophysiology AND Etiologies

A

NSTEMI: partially occlusive thrombus in setting of atherosclerosis (vulnerable plaques are smaller, have ↑lipid + macrophage foam cells, ↓collagen + protein) → ischemia even while at rest; UA is similar, but slowly growing thrombosis

309
Q

Unstable Angina / Non-ST Segment Elevation Myocardial Infarction (UA/NSTEMI): Treatment/Notes

A

More long-term mortality
Tx: aspirin or anticoag (clopidogrel, heparin), β blockers and Ca+ channel blockers, nitrates, if advanced: stenting/bypass/angioplasty

310
Q

ST Segment Elevation Myocardial Infarction (STEMI): Symptoms

A 
Chest pain (angina) / SOB even while at rest, diaphoresis, dyspnea, N/V, palpitations, may be asymptomatic
NSTEMI usually 30
Angina pain = retrosternal pressure/pain ± rad to neck, jaw, arms, ↑with exertion
311
Q

ST Segment Elevation Myocardial Infarction (STEMI): Exam/EKG Findings: acute, hours, days, forever

A

Acute: ST elevation
Hours: ↓R; Q begins
Days: T inversion, deep Q wave, ST normalizes
Weeks: deep Q (permanent)

312
Q

ST Segment Elevation Myocardial Infarction (STEMI): Labs

A

↑↑Troponin

313
Q

ST Segment Elevation Myocardial Infarction (STEMI): Cat

A

Coronary Artery Diseases

314
Q

ST Segment Elevation Myocardial Infarction (STEMI): Pathophysiology AND Etiologies

A

Transmural ischemia, associated with total occlusion of (usually one) artery

315
Q

ST Segment Elevation Myocardial Infarction (STEMI): Treatment/Notes

Lytic by? Balloon by? PPCI by?

A

More short-term mortality
Tx: same as NSTEMI + thrombolytic drugs, e.g. streptokinase and tPA; ACEis, anticoagulants
Goals: primary percutaneous coronary intervention <6-12 hours, door-to-lytic 30 mins, door-to-balloon 90 mins

316
Q

Acute Pericarditis: Symptoms

A

Pleuritic chest pain: retrosternal or left-sided, rad to shoulder, neck, left scapula, positional (↓if lean forward), fever, dyspnea

317
Q

Acute Pericarditis: Exam/EKG Findings

A

Pericardial rub (85%), EKG abnormalities (90%): ST elevation in non-coronary distribution, PR depression, diffuse T inversion

318
Q

Acute Pericarditis: Labs

A

↑WBCs, ESR, CRP, cardiac enzymes

319
Q

Acute Pericarditis: Cat

A

Pericardial/Myocardial Dzs

320
Q

Acute Pericarditis: Pathophysiology

A

Inflammation of pericardium; transudative → exudative effusion → leukocyte infiltration

321
Q

Acute Pericarditis: Etiologies

Most coomon?

A

Echovirus and Coxsackie B most common; TB, bacteria, lupus, Dressler’s syndrome (post-MI), etc.

322
Q

Acute Pericarditis: Treatment/Notes

A

Tx: NSAIDs (ASA, indomethacin, ibuprofen), colchicine, corticosteroids, targeted therapy vs. underlying cause

Hospitalize if T>38C, subacute, chest trauma, tamponade, pericardial effusion, immunocompromised, myocarditis

323
Q

Pericardial Effusion: Symptoms

A

Dull left chest discomfort, dysphagia, dyspnea, hiccups, hoarseness

324
Q

Pericardial Effusion: Exam/EKG Findings

A

↑JVP, distant heart sounds, ↓QRS, Ewart sign: dullness to percussion beneath angle of left scapula

325
Q

Pericardial Effusion: Labs/Imaging

A

↓BP from ↓CO, >200ccs of fluid on CXR (“water-bottle heart”)

326
Q

Pericardial Effusion: Cat

A

Pericardial/Myocardial Dzs

327
Q

Pericardial Effusion: Pathophysiology

A

Non-inflammatory serous/chylous fluid in pericardial sac

328
Q

Pericardial Effusion: Etiologies

A

Pericarditis, trauma, cardiac procedures

329
Q

Pericardial Effusion: Treatment

A

Pericardiocentesis, treat underlying cause

330
Q

Cardiac Tamponade: Symptoms

A

Weakness, fatigue

331
Q

Cardiac Tamponade: Exam

A

Beck’s triad: JVD, hypotension, small quiet heart

332
Q

Cardiac Tamponade: Labs/Imaging/BP

A

↓SV, CO →↑HR, BP

Pulsus paradoxus: systolic BP falls >10 mmHg on inspiration; Echo: RA collapse

333
Q

Pulsus Paradoxus

A

systolic BP falls >10 mmHg on inspiration

334
Q

Cardiac Tamponade: Pathophysiology

A

Severe restriction of cardiac motion due to pericardial effusion

335
Q

Cardiac Tamponade: Etiologies

A

Severe pericardial effusion, post-MI, hemorrhage

336
Q

Cardiac Tamponade: Treatment/Notes

What happens to diastolic pressure?

A

Often fatal, treated with pericardiocentesis; ↑diastolic pressure in all chambers

337
Q

Constrictive Pericarditis: Epi

A

Rare

338
Q

Constrictive Pericarditis: Symptoms

A

Kussmaul sign: ↑JVP during inspiration

339
Q

Constrictive Pericarditis: Exam/Cath Findings

A

Rapid y descent (detectable on cath), “Dip and plateau” in RV/LV pressure, early diastolic “knock”

340
Q

Constrictive Pericarditis: Labs/Imaging/BP

CO? Venous filling pressure?

A

↓CO, ↑venous filling pressure
CT/MRI/CXR: may show thickening
Echo: abnormal septal motion/filling/flow

341
Q

Constrictive Pericarditis: Cat

A

Pericardial/Myocardial Dzs

342
Q

Constrictive Pericarditis: Pathophysiology

A

Pericardium becomes fibrotic → diastolic dysfunction

343
Q

Constrictive Pericarditis: Etiologies

A

Any chronic pericarditis, TB

344
Q

Constrictive Pericarditis: Treatment

A

Often requires surgical removal of pericardium

345
Q

Myocarditis: Cat

A

Pericardial/Myocardial Dzs

346
Q

Myocarditis: Pathophysiology

A

Infection, inflammatory disease, or toxins

347
Q

Myocarditis: Etiologies

A

Coxsackie B most common viral cause

348
Q

Myocarditis: Treatment/Notes

A

Treat underlying cause

349
Q

Atrial Myxoma: Symptoms

A

Often benign; can see emboli, constitutional sx.

350
Q

Atrial Myxoma: Exam

A

Diastolic murmur possible

351
Q

Atrial Myxoma: Imaging

A

Often pedunculated

352
Q

Atrial Myxoma: Cat

A

Pericardial/Myocardial Dzs

353
Q

Atrial Myxoma: Epi

A

Most common primary cardiac tumor (metastases = most common tumor)

354
Q

Sudden Cardiac Death: Epi

A

180-250K in US, 55-85yo

355
Q

Sudden Cardiac Death: Exam/EKG Findings

A

Bradycardia, T wave alternans, acute respiratory failure, risk of PE, CVAs

356
Q

Sudden Cardiac Death: Dx tests

A

Dx with EKG, echo, exercise test, Holter, electrophysiology tests

357
Q

Sudden Cardiac Death: Cat

A

SCD

358
Q

Sudden Cardiac Death: Pathophysiology

How long until death?

A

V.tach→v.fib→asystole, death within one hour of symptoms, no preceding heart failure

359
Q

Sudden Cardiac Death: Etiologies

A

Post-MI, commotio cordis, congenital, cardiomyopathies, long QT, Brugada

360
Q

Sudden Cardiac Death: Treatment

A

Tx: treat underlying cause, antiarrhythmics, ICD, catheter ablation

361
Q

Elastin Insufficiency: Symptoms/Path

A

Peripheral pulmonary stenosis

362
Q

Elastin Insufficiency: Cat

A

Genetic Diseases

363
Q

Elastin Insufficiency: Pathophysiology

A

Elastin mutation

364
Q

Alagille Syndrome: Symptoms/Path

A

Jaundice, stenosis of branched pulmonary arteries

365
Q

Alagille Syndrome: Cat

A

Genetic Diseases

366
Q

Alagille Syndrome: Pathophysiology

Gene?

A

JAG1 mutation

367
Q

Noonan/Costello Synd.: Symptoms

Which valve is displastic?

A

Dysplastic pulmonic valve, HCM, webbed neck, freckles, short

368
Q

Noonan/Costello Synd.: Cat

A

Genetic Diseases

369
Q

Noonan/Costello Synd.: Pathophysiology

Gene?

A

PTPN11 mutation (Ras-MAPK pathway)

370
Q

Noonan/Costello Synd.: Epi

A

Common cause of cardiomyopathy in children

371
Q

Holt-Oram Syndrome: Symptoms

A

Arm/hand birth defects, ASDs, conduction abnormalities

372
Q

Holt-Oram Syndrome: Cat

A

Genetic Diseases

373
Q

Holt-Oram Syndrome: Pathophysiology

Gene

A

TBX5 mutation

374
Q

Neonatal Wolff-Parkinson-White Syndrome (WPW): Symptoms

A

Short PR, Irregular HR, 11 pairs of ribs, macrocephaly, failure to thrive

375
Q

Neonatal Wolff-Parkinson-White Syndrome (WPW): Cat

A

Genetic Diseases

376
Q

Neonatal Wolff-Parkinson-White Syndrome (WPW): Pathophysiology

Gene?

A

20p12.3 de novo mutation → ↓BMP2

377
Q

Marfan’s Syndrome: Epi

A

AD

378
Q

Marfan’s Syndrome: Symptoms

A

Aortic root dilation / dissection, retinal detachment

379
Q

Marfan’s Syndrome: Cat

A

Genetic Diseases

380
Q

Marfan’s Syndrome: Pathophysiology

A

Fibrillin defect → weak connective tissue

381
Q

Marfan’s Syndrome: Treatment/Notes

A

Genetic testing

382
Q

Isolated Hypertrophic Cardiomyopathy: Epi

A

1/500

383
Q

Isolated Hypertrophic Cardiomyopathy: Symptoms

A

1st symptom may be SCD (sudden cardiac death)

384
Q

Isolated Hypertrophic Cardiomyopathy: Exam/EKG Findings

A

HCM

385
Q

Isolated Hypertrophic Cardiomyopathy: Cat

A

Genetic Diseases

386
Q

Isolated Hypertrophic Cardiomyopathy: Pathophysiology

Gene?

A

Sarcomeric genes (Beta-myosin heavy chain, myosin-binding protein C, cardiac troponin T)

387
Q

Isolated Hypertrophic Cardiomyopathy: Epi

A

Most common genetic cardiac disease, most common cause of SCD in children

388
Q

Familial Dilated Cardiomyopathy: Exam/EKG Findings

A

DCM

389
Q

Familial Dilated Cardiomyopathy: Cat

A

Genetic Diseases

390
Q

Familial Dilated Cardiomyopathy: Pathophysiology AND Etiologies

Gene?

A

Diverse genes, some overlap with HCM; LMNA associated with conduction disorders

391
Q

Familial Dilated Cardiomyopathy: Associated w/

A

May be associated with muscular dystrophy

392
Q

Arrhythmogenic RV Cardiomyopathy (ARVC): EKG Findings

A

V.Tach, LBBB

393
Q

Arrhythmogenic RV Cardiomyopathy (ARVC): Cat

A

Genetic Diseases

394
Q

Arrhythmogenic RV Cardiomyopathy (ARVC): Pathophysiology

A

Fibro-fatty replacement of RV myocardium

395
Q

Familial Long QT Syndrome: Epi

A

1/3-5K, AD (AR form also)

396
Q

Familial Long QT Syndrome: Symptoms

A

Pre-syncope, syncope, death, deafness (in AR version)

397
Q

Familial Long QT Syndrome: EKG Findings

A

QTc > 440ms, Torsades de pointes → polymorphic v.tach (v.tach + intermittent sinus)

398
Q

Familial Long QT Syndrome: AR version

A

Deafness

399
Q

Familial Long QT Syndrome: Pathophysiology

Gene?

A

SCN5A GOF or KCN LOF mutations → ↓K channel activity or ↑Na channel activity

400
Q

Familial Long QT Syndrome: Etiologies AND Treatment

Three Classes

A

Type I: emotion, physical activity triggers (BBs, avoid sports)
Type II: sounds during sleep/rest (avoid ↓K+, loud noises)
Type III: most severe, during sleep or rest (mexiletine/flecainide, pacing, AICD)

401
Q

Brugada Syndrome: Epi

A

M>F, AD

402
Q

Brugada Syndrome: Symptoms

A

V.fib, SCD

403
Q

Brugada Syndrome: EKG Findings

A

RBBB, ↑ST in V1-V3

404
Q

Brugada Syndrome: Cat

A

Genetic Diseases

405
Q

Brugada Syndrome: Pathophysiology AND Etiologies

Defect?

A

Mutation in Na + K channels

406
Q

Brugada Syndrome: Treatment/Notes

A

Usually during sleep; Tx: defibrillator

407
Q

Catecholaminergic Polymorphic V.Tach : Symptoms

A

Bi-directional polymorphic VT with exercise, stress; can lead to ventricular arrhythmias, cardiac death

408
Q

Catecholaminergic Polymorphic V.Tach : Cat

A

Genetic Diseases

409
Q

Catecholaminergic Polymorphic V.Tach : Pathophysiology AND Etiologies

Gene?

A

RyR2, calsequestrin mutations; 30% mortality by 30yo

410
Q

Catecholaminergic Polymorphic V.Tach : Treatment/Notes

A

Tx: beta blockers, AICD

411
Q

Ventricular Septal Defect (VSD): Epi

A

1/500

412
Q

Ventricular Septal Defect (VSD): Symptoms

A

Asymptomatic @ birth → CHF (rales, hepatomegaly, S3)

413
Q

Ventricular Septal Defect (VSD): Exam Findings

A

Holosystolic murmur @ LLSB, mid-diastolic rumble, LV heave

414
Q

Ventricular Septal Defect (VSD): Labs/Imaging

A

↑O2 in RV; LV dilation, pulmonary vascular disease

415
Q

Ventricular Septal Defect (VSD): Cat

A

L→R Shunts

416
Q

Ventricular Septal Defect (VSD): Pathophysiology AND Etiologies

A

Hole between ventricles → pulmonary HTN, Eisenmenger’s; severity depends on size, pressure difference

417
Q

Ventricular Septal Defect (VSD): Treatment

A

May self-resolve (50%), if not: digoxin, furosemide, ↑caloric intake, catheter, surgery ± endocarditis prophylaxis

418
Q

Patent Ductus Arteriosus (PDA): Epi

A

1/2500-5000

419
Q

Patent Ductus Arteriosus (PDA): Symptoms

A

R-sided HF from ↑PA pressure

420
Q

Patent Ductus Arteriosus (PDA): Exam

A

Continuous machine-like murmur @ left infraclavicular region (Gibson’s murmur)

421
Q

Patent Ductus Arteriosus (PDA): Cath/Imaging

A

Cardiomegaly, cath: O2 stepup in PA

422
Q

Patent Ductus Arteriosus (PDA): Cat

A

L→R Shunts

423
Q

Patent Ductus Arteriosus (PDA): Pathophysiology

A

Blood flows from aorta to pulmonary artery

424
Q

Patent Ductus Arteriosus (PDA): Etiologies

A

Prematurity, rubella, ↑altitude

425
Q

Patent Ductus Arteriosus (PDA): Treatment/Notes

A

Indomethacin (since prostaglandins keep the ductus open), surgical ligation, transcatheter closure; mnemonic: “a PDA is a machine”

426
Q

AV Canal Defect (AVC): Symptoms

A

Rapidly developing HF

427
Q

AV Canal Defect (AVC): Exam Findings

A

L→R shunt, pulmonary HTN, AV insufficiency

428
Q

AV Canal Defect (AVC): Cat

A

L→R Shunts

429
Q

AV Canal Defect (AVC): Pathophysiology

A

ASD, VSD + common AV valve

430
Q

AV Canal Defect (AVC): Seen with

A

Often seen with Down’s syndrome

431
Q

AV Canal Defect (AVC): Treatment

A

Surgery within 6 months (ASD+VSD closure, repair of AV valves)

432
Q

Atrial Septal Defect (ASD): Epi

A

1/1500

433
Q

Atrial Septal Defect (ASD): Exam/Imaging

A

↑O2 in right side of heart, split S1, side fixed split S2, RV heave, systolic murmur @ LUSB, diastolic murmur @ LLSB, cardiomegaly, RAD/RVH/RBBB, O2 stepup in RA

434
Q

Atrial Septal Defect (ASD): Cat

A

L→R Shunts

435
Q

Atrial Septal Defect (ASD): Pathophysiology AND Etiologies

A

Hole between atria; types: ostium secundum, ostium primum, sinus venosus, coronary sinus, PFO

436
Q

Atrial Septal Defect (ASD): Treatment

A

Close using surgery or catheter-delivered device

437
Q

Eisenmenger’s Syndrome: Symptoms AND Exam

A

CHF initially improves, then cyanosis, hemoptysis, clubbing, loud S2, JVP a wave pulsations, as R→L shunt develops, clear lungs

438
Q

Eisenmenger’s Syndrome: Cat

A

L→R Shunts

439
Q

Eisenmenger’s Syndrome: Pathophysiology AND Etiologies

A

RVH from increased pressure converts any L→R shunt to R→L shunt

440
Q

Eisenmenger’s Syndrome: Treatment/Notes

A

Tx: pulmonary vasodilators, anticoag, inotropes, do NOT close (can→RV failure)

441
Q

Persistent Pulmonary HTN of Newborn (PPHN): Symptoms AND Exam/EKG Findings

A

Cyanosis, low APGAR, neonatal asphyxia, maternal infection

442
Q

Persistent Pulmonary HTN of Newborn (PPHN): Cat

A

R→L Shunts

443
Q

Persistent Pulmonary HTN of Newborn (PPHN): Pathophysiology

A

Pulmonary vasculature fails to relax, R→L shunting at FO and DA

444
Q

Persistent Pulmonary HTN of Newborn (PPHN): Treatment

A

Tx: nitrous oxide, ECMO heart-lung bypass

445
Q

Pulmonic Stenosis (PS): Exam Findings

A

Cyanosis, LUSB systolic ejection murmur

446
Q

Pulmonic Stenosis (PS): Cat

A

R→L Shunts

447
Q

Pulmonic Stenosis (PS): Pathophysiology

A

PV stenotic → RVH

448
Q

Pulmonic Stenosis (PS): Treatment

A

Tx: balloon valvuloplasty vs. surgery

449
Q

Pulmonary Atresia : Symptoms AND Exam Findings

A

Cyanosis, LLSB holosystolic murmur

450
Q

Pulmonary Atresia : Imaging

A

Black lungs on CXR

451
Q

Pulmonary Atresia : Cat

A

R→L Shunts

452
Q

Pulmonary Atresia : Pathophysiology AND Etiologies

A

PV doesn’t open at all → R→L via PFO, blood to lungs via ductus arteriosus

453
Q

Pulmonary Atresia : Treatment

A

Keep ductus arteriosus open with prostaglandins until surgery

454
Q

Tricuspid Atresia: Exam/Imaging/Comorbidity

A

Cyanosis, systolic murmur, small RV, often have VSD, 25% have TGA

455
Q

Tricuspid Atresia: Cat

A

R→L Shunts

456
Q

Tricuspid Atresia: Pathophysiology AND Etiologies

A

Closed TV, R→L via FO

457
Q

Tricuspid Atresia: Treatment/Notes

A

Fontan procedure (bypass RV)

458
Q

Tetralogy of Fallot: Symptoms

A

Cyanotic spells (“Tet spells”), SOB

459
Q

Tetralogy of Fallot: Exam

A

Systolic ejection murmur @ LUSB

460
Q

Tetralogy of Fallot: Imaging/Comes with

A

DiGeorge (25%); CXR: “boot-shaped heart”

461
Q

Tetralogy of Fallot: Cat

A

R→L Shunts

462
Q

Tetralogy of Fallot: Pathophysiology

A

Malalignment of IV septum leads to: VSD, overriding aorta, RVH, pulmonic stenosis

463
Q

Tetralogy of Fallot: Treatment

A

Children will squat to ↑TPR + ↓R→L shunt; surgery to definitively correct

464
Q

Truncus Arteriosus : Exam/comes with

A

Dysplastic valves, cyanosis, regurg murmur, DiGeorge (25%), pulm HTN

465
Q

Truncus Arteriosus : Cat

A

Pulm/Sys Mixing

466
Q

Truncus Arteriosus : Pathophysiology

A

Aorta fused with pulmonary artery + VSD

467
Q

Truncus Arteriosus : Treatment

A

Surgical repair in infancy

468
Q

Total Anomalous Pulmonary Venous Return: Symptoms/Imaging

A

Cyanosis, respiratory distress, CXR white out w/small heart, pulmonary congestion, death

469
Q

Total Anomalous Pulmonary Venous Return: Cat

A

Pulm/Sys Mixing

470
Q

Total Anomalous Pulmonary Venous Return: Pathophysiology

A

Pulmonary veins return to the right heart → R→L shunt @ atria, mixing of blood

471
Q

Total Anomalous Pulmonary Venous Return: Treatment

A

Surgical repair

472
Q

Transposition of Great Arteries (TGA): Symptoms/Exam

Murmur?
When are symptoms better?

A

Cyanosis but no murmur, symptoms better if VSD/ASDs (get more mixing)

473
Q

Transposition of Great Arteries (TGA): Cat

A

Pulm/Sys Mixing

474
Q

Transposition of Great Arteries (TGA): Pathophysiology

A

Aortic, pulmonic arteries connect to wrong ventricles, 2 parallel loops form

475
Q

Transposition of Great Arteries (TGA): Treatment

A

Keep DA open with prostaglandins → balloon atrial septostomy, surgical switch

476
Q

Hypoplastic Left Heart Syndrome: Symptoms AND Exam

Murmur?

A

Mitral + aortic atresia, no murmur, cyanosis, poor pulses

477
Q

Hypoplastic Left Heart Syndrome: Cat

A

Pulm/Sys Mixing

478
Q

Hypoplastic Left Heart Syndrome: Pathophysiology

What does aorta look like?

A

“Shoestring aorta,” left side of heart too small/absent, L→R shunt at PFO

479
Q

Hypoplastic Left Heart Syndrome: Treatment

A

Prostaglandins, surgery

Cardiology (8 decks)

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