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Internal Medicine > Step Up - Cardio > Flashcards

Step Up - Cardio Flashcards

1
Q

What are the major risk factors that predispose a patient to developing stable angina (6)?

A

1) DM
2) Dyslipidemia - high LDL, low HDL
3) Smoking
4) HTN
5) Age (m > 45, w > 55)
6) FamHx of CAD or premature MI

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2
Q

What are prognostic indicators of CAD (stable angina) (2)?

A

1) LVEF (poor if less than 50%)

2) Vessels involved (poor if Left main, 2- or 3-vessel disease)

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3
Q

What are the clinical features of CAD (stable angina) (3)?

A

1) Chest pain or pressure, 1-15 mins in duration
2) Precipitated by exercise or emotional situation
3) Relieved with rest or NO

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4
Q

T or F. Ischemic cardiac pain can be described as a sharp/stabbing pain, that improves with breathing and is worsened with position. The chest wall is typically tender.

A

F - not described as sharp/stabbing, no change with breathing or position. It is not reproduceable with palpation.

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5
Q

What is typically found on the physical exam and resting EKG of a patient with stable angina?

A

Both are normal

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6
Q

What tools are used in the diagnosis of CAD (4)?

A

1) Resting EKG
2) Stress Test - stress EKG, stress Echo, stress myocardial perfusion imaging, pharmacological stress test.
3) Holter monitor - for silent ischemia
4) Cardiac cath with angiography - when stress test positive.

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7
Q

Discuss what constitutes a positive finding for stress EKG, stress Echo, stress myocardial perfusion imaging for the diagnosis of CAD

A

Stress EKG - ST depression
Stress Echo - wall motion abnormalities
Stress Myo perf - myocardial cell uptake of radioisotope (important to determine if this is reversible or irreversible ischemia)

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8
Q

What agents are used in pharmacologic stress tests in the diagnosis of CAD (3)? What are there mechanisms of action on the heart?

A

1) Adenosine and Dipyridamole - vasodilate coronary vessels resulting in steal from the maximally dilated vessels affected by CAD (thus reproducing ischemic symptoms)
2) Dobutamine - Inotrope and Chronotrope, also increases BP (afterload). Thus increases O2 demand of heart.

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9
Q

Outline the medical management of stable angina (5). When is this approach indicated?

A

1) ASA, B-blockers, Nitro, statins, and CCB. Use CCB if symptoms persist on while on nitro and b-blockers.
2) Use this approach for mild disease - normal EF, mild angina, single-vessel disease)

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10
Q

What are the surgical approaches for stable angina (2)? When are they indicated (2)?

A

1) Percutaneous coronary intervention
2) CABG
3) Use if moderate disease not controlled on meds - normal EF, moderate angina, 2-vessel disease
4) Use if severe angina - decreased EF, severe angina, 3-vessel or left main disease.

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11
Q

What distinguishes unstable angina from stable angina (1)? How is unstable angina differentiated from NSTEMI (2)?

A

1) USA has unprovoked onset - O2 supply is limited, whereas in SA O2 demand is increased.
2) NSTEMI will have elevated troponin and CK-MB

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12
Q

Outline the acute medical management of unstable angina (8).

A

1) ASA
2) Anti-platelet -> clopidogrel
3) B-blocker
4) LMWH -> enoxaparin
5) Nitrates
6) O2
7) Morphine (be careful not to mask symptoms)
8) Replace electrolytes if deficient - K and Mg

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13
Q

What are the indications for PCI revascularization in cases of unstable angina (5)?

A

1) persist signs of ischemia on EKG >48 hours after onset
2) hemodynamic instability
3) Ventricular arrhythmia
4) new MR
5) new septal defect

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14
Q

Outline the ongoing medical treatment of unstable angina after an acute event (4)?

A

1) ASA or anti-platelet
2) B-blocker
3) nitrate
4) statin
- Also modify risk factors (obesity, smoking, HTN, etc)

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15
Q

Describe the mechanism of action of Variant (Prinzmetal) Angina? What is seen on EKG? What is associated with variant angina? What is the appropriate medical therapy (2)?

A

1) MOA - transient coronary vasospasm
2) EKG - ST elevation during attack
3) Associated with ventricular dysrhythmia
4) Meds - CCB and nitrates (also modify risk factors - obesity, smoking, DM)

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16
Q

Provide the description of chest pain seen in an MI. Provide other symptoms of MI (6).

A

1) CP - crushing substernal pressure with radiation to neck/jaw/arm/back mainly on left side, may have epigastric pain
2) Dyspnea, diaphoresis, weakness, N/V, sense of doom, syncope

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17
Q

Provide 5 markers on EKG that indicate ischemia/infarct and explain their significance.

A

1) Peaked T waves - early finding, often missed
2) ST seg elevation - transmural injury
3) Q wave - late finding, indicate necrosis
4) T-wave inversion - sensitive but non-specific finding
5) ST seg depression - subendocardial injury

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18
Q

Describe the EKG findings (late and early) for an anterior MI, what leads are involved?

A

1) V1-V4
2) Early - ST seg elevation
3) Late - Q waves

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19
Q

Describe the EKG findings for a posterior MI, what leads are involved?

A

1) V1-V2

2) Large R wave, ST seg depression, prominent T waves

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20
Q

Describe the EKG findings for an Lateral MI, what leads are involved?

A

1) I and aVL

2) Late - Q waves

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21
Q

Describe the EKG findings for an anterior MI, what leads are involved?

A

1) II, III, aVF

2) Late - Q waves

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22
Q

What differentiates STEMI and NSTEMI in terms of involvement of the myocardium?

A

1) STEMI is transmural

2) NSTEMI is Subendocardial (differentiated fro USA based on cardiac enzymes)

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23
Q

What troponins are measured in an MI work-up? When are they first detectable? When do they peak? When do they return to baseline? What advantage do they have over CK-MB measurements?

A

1) I and T
2) 3-5 hrs
3) 24-48 hours
4) 5-14 days
5) Greater sensitivity and specificity than CK-MB

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24
Q

When is CK-MB first detectable in an MI work-up? When does it peak? When does it return to baseline? What advantage does it have over troponin measurements?

A

1) 4-8 hrs
2) 24 hrs
3) 2-3 days
4) Helpful in detecting recurrent infarct as it returns to baseline quicker

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25
Q

When should cardiac enzymes be drawn in a suspected MI?

A

At admission, then every 8 hours for at least 3 measurements

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26
Q

Outline the appropriate medical management for an MI (8). Describe the role of each drug or class of drugs.

A

1) ASA - anti-platelet, prevents thrombus growth
2) B-blockers - negative chronotrope/inotrope, lowers O2 need
3) ACEi - BP control
4) Statins - stabilize plaque, lowers cholesterol
5) O2 - reduces ischemia
6) Nitrates - dilates coronary arteries, venodilation (lowers preload)
7) Morphine - Analgesia, venodilation (lowers preload)
8) LMWH (Enoxaparin) - prevents thrombus progression

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27
Q

Of the medications used to treat MI, which have been shown to decrease mortality (3)?

A

1) ASA
2) B-blocker
3) ACEi

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28
Q

Discussed the 3 methods of revascularization that are used in the case of an acute MI. When are they used?

A

1) PCI - preferred method of treatment, perform within 90 mins
2) Thrombolytic therapy - tPA useful in STEMI when PCI not available or contra-indicated. Best if initiated within 6 hrs.
3) CABG - performed when mechanical complication of acute MI present: cardiogenic shock, life-threatening ventricular arrhythmia, or failure of PCI.

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29
Q

What are the contra-indications to tPA in the treatment of acute MI (5)?

A

1) Recent trauma
2) Prior stroke
3) Recent surgery
4) Dissecting aortic aneurysm
5) Active bleed

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30
Q

The formation of a ventricular thrombus can lead to what complication of an MI?

A

Embolism (PE, stroke)

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31
Q

Expansion of the infarct or ventricular septal defects caused by MI can lead to what complications of MI (2)?

A

1) CHF

2) Cardiogenic shock

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32
Q

Disruption of the electrical conduction system can lead to what complication of an MI?

A

1) Arrhythmia

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33
Q

Infarction of the papillary muscles can lead to what complication of an MI?

A

MR

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34
Q

Free wall rupture or pericardial inflammation can lead to what catastrophic outcome of an MI?

A

Cardiac Tamponade

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35
Q

Provide as many causes of chest pain as you can. Use a systems based approach using the categories: Cardiac, Resp, GI, MSK, Psychiatric, and Meds. Total of 24 causes.

A

1) Cardiac: USA, SA, variant angina, MI, pericarditis, aortic dissection
2) Resp: PE, pneumothorax, pleuritis, pneumonia, status asthmaticus
3) GI: GERD, diffuse esophageal spasm, PUD, esophageal rupture
4) MSK: costochondritis, muscle strain, rib fracture, herpes zoster, thoracic outlet syndrome.
5) Psychiatric: panic attacks, anxiety, somatization
6) Meds: Cocaine

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36
Q

What is the physiologic deficit that exists in systolic dysfunction CHF? What are the causes (5)?

A

1) Impaired contractility (low EF)
2) Ischemic heart disease (MI), HTN creating cardiomyopathy, valvular disease, myocarditis, other (alcohol abuse, radiation, hemochromatosis, thyroid disease)

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37
Q

What is the physiologic deficit that exists in diastolic dysfunction CHF? What are the causes (3)?

A

1) Impaired ventricular filling
2) HTN - myocardial hypertrophy
3) Valvular disease - AS, MS, AR
4) Restrictive cardiomyopathy - amyloidosis, sarcodosis, hemochromatosis

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38
Q

Describe briefly each of the 4 NYHA classifications for CHF.

A

1) Class I: symptoms with vigorous activity only
2) Class II: Symptoms with moderate exertion, slight limitation of activity
3) Class III: Symptoms with ADLs (walking). Marked limitations
4) Class IV: symptoms at rest. Incapacitated.

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39
Q

What are the symptoms of lift-sided heart failure (6)?

A

1) Dyspnea
2) Orthopnea
3) PND
4) Nocturnal cough
5) Confusion and memory loss - inadequate brain perf.
6) Diaphoresis and cool extremities at rest (class IV)

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40
Q

What are the clinical signs of left-side heart failure (6)?

A

1) Displace PMI (to the left)
2) S3 - stiff ventricle, hear at apex with bell, follows S2
3) S4 - atrial systole into stiff ventricle, hear at LSB with bell, precedes S1.
4) Crackels/Rales - pulmonary edema in lung bases
5) Dull to percussion in lower lung fields (pleural effusion)
6) Increase pulmonic component of S2 (pulm HTN)

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41
Q

What are the SSx of right sided heart failure (6)?

A

1) Peripheral pitting edema
2) Nocturia (due to elevaton of legs at night)
3) Jugular venous distention
4) Hepatomegaly/Hepatojugular reflex
5) Ascites
6) RV heave

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42
Q

What tests should be ordered in the patient presenting with suspect CHF (5)?

A

1) CXR - pulm edema, cardiomegaly
2) EKG
3) Cardiac enzymes - r/o MI
4) CBC - anemia
5) Echo - estimate EF

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43
Q

What findings may be found on CXR when done for CHF (4)?

A

1) Cardiomegaly
2) Kerley B lines - pulmonary congestion
3) Prominent interstitial markings
4) Pleural effusion

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44
Q

What important info does an echo provide when working-up CHF (3)?

A

1) Diastolic vs. Systolic dysfunction
2) Estimate EF
3) Shows chamber dilation and/or hypertrophy

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45
Q

Describe the treatment regime for mild CHF (NYHA I-II) (4)?

A

1) Mild salt restriction (less than 4g), physical activity
2) RF modification - wt. loss, smoking cessation, alcohol reduction
3) Loop diuretic - if vol overload or pulmonary congestion
4) ACEi

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46
Q

Describe the treatment regime for Moderate CHF (NYHA II-III) (5)?

A

1) Mild salt restriction (less than 4g), physical activity
2) RF modification - wt. loss, smoking cessation, alcohol reduction
3) Loop diuretic
4) ACEi
5) Add B-blocker if refractory to above treatment

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47
Q

Describe the treatment regime for Sever CHF (NYHA III-IV) (5)?

A

Mild salt restriction (less than 4g), physical activity

2) RF modification - wt. loss, smoking cessation, alcohol reduction
3) Loop diuretic
4) ACEi
5) Add Digoxin and spironolactone

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48
Q

What can be used as an alternative to ACEi in population for which ACEi are ineffective (blacks) (2)?

A

1) Hydralazine and Isosorbide Dinitrate.

2) ARBs used in patient who develop cough

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49
Q

What is the appropriate therapy for CHF due to diastolic dysfunction (2)?

A

1) B-blockers
2) Diuretics
- Digoxin, spironolactone, ACEi and ARBs not used
- No drugs improve mortality

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50
Q

Which drugs used in the treatment of CHF (Systolic) have been shown to reduce mortality (4)?

A

1) B-blocker
2) ACEi and ARBs
3) Hydralazine and Nitrates
4) Spironolactone (aldosterone antagonists)
- loop diuretics and digoxin do not decrease mortality

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51
Q

What are the findings on EKG for premature atrial complexes? What can they cause (2)? What is the treatment for those who are symptomatic?

A

1) P-waves of different morphology (not originating in SA node)
2) Can cause palpitations and PSVT
3) B-blockers

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52
Q

What are some causes of PVCs (6)? What is the concern of frequent PVCs in a patient with underlying heart disease? How are symptomatic (eg. palpitations, dizziness) PVCs treated?

A

1) Causes: hypoxia, electrolyte abnormalities, stimulants, caffeine, meds, structural heart disease
2) Sudden death due to arrhythmia (VFib)
3) B-block

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53
Q

What are the symptoms of Afib (6)? What is seen on the EKG (2)? What is the primary concern?

A

1) Sx: fatigue, exertional dyspnea, palpitations, dizziness, angina, syncope
2) No P-wave, irregularly irregular rhythm
3) Formation of intramural thrombus which can embolize (CVA).

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54
Q

How is acute Afib treated in the hemodynamically unstable patient?

A

Cardioversion

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55
Q

How is acute Afib treated in the hemodynamically stable patient (3)?

A

1) Rate Control - B-blocker or CCB
2) Cardioversion - use in unstable patient, those with worsening Afib, or those with first episode of Afib.
3) Anticoagulation - Warfarin, goal INR 2-3

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56
Q

How is chronic Afib treated (2)

A

1) Rate control - B-blocker or CCB
2) Anticoagulate - Warfarin
- ‘lone’ Afib (no heart disease, age less than 60) does not require anticoagulation

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57
Q

What are the causes of Atrial flutter (5)? What is the typical atrial rate? What is seen on EKG? What is the treatment (1)?

A

1) Causes: HF, rheumatic heart disease, CAD, COPD, ASD
2) 300 bpm
3) Saw-tooth pattern with 2:1 or 3:1 P-waves to QRS
4) Similar to AFib

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58
Q

Multifocal Atrial Tachycardia is associated with what other disease? What is seen on EKG that is diagnostic?

A

1) pulmonary disease - COPD

2) P-waves with at least 3 different morphologies

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59
Q

Describe the difference between orthodromic and antidromic with respect to AV nodal re-entrant tachycardia. In which are p-waves visualized on EKG?

A

1) Orthodromic - re-entry pathway passes first through AV, then return to atria via the accessory pathway.
2) Antidromic - re-entry pathway psses to ventricles via the accessory pathway, then retrograde via the AV.
- p-waves in orthodromic tachy

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60
Q

Provide 4 causes of Paroxysmal Supraventrical Tachycardia (PSVT).

A

1) Ischemic heart disease
2) Re-entry / accessory pathway
3) Atrial flutter
4) Caffeine / Alcohol

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61
Q

Provide the non-pharmacologic mechanisms (4), pharmacologic therapies (4), and prevention therapies for PSVTs (2)

A

1) Valsalva, carotid sinus massage, breath holding, cold water immersion
2) IV adenosine, IV verapamil, IV esmolol, digoxin
3) Prevention: verapamil, b-blocker

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62
Q

What differentiates sustained versus nonsustained VT? Provide a unique physical finding in the neck that indicates VT. What is seen on EKG in VT?

A

1) sustained if >30sec
2) Cannon A waves
3) Wide complex QRS (>0.12)

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63
Q

How is sustained VT treated (hemodynamically stable versus unstable)?

A

1) stable - IV amiodarone, IV procainamide, IV sotalol
2) unstable - DC cardioversion with IV amiodarone
- ICD placement

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64
Q

How is nonsustained VT treated (heart disease versus no heart disease)?

A

1) disease - ICD

2) no disease - nothing

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65
Q

What precedes most instances of VFib? How does the treatment change if the instance of VFib is associated with an acute MI or not?

A

1) VFib preceded by VT typically
2) If no associated MI - high recurrence risk, treat with antiarrhthmic (amiodarone) or implantable defibrillator
3) If MI up to 48 hours before - low recurrence risk, no chronic therapy needed.

66
Q

How is VFib managed acutely (4)?

A

1) Emergency! Defibrillate.
2) CPR
3) IV epi and shock
4) IV amiodarone and shock if refractory

67
Q

What findings on EKG are seen for first-degree AV block (2)? Where is the deficit in the conduction system? What is the appropriate therapy?

A

1) p-wave >0.2sec, p-wave before every QRS
2) AV node
3) No therapy needed

68
Q

What findings on EKG are seen for second-degree AV block (Mobitz type 1, Wenckebach)? Where is the deficit in the conduction system? What is the appropriate therapy?

A

1) progressive prolongation of PR interval until p-wave fails to conduct.
2) Deficit in AV node
3) Benign, no treatment needed

69
Q

What findings on EKG are seen for second-degree AV block (Mobitz type 2)? Where is the deficit in the conduction system? What is the appropriate therapy?

A

1) No prolongation of PR interval, sudden drop of QRS
2) Deficit in His-Purkinje system
3) Can lead to complete block, requires pacemaker implantation

70
Q

What findings on EKG are seen for third-degree AV (complete) block? Where is the deficit in the conduction system? What is the appropriate therapy?

A

1) No correspondence between p-waves and QRS complex
2) Complete AV dissociation
3) Heart is paced by ventricular escape rhythm, requires pacemaker implantation.

71
Q

What is the most common cause of dilated cardiomyopathy? What are some clinical features of the disease (5)?

A

1) 50% of cases idiopathic
2) Clinically: symptoms of CHF, additional heart sounds (S3, S4, tricuspid and mitral insufficiency), cardiomegaly, coexisting arrhythmia, sudden death.

72
Q

How is dilated cardiomyopathy diagnosed? How is it treated?

A

1) Dx: EKG, CXR, echo consistent with CHF

2) Tx: similar to CHF - digoxin, diuretics, vasodilators, anticoagulation, transplant.

73
Q

Describe the pathophysiology of hypertrophic cardiomyopathy (3).

A

1) Diastolic dysfunction due to stiff and hypertrophied venticle
2) Worsens with increased HR or contractility (exercise), or decreased LV volume (Valsalva)
3) May have outflow obstruction

74
Q

Describe the symptoms (7) and signs (4)

A

1) Symp: dyspnea, chest pain, syncope, palpitations, arrhythmias (AFib), cardiac failure, sudden death - all worsened with exertion.
2) Sign: sustained PMI, loud S4, Systolic ejection murmur, carotid pulse with two upstrokes.

75
Q

How is the quality of the systolic ejection murmur affected by the following: squatting/lying down, valsalva/standing, and sustained hand grip? What is the mechanism associate with the change?

A

1) Squatting/Lying - decreases murmur due to decreased outflow obstruction
2) Valsalva/Standing - increases murmur due to decreased LV size
3) Sustained handgrip - decreases murmur due to decreased pressure gradient across aortic valve (raises SVR).

76
Q

What is the appropriate treatment for those diagnosed with hypertrophic cardiomyopathy (5)?

A

1) No treatment if assymptomatic
2) Avoid competitive sports or vigorous activity
3) B-blockers or CCB if symptomatic (increase time in diastole)
4) Diuretics if fluid overload
5) Treat AFib if present

77
Q

What is the pathophysiology behind restrictive cardiomyopathy? What are the 7 causes?

A

1) Infiltration of myocardium results in impaired diastolic ventricular filling due to decreased compliance
2) Amyloidosis
3) Sarcoidosis
4) Hemochromatosis
5) Scleroderma
6) Carcinoid Syndrome
7) Chemotherapy/radiation
8) Idiopathic

78
Q

What are the clinical features of restrictive cardiomyopathy (2)? How is it diagnosed (3)?

A

1) Sx: dyspnea and exercise intolerance
2) Dx: Echo - thick myocardium, dilated atria, normal ventricle size
3) Dx: EKG - low voltage, conduction abnormalities, arrhythmias, AFib
4) Endomyocardial biopsy

79
Q

How is restrictive cardiomyopathy treated (2)?

A

1) Treat underlying cause

2) Digoxin if systolic dysfunction is present

80
Q

What are the clinical features of acute pericarditis (3)?

A

1) Chest Pain - pleuritic, positional (relieved with sitting up and leaning forward), retrosternal with radiation to trapezius and neck
2) Fever and leukocytosis
3) Pericardial friction rub

81
Q

What is seen on EKG during the course of acute pericarditis (3)? What is seen on Echo?

A

1) EKG:
a) ST elevation, PR depression
b) ST elevation returns to normal within 1 week
c) T wave inversion, then returns to normal
2) Echo - typically normal, may find pericardial effusion

82
Q

How is actue pericarditis treated (4)?

A

1) Usually self-limited 2-6 weeks
2) NSAIDs or colchicine
3) Glucocorticoids if refractory to NSAIDs
4) Treat as inpatient if symptoms are worrisome - fever, leukocytosis, pericardial effusion

83
Q

Describe the pathophysiology of constrictive pericarditis. What are the common causes (2)?

A

1) Fibrous scarring of pericardium leads to rigidity that restricts late diastolic ventricular filling
2) Idiopathic or past viral infection

84
Q

Describe the clinical SSx of constrictive pericarditis (5).

A

1) Patient may have signs of fluid overload - edema, ascites, pleural effusion
2) Patient may have signs of diminished cardiac output - dyspnea, fatigue, low exercise tolerance, cachexia
3) JVD
4) Kussmaul sign - JVP fails to decrease with inspiration
5) Pericardial knock

85
Q

What is seen on different investigative modalities used to Dx constrictive pericarditis (4) - Echo, EKG, CT/MRI, Cath?

A

1) EKG - low QRS voltage, T-wave flattening, AFib
2) Echo - pericardial thickening, halt in ventricular filling, atrial enlargement
3) CT/MRI - pericardial thickening and calcification
4) Cath - elevated and equalized diastolic pressures, “square root sign” on ventricular pressures.

86
Q

How is constrictive pericarditis treated (3)?

A

1) Treat underlying disease if identified
2) Diuretics for fluid overload symptoms
3) Surgical pericardiectomy

87
Q

What are the clinical features of pericardial effusion (4)?

A
  • All non-specific findings:
    1) Muffled heart sounds
    2) Soft PMI
    3) Dullness at left lung base (due to compression)
    4) Pericardial friction rub (maybe)
88
Q

What is seen on Echo, CXR, and EKG when a pericardial effusion is present? What can be done to help determine the etiology of the effusion?

A

1) Echo - Very sensitive (detects 20ml)
2) CXR - Enlarged cardiac silhouette (if effusion > 250ml). “Water bottle sign”
3) EKG - low QRS voltage, T-wave flattening. Not useful in Dx.
4) Tap fluid and send for analysis to determine etiology

89
Q

What is the treatment for pericardial effusion (2)?

A

1) If unstable - pericardiocentesis

2) If stable and effusion small - conservative mgmt, repeat echo in 1-2 weeks.

90
Q

Describe the pathophysiology of cardiac tamponade (4).

A

1) Rate of effusion collection is very important
2) Ventricles, atriums, and pericardium equalize in pressure during diastoly
3) Results in impaired ventricular filling throughout diastole
4) Decreased diastolic filling results in low SV and CO.

91
Q

How does the diastolic filling impairment differ between constrictive pericarditis and cardiac tamponade?

A

1) Constrictive pericarditis - diastolic filling impairment in late diastole only
2) Cardiac tamponade - diatolic filling impairment throughout diastole

92
Q

What are the causes of cardiac tamponade (4)?

A

1) Penetrating or blunt trauma - gun shot, VMA
2) Iatrogenic - central line placement, pacemaker insertion
3) Pericarditis - idiopathic, neoplastic, uremic
4) Post-MI free wall rupture

93
Q

What are the clinical features of cardial tamponade (5)?

A

1) High JVP
2) Narrow pulse pressure
3) Pulsus paradoxus (>10mmHG drop on inspiration)
4) Muffled heart sounds
5) Tachypnea, tachycardia, hypotension

94
Q

What is Beck’s triad?

A
  • related to cardiac tamponade
    1) Hypotension
    2) Muffled heart sounds
    3) JVD
95
Q

What is seen on Echo, CXR, EKG, and cath for cardiac tamponade?

A

1) Echo - very sensitive
2) CXR - enlarged cardiac silhouette when >250ml, clear lungs
3) EKG - electrical alternans
4) Cath - shows equalization of pressures in chambers

96
Q

How is cardiac tamponade treated (hint: dependent on presentation) (3)?

A

1) If nonhemorrhagic, stable - monitor, dialysis if renal failure present
2) If nonhemorrhagic, unstable - pericardiocentesis, fluid challenge to improve symptoms
3) If hemorrhagic - emergent surgery

97
Q

What is the primary cause of mitral stenosis? What is seen on CXR (1) and Echo (3)?

A

1) Rheumatic fever cause of nearly all cases
2) CXR - LA dilation
3) Echo -
a) LA dilation
b) Narrow orifice, calcified and thickened valve
c) Signs of RVF in advanced disease

98
Q

What are the clinical features of mitral stenosis (4)?

A

1) Pulm HTN - exertional dyspnea, orthopnea, PND, hemoptysis (rupture of anastomoses of small bronchial veins)
2) RVF - ascites, edema, JVD, RV heave
3) AFib - Thromboemolism
4) Murmur

99
Q

Describe the murmur of mitral stenosis (5).

A

1) Opening snap
2) low-pitched diastolic rumble
3) heard with bell in left lateral decubitus
4) Loud S1
5) Loud P2 if pulm HTN

100
Q

Describe the management for mitral stenosis (3).

A

1) Treat only if symptomatic
2) Medical - diuretics, B-blockers, treat AFib
3) Surgical - balloon valvuloplasty, mitral valve replacement

101
Q

Describe the pathophysiology of Aortic Stenosis (3). What are the causes (3)

A

1) Pathophys: outflow obstruction -> LVH -> LV dilation -> MR (also, LVF)
2) Causes: calcification of congenital bicuspid aorta, calcification of normal aorta in elderly, rheumatic fever

102
Q

What are the clinical features of aortic stenosis (7)?

A

1) Angina
2) Syncope (exertional)
3) LVF - dyspnea, orthopnea, PND
4) Murmur
5) Parvus et Tardus (low and late carotid upstroke)
6) Sustained PMI
7) Precordial thrill

103
Q

Describe the murmur of aortic stenosis (4).

A

1) Harsh crescendo-decrescendo, systolic
2) Heard in right intercostal space
3) Radiates to carotids
4) Soft S2, S4 present

104
Q

What is seen on CXR, EKG, Echo, and Cath in the work-up for aortic stenosis?

A

1) CXR - calcified aortic valve, enlarged LV/LA
2) EKG - LVH, LA dilation
3) Echo - LVH, thickened aortic valve, dilated ortic root
4) Cath - concerning if area less than 0.8cm2.

105
Q

What is the treatment for aortic stenosis?

A

Surgical replacement when symptomatic

106
Q

Describe the pathophysiology of aortic regurg (insufficiency). What are the acute causes (4)?

A

1) backflow of blood through incompetent valve -> LVH -> LV dilation -> LVF + pulmonary HTN.
2) Infective endocarditis, trauma, aortic dissection, post-MI, iatrogenic

107
Q

What is seen clinically in aortic regurgitation (6)?

A

1) LVF - dyspnea on exertion, PND, orthopnea
2) Palpitations
3) Angina
4) Wide pulse pressure / water-hammer pulse
5) Murmur
6) Displaced PMI

108
Q

Describe the murmur of aortic regurgitation (3)

A

1) Diastolic decrescendo murmur, heard at LSB
2) S3
3) Murmur increases with hand grip (increased SVR).

109
Q

Outline the treatment for aortic regurg (3).

A

1) If stable and assymptomatic - medical therapy (salt restrict, vasodilators, digoxin, ACEi, activity restriction)
2) If symptomatic or low EF - surgical valve replacement
3) If acute AR - valve replacement, medical emergency

110
Q

Describe the pathophysiology in acute and chronic mitral regurg.

A

1) Acute -> abrupt inc in LA pressure -> pulm HTN, loss in CO (may result in shock)
2) Chronic -> gradual inc in LA pressure -> dilated LA and LV -> LVF due to dilation, ,ay have pulm HTN

111
Q

What are the causes of acute (3) and chronic (4) mitral regurg?

A

1) Acute - Endocarditis (staph), Papillary muscle rupture (infarct), Chordae tendinae rupture
2) Chronic - Mitral valve prolapse, rheumatic fevef, marfans, cardiomyopathy

112
Q

What are the symptoms of mitral regurgitation (5)?

A

1) LVF - dyspnea on exertion, PND, orthopnea
2) Palpitations
3) Pulmonary edema
4) Murmur
5) AFib

113
Q

Describe the murmur of mitral regurgitation (2)

A

1) Holosystolic, loudest at Apex

2) Radiates to back or clavicular area

114
Q

What is the appropriate treatment for mitral regurgitation (2)?

A

1) Medical - vasodilators, treat AFib

2) Surgical - replace valve

115
Q

What are the clinical features of tricuspid regurgitation (6)?

A

1) Typically assymptomatic unless RHF or pulm HTN present
2) SSx of RVF - ascites, edema, hepatomegaly, JVD
3) Pulsatile liver
4) Murmur
5) RV pulsation at LLSB
6) AFib

116
Q

Describe the murmur of tricuspid regurgitation (3).

A

1) Blowing holosystolic murmur at LLSB
2) Intensifies with inspiration, lessened with valsalva
3) Inspiratory S3 at LLSB

117
Q

What are the causes of tricuspid regurgitation (4)?

A

1) RV dilation - inferior MI, LHF, RHF, pulm HTN
2) Tricuspid endocarditis - IV drugs
3) Rheumatic heart disease
4) Epstein Anomaly - downward displacement of valve into RV

118
Q

How is tricsupid regurg treated (3)?

A

1) Treat underlying cause
2) Diuretics if fluid overloaded
3) Surgery - valve repair, valvuloplasty, valve replacement

119
Q

What are the causes of mitral valve prolapse (3)? What is it associated with?

A

1) Connective tissue disease - Marfans, osteogenesis imperfecta, ehlers-danlos
2) MR

120
Q

What are the symptoms of mitral valve prolapse (3)?

A

1) Most are asymptomatic
2) May have chest pain and palpitations
3) Rarely TIA due to emboli

121
Q

Describe the murmur of mitral valve prolapse (2)? What accentuates and diminishes the sound of the murmur (2)?

A

1) Midsystolic or late systolic click
2) Mid-to-late systolic murmur
3) Standing and Valsalva accentuate
4) Squatting reduces

122
Q

What is the treatment for mitral valve prolapse (3)?

A

1) Nothing. Most are asymptomatic
2) B-block if chest pain, but rare
3) Very rarely - surgery

123
Q

What is the cause of rheumatic fever? What areas of the heart does it affect (3)?

A

1) Complication of GAS pharyngitis

2) Mitral > Aortic > Tricuspid

124
Q

How is rheumatic fever diagnosed? Provide the Jones criteria (5 + 6).

A

1) Jones criteria - 2 major, or 1 major + 2 minor
2) Major: migratory polyarthritis, erythema marginatum, cardiac involvement (pericarditis, CHF), chorea, subcutaneous nodules
3) Minor: Fever, high ESR, polyarthralgias, prior Hx of RF prolonged PR, evidence of preceding GAS infection.

125
Q

How is acute rheumatic fever treated (3)?

A

1) GAS - Penicillin or erythromycin
2) acute RF - NSAIDs, monitor CRP
3) treat valvular pathology

126
Q

What organisms are responsible for infective endocarditis (acute vs. subactue, native vs prosthetic valves, IV drug users) ?

A

1) Acute - S. aureus, fatal within 6 weeks
2) Subactue - S. viridans, enterococcus
3) Native - S. viridans > Staph > Enterococci
4) Prosthetic - Staph in early-onset, Strep in late-onset
5) IV drug users - S. aureus

127
Q

Describe the Duke criteria for diagnosing infective endocarditis (2 major, 6 minor).

A

1) Dx - requires 2 major, 1 major + 3 minor, or 5 minor criteria.
2) Major: Sustained bacteremia, endocardial involvement (echo, or new murmur)
3) Minor: Predisposing condition, fever, vascular phenomena (janeway lesion), immune phenomena (GN, olser nodes, roth spots, RF+), positive blood culture, positive echo

128
Q

How is infective endocarditis treated (2)?

A

1) ABx based on culture for 4-6wks

2) If culture negative, but suspicion high - treat empirically with penicillin or vanco AND an aminoglycoside

129
Q

What is required to consider Abx prophylaxis for infective endocarditis in a patient (2)?

A

1) Qualifying cardiac indications - prosthetic valve, Hx of infective endocarditis, congenital heart disease, cardiac transplant with valvulopathy
2) Qualifying procedure - Dental, procedures involving respiratory mucosa, procedures involving infected skin or MSK tissue.

130
Q

Describe the clinical features of an atrial septal defect (5).

A

1) Typically asymptomatic until 40
2) Symptoms: exercise intolerance, dyspnea, fatigue
3) Mild systolic ejection murmur (incr. pulm flow)
4) Fixed S2
5) RVF and Afib in advanced disease

131
Q

What is seen on CXR and EKG in a patient with an atrial septal defect? How is it typically diagnosed?

A

1) CXR - increase pulm vasc
2) EKG - RBBB and right axis deviation, AFib/flutter
3) Dx - Echo - TEE > TTE

132
Q

What are the complications (4) and treatment for atrial septal defects?

A

1) Pulm HTN
2) Eisenmenger disease (reversal of shunt leading to cyanosis)
3) RHF
4) AFib/flutter with associated stroke (emboli)
5) Tx - repair if shunt large or pt symptomatic

133
Q

Discuss the clinical features of ventricular septal defects (4). What is seen on EKG and CXR?

A

1) large shunt w/o high PVR - CHF, growth failure, recurrent LRTI
2) Large shunt w/ high PVR - Eisenmenger reaction, SOB, dyspnea, CP, syncope, cyanosis
3) Harsh holosystolic murmur
4) Loud P2 as PVR increases
5) EKG - RVH, LVH
6) CXR - enlarged cardiac silhouette and pulmonary artery

134
Q

What is the treatment for ventricular septal defects (2)?

A

1) If asymptomatic - nothing

2) If shunt large or pt symptomatic, fix surgically

135
Q

What are the clinical features of coarctation of the aorta (6)?

A

1) Upper limb HTN, lower limb hypotension
2) Well developed upper body, poorly developed lower body
3) Midsystolic murmur
4) Delayed femoral pulse
5) Leg claudication, fatigue
6) Association with Turners

136
Q

What is seen on CXR and EKG in coarctation of the aorta? How is it treated (2)?

A

1) CXR - notching of ribs
2) EKG - LVH
3) Tx - surgical repair, valvuloplasty

137
Q

What are the clinical features of patent ductus arteiosus (6)?

A

1) May be asymptomatic
2) Pulm HTN - leading to loud S2 and RHF
3) LVH
4) Continuous machinery murmur
5) Wide pulse pressure
6) Lower-extremity clubbing - cyanotic toes

138
Q

What is seen on CXR in patent ductus arteriosus (3)? How is it treated (2)?

A

1) CXR - increased pulm vasc, increased pulm artery size, increased cardiac silhouette
2) Tx if no pulm HTN - surgical ligation
3) Tx if pulm HTN - surgery contraindicated, Indomethacin (NSAID) for closure

139
Q

What are the abnormalities seen in tetralogy of Fallot (4)? What are the clinical features (3)?

A

1) VSD, RVH, pulm artery stenosis, over-riding aorta

2) Cyanosis, Tet Spells, Crescendo-decrescendo systolic murmur

140
Q

What is seen on CXR in tetralogy of Fallot? How is ToF treated?

A

1) CXR - boot shaped heart

2) Surgery within 1st year of life

141
Q

Define hypertensive emergency. What systems should be investigated in the work-up (5)?

A

1) BP >220 and/or >120 diastolic with evidence of end-organ damage
2) Systems: (Eyes - papilledema, CNS - altered mental status, kidneys - failure, Heart, lungs - edema)

142
Q

What are the clinical features of a hypertensive emergency (3)? How is it treated (3)?

A

1) SSx: headache, vision change, altered mental status
2) Tx - reduce BP by 25% in 1-2 hours
3) IV agents - B-blockers, hydralazine, NO
4) Get brain imaging to look for cerebral encephalopathy

143
Q

What are the clinical features of Aortic dissection (5)?

A

1) Severe stabbing pain in anterior chest or interscapular
2) Diaphoresis
3) BP difference between upper and lower limbs
4) Aortic regurg
5) Neurologic manifestations

144
Q

Describe a Type A aortic dissection. How is it treated (2)?

A

1) Involves ascending aorta
2) IV meds - B-blockers and sodium nitroprusside
3) Surgical correction

145
Q

Describe a Type B aortic dissection. How is it treated (2)?

A

1) Involves descending aorta
2) IV meds - B-blockers and sodium nitroprusside
3) Mgmt is medical including drugs llisted above and morphine for pain control

146
Q

How is aortic dissection diagnosed (4)?

A

1) CXR - widened mediastinum (>8mm)
2) TTE - bedside test
3) CT - highly sensitive
4) Aortic angio - invasive, but most accurate

147
Q

What are the clinical symptoms of an abominal aortic aneurysm ()? How is it diagnosed

A

1) Usually asymptomatic
2) Sense of fullness
3) May have pain - hypogastric/lower back
4) Pulsatile abdo mass
5) Gray turner and Cullen sign (impending rupture)
6) rupture
7) Dx - ultrasound

148
Q

What is the appropriate treatment for an AAA in a stable (2) and unstable patient?

A

1) Stable - surgery if symptomatic or >5cm

2) Unstable - surgical repair (emergency)

149
Q

How is a ruptured AAA diagnosed (3)?

A

1) Clinically - abdo pain, hypotension, palpable pulsatile abdo mass

150
Q

What are the common sites of occlusion in peripheral vascular disease (3)? What are the largest risk factors (5)?

A

1) Sites - superficial femoral, popliteal, aortoiliac

2) RF - smoking, CAD, hyperlipidemia, HTN, DM

151
Q

How is peripheral vascular disease diagnosed (2)?

A

1) Ankle-to-brachial index (ABI). ABI under 0.7 - claudication, ABI under 0.4 - rest pain
2) Arteriography

152
Q

How is peripheral vascular disease treated? Contrast intermittent claudication treatment (5) with rest pain treatment (2).

A

1) Intermittent claudical - treat conservatively
a) stop smoking
b) exercise program
c) foot care
d) atherosclerotic RF reduction (hyperlipidemia, HTN, wt, DM)
e) ASA
2) Rest pain - surgical treatment
a) Angioplasty w/ or w/o stent
b) Bypass graft

153
Q

Describe the 6 Ps of the presentation of acute arterial occlusion.

A

1) Pain (acute onset)
2) Pallor
3) Polar
4) Paralysis
5) Paresthesia
6) Pulselessness

154
Q

What is the treatment for acute arterial occlusion (3)?

A

1) Repurfuse within 6 hours
2) Surgical embolectomy with Fogarty balloon cath
3) IV heparin (anticoagulate)
- common femoral is most common site

155
Q

Describe the pathophysiology of chronic venous insufficiency (2)?.

A

1) Caused by history of DVT (may not be documented)

2) Destruction of valves in venous system leading to ambulatory HTN resulting in edema and pigmentation of the skin

156
Q

Describe the skin changes of venous insufficiency (4).

A

1) Thin and atrophic
2) Shiny
3) Cyanotic
4) Brawny pigmented induration

157
Q

Provide the direction of change in cardiac output, SVR, and JVP for cardiogenic shock.

A

1) CO - down
2) SVR - up
3) JVP - up

158
Q

Provide the direction of change in cardiac output, SVR, and JVP for hypovolemic shock.

A

1) CO - down
2) SVR - up
3) JVP - down

159
Q

Provide the direction of change in cardiac output, SVR, and JVP for septic shock.

A

1) CO - up
2) SVR - down
3) JVP - down

160
Q

Provide the direction of change in cardiac output, SVR, and JVP for neurogenic shock.

A

1) CO - down
2) SVR - down
3) JVP - down

161
Q

Provide the criteria for SIRS (4).

A

1) T >38, or less than 36
2) RR >20
3) HR >90
4) WBC >12, or less than 4.
- SIRS requires 2 of the above

162
Q

Describe the relationship between SIRS, sepsis, septic shock, and multiple organ dysfunction syndrome

A

1) SIRS - 2 of 4 criteria (elevated T, RR, HR, WBC)
2) Sepsis - SIRS + source of infection
3) Septic Shock - hypotension induced by sepsis
4) MODS - organ dysfunction resulting from septic shock

Internal Medicine (9 decks)

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