Cardiology Flashcards
1
Q
Hypovolemic shock is caused by what?
A
Hemorrhage, loss of plasma, or loss of fluid and electrolytes, resulting in decreased intravascular volume. This may be caused by obvious loss or by “third-space” sequestration
2
Q
Causes of cardiogenic shock
A
MI, dysrhythmias, heart failure, defects in the valves or septum, hypertension, myocarditis, cardiac contusion, rupture of the ventricular septum, or cardiomyopathies
3
Q
Causes of obstructive shock
A
Tension pneumothorax, pericardial tamponade, obstructive valvular disease, and pulmonary problems, including massive pulmonary embolism
4
Q
Distributive shock includes what?
A
Septic shock, systemic inflammatory response syndrome (SIRS), anaphylaxis, and neurogenic shock
5
Q
Septic shock has a high mortality rate (30-87%). It is most often associated with what?
A
Gram-negative sepsis
6
Q
Causes of neurogenic shock
A
Spinal cord injury or adverse effects of spinal or epidural anesthesia
7
Q
Definition of postural hypotension
A
Greater than 20 mm Hg drop in systolic BP or a drop greater than 10 mm Hg in diastolic BP between supine and sitting and/or standing measurements
8
Q
In postural hypotension, if there is a rise in pulse of more than 15 bpm, what is the probable cause?
A
Depleted circulating blood volume
9
Q
In postural hypotension, if there is no change in the pulse rate, what causes should be considered?
A
Medications, central autonomic nervous system disease (e.g., Parkinson disease or Shy-Drager syndrome), or peripheral neuropathies (e.g., diabetic autonomic neuropathy)
10
Q
New York Heart Association Functional Classification of Heart Disease: Class I
A
No limitation of physical activity; ordinary physical activity does not cause undue fatigue, dyspnea, or anginal pain
11
Q
New York Heart Association Functional Classification of Heart Disease: Class II
A
Slight limitation of physical activity; ordinary physical activity results in symptoms
12
Q
New York Heart Association Functional Classification of Heart Disease: Class III
A
Marked limitation of physical activity; comfortable at rest, but less than ordinary activity causes symptoms
13
Q
New York Heart Association Functional Classification of Heart Disease: Class IV
A
Unable to engage in any physical activity without discomfort; symptoms may be present even at rest
14
Q
End-organ damage in untreated HTN includes what
A
Heart failure, renal failure, stroke, dementia, aortic dissection, artherosclerosis, and retinal hemorrhage
15
Q
When is a two-drug regimen started in hypertension?
A
Stage 2 HTN (≥160 mm Hg systolic or ≥100 mm Hg diastolic)
16
Q
Diuretics help reduce plasma volume and chronically reduce peripheral resistance. Thiazide diuretics are normally the DOC. When would loop diuretics be used?
A
In those with renal dysfunction and when close electrolyte monitoring is assured
17
Q
Beta blockers tend to be more effective at treating HTN in what patients?
A
Whites
18
Q
Beta blockers must be used with caution with what patients?
A
In those with pulmonary disease or diabetes
19
Q
ACEI I becoming increasingly the treatment of choice for what circumstances of HTN?
A
- For mild to moderate HTN
- For whites
- When diuretics are insufficient
20
Q
Calcium channel blockers cause peripheral vasodilation. They are preferable in what type of patients?
A
In African Americans and elderly patients
21
Q
What is Aliskiren?
A
It is a renin inhibitor used for refractory cases of HTN or special situations; it is approved for mono- or combination therapy
22
Q
What are the preferred agents for hypertensive urgencies and emergencies?
A
Sodium nitroprusside and, if myocardial ischemia is present, nitroglycerin or a beta blocker
23
Q
Other acceptable agents used in hypertensive urgencies and emergencies?
A
Nicardipine, enalaprilat, diazoxide, trimethaphan, and loop diuretics
24
Q
Aortic dissection usually call for what treatment?
A
Nitroprusside and a beta blocker, usually labetalol or emolol, and urgent surgery
25
What is the preferred medication for HTN during pregnancy?
Hydralazine
26
What oral agents are used for less severe HTN?
Clonidine, captopril, and nifedipine
27
Metabolic syndrome is a major contributor to coronary heart disease and at least three of the criteria have to be met to diagnose this. What is the criteria?
1. Abdominal obesity
2. Triglycerides greater than 150 mg/dL
3. HDL 110 mg/dL
5. HTN
28
Patients are considered at high risk for ischemic heart disease if they have which medical conditions?
Cerebrovascular disease, peripheral arterial disease, abdominal aortic aneurysm, chronic or end-stage renal disease or diabetes
29
Prinzmetal (or variant) angina is caused by what?
Vasospasm at rest, with preservation of physical activity. These are typically younger patients.
30
What are the three common patterns of presentation of unstable angina (UA)?
1. Angina at rest
2. New onset of angina symptoms
3. Increasing pattern of pain in previously stable patients
31
The American Heart Association (AHA) report what as the most common presentation of unstable angina?
Angina at rest
32
When is unstable angina suspected?
When the pain is less responsive to NTG, lasts longer, and occurs at rest or with less exertion than previous episodes of angina
33
Stable angina pectoris usually lasts how long?
Less than 3 minutes
34
What ECG changes during an angina attack is among the most sensitive clinical signs?
Horizontal or downsloping ST-segment depression on the ECG
35
What is considered to be a positive test in a stress test?
ST-segment depression of 1 mm (0.1 mV)
36
What is the definitive diagnostic procedure for ischemic heart disease?
Coronary angiography
37
What medication is the first-line therapy for chronic angina?
Beta blockers
38
What antiplatelet medications should be used in all patients with ischemic heart disease unless a contraindication exists?
ASA, Clopidogrel (Plavix)
39
What does Ranolazine (Ranexa) do for angina?
It prolongs exercise duration and time to angina and is useful for symptom control
40
What is the usual cause of death in MI patients?
Ventricular fibrillation
41
What are some atypical symptoms that elderly patients may present with?
Altered mental status, generalized weakness, stroke, or syncope
42
Dressler syndrome (post-MI syndrome) consists of what?
Pericarditis, fever, leukocytosis, and pericardial or pleural effusion. Usually comes 1-2 weeks post-MI
43
A patient who presents with transient ST-segment changes of ≥0.5 mm that develop during a symptomatic episode and resolve when the patient becomes asymptomatic is highly suggestive of what?
Acute ischemia and CAD
44
What on an ECG is highly suspicious for a new MI?
New left bundle branch block
45
Inferior ECG leads
II, III, aVF
46
Posterior ECG leads
V1-V2
47
Anteroseptal ECG leads
V1-V2
48
Anterior ECG leads
V1-V3
49
Anterolateral ECG leads
V4-V6
50
What is the timing of initial elevation (in hours) for myoglobin, cardiac troponin I, cardiac troponin T and CK-MB?
Myoglobin: 1-4 hours
Cardiac troponin I: 3-12 hours
Cardiac troponin T: 3-12 hours
CK-MB: 3-12 hours
51
What is the peak elevation for myoglobin, cardiac troponin I, cardiac troponin T and CK-MB?
Myoglobin: 6-7 hours
Cardiac troponin I: 24 hours
Cardiac troponin T: 12-48 hours
CK-MB: 24 hours
52
When does myoglobin, cardiac troponin I, cardiac troponin T, and CK-MB return to normal?
Myoglobin: 24 hours
Cardiac troponin I: 5-10 days
Cardiac troponin T: 5-14 days
CK-MB: 48-72 hours
53
TIMI (Thrombolysis in Myocardial Infarction) is used for risk stratification in ACS patients. One point is given for certain factors. What are these factors?
- Age 65 and older
- Three or more risk factors for CAD
- Use of ASA within the last 7 days
- Known CAD with stenosis 50% or greater
- More than one episode of rest angina within the last 24 hours
- ST segment deviation
- Elevated cardiac markers
54
What score is considered high risk when using TIMI?
3 or more
55
What are the most commonly used thrombolytic agents used in STEMI?
Alteplase, reteplase, and tenecteplase
56
Absolute contraindications to thrombolytic agents?
Previous hemorrhage or stroke, any stroke within the past year, known intracranial neoplasm, active internal bleeding, or suspected aortic dissection
57
Relative contraindications to thrombolytic agents?
Known bleeding diathesis, trauma within the past 2-4 weeks, major surgery within the past 3 weeks, prolonged or traumatic CPR, recent internal bleeding, noncompressible vascular puncture, active diabetic retinopathy, pregnancy, active PUD, current use of anticoagulants, and BP greater than 180/110
58
What are the four cyanotic congenital anomalies?
1. Tetralogy of Fallot
2. Pulmonary atresia
3. Hypoplastic left heart syndrome
4. Transposition of the great vessels
59
Tetralogy of Fallot consists of what?
Ventricular septal defect, aortic origination over the defect, right ventricular outflow obstruction, and right ventricular hypertrophy
60
Pulmonary atresia
- Most often occurs with an intact ventricular septum
| - The pulmonary valve is closed; an atrial septal opening and patent ductus arteriosus are present
61
Hypoplastic left heart syndrome
Group of defects with a small left ventricle and normally placed great vessels
62
Transposition of the great vessels
Most commonly a complete transposition of the aorta and pulmonary artery
63
Tetralogy of Fallot murmur
Crescendo-decrescendo holosystolic at LSB, radiating to back
64
Tetralogy of Fallot physical findings
Cyanosis, clubbing, increased RV impulse at LLSB, loud S2
65
Tetralogy of Fallot important clinical information
Polycythemia is usually present; tet (hypercyanotic) spells include extreme cyanosis, hyperpnea, and agitation (this is a medical emergency!!)
66
Pulmonary atresia murmur
Depends on presence of tricuspid regurgitation
67
Pulmonary atresia physical findings
Cyanosis with tachypnea at birth, tachypnea without dyspnea, hyperdynamic apical impulse, single S1 and S2
68
Pulmonary atresia important clinical information
Sudden onset of severe cyanosis and acidosis requires emergency treatment
69
Hypoplastic left heart syndrome murmur
Variable; not diagnostic
70
Hypoplastic left heart syndrome physical findings
Shock, early heart failure, respiratory distress, single S2; presentation varies with specific syndrome
71
Hypoplastic left heart syndrome important clinical information
Occurs more often in males; accounts for 1/4 of cardiac deaths before age 7
72
Transposition of the great vessels murmur
Systolic murmur if associated with VSD; systolic ejection murmur if with pulmonary stenosis
73
Transposition of the great vessels physical findings
Cyanosis in newborn is most common sign; tachypnea without respiratory distress; if large VSD, symptoms of CHF and poor feeding; single loud S2; absent LE pulses if with aortic arch obstruction
74
What are the 5 noncyanotic congenital heart anomalies?
1. Atrial septal defect
2. Ventricular septal defect
3. Atrioventricular septal defect
4. Patient (persistent) ductus arteriosus
5. Coarctation of the aorta
75
Atrial septal defect
Opening between the right and left atria. Of the four main types, ostium secundum is the most common
76
Atrial septal defect murmur
Systolic ejection murmur at 2nd LICS; early to middle systolic rumble
77
Atrial septal defect physical findings
Failure to thrive, fatigability, RV heave, wide fixed split S2
78
Ventricular septal defect
May be perimembranous (most common), muscular, or outlet openings between the ventricles
79
VSD murmur
Systolic murmur as LLSB; others depend on severity of defect
80
VSD physical findings
Depends on the size of the defect - from asymptomatic to signs of CHF
81
VSD important clinical information
Outlet VSDs are more common in Japanese and Chinese
82
Patent ductus arteriosus
Failed or delayed closure of the channel bypassing the lungs, which allows placental gas exchange during the fetal state. Unlike other congenital anomalies, surgical treatment is usually not indicated as many patients respond to IV indomethacin
83
PDA murmur
Continuous (machinery) murmur in patients with isolated PDA
84
PDA physical findings
Wide pulse pressure, hyperdynamic apical pulse
85
Coarctation of the aorta
It involves narrowing of the proximal thoracic aorta
86
Coarctation of the aorta murmur
Systolic, LUSB, and left interscapular area; may be continuous
87
Coarctation of the aorta physical findings
Infants may present with CHF; older children may have systolic hypertension or murmur of underdeveloped lower extremities
88
Coarctation of the aorta important clinical information
Differences between arterial pulses and blood pressure in UE and LE pathognomonic
89
Aortic stenosis
Narrows the valve opening, impeding the ejection fraction of the left side of the heart.
90
What is the most common valvular disease in the U.S. and second most frequent cause for cardiac surgery?
Aortic stenosis
91
Aortic insufficiency (regurgitation)
Results in volume overloading due to the retrograde blood flow into the left ventricle
92
Mitral stenosis
Impedes blood flow between the left atrium and ventricle
93
Mitral insufficiency (regurgitation)
Allows retrograde blood flow and volume overload of the left atrium
94
Mitral valve prolapse
Usually is asymptomatic, but it may be associated with mitral regurgitation
95
Causes of mitral and aortic valve disorders
Most frequent causes are congenital defects; other causes include rheumatic heart disease, connective tissue disorders, infection, and senile degeneration
96
Which valvular disorder presents with thready carotid pulses?
Aortic stenosis
97
Which valvular disorder presents with bounding pulses and widened pulse pressures?
Aortic regurgiation
98
Aortic stenosis murmur location
2nd RICS
99
Aortic stenosis radiation
To neck and LSB
100
Aortic stenosis intensity
Often loud with a thrill (grades 4-6)
101
Aortic stenosis pitch/quality
medium pitch; harsh
102
Aortic stenosis aids to hearing
Patient sitting and leaning forward
103
Aortic stenosis timing
midsystolic
104
Aortic regurgitation murmur location
2nd-4th LICS
105
Aortic regurgitation radiation
To apex and RSB
106
Aortic regurgitation intensity
Grades 1-3
107
Aortic regurgitation pitch/quality
High pitch; blowing
108
Aortic regurgitation aids to hearing
Patient sitting and leaning forward; full exhalation
109
Aortic regurgitation associated findings
Midsystolic or Austin Flint murmur suggests large flow; arterial pulses large and bounding
110
Aortic regurgitation timing
Systolic (soft) and diastolic decrescendo
111
Mitral stenosis murmur location
Apex
112
Mitral stenosis radiation
Little or none
113
Mitral stenosis intensity
Grades 1-4
114
Mitral stenosis pitch/quality
Low pitch
115
Mitral stenosis aids to hearing
Patient in left lateral position; full exhalation
116
Mitral stenosis associated findings
S1 accentuated; opening snap follows S2
117
Mitral stenosis timing
Middiastolic
118
Mitral regurgitation murmur location
Apex
119
Mitral regurgitation radiation
To left axilla
120
Mitral regurgitation intensity
Soft to loud
121
Mitral regurgitation pitch/quality
Medium to high pitch; blowing
122
Mitral regurgitation associated findings
S2 often decreased; apical impulse prolonged
123
Mitral regurgitation timing
Pansystolic
124
Tricuspid regurgitation murmur location
LLSB; holosystolic
125
Tricuspid regurgitation radiation
To right sternum and xiphoid area
126
Tricuspid regurgitation intensity
Variable
127
Tricuspid regurgitation pitch/quality
Medium; blowing
128
Tricuspid regurgitation aids to hearing
Increases slightly with inspiration
129
Tricuspid regurgitation associated findings
JVP often elevated
130
Tricuspid regurgitation timing
Pansystolic
131
Pulmonic stenosis murmur location
2nd-3rd ICS; mid-systolic crescendo-decrescendo
132
Pulmonic stenosis radiation
To left shoulder and neck
133
Pulmonic stenosis intensity
Soft to loud, possibly associated with thrill
134
Pulmonic stenosis pitch/quality
Medium; harsh
135
Pulmonic stenosis associated findings
Early pulmonic ejection sound common
136
Pulmonic stenosis timing
Systolic
137
Underlying conditions in pulmonic and tricuspid disorders that cause pulmonary HTN are treated with what?
Arterial vasodilators (hydralazine, nitroprusside) or positive inotropric agents (amiodarone, digitalis, digoxin)
138
Class Ia antiarrhythmic drugs action
Sodium channel blockers; depress phase 0 depolarization; slow conduction; prolong repolarization
139
Class Ia antiarrhythmic drugs indications
Supraventricular tachycardia; V tach; prevention of V fib; symptomatic ventricular premature beats
140
Class Ia antiarrhythmic drugs examples
Quinidine, procainamide, dispyramide, moricizine
141
Class Ib antiarrhythmic drugs action
Shorten repolarization
142
Class Ib antiarrhythmic drugs indications
V tach; prevention of V fib; symptomatic ventricular premature beats
143
Class Ib antiarrhythmic drugs examples
Lidocaine, mexiletine
144
Class Ic antiarrhythmic drugs action
Depress phase 0 repolarization; slow conduction
145
Class Ic antiarrhythmic drugs indications
Life-threatening V tach or V fib, refractory supraventricular tachycardia
146
Class Ic antiarrhythmic drugs examples
Flecainide, propafenone
147
Class II antiarrhythmic drugs action
Beta blockers; slow AV conduction
148
Class II antiarrhythmic drugs indications
Supraventricular tachycardia; may prevent ventricular fibrillation
149
Class II antiarrhythmic drugs examples
Esmolol, propranolol, metoprolol
150
Class III antiarrhythmic drugs action
Potassium channel blockers; prolong action potential
151
Class III antiarrhythmic drugs indications
Refractory V tach; supraventricular tachycardia; individual agents have specific indications
152
Class III antiarrhythmic drugs examples
Amiodarone, sotalol, dofetilide, ibutilide
153
Class IV antiarrhythmic drugs action
Slow calcium channel blockers
154
Class IV antiarrhythmic drugs indications
Supraventricular tachycardia
155
Class IV antiarrhythmic drugs examples
Verapamil, diltiazem
156
Class V antiarrhythmic drugs action
Adenosine: slows conduction time through AV node, interrupts reentry pathways; digoxin: direct action on cardiovascular system via ANS
157
Class V antiarrhythmic drugs indications
supraventricular tachycardia
158
Class V antiarrhythmic drugs examples
Adenosine, digoxin
159
What is the holiday heart syndrome?
It is an arrhythmia that is caused by alcohol excess or withdrawal; most commonly it is atrial fibrillation
160
Atrial flutter usually occurs in what patients?
In those with COPD, heart failure, ASD, or CAD
161
Junctional rhythms occur in what patients?
In patients with normal hearts or those with myocarditis, CAD, or digitalis
162
Signs and symptoms of an unstable rhythm
Chest pain, dyspnea, altered mental status, and hypotension
163
Patients with unstable bradycardia leading to hypotension, shock, altered mental status, angina, or heart failure should be treated with what?
A vagolytic (i.e., atropine) or positive chronotropic (i.e., epinephrine or dopamine). Transcutaneous or transvenous pacing is often indicated and may need to be followed by permanent pacing
164
Treatment of a regular, narrow-complex tachycardia in a stable patient
- First, Valsalva maneuvers may be attempted.
- The initial medication of choice is adenosine administered via rapid IV push
- If adenosine is ineffective, beta blockers or CCB can also be used
165
Treatment of a regular, narrow-complex tachycardia in an unstable patient
synchronized cardioversion
166
Treatment of sustained or recurrent PSVT
Refer for catheter ablative surgery
167
If a patient with significant tachycardia is stable and the QRS complex is wide, what is the treatment of choice?
An antiarrhythmic infusion of procainamide, amiodarone, or sotalol
168
Rate control methods for afib in the presence of heart failure
Use of digoxin, amiodarone, or dronedarone
169
Rate control methods for afib in the absence of heart failure
Beta blockers (i.e., metoprolol or esmolol) or CCB (diltiazem or verapamil)
170
What is the primary antiarrhythmic therapy in chronic atrial flutter?
Dofetilide
171
Brugada syndrome
Genetic disorder that causes syncope, ventricular fibrillation, and sudden death, often during sleep. It is more common in Asian men.
172
What is the treatment for ventricular premature beats and sustained V tach w/o heart disease or electrolyte abnormalities?
Usually not treated. If the patient is having symptoms, can give a beta blocker or CCB
173
Treatment of V tach with severe hypotension or loss of consciousness
Synchronized cardioversion; ventricular overdrive pacing may help
174
Pulseless v tach treatment
Immediate defibrillation along with CPR
175
Preferred pharmacologic interventions for acute V tach (in order)
1. Amiodarone
2. Lidocaine
3. Procainamide
176
An ICD may be indicated for recurrent sustained V tach with what conditions?
In patients with structural heart disease or without a reversible cause, for congenital long QT syndrome, and for Brugada syndrome
177
Treatment of acquired long QT syndrome
Treatment of electrolyte abnormalities and discontinuation of drugs that prolong the QT interval
178
What is the initial treatment for torsades de pointes?
IV magnesium, correction of electrolyte abnormalities (hypokalemia or hypomagnesemia), and withdrawal of drugs that may have precipitated the event
179
What treatment may be indicated after initial treatment of torsades?
Isoproterenol infusion and overdrive pacing
180
Treatment for recurrent torsades
Permanent pacemaker
181
In sick sinus syndrome, besides scarring of the heart's conduction system or infants who have had heart surgery, what are other causes or exacerbations?
Digitalis, CCB, beta blockers, sympatholytic agents, antiarrhythmic drugs, and aerosol propellant abuse. It may also result from underlying collagen vascular or metastatic disease, surgical injury, or, rarely, coronary disease
182
What are some reversible causes of sick sinus syndrome?
Digitalis, quinidine, beta blockers, or aerosol propellants
183
Dilated cardiomyopathies are the most common type of cardiomyopathies (95%). What is is associated with?
Reduced strength of ventricular contraction, resulting in dilation of the left ventricle
184
Causes of dilated cardiomyopathies
Excessive alcohol consumption, postpartum state, chemotherapy toxicity, endocrinopathies, and myocarditis; it may be idiopathic
185
Hypertrophic cardiomyopathy demonstrates what?
Massive hypertrophy (particularly of the septum), small left ventricle, systolic anterior mitral motion, and diastolic dysfunction
186
What in hypertrophic cardiomyopathy promotes the development of an arrhythmia?
Microscopic myocardial abnormalities
187
Restrictive cardiomyopathy results from what?
From fibrosis or infiltration of the ventricular wall because of collagen-defect diseases, most commonly amyloidosis, radiation, postoperative changes, diabetes, and endomyocardial fibrosis
188
How is the left ventricle in restrictive cardiomyopathy?
Small or normal, with mildly reduced function
189
Signs and symptoms of dilated cardiomyopathy
It results in signs and symptoms of left or biventricular congestive failure; the most common presentation is dyspnea. Patients may have an S3 gallop, pulmonary crackles (rales), and increased JVP
190
Takotsubo cardiomyopathy presents with what?
Retrosternal chest pain indistinguishable from acute MI
191
Patients with hypertrophic cardiomyopathy may present with what symptoms?
Dyspnea and angina. Syncope and arrhythmias are common. It may be asymptomatic. Sudden death may be the initial presentation
192
Physical exam in hypertrophic cardiomyopathy
Sustained PMI or triple apical impulse, loud S4 gallop, variable systolic murmur, a bisferiens carotid pulse, and jugular venous pulsations with a prominent "a" wave
193
Presentation for restrictive cardiomyopathy
Decreased exercise tolerance; in advanced disease, patients develop right-sided congestive failure; pulmonary HTN is usually present
194
What does cardiac catherization reveal in Takotsubo cardiomyopathy?
Hypocontractility of the left ventricular apex and patent coronary arteries
195
What does the echocardiogram reveal in hypertrophic obstructive cardiomyopathy?
LVH, asymmetric septal hypertrophy, small left ventricle, and diastolic dysfunction
196
What study may be necessary in restrictive cardiomyopathy to differentiate restrictive disease from other forms of cardiomyopathy or pericarditis?
Endomyocardial biopsy
197
Treatment of dilated cardiomyopathy
1. Abstinence from alcohol is essential
2. Underlying disease should be treated
3. CHF requires supportive treatment
198
Takotsubo cardiomyopathy treatment
Usually treated with supportive care. Inotropes should generally be avoided. Most patients return to baseline within 2 months
199
Hypertrophic cardiomyopathy treatment
1. Initial treatment employs beta blockers or CCBs; disopyramide is used for its negative inotropic effects
2. Surgical or nonsurgical ablation of the hypertrophic septum may be required
3. Dual chamber pacing, implantable defibrillators, or mitral valve replacement may be indicated
200
What medication may help patients with restrictive cardiomyopathies?
Diuretics
201
Pericardial effusion is secondary to what?
Pericarditis, uremia, or cardiac trauma
202
Pericardial effusion produces what?
Restrictive pressure on the heart
203
What occurs in cardiac tamponade?
The fluid that accumulates compromises cardiac filling and impairs cardiac output
204
What is the primary presenting symptom of acute pericarditis?
Sharp, pleuritic substernal radiating chest pain often relieved by sitting upright and leaning forward; a cardiac friction rub is characteristic
205
Electrical alternans is pathognomonic of what?
Effusion
206
In the presence of hemodynamic compromise, what is the treatment of an effusion?
Pericardiocentesis
207
What is the treatment of recurrent effusions?
May be treated surgically with a pericardial window
208
Strictly inflammatory conditions in a pericardial effusion may be treated with what?
Steroids or NSAIDs
209
Pericardiectomy may be performed when?
To relieve constrictive pericarditis
210
Most cases of native valve infective endocarditis (IE) are caused by what pathogens?
Streptococcus viridans, Staphylococcus aureus, and enterococci
211
In IV drug users, what is the most common pathogen and what valve is frequently involved?
S. aureus and the tricuspid valve is frequently involved
212
Approximately 90% of IE patients have what sign?
A stable murmur, but this may be absent in right-sided infections. A changing murmur is rare but diagnostically significant
213
Classic features of IE
1. Palatal, conjunctival or subungal petechiae
2. Splinter hemorrhages
3. Osler nodes
4. Janeway lesions
5. Roth spots
214
Osler nodes
Painful, violaceous, raised lesions of the fingers, toes or feet
215
Janeway lesions
Painless red lesions of the palms or soles
216
Roth spots
Exudative lesions in the retina
217
What study has no specific diagnostic features in infective endocarditis?
ECG
218
Patients must have what in the Duke criteria to be considered "definite" in the diagnosis of IE?
1. Two major criteria
2. One major and three minor OR
3. Five minor criteria
219
IE is considered "possible" with what in the Duke criteria?
1. One major and one minor
| 2. Three minor
220
Major criteria of IE
1. Two positive blood cultures of a typical causative microorganism
2. Echocardiographic evidence of endocardial involvement including new valvular regurgitation
221
Minor criteria of IE
1. Predisposing factor
2. Fever higher than 100.4 F (38 C)
3. Vascular phenomena (e.g., embolic disease or pulmonary infarction)
4. Immunologic phenomena (e.g., glomerulonephritis, Osler nodes, Roth spots)
5. Positive blood culture not meeting major criteria
222
What is an appropriate initial therapy for patients with suspected IE?
Gentamicin with ceftriaxone OR vancomycin
223
What is an appropriate therapy for acutely ill patients with heart failure pending blood cultures?
Gentamicin, vancomycin plus cefepime
224
Antibiotic prophylaxis is recommended in what patients?
Prosthetic valves, previous IE, some congenital heart conditions, some acquired valve disorders, hypertrophic cardiomyopathy, and cardiac transplant recipients with valvulopathy. Amoxicillin is the usual drug of choice
225
Valve replacement (especially of the aortic valve) may be necessary in what patients with IE?
If the IE does not resolve with antibiotic therapy, if an abscess develops, or if a fungal infection is the cause
226
What systems are most commonly affected in rheumatic heart disease?
Heart, joints, skin, and CNS
227
What ages are most commonly affected by rheumatic heart disease?
Children from ages 5-15 years
228
What is the typical lesion in rheumatic valve disease?
Perivascular granuloma with vasculitis
229
What are the most commonly involved valves in rheumatic heart disease?
Mitral valve ( 75-80%) followed by the aortic valve (30%)
230
How many of the Jones criteria is required to make the diagnosis of rheumatic fever?
Two major or one major and two minor
231
Major Jones criteria for rheumatic fever
Carditis, erythema marginatum, subcutaneous nodules, chorea, and polyarthritis
232
Minor Jones criteria for rheumatic fever
Fever, polyarthralgias, reversible prolongation of the PR inteval, rapid ESR, or C-reactive protein
233
What part of treatment is essential in rheumatic fever?
Strict bed rest
234
Antibiotic treatment of rheumatic fever
IM penicillin is used for documented streptococcal infection; in patients who are allergic to penicillin, erythromycin is appropriate
235
What do salicylates do in rheumatic fever?
Reduce fever and relieve joint problems
236
What do corticosteroids do in rheumatic fever?
Relieve joint symptoms but do not prevent cardiac disease
237
Prevention of rheumatic fever
Early treatment of streptococcal pharyngitis
238
Prevention of the recurrence of rheumatic fever is essential to prevent heart damage. What antibiotic is given for prophylaxis?
Benzathine penicillin every 4 weeks
239
What are signs of peripheral arterial disease?
- Femoral and distal pulses will be weak or absent; an aortic, iliac, or femoral bruit may be present.
- Skin changes to the lower extremity includes loss of hair, shiny atrophic skin, and pallor with dependent rubor
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What is Leriche syndrome?
Iliac artery disease; erectile dysfunction may occur in this syndrome
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Acute arterial occlusion threatens limb viability and results in what signs and symptoms?
Pain, pallor, pulselessness, paresthesias, poikilothermia, and paralysis
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An ABI of what indicates significant PAD?
≤0.9
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What is the gold standard study for PAD?
Angiography
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Although it is not regularly used for screening, an elevation of what has a strong association with incidence and progression of PAD?
Homocysteine
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What aggressive risk factor modification is used for PAD?
Tobacco use must be discontinued; DM, HTN, and HLD must be controlled
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What has been shown to be helpful at reducing symptoms of claudication in PAD?
Beta blockers, ACE inhibitors, statins, progressive exercise, and supervised exercise programs
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What medication(s) should be used in all patients with PAD (unless there is a contraindication)?
ASA and/or clopidrogel
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What medication can be added to help with symptom relief of PAD (primarily improved pain-free walking distances)?
Cilostazol (phosphodiesterase 3 inhibitor)
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What are risk factors for varicose veins?
Women who have been pregnant, obesity, family history, prolonged sitting and standing, and history of phlebitis
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The main mechanisms of varicose veins?
Superficial venous insufficiency and valvular incompetence
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What test differentiates saphenofemoral valve incompetence from perforator vein incompetence?
Brodie-Trendelengurg test
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Small venous ulcers in varicose veins heal with what treatment?
Leg elevation and compression bandages
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Large venous ulcers in varicose veins require what treatment?
Compression boot dressing (Unna boot) or skin grafts
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Interventional techniques for varicose veins
Endovenous radiofrequency or laser ablation, compression sclerotherapy, and sometimes surgical stripping of the saphenous tree
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Virchow triad
Stasis, vascular injury, and hypercoagulability
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What study is the most accurate method for definitive diagnosis of DVT?
Venography; however it is associated with increased risk and is rarely needed.
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Studies used in pulmonary embolism
1. Pulmonary angiography (gold standard)
2. CT angiography (most commonly used)
3. V/Q scanning
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Treatment of superficial thrombophlebitis
1. Bed rest, local heat, elevation of the extremity, and NSAIDs
2. Antibiotics may be required if evidence of infection exists
3. More serious disease may require surgical intervention
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Preferred treatment for DVT
Anticoagulation with enoxaparin (a low-molecular-weight heparin) or unfractioned heparin followed by warfarin
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Skin changes in chronic venous insufficency
Shiny, thin, and atrophic with dark pigmentary changes and subcutaneous induration
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Nonclassic symptoms of giant cell arteritis
Respiratory tract problems, mononeuritis complex (peripheral neuropathy), fever of unknown origin, or unexplained neck and head pain
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What do lab studies show in giant cell arteritis?
- ESR and CRP will be markedy elevated
| - Most patients have a normochromic normocytic anemia and thrombocytosis; some have elevated alkaline phosphatase
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Treatment of giant cell arteritis
High dose prednisone (1-2 months before tapering) and low dose ASA. Treatment should be initiated immeidately and not delayed for biopsy results
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Aortic aneurysm is what?
A weakness and subsequent dilation of the vessel wall
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Causes of aortic aneursym
Artherosclerosis is the most common cause, although some exist as congenital defects or as a result of syphilis, giant cell arteritis, vasculitis, trauma, Marfan syndrome, or Ehlers Danlos syndrome
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Where do the majority of aortic aneurysms occur in?
The abdomen (90% compared to 10% in the thoracic area)
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What is the study of choice for abdominal aneurysms?
Abdominal ultrasonography
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Current recommendation for abdominal aortic aneurysm screening
Single abdominal U/S for men older than the age of 65 years who have ever smokes; this may be followed by contrast-enhanced CT
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Diagnostic studies for thoracic aneursyms
It may require aortography for diagnosis; CT and MRI are preferred over U/S
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Treatment of aortic aneurysm
- The only effective treatment is endovascular or open surgical repair
- Five year survival after repair is greater than 60%
