Cardiology Part 1 Flashcards
(473 cards)
1
Q
Hypertension Module
A
x
2
Q
dx
A
x
3
Q
what is the measure that raises concern for HTN?
A
BP > 140/90
4
Q
how many readings do you need to make the dx of HTN?
A
> 140/90 on 3-6 readings over a period of weeks to months.
tyypically >=2 BP readings are necessary
5
Q
define
A
x
6
Q
what are the two categories of HTN?
A
primary (essential) or secondary
7
Q
causes
A
x
8
Q
what are the causes of secondary HTN?
A
coarctation of aorta, renal or renovascular disease, sleep apnea, pheochromocytoma, cushing syndrome, endocrine disorders
9
Q
PE
A
x
10
Q
what are important PE findings to pursue in HTN?
A
fundoscopic exam (HTN retinopathy), pulse palpation (coarctation of aorta), cardiac exam (LVH), abd exam (renal artery bruit)
11
Q
what type of PE should be done for HTN?
A
full physical exam
12
Q
workup
A
x
13
Q
what are important workup labs for HTN module to order?
A
CBC, BMP, UA, lipid profile, and 12 lead EKG, may need microalbumineria screening in diabetics
14
Q
what imaging should be ordered for HTN?
A
echocardiogram
15
Q
Management
A
x
16
Q
first line management for HTN is?
A
lifestyle mods (low salt, regular excercise, no smoking, no alcohol, calorie restriction, low fat diet)
17
Q
if lifestyle mods fail to alter HTN, what is second line management?
A
pharmacotherapy
18
Q
what is considered stage I HTN? what is best pharmacotherapy?
A
BP: 140-159/90-99, monotherapy with ACEi/ARB/CCB
19
Q
what is considered stage II HTN? what is best pharmacotherapy?
A
BP: >=160/>=100, start two drug therapy ACEi/ARB +CCB
20
Q
Goal of HTN therapy
A
x
21
Q
what is goal BP for those < 60y.o. and CKD or DM?
A
<140/90
22
Q
what is goal BP for those >= 60y.o.?
A
<150/90
23
Q
preferred drugs in select situations
A
x
24
Q
what is the preferred drug in afib/flutter for BP control?
A
b-blocker, nondihydropyridine CCB
25
what is the preferred drug in angina pectoris for BP control?
b-blocker, CCB
26
what is the preferred drug in MI for BP control?
ACEi/ARB, b-blocker, or aldosterone antagonist
27
what is the preferred drug in CHF for BP control?
ACEi/ARB, b-blocker, diuretic or aldosterone antagonist
28
what is the preferred drug in DM (no proteinuria) for BP control?
diuretic or ACEi
29
what is the preferred drug in proteinuria for BP control?
ACEi or ARB
30
what is the preferred drug in osteoperosis for BP control?
thiazide diuretic
31
what is the preferred drug in BPH for BP control?
alpha blocker (prazosin, terazosin, or doxasozin)
32
Hypertension
x
33
managment
x
34
what is the most effective non pharm way to decrease BP?
10% weight loss (drops SBP by 5-20mm Hg per 10 kg loss)
35
what is the second most effective non pharm way to decrease BP?
```
DASH diet (diet high in fruits and veggies and low saturated fat and total fat, high in potassium, calcium and dietary fiber).
Drops SBP by 8-14mm Hg
```
36
what is the third most effective non pharm way to decrease BP?
excercise . 30 minutes /day for 5-6 days/week drops SBP by 4-9 mmHg
37
what is the fourth most effective non pharm way to decrease BP?
dietary sodium (<3g/day). Drops SBP by 2-8mmHg
38
what is the fifth most effective non pharm way to decrease BP?
alcohol intake (2drinks/day in men and 1 drink / day in women) drops SBP by 2-4mmHg
39
trx
x
40
when treating blood pressure in patients what is an effective combination?
ACE inhibitor/ARB + CCB (i.e. amlodipine)
41
Recommendations for treating hypertension
x
42
if Age >=60y.o. , at what BP reading do you initiate treatment of BP?
>=150 mm Hg SBP or >90 mm Hg DBP
43
what is the goal BP if age >= 60 y.o.?
< 150/90 mm Hg
44
if age <60 y.o., CKD , or DM at what BP reading do you initiate treatment of BP?
>=140 mm Hg SBP or >90 mm Hg DBP
45
if age <60 y.o., CKD , or DM what is the goal BP?
<140/90 mm Hg
46
initial anti HTN trx choice in certain populations
x
47
initial treatment for black patients?
thiazide diuretics or CCB, alone or in combination (ACEi/ARB, not first line)
48
initial treatment for other ethnicities ?
thiazide diuretics, ACEi, ARB, or CCB, alone or in combination
49
treatment of all ethnicities with CKD or DM?
ACEi or ARB, alone or in combination with other drug classes
50
Cyanide Accumulation and Toxicity
x
51
risk
x
52
what is the risk of cyanide toxicity?
HTN emergency treated with nitroprusside in the setting of chronic renal failure or those receiving a high dose or prolonged infusion (>2ug/kg/min)
53
pathophys
x
54
what is the pathophys of cyanide accumulation in HTN emergency?
nitroprusside infusion to treat high BP. Nitroprusside is metabolized to cyanide, which may accumulate and can be toxic
55
syx
x
56
what are syx of cyanide toxicity?
- Skin: Flushing (cherry red color), cyanosis (occurs later)
- CNS: headache, AMS, seizures, coma
- Cardiovascular: Arrythmias
- Respiratory: Tachypnea followed by respiratory depression, pulm edema
- GI: Abd pain, nausea, vomiting
- Renal: Met Acidosis (f
57
trx
x
58
what is the trx of cyanide accumulation?
sodium thiosulfate
59
Nitroprusside
x
60
pathophys
x
61
what is the pathophys of nitroprusside ?
potent vasodilator that works on arterial venous circulation
62
Hypertensive emergency
x
63
ED visit
x
64
what are initial ED orders for HTN emergency prior to physical exam?
IV access, oxygen, pulse ox, cardiac monitoring, BP monitor
65
syx
x
66
what are the symptoms of htn emergency?
insidious onset of headaches, nausea, vomiting, which can progress to restlessness, confusion, agitation, seizures, coma.
67
dx
x
68
how is HTN emergency different than urgency?
HTN urgency: SBP >180 and/or DBP>120 with no end organ damage
HTN emergency is DBP > 120 with end organ damage
69
PE
x
70
what are most important physical exam findings in HTN emergency?
fundoscopy, Cardiovascular, and CNS exam.
End organ damage: retinal hemorrhage, papilledema, HTN encephalopathy (n/v, headache, confusion) stroke, malignant nephrosclerosis
71
work up
x
72
what is the work up for HTN emergency?
EKG, CTH, CXR, UA, CBC, BMP, lipid profile (assess for stroke, pulmonary edema, renal impairment, and hemolysis)
73
what additional orders should be given to a HTN emergency patient?
NPO, complete bed rest, monitor urine output
74
trx
x
75
what is the trx for hypertensive emergency?
rapidly lower diastolic pressure to 100-105 mm Hg over 2-6 hours, with a total drop in blod pressure being no more than 25% of the initial value.
76
what is first line IV BP lowering meds and next steps in addressing HTN crisis?
IV nitroprusside to lower BP by 25% while in ICU with arterial line place.
Then transfer to wards to lower BP further with PO meds. D/C art line.
Goal is to lower DBP to 85-90 . over 2-3 months.
77
what are next steps once BP is under control?
discharge home, lipid profile, counseling (medication compliance, smoking cessation, excercise, limit alcohol intake, low salt diet)
78
if you drop the BP too far what happens?
ischemic events (cerebral ischemia, myocardial infarction), AMS, generalized seizures
79
what are the initial meds used to lower BP?
IV nutroprusside, IV hydralazine
80
what is major side effect of fast acting BP lowering meds?
reflex tachycardia
81
what are alternaive BP lowering meds ?
IV labetalol, IV nicardipine
82
x
x
83
Intracerebral hemorrhage
x
84
syx
x
85
what are the syx of intracerebral hemorrhage?
focal neuro deficits, hemiplegia or paresis and hemianopsia.
86
TCA (tricyclic antidepressant) overdose
x
87
syx
x
88
what are the CNS syx of TCA overdose?
-CNS: AMS (drowsiness, delirium, coma); seizures, respiratory depression.
89
what are the Cardio syx of TCA overdose?
#NAME?
90
what are the Anticholenergic syx of TCA overdose?
#NAME?
91
complications
x
92
what are the complications of TCA overdose?
- acidemia, which can increase serum potassium due to cellular exchange of hydrogen and potassium.
- also prolongs QRS interval (>100 ms) and causes arrythmias (eg Vtach, Vfib)
- can also decrease calcium influx into the myocardium and increase periophera
93
management
x
94
what is the management of TCA overdose?
- supplemental oxygen, intubation.
- IV fluids
- Activated charcoal for patients within 2 hours of ingestion (unless ileus present)
- IV sodium bicarb for QRS widening or ventricular arryhtmia
95
how does sodium bicarb owrk?
it increases serum pH and extracellular sodium, thereby modifying TCA to their neutral (non-ionized) form, making them less available to bind to the rapid sodium channels.
96
if patients are refractory to sodium bicarb, what could they respond to?
adjuvant magnesium or lidocaine
97
Salicylate toxicity
x
98
managment
x
99
what do you treat salicylate toxicity with?
sodium bicarb , which can alkalanize the urine and enhance salicylate excretion by the kidney
100
Hyperkalemia
x
101
trx
x
102
what is the treatment of hyperkalemia with EKG changes (peaked T waves, short QT, increased QRS intervals)?
sodium bicarb
103
Paroxysmal Supraventricular Tachycardia (PSVT)
x
104
subtypes
x
105
what are the subtypes of PSVT?
atrioventricular nodal reentrant tachycardia (AVNRT), atrioventricular reentrant tachycardia (AVRT), and atrial tachycardia
106
pathophys
x
107
what is the pathophys of PSVT?
result from secondary conduction pathway that allows abnormal cycling of cardiac conduction and formation of a reentrant circuit
108
syx
x
109
what are the syx of PSVT?
- intermittent , abrupt onset palpitations accompanied by a sensation of a rapid heartbeat.
- dyspnea, lightheadedness, chest pain, or rarely syncope, presyncope
110
PE
x
111
what are physical exam findings of PSVT?
HR> 150
112
dx
x
113
what are EKG findings ?
- narrow complex tachcyardia with regular RR intervals .
| - may show retrograde P waves that are typically inverted in the inferior leads (II, III, avF)
114
trx
x
115
what is the trx for PSVT in HD stable patients?
- vagal maneuvers (eg valsalva) can be done
| - adenosine administered to slow the AV node and allow for easier idenitifcation of the arrythmia on cardiac monitoring
116
what is the trx for PSVT in HD unstable patients?
- undergo urgent synchronized cardioversion.
| - if needed, cardiac ablation is the definitive treatment of choice
117
Atrioventricular reentrant tachycardia (AVRT)
x
118
dx
x
119
what are EKG findings of AVRT?
can have marked ST segment depression during tachycardia, occurs in young patients in the absence of CAD and does not represent MI
120
Atrial Fibrillation
x
121
dx
x
122
what are the EKG findings of Afib?
irregular rhythm and absent P waves
123
what is a drug approved for pharmacologic cardioversion of afib?
ibutilide (class III antiarrhythmic)
124
Atrial Flutter
x
125
trx
x
126
what is a good short acting med for trx of Atrial Flutter?
esmolol (ultra short acting beta blocker)
127
what is a drug approved for pharmacologic cardioversion of aflutter?
ibutilide (class III antiarrhythmic)
128
dx
x
129
what are the EKG findings of Aflutter?
flutter waves in a sawtooth pattern with a HR> 150 due to 2:1 atrial to ventricular conduction
130
Multifocal atrial tachycardia
x
131
association
x
132
what is the associated disease with multifocal atrial tachycardia?
COPD
133
dx
x
134
what does EKG show for multifocal atrial tachycardia?
irregular, narrow complex tachycardia with variable P wave morphology (p waves higher or lower than others)
135
Sinus Tachycardia
x
136
dx
x
137
what is the EKG pattern of sinus tachycardia?
narrow QRS complexes but normal p waves and often gradual (rather than abrupt) onset.
138
Wolf Parkinson White Syndrome (WPW Syndrome)
x
139
define
x
140
what is WPW syndrome a type of?
a type of tachyarrythmia
141
syx
x
142
what are the symptoms of WPW Syndrome?
syncope, pounding sensation in the chest, nausea, and vomiting
143
dx
x
144
what are the classic EKG findings of WPW?
classic triad = short PR interval + slurred upstroke of the QRS complex + widening of the QRS complex.
145
what is WPW syndrome?
classic triad + symptomatic tachyarrythmia
146
pathophys
x
147
what is the pathophys of WPW?
due to an extranodal accessory conduction pathway that directly connects the atria and ventricles, bypassing the atrioventricular node.THe accessory pathway conducts faster than the AV node and excites the ventricles prematurely, manifesting on EKG as short PR interval with delta wave and widened QRS complex
148
risk
x
149
what is the risk of WPW syndrome turning into Afib?
due to alcohol ingestion, WPW develop afib and conduct down the accessory pathway from the atria to ventricle at such a fast rate that you see syncope
150
association
x
151
what is the typical rhythm associated with WPW?
Atrioventricular reentrant tachycardia (AVRT)
152
trx
x
153
what is the treatment of WPW that continues to convert to AFib leading to tachyarrythmias causing lightheadedness?
catheter ablation (~90% efficacy rate and <5% risk of complications, replacing surgical ablation as the preferred treatment).
154
Cardiac Risk Stratification for Noncardiac surgical procedures
x
155
dx
x
156
what is dx when determining perioperative cardiovascular risk ?
requires consideration of the type of surgery being performed as well as the clinical comorbidities and functional status of the patient
157
risk
x
158
what are considered low risk (<1%) surgeries of experiencing cardiac death or nonfatal MI?
breast, cataract, endoscopic procedure, or ambulatory or superficial procedure
159
what are considered intermediate risk (1-5%) surgeries of experiencing cardiac death or nonfatal MI?
CEA, head and neck, intraperiotoneal and intrathoracic, orthapedic, prostate
160
what are considered high risk (>5%) surgeries of experiencing cardiac death or nonfatal MI?
aortic or other major vascular, peripheral vascular
161
management
x
162
in patients undergoing low risk surgeries without acutely active cardiac disease (eg decompensated heart failure, unstable angina), what do you do regarding perioperative cardiovascular risk?
no further cardiac workup regardless of underlying comorbidities
163
Moderate- or high-risk patients (ie, with an estimated risk of cardiac death, nonfatal cardiac arrest, or nonfatal MI >1%) may need additional evaluation depending on?
functional status
164
what is considered good functional status?
>=4 METs of activity (eg brisk walking, climbing 2 flights of stairs)
165
if assesing for reduced excercise capacity, what would be appropriate tests?
stress testing (excercise EKG, Myocardial perfusion imagin) or repeat echocardiogram
166
Subacute Stent Thrombosis
x
167
syx
x
168
what are the symptoms of subacute stent thrombosis?
substernal chest pressure , mild nausea, all post stenting
169
dx
x
170
what does EKG show for subacute stent thromobosis?
ST elevation in leads II, III, aVF
171
risk
x
172
risk of subacute stent thrombosis occurs how soon after stent placement?
within 30 days
173
what is the risk of subacute stent thrombosis?
premature cessation of dual antiplatelet therapy with aspirin and platelet P2Y12 receptor blocker (i.e. clopidogrel, prasugrel, ticagrelor)
174
Acute Decompensated Heart Failure (ADHF)
x
175
syx
x
176
what are the symptoms of acute decompensated heart failure?
- acute dyspnea, orthopnea, paroxysmal nocturnal dyspnea
- HTN common, hypotension suggests severe disease
- acute SOB
177
PE
x
178
what are the physical exam findings of acute decompensated heart failure?
- anxious appearing, diaphoretic
- JVD, S3 gallop, faint holosystolic murmur over the apex
- crackles to the midlung level bilaterally, decreased SpO2
- pitting edema LE
179
what does the S3 gallop and holosystolic murmur suggest?
dilated cardiomyopathy with functional mitral regurg
180
risk
x
181
what are the risk factors that lead to Acute Decompensated Heart Failure?
coronary ischemia, HTN cardiomyopathy, excessive preload(excessive volume resuscitation) or afterload (severe HTN)
182
pathophys
x
183
what is the pathophys of ADHF?
LV systolic and/or diastolic dysfunction (i.e. coronary ischemia, HTN cardiomyopathy), with or without coexisting valvular or coronary heart disease.
184
a sudden increase in pulmonary capillary wedge pressure (along with atrial and ventricular filling pressures or LV preload) leads to what?
accumulation of fluid in pulmonary interstitial and alveolar spaces
185
treatment
x
186
what is the treatment of normal or elevated BP with adequate end organ perfusion?
supplemental O2
IV loop diuretics (eg furosemide)
Consider IV vasodilator (eg nitroglycerin)
187
what is the treatment for hypotension or signs of shock?
supplemental O2
IV loop diuretics (eg furosemide) as appropriate
IV vasodilator (eg norepinephrine)
188
when improving symptoms of ADHF, what is the most appropriate next steps pathophysiologically?
#NAME?
189
when do you need to imporve myocardial contractility with dobutamine and milrinone?
- in severe LV dysfunction and low cardiac output which leads to low cardiac output causing poor peripheral perfusion and end organ dysfunction
- in patients with inadequate response to diuretic therapy
190
management
x
191
what role does nitroglycerin have in ADHF?
venous dilator that leads to decrease in cardiac preload resulting in reduced intracardiac filling pressures and improvement of pulmonary edema
192
what role does milrinone have in ADHF?
selective phosphodiesterase 3 inhibitor that causes positive inotropy (as well as reduction in preload and afterload). It can be useful for severe ADHF due to LV systolic dysfunction
193
what med is contrainidcated in acute decompensated heart failure?
beta blockers
194
Heart Failure with Preserved Ejection Fraction (HFpEF)
x
195
cause
x
196
what is the cause of HFpEF?
caused by LV diastolic dysfunction
197
pathophys
x
198
what is the pathophys of HFpEF?
prolonged systemic HTN causes LVH and impaired diastolic filling, eventually leading to decompensated volume overload despite normal LV EF>50%
199
association
x
200
what are common associated diseases?
obesity, DM, OSA
201
dx
x
202
how do you dx CHF?
largely based on history and physical exam
203
what do you see on CXR?
pleural effusions or pulm edema (kerley b lines=horizontal lines representing interstitial edema)
204
what does echo show?
concentric LVH , left atrial enlargement, and LVEF >50%
205
what are BNP levels usually?
BNP >100 pg/mL (however obesity lowers BNP levels, making it an unreliable test in these patients)
206
syx
x
207
what are the symptoms of HFpEF?
dyspnea, orthopnea, PND
208
PE
x
209
what are physical exam findings of CHF?
elevated JVP, lower extremity edema, S3
210
Obesity Hypoventilation Syndrome (OHS)
x
211
syx
x
212
what are the syx of OHS?
dyspnea
213
PE
x
214
what aer the PE of OHS?
right sided HF leading to LE edema, hepatomegaly, elevated JVD
215
ST elevation myocardial infarction (STEMI)
x
216
syx
x
217
what are the symptoms of STEMI?
CP like a pick up is right on top of chest, diaphoretic, chest tightness
218
PE
x
219
what are the PE findings of STEMI?
diffuse mild chest tenderness, low pitched sound at the apex just before S1
220
Dx
x
221
what are the classic EKG findings of STEMI?
ST elevation of 1.5mm in leads I and aVL with reciprocal changes 1-mm ST depression in II, III, and aVF
222
what are the EKG findings that diagnose STEMI?
- New ST elevation at the J point in >=2 anatomically contiguous leads with the following threshold:
- ->All leads except V2 and V3: > 1 mm (0.1 mV)
- ->Leads V2 and V3: > 1.5 mm in women, >2 mm in men age >40, and >2.5 mm in men age <40
- New left bun
223
what is the J point?
point where QRS complex meets the ST segment
224
how tall is each little box on EKG? big box on EKG?
little box: 1mm
| big box: 5mm
225
trx
x
226
what is optimal therapy for STEMI?
percutaneous coronary intervention (PCI) within 90 minutes of first medical contact or within 120 mintues for patients who require rapid transfer to a PCI capable facility
227
what are types of fibrinolytic therapy?
tenecteplase, alteplase, reteplase
228
when are cardiac enzymes and serial EKGs appropriate?
patients with suspected but undiagnosed ACS
229
Acute Inferior wall STEMI
x
230
pathophys
x
231
what is the pathophys of sinus brady in acute inferior wall STEMI ?
due to ischemia of the SA node and right ventricular wall triggering an increase in vagal tone
232
dx
x
233
what is the diagnosis of acute inferolateral wall STEMI?
ST elevation in leads II, III, aVF
234
complications
x
235
what is a common complication of acute inferior wall STEMI?
bradyarrhythmias, typically transient
236
acute inferior wall STEMI can lead to severe bradycardia leading to inadequate LV cardiac output causing what?
pulmonary edema (evidenced by bibasilar crackles) and cardiogenic shock
237
trx
x
238
how do you treat acute inferolateral wall STEMI?
IV atropine
239
Acute Anterior wall MI
x
240
trx
x
241
do these patients respond to atropine in setting of bradycardia?
no they don't becasue the bradyarrhyhtmias of anterior wall MI are commonly due to damage to the conduction system below the AV node (AV block in this setting is unlikely to respond to atropine)
242
once cardiac pacing is initiated for bradycardia, what is the next step in the setting of ST elevation in either lateral or inferior leads?
PCI
243
Persistent bradycardia secondary to anterior or inferior wall acute MI?
x
244
trx
x
245
what is the trx of choice?
cardiac pacing if syx (hypotenision, dizziness, heart failure, syncope) and not responsive to atropine
246
Post MI Sexual Activity
x
247
issue
x
248
what is the issue after an MI in engaging in sexual activity?
sexual activity associated with increased in HR and BP, and a small but measurable absolute increase in teh risk of MI
249
metabolic equivalents
x
250
what is the metabolic equivalents for sexual activity?
3-4 METs
251
what is the metabolic equivalents for rest?
1 METs
252
what is the metabolic equivalents for walking?
2 METs
253
what is the metabolic equivalents for housework?
2-4 METs
254
what is the metabolic equivalents for moderate walking, sexual intercourse?
3-4 METs
255
what is the metabolic equivalents for climbing stairs, golf, ballroom dancing?
4-5 METs
256
what is the metabolic equivalents for weight lifting?
5-7 METs
257
what is the metabolic equivalents for aerobic sports (cycling, tennis, basketball)?
8-10 METs
258
what is the metabolic equivalents for running?
8-12 + METs
259
CVD status and sexual activity
x
260
CVD status in regards to sexual activity can be divided into three categories. what are they?
Low risk
High Risk
Indeterminant/Intermediate Risk
261
What are low risk patients?
light intensity excercise without syx and should be able to initiate or resume sexual activity (ex include-those with few CVD risk factors, controlled hypertension, asymptomatic left ventricular dysfunction, or successful revascularization of clinically significant lesions (>50%-60%))
262
what are high risk patients?
referred for a detailed assessment prior to advising on activity. Examples include (refractory angina, NYHA class IV heart failure, significant arrythmias, severe valvular disease)
263
what are indeterminate/intermediate risk patients?
stress testing recommended to reclassify them as low or high risk and to help guide decisions
264
managment
x
265
what do you tell low risk patients about resuming sexual activity post MI?
safely resume intercourse soon after the MI, within 3-4 weeks and possibly as early as 1 week
266
Acute Pericarditis
x
267
dx
x
268
what are the EKG findigns of acute pericardiits?
diffuse ST elevation with PR depression
269
what does echo show for acute pericarditis?
pericardial effusion
270
PE
x
271
what does PE findings show Acute Pericarditis?
pleuritic CP (decreases with sitting), pericardial friction rub (highly specific)-scratchy sound heard during ventricular systole along the left sternal border
272
causes
x
273
what are the causes of acute pericarditis?
viral or idiopathic, autoimmune disease (eg SLE), uremia (acute or chronic renal failure), post MI (early: peri-infarction pericardiits; late: dressler syndrome)
274
trx
x
275
what is the treatment for acute pericarditis?
NSAIDs and colchicine for viral or idiopathic, variable for other etiologies
276
Acute Pericarditis Module
x
277
syx
x
278
what are syx of Acute Pericarditis?
sharp, retrosternal chest pain worsened with inspiration and relieved by leaning forward, fever
279
what are common preceding syx of viral Acute Pericarditis ?
preceding flu like illness , febrile over the days prior to admission
280
DDx
x
281
what is on the differential for Acute Pericarditis?
Acute MI, Pulm Embolism, PNA, GERD, MSK pain
282
initial orders
x
283
what are important initial orders for Acute Pericarditis?
IV access, Oxygen therapy, pulse ox, cardiac monitoring, EKG
284
Dx
x
285
what does EKG for Acute Pericarditis classically show?
diffuse ST segment elevation
286
PE
x
287
what do you appreciate on Physical exam for Acute Pericarditis?
pericardial friction rub
288
causes
x
289
what are causes of Acute Pericarditis?
viral agents, neoplasm, uremia, autoimmune disease, TB, bacteria, acute MI, and trauma
290
workup
x
291
what are important initial dx orders for Acute Pericarditis?
CBC (infxn, inflammation), BMP (to evaluate uremia), CXR, echo (to rule out cardiac tamponade), blood culture (in febrile patients), ESR.
292
where do you admit patient after ordering those labs for Acute Pericarditis?
into the wards
293
what are other important labs to order in Acute Pericarditis in whcih the underlying cause is not readily apparent (URI, uremia, post MI, cardiac surgery)?
ANA, HIV, TB skin testing
294
management
x
295
when is pericardiocentesis indicated in Acute Pericarditis?
if echo shows cardiac tamponade
296
what are the criteria for hospitilization of Acute Pericarditis ?
fever >100.4, cardiac tamponade, failure to respond to NSAIDs within one week, immunosuppressed, anticoagulated, acute trauma, elevated cardiac trops
297
what is initial best management for Acute Pericarditis?
NSAIDs and colchicine for idiopathic or viral pericarditis,
298
how long do you continue NSAIDs and colchicine in Acute Pericarditis?
NSAID should be continued while the patient is symptomatic . (generally <2 weeks)
colchicine should continued for 3 months
299
in which patient population of Acute Pericarditis should you avoid NSAIDs (other than aspirin)?
post-MI pericarditis
300
in which patient population of Acute Pericarditis do you use steroids as second line ?
idiopathic or viral pericariditis that is resisitant to NSAIDs and colchicine
301
in which patient population of Acute Pericarditis do you give steroids as first line trx?
in autoimmune disease Acute Pericarditis
302
if you have uremia induced Acute Pericarditis, what do you manage with ?
dialysis
303
Peri-infraction Pericarditis (PIP)
x
304
timing
x
305
when does pericardiits typically occur post MI?
<4 days following MI
306
risk
x
307
what increases the risk of developing PIP?
delayed coronary reperfusion following STEMI (eg >3 hours from symptom onset)
308
syx
x
309
what are the symptoms of PIP?
pleuritic CP that worsens with deep inspiration and improves with sitting up. Pain is usually located retrosternally and often radiates posteriorly to the bilateral trapezius ridges (lower porition of the scapulae). +/- low grade fever
310
PE
x
311
what does cardiac ausculation show?
triphasic pericardial friction rub(heard in atrial systole, ventricular systole, and early ventricular diastole
312
trx
x
313
what is the trx for those with significant discomfort?
high dose aspirin (650mg 3x/day)=analgesia and anti-inflammatory effects
314
for patients with persistent symptoms despite high dose aspirin, what is the trx?
colchicine or narcotic analgesics (eg oxycodone)
315
why is aspirin a better choice over other NSAIDs?
Other anti-inflammatory agents (eg, other nonsteroidal anti-inflammatory drugs, glucocorticoids) should be avoided as they may impair myocardial healing and increase the risk of ventricular septal or free wall rupture.
316
complications
x
317
what are the complications of PIP?
right ventricular failure (acute), papillary muscle rupture (acute or within 3-5 days), interventricular septum rupture (acute or w/n 3-5 d), free wall rupture (within 5d-2wks), left ventricular aneurysm (up to several months),
318
Right Bundle Branch Block (RBBB)
x
319
dx
x
320
what are the EKG findings of RBBB?
R prime wave (second R wave) in V1 accompanied by a widened S wave in V6
321
association
x
322
what are the associated RBBB inducing diseases?
pHTN or acute PE
323
Right Heart Strain
x
324
dx
x
325
what are EKG findings of right heart strain?
T wave inversion in Leads II,III, aVF
326
Ventral Septal Defect (VSD)
x
327
PE
x
328
what are the physical exam findings of VSD?
a harsh, 4/6 holosystolic murmur is heard at the 4th left intercostal space close to the sternal border accompanied by a thrill
329
the murmur is ___ in a small restrictive VSD, but the murmur is ___ in a large nonrestrictive VSD?
small VSD has a loud murmur
| large VSD has a soft murmur (due to equalization of right and left ventircular pressures)
330
epid
x
331
what is the epidemiology of VSD?
most common congenital heart defect at birth
332
trx
x
333
what is the trx for VSD?
spontaneous closure in 40-60% of patients during early childhood
334
syx
x
335
what are syx of VSD?
asyx
336
dx
x
337
what does the echo show for VSD?
right ventricle dilation along with enlargement of the left ventricle, left atrium, and pulmonary arteries due to volume overload in pulm circulation
338
Atrial Septal Defect (ASD)
x
339
PE
x
340
what is murmur heard on exam for ASD with large left to right shunt and normal pulm artery pressure?
wide and fixed splitting of the second heart sound
341
what is the auscultation sounds of ASD?
mid-systolic ejection murmur resulting form increased flow across the pulmonic valve, and a mild diastolic rumble from increased flow across the tricuspid valve
342
what does the murmur of ASD sound like if there is a left to right shunt?
mid- systolic murmur at the left upper sternal border with right atrial and ventricular dilation
343
pathophys
x
344
what is the pathophys of ASD?
left to right shunt with increased flow through the pulmonic valve.
345
syx
x
346
what are the syx of ASD?
most patients asyx. those with significant shunt flow have decreased excercise tolerance (dyspnea and fatigue), other complicatoins like pulm HTN, right CHF, stroke due to paradoxical embolization, atrial arrythmias (afib or aflutter)
347
dx
x
348
what does Echo show?
normal LV size and function and right atrial and ventricular dilation
349
what does EKG show?
Afib with RVR
350
Mitral Valve Prolapse (MVP)
x
351
PE
x
352
what is the murmur heard on exam for MVP?
single or multiple non ejection clicks (due to snapping of the mitral chordae as the valve cusps extend into the atrium during systole) and/or mid to late systolic murmur of mitral regurg that is best heard at or just medial to the cardiac apex.
353
what maneuvers cause the systolic murmur of MVP start earlier (and is longer and softer) from decreased venous return ?
standing, valsalva, inhalation of amyl nitrate
354
what maneuvers cause the systolic murmur of MVP to be delayed in onset (late in systole) or may not be reached at all (dissapearance of the click)?
squatting, leg elevation, and handgrip
355
pathohpys
x
356
what is the most important factor in affecting the onset of the click (early vs late) in MVP?
LVEDV (LV end diastolic volume).
- The LVEDV is relatively high with increased venous return (squatting, supine leg raise), causing a later click in systole of the MVP murmur.
- The LVEDV is relatively low with decreased venous return (eg standing, valsalva), causing an earlier click in systole of the MVP murmur
357
x
x
358
Tetralogy of Fallot (TOF)
x
359
epid
x
360
what is the frequency of Tetralogy of Fallot ?
most common cyanotic congenital heart defect
361
dx
x
362
what are the components of TOF?
right ventricular outflow tract (RVOT), overriding aorta, right ventricular hypertrophy, and VSD
363
pathophys
x
364
what is the pathophys of TOF?
as RVOT obstruction increases , it leads to decreased pulm blood flow, resulting in cyanosis early in life.
365
Tricuspid Regurgitation
x
366
PE
x
367
what is the physical exam sound of tricuspid regurg?
holosytolic murmur at the lower sternum that increases with inspiration
368
Tricuspid Valve Stenosis
x
369
dx
x
370
what is the heart murmur associated with tricuspid valve stenosis?
mid-diastolic rumble best heard along the left sternal border
371
Anomalous Coronary Artery/Anomalous Aortic Origin of a Coronary Artery (AAOCA)
x
372
syx
x
373
what are common syx
exertional angina, lightheadedness, or syncope. Sudden cardiac death in young athletes
374
epid
x
375
what population is most commonly affected?
young athletes (<35y.o. )
376
pathophys
x
377
what is the pathophys of AAOCA?
-Two types of AAOCA commonly associated with Sudden Cardiac Death are the left main coronary artery originating from the right aortic sinus (with right coronary artery also originating from the same side) and the right coronary artery originating from the
378
dx
x
379
what does the EKG of AAOCA normally show?
resting EKG is typically unremarkable
380
Brugada Syndrome
x
381
dx
x
382
what are the EKG findings of Brugada Syndrome?
- right bundle branch block
| - ST elevation in leads V1-V3
383
Long QT syndrome
x
384
dx
x
385
what are the EKG findings of Long QT syndrome?
Men: QTc>450 ms
Women: QTc>470 ms
386
syx
x
387
what is an uncommon presentation of long QT syndrome?
sudden cardiac death
388
Hypertrophic Obstructive Cardiomyopathy (HOCM)
x
389
epid
x
390
what population is most commonly affected?
young athletes
391
what is the most common cause of sudden SCD in young athletes?
HOCM
392
genetics
x
393
what is the genetic mutaiton?
myosin gene
394
dx
x
395
what do you see on EKG?
LV hypertrophy ( Add the R wave in aVL and the S wave in V3. If the sum is greater than 28 millimeters in males or greater than 20 mm in females, LVH is present. Or look at increased voltage in precordial leads (V1-V5)
396
what do you see on Echo?
small left ventricular cavity, LV hypertrophy (often asymmetric and involving the septum), and increased LV outflow tract gradient pressure that increases with valsalva.
397
what else do you see on echo for HOCM?
echo shows left atrial enlargement , intraventricular septal thickness increased, and posterior left ventricular wall thickness increased. There is a systolic anterior moition of the mitral valve.
398
PE
x
399
what do you hear on PE for HOCM?
harsh crescendo-decresendo systolic murmur heard best at the apex and lower left sternal border.
murmur increases in intensity with valsalva and also when rising from sitting or squatting position
400
what maneuvers increase murmur intensity?
decrease preload: which decrease LV Blood volume: valsalva, abrupt stending , nitroglycerin administration
401
what maneuvers decrease murmur intensity?
increase afterload: sustained hand grip
squatting: increase afterload and preload
passive leg raise: increase preload
All increase LV blood volume, which decrease murmur intensity
402
Syx
x
403
what are the symptoms of HOCM?
asyx or severe fatigue, exertional dyspnea, CP, palpitations, presyncope, or syncope
404
Trx
x
405
what is the treatment of HOCM?
negative inotropic agents (beta blockers, verapamil or disopyramide)
usually start with beta blockers and then add verapamil or disopyramide
406
what is the treatment in those with refractory HOCM?
-Alcohol septal ablation (injecting ethanol into the first or second septal perforator artery to cuase a localized MI in the basal septum leading to localized scarring and remodeling over time and leads to a reduction in LVOT gradient with improvment in s
407
what are indications for ICD (implantable cardioverter -defibrillator)?
prevention of SCD in patients with hx of cardiac hx or sustained VT. HCM patients have high risk of malignant arrythmias (fam hx of SCD, recurrent or exertional syncope, nonsustained VT, hypotension w excercise, extreme LVH)
408
Constrictive Pericarditis
x
409
cause
x
410
what is the cause of constrictive pericarditis?
- idiopathic or viral pericarditis
- cardiac surgery or radiation therapy
- TB pericarditis (in endemic areas)
411
syx
x
412
what are the symptoms?
fatigue, DOE, peripheral edema
413
PE
x
414
what are the physical exam findings of constrictive pericarditis?
increased JVD, pericardial knock (mid diastolic sound) may be heard, pulsus paradoxus, kussmaul's sign (increa or lack of decrease in JVP on inspiration), hepatic congestion with hepatomegaly
415
what does cardiac auscultation show?
mid diastolic murmur
416
dx
x
417
what are EKG findings for constrictive pericarditis?
nonspecific or show atrial fibrillation or low voltage QRS complex
418
what are CXR findings for constrictive pericarditis?
calcified cardiac borders
419
what does jugular venous pulse tracings show?
prominent x and y descents
420
what does echo show for constrictive pericarditis?
pericardial thickening and calcification , atrial enlargement, and abnormal septal motion
421
what is considered elevated JVD?
>8cm H20
422
risk
x
423
what is a common risk for constrictive pericarditis?
post op from CABG
424
pathophys
x
425
what is the pathophys of constrictive pericarditis post CABG surgery?
post pericardial effusions commonly form and eventually continued inflammation over months may lead to development of thickened, fibrous pericardium and constrictive pericarditis
426
trx
x
427
what are the treatment options for constrictive pericarditis?
- supportive care (anti-inflammatory agents)
| - pericardiectomy for refractory causes
428
Amiodarone Toxicity
x
429
side effects
x
430
what are side effects of amiodarone?
thyroid dysfunction, hepatotoxicity, cardiac bradyarryhtmias, chronic interstitial pneumonitis, neuorlogic symptoms (eg ataxia, peripheral neuropathy), blue-gray skin discoloration, and visual disturbances.
431
timeline
x
432
what is the timeline for amiodarone toxicity?
prolonged treatment
433
syx
x
434
what are syx of amiodarone toxicity?
photosensitivity, skin discoloration, bone marrow suppression, thyroid dysfunction, abnormal liver function tests, and pulmonary toxicity
435
Pulmonary Toxicity from Amiodarone
x
436
forms
x
437
what are forms of Pulmonary Toxicity from Amiodarone?
chronic interstitial pneumonitis, organizing pneumonia, acute respiratory distress syndrome, and rarely with a solitary pulmonary mass
438
which is the most common form of Pulmonary Toxicity from Amiodarone?
Chronic interstitial pneumonitis,
439
Chronic interstitial pneumonitis
x
440
features
x
441
what are features of Chronic interstitial pneumonitis?
nonproductive cough, fever, pleuritic chest pain, weight loss, dyspnea on exertion and a focal or diffuse interstitial opacity on the chest radiograph
442
risk
x
443
what is the risk dose of amiodarone to lead to pulm toxicity?
higher maintenance doses (more than 400 mg/day)
444
management
x
445
what is the mainstay of management of Pulmonary Toxicity from Amiodarone?
`Discontinuation of amiodarone is the mainstay of treatment for amiodarone-induced pulmonary toxicity
Corticosteroids can be used in patients with severe or life-threatening pulmonary disease
446
prognosis
x
447
what is the prognosis of Pulmonary Toxicity from Amiodarone?
good , majority of patients either stabilize or improve after the complete withdrawal of the drug
448
Cardiac Amyloidosis
x
449
dx
x
450
what would EKG show?
low voltage on EKG
451
what woudl Echo show?
increased ventricular wall thickness with normal LV cavity dimensions
452
syx
x
453
what do syx of cardiac amyloidosis show?
unexplained CHF
454
Superior Vena Cava Syndrome
x
455
pathophys
x
456
what is the pathophys of SVC Syndrome?
obstruction of blood flow (typically due to external compression from a tumor)
457
syx
x
458
what are the SVC syndrome syx?
facial swelling, JVD, distended chest wall veins
459
Blunt Cardiac Injury
x
460
risk
x
461
what is the major risk of blunt cardiac injury?
Motor Vehicle Collision
462
syx
x
463
what are the syx of Blunt Cardiac Injury?
acute heart failure, cardiac arrythmias, myocardial ruputure, superficial injuries across chest
464
complications
x
465
what are the complications of blunt cardiac injury?
pericardial effusion, tamponade, and cardiogenic shock
466
what are the rapidly fatal injuiries in blunt cardiac injury?
pneumothorax, aortic dissection, hemoperitoneum, pericardial effusion leading to tamponade
467
dx
x
468
what is the best initial dx test to rapidly identify rapidly fatal injuires in blunt cardiac injury?
FAST (bedside U/S)
469
what happens to cardiac biomarkers in blunt thoracic trauma?
elevated troponins (non specific)
470
what are the best proceeding dx test to after FAST to identify rapidly fatal injuires in blunt cardiac injury?
CXR, CT scan of chest
471
PE
x
472
what are the physical exam findings of blunt cardiac injury?
bruises over the anterior chest
473
x
x
