Cardiology Flashcards
1
Q
Jugular Venous Distention
A
> 7cm above sternal angle
- suggests right HF, pulmonary HTN, volume overload, tricuspid regurgitation, pericardial disease
2
Q
Hepatojugular reflex
A
- fluid overload
- impaired right ventricular compliance
3
Q
Kussmaul’s sign
A
- increased JVP with inspiration suggests: - right ventricular infarction - post-op cardiac tamponade - tricuspid regurgitation - constrictive pericarditis
4
Q
Aortic stenosis
A
- harsh systolic ejection murmur that radiates to carotids
5
Q
Mitral regurgitation
A
- holosystolic murmur that radiates to the axilla or carotids
6
Q
Mitral valve prolapse
A
- midsystolic or late systolic murmur with a preceding click
7
Q
Flow murmur
A
- very common
- doesn’t imply cardiac disease
8
Q
Aortic regurgitation
A
- early decrescendo diastolic murmur
9
Q
Mitral stenosis
A
- mid to late, low-piched diastolic murmur
10
Q
S3 gallop
A
- dilated cardiomyopathy (floppy ventricle)
- often normal in younger patient and in high output states (e.g. pregnancy)
- mitral valve disease
11
Q
S4 gallop
A
- seen in hypertension
- diastolic dysfunction (stiff ventricle)
- aortic stenosis
- often normal in younger patients and in athletes
12
Q
Pulmonary edema
A
- left heart failure (fluid “backs up” into lungs
13
Q
Peripheral edema
A
- right heart failure
- biventricular failure (fluid “backs up” into the periphery)
- Peripheral Venous Disease
14
Q
Increased peripheral pulses
A
- compensated aortic regurgiation
- coarctation (arms > legs)
- PDA
15
Q
Decreased peripheral pulses
A
- peripheral arterial disease
- Late stage heart failure
16
Q
Pulsus Paradoxus
A
- decreased systolic BP with inspiration seen in: - pericardial tamponade - COPD and asthma - Tension pneumothorax - Foreign body in airway
17
Q
Pulsus alternans
A
- alternating weak and strong pulses
- cardiac tamponade
- LV systolic function
- Poor prognosis
18
Q
Pulsus parvus et tardus
A
- Weak and delayed pulse
- Aortic stenosis
19
Q
CHF
A
- caused by inability of heart to pump enough blood to maintain fluid and metabolic homeostasis
- risk factors: CAD, HTN, cardiomyopathy, valvular heart disease
20
Q
Systolic Dysfunction
A
- decreased EF (< 50%)
- increased LV EDV
- caused by inadequate LV contractility or increased afterload
21
Q
Management options for A-Fib
A
"ABCD" A-anticoagulate B- beta blockers C- cardiovert/calcium channel blockers D- digoxin
22
Q
Hx and PE: CHF
A
- exertional dyspnea is earlist and most common symptom
- can progress to orthopnea, paroxysmal nocturnal dyspnea
- S3/S4 gallop, JVD, and peripheral edema
23
Q
Sinus bradycardia: etiology
A
- normal response to cardiovascular conditioning
- result form sinus node dysfunction
- from B-blockers or calcium channel blockers
24
Q
Sx: sinus bradycardia
A
- may be asymptomatic
- present w/ lightheadedness, syncope, chest pain, or hypotension
25
Ecg findings: sinus bradycardia
- sinus rhythm
| - ventricular rate < 60 bpm
26
1st degree AV block: etiology
- can occur in normal individuals
| - associated with incr. vagal tone and with B-blocker or CCB use
27
1st degree AV block: signs/sx
asymptomatic
28
1st degree AV block: ECG findings
PR interval > 200msec
29
Tx: 1st degree AV block
None necessary
30
Etiology: 2nd degree AV block
- Drug effects (digoxin, B-blockers, CCBs)
- Incr. vagal tone
- Right coronary ischemia or infarction
- usually asymptomatic
31
ECG: 2nd degree AV block (Mobitz I)
- Progressive PR lengthening until a dropped beat occurs;
| the PR interval then resets
32
Tx: 2nd degree AV block (Mobitz I)
- stop offending drug
| - atropine as clinically indicated
33
Etiology: 2nd degree Av block (Mobitz II)
- results from fibrotic disease of conduction system or acute, subacute, or prior MI
34
Sx: 2nd degree AV block (Mobitz II)
- Occasionally syncope
| - Frequent progression to third degree AV block
35
ECG findings: 2nd degree AV block (Mobitz II)
Unexpected dropped beat(s) w/o a change in PR interval
36
Tx: 2nd degree AV block (Mobitz II)
Pacemaker placement
37
Etiology: 3rd degree AV block (complete)
- no electrical communication btwn the atria and ventricles
38
Sx: 3rd degree AV block (complete)
- syncope
- dizziness, acute heart failure
- hypotension
- cannon A waves
39
ECG findings: 3rd degree AV block (complete)
No relationship between P waves and QRS complexes
40
Tx: 3rd degree AV block (complete)
Pacemaker placement
41
Etiology: sick sinus syndrome/tachycardia-bradycardia syndrome
Heterogenous disorder that leads to intermittent supraventricular tachy- and bradyarrhythmias
42
Sx: Sick sinus syndrome/ tachycardia -bradycardia syndrome
- Secondary to tachycardia or bradycardia;
| May include syncope, palpitations, dyspnea, chest pain, TIA, and stroke
43
Tx: sick sinus syndrome/ tachycardia-bradycardia syndrome
Pacemaker placement
44
Etiology: sinus tachycardia
normal physiologic response to fear, pain and exercise
| - can be secondary to hyperthyroidism, volume contraction, infection or pulmonary embolism
45
Sx: sinus tachycaria
- palpitations
| - SOB
46
ECG findings: sinus tachycardia
- sinus rhythm
| - ventricular rate > 100 bpm
47
Tx: sinus tachycardia
- treat the underlying cause
48
Etiology: atrial fibrillation
```
Acute AF: "PIRATES"
P-pulmonary disease
I- ischemia
R- rheumatic disease
A - anemia/atrial myxoma
T - thyrotoxicosis
E - ethanol
S - sepsis
```
49
Sx: atrial fibrillation
- often asymptomatic
- may present w/ SOB, chest pain, or palpitations
- irregularly irregular pulse
50
ECG findings: atrial fibrillation
no discernible P waves with variable and irregular QRS response
51
Tx: atrial fibrillation
- Estimate risk of stroke using CHADS2 score
- anticoagulate if score > 48 hrs ( to prevent CVA)
- rate control (B-blockers, CCBs, digoxin)
- Initiate cardioversion only if only new onset
52
Etiology: atrial flutter
- Circular movement of electrical activity around atrium at a rate of approx 300 times per minute
53
Sx: atrial flutter
- usually asymptomatic, but can present with palpitations, syncope, and lightheadness
54
ECG findings: atrial flutter
Regular rhythm
"sawtooth appearance" of P waves can be seen
- atrial rate is usually 240-32 bpm and the ventricular rate ~ 150 bpm
55
Tx: atrial flutter
anticoagulation,
rate control
cardioversion guidelines
56
Etiology: multifocal atrial tachycardia
multiple atrial pacemakers or reentrant pathways
| - COPD and hypoxemia
57
Sx: multifocal atrial tachycardia
- may be asymptomatic
| - at least 3 different P wave morphologies
58
ECG findings: multifocal atrial tachycardia
- 3 or more unique P wae morphologies
| - rate > 100 bpm
59
Tx: multifocal atrial tachycardia
- treat underlying disorder
| - verapamil or B-blockers for rate control and suppression of atrial pacemakers (not very effectors)
60
Etiology: atrioventricular nordal reentry tachycardia (AVNRT)
- a reentry circuit in the AV node depolarizes the atrium and ventricle simultaneously
61
Sx: AVNRT
```
palpitations
SOB
Angina
Syncope
Lightheadedness
```
62
ECG findings: AVNRT
- rate 150 - 250 bpm
| - P wave is often buried in QRS or shortly after
63
Tx: AVNRT
- cardiovert if hemodynamically unstable
| - carotid massage, Valsalva, or adenosin can stop the arrhythmia
64
Etiology: atrioventricular reciprocating tachycardia (AVRT)
- an ectopic connection between the atrium and ventricle that causes a reentry circuit
- seen in WPW
65
Sx: AVRT
- palpitations
- SOB
- angina
- lightheadedness
- syncome
66
Tx: AVRT
Cardiovert vs. procainamide
- blockage of AV node (CCBs, adenosines, digoxin)
thru ectopic P waves
67
Ecg: AVRT
- Retrograde P wave is often seen after a normal QRS
| - pre-excitation delta wave is characteristically seen in WPW
68
Mitral stenosis
mid diastolic rumbling murmur heard at apex
| - can often lead to LA dilitation
69
Atrial fibrillation
- irregularly irregular rhythm and loss of P waves
70
Aortic dissection
- presents with tearing chest pain radiating to back
| - may include cardiac tamponade, acute aortic regurgitation stroke, and renal failure
71
Order of ECG
1. Rate
2. Rhythm (P wave before QRS complex)
3. Axis
72
Normal Axis on ECG
1. Upright QRS on leads I and AVF
73
Left-axis deviation
Upright QRS in lead I and downward QRS
| * up to -30 degrees is normal variant
74
Right axis deviation
A downward QRS in lead I and upright QRS lead in AVF (up to +105 degrees is considered nrl variant)
75
Normal intervals
PR interval btwn 120 and 200ms
| QRS < 120 msec
76
AV block
PR > 200msec
| P with no QRS afterwards
77
Left bundle branch block
1. QRS > 120msec
no R wave in V1
tall R waves in I, V5, V6
78
Right bundle branch block on ECG
QRS duration > 120 msec
RSR' complex ("rabbit ears")
qR or R morphology with wide R wave in V1
QRS pater with a wide S wave I, V5, V6
79
Long QT syndrome on ECG
QTc > 440msec
| - underdiagnosed congenital disorder that predisposes to ventricular tachyarrhythmias
80
Ischemia on ECG
new inverted T wave
poor R wave progression in precordial leads
ST segment changes (elevation or depression)
81
Transmural infarct on ECG
Significant Q waves > 40msec or more than 1/3 of the QRS amplitude
ST elevations with T wave inversions
82
Atrial enlargement: right atrial abnormality (P pulmonale)
P wave amplitude in lead II is > 2.5 mm
83
Left atrial enlargement on ECG
P wave width in lead II is > 120 msec or
terminal negative deflection in V1 is > 1mm in amplitude and > 40msec in duration
Nothced P waves can be frequently seen in lead II
84
Signs of LVH on ECG
- amplitude of ( S in V1 )+ (R in V5 or V6 )is > 35mm
OR:
- amplitude of R in AVL + S in V3 is > 28mm
85
Right ventricular hypertrophy
right axis deviation and R wave in V1 > 7mm
86
College age male "passed out" while playing basket ball and had no prodromal symptoms or signs of seixure. His cardiac exam is unremarkable. ECG shows a slurred upstroke of QRS. Next step?
Wolf-Parkinson Syndrome
- advise against vigorous physical activity
- treat arrhythmias w/ procainadmide
- refer for electrophysiology study
87
Systolic dysfunction
- decreased EF (< 50%) and increased LEDV
88
Etiology of systolic dysfunction
- Inadequate left ventricular contractility or increased afterload
- headrt compensated for decr. EF and increased preload through hypertrophy and ventricular dilitation
- eventually compensation fails leading to incr. myocardial work and worsening systolic dysfunction
89
CHF: Hx
Exertional dyspnea is earliest and most common presenting symptom
- progresses to orthopnea, paroxysmal nocturnal dyspnea (PND) and rest dyspnea
90
CHF: PE
- parasternal lift
- an elevated and sustained LV impulse
- S3/S4 gallop
- Peripheral edema
91
Man was admitted for CHF exacerbation w/ low EF
| Patient now ready for discharge, and his meds include furosemide and metoprolol. Next step in management?
```
Add ACE inhibitors to current regiment
- ACEis have positive mortality benefit when used with beta blockers in NYHA class II-IV heart failure patients
```
92
CHF: Diagnosis
- clinical syndrome
- CXR: shows cardiomegaly, cephalization of pulm vessels, vascular congesion
- Echo: decr. EF and ventricular dilitation
93
Lab values associated w/ CHF
BNP > 500 pg/mL
- increased creatinine
- decreased sodum
94
Acute CHF Management
LMNOP
- Lasix
- Morphine
- Nitrates
- Oxygen
- Position (upright)
95
Acute treatment of CHF
1. Treat underlying cause (e.g. arrhytmias, MI and drugs)
2. Diurese aggressively with loop and thiazide diuretics
3. Give diuretics to patients who can tolerate them
4. Use LMNOP for pulmonary congestion
96
NYHA Class I
no limitation of activiy
| no symptoms w/ normal activity
97
NYHA Class II
Slight limitation of activity
| Comfortable at rest or w/ mild exertion
98
NYHA Class III
Marked limitation of activity
| Comfortable only at rest
99
NYHA Class IV
Any physical activity brings on discomfort;
| symptoms present at rest
100
Chronic Tx of CHF
- Long term B-blockers and ACEis/ ARBS help prevent remodeling of heart and decrease mortality for NYHA Class II-IV
- daily ASA and statin if underlying cause of prior MI
- Chronic diuretics (loops +/- thiazides)
- low dose spironolactone decr mortality risk in patients
101
When should you consider ICDs in CHF patient?
Patients w/ EF < 35%
102
Systolic dysfunction: common factors
```
Pts < 65 y/o
Co-morb: Dilated cardiomyopathy, valvular heart dz
PE: Displaced PMI, S3 gallop
CXR: Pulmonary congestion, cardiomegaly
ECG/Echo: Q waves, decr (< 40%)
```
103
Nonsystolic dysfunction: common characteristics
Often > 65 y/o
Co-morb: Restrictive or hypertrophic cardiomyopathy, renal dz, or HTN
PE: Sustained PMI, S4 gallop
CXR: Pulmonary congestion, normal heart size
ECG/Echo: LVH, normal EF (> 55%)
104
Left-Sided CHF: symptoms
1. Left sided S3/S4 gallop
2. Bilateral basilar rates
3. Pleural effusions
4. Pulmonary edema
5. Orthopnea, paroxysmal nocturnal dyspnea
105
Right-Sided CHF: symptoms
1. Right sided S3/S4 gallop
2. JVD
3. Hepatojugular reflex
4. Peripheral edema
5. Hepatomegaly, ascites
106
Loop diuretics
- acts on Loop of Henle
107
Loop diuretics : mechanism of actiion
- decreases Na/K/2CL co-transported
- decreases urine concentration
- increases calcium excretion
108
Loop diuretics: side effects
- Ototoxicity
- Hypokalemia
- Hypocalcemia
- Dehydration
- Gout
109
Thiazide diuretics: sites of action
Early distal tubule
110
Thiazide: mechanism of action
- decreases NaCL reabsorption leading to decreased diluting capacity of nephron;
- decreased Ca excretion
111
Thiazide: side effects
```
Hypokalemic metabolic alkalosis
Hyponatremia
HyperGLUC
- hyperglycemia
- hyperlipidemia
- hyperuricemia
- hypercalcemia
```
112
K-sparing agents
spironolactone
triamterene
amiloride
113
K-sparing agents: site of action
cortical collecting tubule
114
Spironolactone: MOA
- aldosterone receptor antagonist
115
Triamterene and Amiloride
Block Na channels
116
K-sparing agents: side effects
- Gynceomastia
- Hyperkalemia
- Sexual dysfunction
117
Carbonic anhydrase inhibitors
Acetazolamde
118
Carbonic anhydrase inhibitors: Site of aCtion
Proximal convoluted tubule
119
Carbonic anhydrase inhibitors: MOA
NaHCO3 diuresis decreases total body NaHCO2
120
Carbonic anhydrate inhibitors: Side effect
Hypercholeric metabolic acidosis
Neuropathy
NH3 toxicity
Sulfa allergy
121
Osmotic agents
mannitol
122
Osmostic agents: site of action
proximal tubule
123
Osmotic agents: MOA
Creates increased tubular fluid osmolaity, leading to increased urine flow
124
Osmotic agents: side effects
Pulmonary edema
Dehydration
Contraindicated in anuria and CHF
125
Nonsystolic dysfunction: Hx and PE
- associated with stable and unstable angina
- SOB
- Dyspnea on exertion
- Arrhythmias
- Heart failure
- Sudden failure
126
Nonsystolic dysfunction: Tx
Diuretics (first line therapy)
- Maintain rate and BP via B-blockers, ACEis, ARBs, or CCBs
- Digozxin is not useful in patients
127
S3 gallops
signifies rapid ventricular filling in the setting of fluid overload and is associated w/ dilated cardiomyopathy
128
Loop diuretics vs Thiazide
Loops LOSE Calcium
| Thiazides take it in Ca
129
Common causes of dilated cardiomyopathy
- Ischemia
| - Long standing hypertension
130
Drugs associated w/ dilated cardiomyopathy
Doxorubicin
AZT
Cocaine
131
Infection associated w dilated cardiomyopathy
- Coxsackievirus
- HIV
- Chagas' disease
- Parasites
132
Dilated Cardiomyopathy: Hx and PE
- often presents w/ gradual sx of CHF
- displacement of LV impulse
- S3/S4 gallop
- Mitral/tricuspid regurgitation
133
Dilated Cardiomyopathy
- impaired contractility
- very increased LV- EDV
- very increased LV - ESV
- very decreased EF
- decreased wall thickness
134
Hypertrophic cardiomyopathy
- impaired relaxation
- decreased LV - EDV
- very decreased LV - ESV
- increased or unchanged EF
- very increased wall thickness
135
Restrictive Cardiomyopathy
- impaired elasticity
- increased LV - EDV
- increased LV - ESV
- decreased or normal EF
- increased wall thickness
136
Dilated Cardiomyopathy: Diagnosis
1. ECHO
2. ECG show ST-T changes, low voltage WRS, sinus tachycadia, and ectopy (LBBB is comon)
3. CXR show enlarged balloon-like heart and pulm congestion
137
Dilated cardiomyopathy: Tx
Address underlying etiology
- treat sx with CHF meds (ACEis/ARBs and B-blockers)
- AVOID CCBs in heart failure
- Consider anticoagulation to decr thrombus risk if AF or IV thrombus
- Consider ICD if < 35%
138
A woman w/ hypertension and prior MI has an exam notable for displaced PMI, S3, nonelevated JVP and bibasilar rale. Next best step in dx?
Dilated cardiomyopathy
| - next best step is echocardiogram
139
Common HOCM scenario
most common cause of sudden death in young, healthy athletes in the United States
140
Hypertrophic Cardiomyopathy
- impaired LV relaxation and filling (nonsystolic dysfunction)
- involves interventricular septum
- leading to LV outflow tract obstruction and impaired ejection of blood
141
Hypertrophic cardiomyopathy: Hx and PE
- may be assymptomatic byt present w/ dyspnea, palpitations, angina or sudden cardiac death
- sustained apical impulse, S4 gallop
- crescendo-decrendo systolic murmur increases w/ decreases preload
142
Hypertrophic cardiomyopathy: Dx
Echocardiogram - show asymmetrical septum and obstruction of blood flow
- ECG shows LVH
- CXR reveal left atrial enlargement 2/2 mitral regurgitation
143
Hypertrophic cardiomyopathy: Tx
B-blockers are initial therapy for symptomatic relief: CCBs are second line
- surgical ablation: dual chamer pacing, partial excision or alcohol ablation
- should avoid intense competition
144
Hypertension
systolic BP > 140 mmg Hg and/or diastolic BP > 90 mm Hg based on 2 measurements separated by time
145
Hypertension: Hx and PE
- asymptomatic until complications
- pts should be evaluated for end-organ damage to brain, eye, heart, and kidneys
- renal bruits may signify stenosis
146
Ocular signs of hypertension
Cotton-wool exudates
| Hemorrhage
147
Heart signs of hypertension
LVH
148
Renal signs of HTN
Proteinuria
| Chronic kidney disease
149
Neuro signs of HTN
- Stroke
| - Dementia
150
Dx of HTN
To assess extent of end-organ damage
- Obtain UA
- BUN/CR
- CBC
- Electrolytes
151
Tx of HTN
After ruling on secondary causes:
1. Lifestyle modifications
2. Diuretics, ACEis and B-blockers decrease mortablity in uncomplicated HTN
3. Periodically test for end-organ damage
152
Tx for Stage 2 HTN (SBP > 160 or DBP > 100)
Two drug combo
| - thiazide plus ACEi, ARB, B-blocker, or CCB
153
Tx of HTN
```
ABCD
ACEIs/ARBs
B-blockers
CCBs
Diuretics
```
154
Causes of 2 hypertension
```
CHAPS
Cushing's Syndromes
Hyperaldosteronism
Aortic coarctation
Pheochromocytopma
Stenosis of renal arteries
```
155
Primary Renal Disease
-often unilateral renal parenchymal disease
156
Management of primary renal disease
treat w/ ACEis which slow progression of disease
157
Renal artery stenosis
especially common in patients < 25 and > 50 o age with recent onset hypertension
- include fibromuscular dysplasia (younger patients) and atherosclerosis (older patients)
158
Mgmt renal artery stenosis
Diagnose w/ MRA or Renal Artery Dopplyer
- Treat w/ angioplasty or stenting
- Consider stenting in undilateral diz
159
Why should ACEis be used in renal artery stenosis?
ACEis can accelerate kidney failure by preferential dilation of efferent arteriole
160
OCP use in HTN
Common in woman > 35 yo, obse woman and those w. longstanding use
161
Tx of OCP associated HTN
Discontinue OCPs - effect may be delayed
162
Pheochromocytoma
adrenal gland tumor that secretes epinepherine and norepipnepherine
- leads to episodic headaches
- sweating
- tachycardia
163
Mgmt of pheochromocytoma
Diagnose with urinary metanepherine and catecholemine levels or plasma metanepherine
- Surgical removal of tumor after tx with both alpha and beta blockers
164
When removing pheochromocytoma what should be done?
Administer both alpha and beta blockers before surgical removal of tumor
165
Conn's syndrome (hyperaldosteronism)
Most often secondary to aldosterone producing adrenal adenoma
166
Conn's syndrome triad
- Hypertension
- Unexplained hypokalemia
- Metabolic alkalosis
167
Conn's syndrome management
Metabolic workup w/ plasma aldosterone and renin level
- increased aldosterone and decreased renin levels suggest hyperaldosteronism
- Surgical removal of tumor
168
Cushing's syndrome
due to ACTH producing pituitary tumor OR
ectopic ACTH-secreting tumor
cortisol secretion by adrenal adenoma or carcnoma
also cause by exogenous steroids
169
Tx of Cushing's syndrome
Surgical removal of tumor
| Removal of exogenous tumor
170
Hypertensive Crisis
clinical presentation of elevated BPs leads to end organ damage
171
Hypertensive Crisis: History and PE
present w/ end-organ damage revealed by renal disease, chest pain (ischemia or MI), back pain (aortic dissection) or changes in mental status (hypertensive encepholapty)
172
Hypretensive urgency: Dx
Elevated BP with mild to moderate sx (headache, chest pain) w/o end organ damage
173
Hypertensive emergency: Dx
Elevated BP with signs or symptoms of impending end-organ damage such as acute kidney injury, intracranial hemorrhage, papilledema or ECG changes suggestive of ischemia
174
Hypertensive urgency: Tx
can be treated w/ oral hypertensive with goal of gradually lower BP over 24-48 hrs
175
Hypertensive emergencies: tx
Treat w/ IV meds (labetalol, nitroprusside, nicardipine) w/ goal of lowering MAP by no more than 25% over first 2 hrs to prevent cerebral hypoperfusion on coronary insufficiency
176
NSTEMI
- chest pain at rest
- absence of ST elevation on EKG
- elevated biomarkers of myocardial injury
- ST depression on EKG
177
Acute pericarditis diagnosis
2 of 3 classic features:
- pleuritic chest pain
- friction rub (can be squeaky, scratchy or high pitched)
- diffuse concordant ST-segment elevation on EKG
178
Management of STEMI
- Percutaneous Angioplasty and stent placement are preferred therapies
179
STEMI
- chest pain at rest
- elevated cardiac biomarkers
- ST-segment elevation in inferior leads II, III, aVF
180
Contraindications to thrombolytic therapy
- Prior intracranial hemorrhage
- Ischemic stroke within 3 months
- Suspected aortic dissection
- Active bleeding
181
Ischemic heart disease
- chest pain in relation to exercise and relief with rest of nitroglycerin
182
Right ventricular MI
- hypotension
- clear lung fields
- elevated CVP
* * ST segment elevation on right sided EKG
183
Treatment of right ventricular MI
Volume expansion (w/ normal saline)
184
First step in management of esophageal noncardiac chest pain
Prescribe PPI
185
Third degree block
- complete absence of conduction of atrial impulses to ventricles (no P waves)
- most common cause of marked bradycardia
186
Lyme carditis
- presence of skin rash (erythema migrans) with known hx of tick bite (presence in endemic regions)
- caused by Borrelia burgdoferi
- manifested by acute, high grade AV conduction defects occasionally associated with myocarditis
187
Panic disorder
- recurrent, unexpected panic attacks that feature abrupt onset of numerous somatic symptoms such as palpitations, sweating, tremulousness, dyspnea, chest pain, nausea, dizziness, and numbness
188
Mobitz type I (second degree AV block)
progressive prolongation of PR interval until dropped beat occurs
189
Mobitz type II second degree AV block
regularly dropped beat (i.e. nonconducted P wave every 2nd or 3rd beat) without progressive prolongation of PR interval
190
Therapy for chronic stable CAD
Anti-anginals: B-blockers, CCBs, and nitrates
| Vascular protective: aspirin, ACE, and statins
191
B-blockers in tx of chronic stable angina
should be titrated to achieve resting heart rate of approximately 55 - 60 /min and approximately 75% of heart rate
192
Sx of pulmonary embolism
- assymetric leg edema
- elevated CVP
- tachypnea and tachycardia
193
Best diagnostic test
Pulmonary embolism
194
Causes of pericarditis
```
CARDIAC RIND
Collagen vascular disease
Aortic dissection
Radiation
Drugs
Infections
Acute renal failure
Cardiac (MI)
Rheumatic fever
Injury
Neoplasms
Dressler's syndrome
```
195
Pericarditis
- inflammation of the pericardial sac
| - can compromise cardiac output via tamponade or constrictive pericarditis
196
Pericarditis: Hx and PE
- may present pleuritic chest pain, dyspnea, cough and fever
- chest pain tends to worsen in supine position and w/ inspiration
- exam reveals pericardial rub
- elevated JVP and pulsus paradoxus
197
Pericarditis: Diagnosis
CXR, ECG and echo to r/o MI and pneumonia
- EKG changes include DIFFUSE ST-SEGMENT ELEVATION AND PR-SEGMENT DEPRESSIONS followed by T-wave inversions
- pericardial thickening or effusion may be evident
198
20 y/o M presents with an initial BP of 150/85 mm Hg and repeat measurement yields 147/85 mm Hg. Potassium level is 3.2 mg/dl Next step?
Hyperaldosteronism workup with serum aldosterone and renin levels is an appropriate next diagnostic step
199
Hypertensive crises are diagnosis on what basis?
Basis of end-organ damage, not BP measurement
200
B-blockers
- decrease cardiac contractility and renin release
201
B-blockers: side effects
Bronchospasm (in severe active asthma), bradycardia, CHF exacertbation, impotence, fatigue, depression
202
ACE inhibitors (e.g. captopril, enalapril, fosinopril, benzanapril)
block aldosterone formation, reducing peripheral resistance and salt/water retention
203
ACE inhibitors: side effects
Cough, rashes, leukopenia, hyperkalemia
204
ARBs (e.g. losartan, valsartan, irebsartaN
Block aldosterone effect, reducing peripheral resitance and salt/water retention
205
ARBs: side effects
Rashes
Leukopenia
Hyperkalemia but no cough
206
Calcium channel blockers
| e. g. dihydropyridines -- nifedipine, felodipine, amlodipine
(e. g. nondihydropyridines -- diltiazem, verapramil)
decreased smooth muscle tone and cause vasodilation;
| may also decrease cardiac output
207
Calcium channel blockers: side effects
Dihydropyridines: headaches, flushing, peripheral edema
Nondihydropyridines: decreased contractility
208
Vasodilators (e.g. hydralazine, minoxidil)
decrease peripheral resistance by dilating arteries/arterioles
209
Vasodilators (e.g. hydralazine, minoxidil)
Hydralazine: headache, lupus-like syndrome
Minoxidil: orthostasis, hirsuitism
210
Alpha1- adrenergic blockers (e.g. prazosin, terazosin, phenoxybenzamine)
cause vasodilation by blocking actions of norepinepherine on vascular smooth tone
211
Alpha 1 adrenergic blockers: side effects
Orthostatic hypotension
212
Centrally acting adrenergic agonists (e.g methyldopa, clonidine)
inhibit sympathetic nervous system via centrial alpha 2 adrenergic receptors
213
Centrally acting adrenergic agonists
somnolence
Orthostatic hypotenson
Impotence
Rebound hypertension
214
Pericarditis: Tx
- address underling cause (e.g steroids for SLE, dialysis for uremia) or sx (ASA for post-MI carditis)
- pericardial effusions w/o symptoms can be monitored by evidence of tamponade
215
Cardiac tamponade
excess fluid in the pericardial sac, leading to compromised ventricular filling and decreased cardiac output
- rate of fluid formation is more important than size
216
Risk factors for cardiac tamponade
```
Pericarditis
Malignancy
SLE
TB
Trauma (stab wounds medial to left nipple)
```
217
Cardiac tamponade: Hx and PE
- presents with fatigue, dyspnea, anxiety, tachycardia, and tachypnea that progresses from shock to death
- Beck's triad (hypotension, JVD, and muffled heart sounds)
- narrow pulse pressure, pulsus paradoxus, and Kussmaul's sign (JVD on inspiration)
218
Cardiac tamponade: diagnosis
Echo shows right atrial and right ventricular diastolic collapse
- CXR shows enlarged, globular, water bottled shaped heart w/ large effusion
- Electrical alternans on ECG
219
Cardiac tamponade: Tx
- Aggressive volume expansion w/ IV fluids
- urgent pericardiocentesis (aspirate will be nonclotting blood)
- decompensation may warrant pericardial window
220
Aortic stenosis: Etiology and Hx
- most often seen in elderly
- unicuspid/bicuspid valves leads to earlier presentation
- may be asymptomatic for years
- once symptomatic progresses from angina --> CHF --> syncope within 5 years
221
Aortic Stenosis: Ex
PE: pulsus parvus et tardus (weak, delayed, carotid upstroke) and paradoxically split S2 sound
- systolic murmur radiating to carotids
Dx: Echocardiogram
222
Aortic Stenosis: Tx
Aortic valve replacement
223
ACUTE Aortic regurgitaton: Etiology
Infective endocarditis
Aortic dissection
Chest trauma
224
CHRONIC Aortic Regurgitaiton: Etiology
Valve malformations,
rheumatic fever,
connective tissue disorders
225
ACUTE Aortic Regurgitation: Hx
Rapid onset of pulmonary congestion, cardiogenic shock, chest trauma
226
CHRONIC Aortic Regurgitation
Slowly progressive onset of dyspnea on eertion, orthopnea, and PND
227
Aortic Regurgitation: PE
- Blowing diastolic murmur at LSB
- mid-diastolic rumble (Austin Flint Murmur)
- mid systolic apical murmur
- Widened pulse pressure causes de Muzzet's sign, Corrigan's signs and Duroziez's sign
228
de Musset's sign
- associated with aortic regurgitation
| - head bob with heartbeat
229
Corrigan's sign
- associated with aortic regurgitation
| - water-hammer pulse
230
Duroziez's sign
- associated with aortic regurgitation
| - femoral bruit
231
Aortic Regurgitation: Dx
Echocardiogram
232
Aortic Regurgitation: Tx
Vasodilator therapy (dihydropyridines or ACES) for isolated AR until sx become apparent enough for valve replacement
233
Mitral valve stenosis
- most common etiology is rheumatic fever
| - symptoms range from dyspnea, orthopnea, and PD to infective endocarditis and arrhythmias
234
Mitral valve stensosis: PE and Dx
- opening snap and mid-diastolic murmur at apex, pulmonary edema
- diagnosed with echocardiogram
235
Mitral valve stenosis: Tx
Antiarrhythmics (B-blockers, digoxin) for symptomatic relief
| Mitral valve ballon valvotomy and valve replacement are effective for severe cases
236
Mitral valve regurgitation
primary secondarily to rheumatic fever or chordae tendinae rupture after MI
- infective endocarditis
237
Mitral valve regurgitation: HX
patients present with dyspnea, orthopnea, ad fatigue
238
Mitral valve regurgitation: PE and Dx
- holosystolic murmur radiating to axilla
- diagnosed with echo will demonstrate regurgitant flow;
- angiography can assess severity
239
Mitral valve regurgitation: tx
Antiarrhythmics if necessary
(A-fib is common w/ LAE)
- Nitrates and diuretics to decrease preload
- Valve repair or replacement for severe cases
240
Unstable angina
- defined as chest pain with new onset, is accelerated with less exertion, lasts longer
- signals presence of impending infarction
241
NSTEMI (non ST elevated MI)
- myocardial necrosis marked by elevations in tropnonin I and CKMB without ST elevations on EKG
242
NSTEMI: Dx
- should risk stratified according to TIMI score
| - serial cardiac enzyme elevations and KEG
243
Unstable angina: Dx
suddent onset chest pain associated with exertion, longer lasting or nonresponsive to meds
- NO elevation in cardiac enzymes on EKG
244
Unstable angina: Tx
Clopidogrel
Unfractionated heparin
Enoxaparin
245
NSTEMI
- patients with chest pain refractory to meds, TIMI score > 3, or ST changes > 1mm should be given IV heparin and scheduled for angiography, PCI or CABG
246
ST- Elevations MI
defined as ST segment elevations and cardiac enzymes release secondary to prolonged ischemia and necrosis
247
ST- Elevation MI: Hx and PE
- acute onset chest pain with tightness or pressure that radiates to left arm, neck, or jaw
- associated with diaphoresis, SOB, lightheadness, N/V, and syncope
- PE may show arrhythmias, hypotension, and new onset CHF
248
Best predictor of STEMI survival
LVEF
249
Med Management of MI
MONA
- Morphine
- Oxygen
- Nitrates
- Aspirin
250
STEMI: Dx
- ECG: ST segment elevations or new LBBB
- Sequence of ECG changes
- Cardiac enzymes (Troponin and CK-MB)
251
ECG changes after STEMI
1. peaked T waves
2. ST elevations
3. Q waves
4. T wave inversion
5. ST segment normalization
6. ST wave normalization
252
Cardiac enzymes after STEMI
- Troponin > CK-MB more sensitive to STEMI
| - can take up to 6 hours to rise
253
ST segment elevation in leads II, III, aVF
- signifies INFERIOR MI (involving RCA/PDA)
| - get right sided ECG to look for RV infarct
254
ST segment elevation in leads V1 - V4
- signifies ANTERIOR MI (involving (LAD and diagonal branches)
255
ST segment elevation in leads I, aVL, and V5 - V6
- signifies LATERAL MI (involving LCA)
256
ST segment elevation in leads V1 - V2 (anterior leads)
- acute TRANSMURAL INFARCT in POSTERIOR WALL
| - obtain ECG leads V7 - V9 to assess for ST segment elevations
257
Ddx chest pain
- MI
- GERD
- Esophageal pain
- MSK disorders (costochrondritis, trauma)
- Pneumonia
258
Woman is found w/ pulseless electrical activity on HD # 7 suffering lateral wall STEMI. ACLS protocol is initiated. Next best step?
LV free wall rupture with acute cardiac tamponade
| - emergent pericardiocentesis is next best therapeutic and diagnostic step
259
Main meds for STEMI
BC MONA
- Beta-blockers
- Clopidogrel
- Morphine
- Oxygen
- Nitrates
- Aspirin
260
Pt had STEMI but is in heart failure or cardiogenic shock. What medication should not be given?
B-blockers are contraindicated give ACEis instead if patient is not hypotensie
261
STEMI: Tx
- BC MONA meds
| - Emergent angiography and PCI
262
PT has STEMI but lives 3 hours away from closest hospital with cath lab. Next best step?
TPA -- if patient doesn't have contraindications to thrombolysis (hx of hemorrhagic stroke, recent ischemic stroke, severe HF, or cardogenic shock
** must be given within 3 hours of chest pain onset
263
Indications for CABG
"ULTD"
- Unable to perform PCI (diffuse disease)
- Left main coronary artery disease
- Triple vessel disease
- Depressed ventricular function
264
Complications of MI
- Arrhythmia (lethal ones MCC of death post-MI)
- Dressler's syndrome
- LV rupture, papillary muscle rupture, VSD, etc
265
Dressler's syndrome
autoimmune process that occurs 2- 10 wks post MI presents with fever, pericarditis, pleural effusion leukocytosis, and increased ESR
266
Complication of Post MI Day #1
Heart failure
267
Complication of post MI day # 2-4
Arrhythmia, pericarditis
268
Complication of post MI day # 5 - 10
LV wall rupture (acute pericardial tamponade causing electrical alternans, PEA)
Papillary muscle rupture (severe MR)
269
Complications of post MI weeks to months
Ventricular aneurysm (CHF, arrhythmia, persistent ST segment elevation, MR, thrombus formation)
270
Dyslipidemia
- total cholesterol > 200
- LDL > 130 mg/DL
- Triglycerides > 150 mg/dL
271
Dyslipidemia: Risk factors
CAD Risk factors
- Obesity, DM,
- Hypothyrodism, Nephrotic syndrome
- Cushing's syndrome,
272
Dyslipidemia: Hx and PE
- NO SPECIFIC SIGNS OR SYMPTOMS
- patients with extremely high triglyceride or LDL levels may have xanothomas (eruptive nodules on skin over tendons)
- xanthelasmas (yellow fatty deposits in skin around eyes)
- lipidemia retinals (creamy appearance of retinal vessels)
273
Dyslipidemia: Dx
- conduct fasting lipid profile for pts > 35 yrs in age or > 20 w/ CAD risk factors (repeat q 5 yrs)
- total serum cholesterol > 200 on 2 different occasions
- LDL > 130 or HDL < 40 even if total cholesterol is < 200
274
Dyslipidemia:: Tx
In patients with no known atherosclerotic disease - 12 week trial of diet and exercise
275
HMG-COA reductase (e.g. atorvastain, simvastatin)
- inhibit rate limiting step in cholesterol synthesis
| - decreases LDL and triglycerides
276
HMG-COA reductase side effects
- increase LFTs, myositis, warfarin potentiation
277
Lipoprotein lipase stimulators ./ Fibrates
| e.g. gemfibrozil
- increase lipoprotein lipase leading to increasing VLDL and triglyceride catabolism
- decrease triglycerides and increased HDL
278
Lipoprotein lipase stimulators: side effects
GI upset
Cholelithiasis
Myositis
Increased LFTs
279
Cholesterol absorption inhibitors (e.g. Ezetimibe)
- decreased absorption of cholesterol at the small intense brush border
- decreased LDL
280
Cholesterol absorption inhibitors: side effects
Diarrhea
Abdominal pain
Can cause angioedema
281
Niacin (e.g. niaspan)
- decreased fatty acid release from adipose tissue
- decreased hepatic synthesis of LDL
- increase HDL
- decrease LDL
282
Niacin: side effects
```
Skin flushing (can be prevented with ASA)
Parasthesias
Pruritis
GI upset
Increased LFTs
```
283
Bile acid resins (cholestyramine, colestipil)
- bind instestinal bile acids
- leads to decreaed bile acid stones and increased catabolism of LDL from plasma
- decreased LDL
284
Bile acid resins: side effects constipation
```
Constipation
GI upset
LFT abnormalities
Myalgias
- can decreae absorption of other drugs from small intestine
```
285
Aortic dissection
- transverse tear in intima of vessel that reults in blood enterine media creating false lumen
- SECONDARY TO HYPERTENSION
286
Common sites of aortic dissection
- aortic valve
| - distal to left subclavian arter
287
Aortic Dissection: Hx and PE
- sudden tearing/ripping pain in anterior chest
- typically hypertensive
- ASYMMETRIC PULSES AND BP MEASUREMENTS
- Neuro deficits seen if aortic arch or spinal arteries are involved
288
Aortic Dissection: Dx
CT angiography
Type A Aortic dissections are proximal to left subclavian artery
Type B Aortic dissections are distal to left subclavian artery
289
Aortic Dissection Tx
- monitor and medically manage BP and HR as necessary
| - begin B- blockage before starting vasodilators to prevent reflex tachycardia
290
When aortic dissection a surgical emergency?
When aortic disesection involves ascending aortia
| Descending aorta dissections can be managed with BP and HR control
291
Deep Vein Thombosis
- clot formation in large veins of extremities or pelvis
| - Virchow's triad (venous stasis, endothelial trauma, or hypercoaguable state)
292
Risk factors for DVT
```
Venous stasis
- immobilization, bed rest, incompetent valves
Endothelial injury
- surgery, injury to lower extremities
Hypercoagulable states
- malignancy, pregnancy, OCP use
```
293
DVT: Hx and PE
- presents with unilateral lower extremity pain and swelling
| - Homan's sign (calf tenderness w/ passive foot dorsiflexion)
294
DVT: Dx
- Doppler U/S
| - spiral CT or V/Q scan may be used to eval
295
DVT: Tx
- Anticoagulate with IV unfractionated heparin or SQ LMWH followed by PO warfarin for 3-6 months
- if anticoagulants are contraindicated: IVC filters
296
In low risk patients, what test can be used to rule out PE in low risk patients?
Negative D-dimer test
297
Peripheral arterial disease
- restriction of blood supply to extremities by atherosclerosis
- lower extremities most commonly affect
298
Peripheral arterial disease: Hx and PE
- intermitent claudication (reproducible w/ walking and relieved with rests)
- progression of disease causes pain at rest
- dorsal foot ulcers cause poor perfusion
- painful, cold, numb foot is sign of limb ischemia
299
Aortoiliac disease
- buttock claudication
- decreased femoral pulses
- male impotence (Leriche's syndrome)
300
Femoropopliteal disease
- calf claudication
| - decreased pulses below the femoral artery
301
Acute ischemia
- often caused by embolization from the heart
- commonly occurs at bifurcations distal to the last palpable pulse
- may be secondary to cholesterol atheroembolism ("blue toe syndrome")
302
Chronic ischemia
- lack of blood perfusion leads to muscle atrophy
| - leads to: pallor, cyanosis, hair loss, and gangrene necrosis
303
Peripheral arterial disease: Dx
Ankle-Brachial Index (ABI) to provide evidence of atherosclerosis
- rest pain with ABI < 0.4
- Doppler U/S identifies stenosis and occlusion
(normal doppler readings > 90% brachial)
304
Peripheral arterial disease: Tx
- control underlying conditions (DM, tobacco) and institute gangrene and foot care
- ASA, Cilostazol, and thromboxane inhibitors may improve symptoms
- angioplasty and stenting have variable success rate
- surgery and amputation employed when medical management fails
305
Lymphedema
- disruption of lymphatic circulation that results in peripheral edema and chronic infxn of extremities
- often complication of lymph node dissection
306
Lymphademia: Hx and PE
- postmatectomy pts present w/ unexplained swelling of upper extremity
- immigrants presents with progressive lower extremity wswelling with no cardiac abnormalities (e.g. filarisis)
- children with b/l swelling of extremities
307
Lymphedema: Dx
Clinical
| - diagnosis of exclusion after ruling out cardiac and metabolic disorders`
308
Lymphedema: Tx
- symptom management (exercise, massage, and pressure garments ) to mobilize and reduce fluid accumulation
- diuretics are contraindicated
- maintain vigilance for cellulitis
309
Syncope
- sudden termporary loss of consciousness and postural tone secondary to cerebral hypoperfusion
310
Cardiac etiologies: syncope
```
Valvular lesions
Arrhythmias
PE
Cardiac tamponade
Aortic dissection
```
311
Noncardiac etiologies
Orthostatic/hypovolemic
Hypotension
Neurologic (TIA, Stroke)
Metabolic abnormalities
312
Syncope: Hx and PE
- triggers, prodromal symptoms and associated
- cardiac causes associated with brief or absent prodromal sx, hx of exertion, lack of association with changes in position and hx of cardiac disease
313
Syncope: Dx
Depends on etiology
- Arrhythmias (Holter monitors / event recorders)
- Echocardiograms (structural)
- Stress tests (ischemia)
- Tilt table testing (mediated syncope)
314
Syncope: Tx
Commonly B-blockers for heart rate control
315
PVC
ectopic beart aise from ventricular foci
| - associated with hypoxia, electrolyte abnormalities, and hypoerthyroidism
316
PVC: ECG finds
Early wide QRS note preceded by P wave
| - often followed by compensatory pause
