Final Flashcards

(407 cards)

1
Q

What are the sx of myocarditis

A

Fatigue, chest pain, unexplained tachycardia, S3 or 4 gallop, ab ekg/echo, new cardiomegaly, arrhythmia, shock, resp distress, hepatomegaly

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2
Q

What will you find on PE of someone with myocarditis

A

Systolic CHF; orthopnea, dyspnea, crackles, paroxysmal notctural dyspnea

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3
Q

What is the most common arrhythmia to present with myocarditis

A

Sinus tach

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4
Q

What does echo measure

A

Ventricular function

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5
Q

What labs would you order for suspected myocarditis

A

CBC, cardiac enzymes, BNP, CPK (assesses m damage), ESR and CRP

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6
Q

What can confirm a diagnosis of myocarditis

A

Endomyocardial bx

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7
Q

What are complications of myocarditis

A

Dilated cardiomyopathy, myopericarditis, sudden death

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8
Q

How do you treat myocarditis

A

Beta blocker, ACEI, diuretics *avoid NSAIDs, EtOH, exercise

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9
Q

What is the prognosis of myocarditis dependent on

A

Clinicopathologic types of myocarditis

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10
Q

What are the most common causes of myocarditis

A

Coxsackie B, T cruzi, trichinella spiralis

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11
Q

What are the features of Coxsackie B

A

Positive sense ssRNA; naked; fecal oral; *pleurodynia (devil’s grip), aseptic meningitis

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12
Q

What are the features of trichinella spiralis

A

Nematode; ingestion of cysts from raw pork -> develop in gut and invade mm *consider dx if periorbital edema, myositis, eosinophilia; dx with ELISA, latex agglutination, CPK levels, muscle biopsy

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13
Q

What is the presentation of pericarditis

A

Positional chest pain (relieved by leaning forward), fever, palpitations

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14
Q

What is present on a PE of a patient with pericarditis

A

Friction rub, rapid or irregular pulse

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15
Q

Will you see anything on an XR of someone with pericarditis

A

No *except pericardial effusion >250 mL will cause symmetrically enlarged cardiac silhouette *water bottle sign

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16
Q

What will an EKG of someone with pericarditis show

A

Diffusion ST elevations with reciprocal depressions in leads aVR and V1 with PR depression

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17
Q

What are the complications of pericarditis

A

Cardiac tamponade: treated with pericardiocentesis

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18
Q

What is the treatment for pericarditis

A

High dose aspirin TID colchicine

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19
Q

What is contraindicated in patients with pericarditis

A

Anticoagulants

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20
Q

What are the most common causes of pericarditis

A

Coxsackie B (serous), mycobacterium TB (caseous)

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21
Q

What are the features of mycobacterium TB

A

Acid fast, obligate aerobes, faculative intracellular; virulence: sulfatides, cord factor, surface protein can cause delayed hypersensitivity (used for PPD), wax D; stains: acid fast (ziehl-Nielsen, kinyon) - red rods; auramine rhodamine stain - apple green

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22
Q

What a re the risk factors for IE

A

Age >60, Male, poor dentition, IV drugs, structural heart dz, prosthetic valve

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23
Q

What are the complications of IE

A

CHF, abscess formation, hematogenous spread, embolism, systemic immune reaction, death

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24
Q

What diagnostic tests would you run for IE

A

Blood culture x 3, CBC with diff, CMP, EKG, CRP, UA, transesophageal echo, CXR

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25
What is the duke criteria
For dx of IE: must meet 2 major OR 1 major and 3 minor OR 5 minor
26
What is the treatment for IE
If in cardiogenic shock surgery ASAP; if not, start empiric abx -> vanco + gentamicin; for subacute dont have to start empiric - can wait for cultures
27
What abx can be given prophylactically prior to dental procedures to prevent IE
- if can tolerate PO: amoxicillin - if cant take PO and need IV: ampicillin or cefazolin or ceftriaxon - if allergic to penicillin: desensitize or cephalexin or clindamycin or azithromycin
28
What are the virulence factors of staph aureus
Protein A, coagulase (forms fibrin clot around organism), catalase, hemolysins, leukocydins
29
How does staph aureus invade tissue and blood
- hyaluronidase: breaks down connective tissue - staphylokinase: lyses formed clots - lipase: breaks down fat
30
What are the features of s viridans
Gram positive cocci in chains; alpha hemolytic; catalase negative, faculative anaerobe, optochin resistant Virulence: extracellular dextran binds heart valves
31
What is the treatment for s viridans
Penicillin
32
What are the features of s epidermidis
Gram positive cocci, coagulase negative, catalase positive, novobicin sensitive, faculative anaerob Virulence: adhesion polysaccharide capsule - biofilm formation
33
Who is susceptible to s epidermis
Neutropenic patient
34
What is the treatment for s epidermidis
Vanco
35
What are the features of enterococcus
Group D strep; faecalis: gram positive cocci, catalase negative, faculative anaerobe; virulence: extracellular dextran; UTI and biliary tract infections; can grown in 40% bile and 6.5% NaCl
36
What is strep Bovis
Non-enterococci Group D strep; assoc with colon cancer and IBD, gram positive cocci in chains, catalase negative, faculative anaerobe, virulence: extracellular dextran; 40% bile and blood agar
37
What are the features of HÁČEK
Gram negative bacilli, suspected cause of culture negative endocarditis; chocolate agar (factors V and X and Hemin); haemophilus cannot grow on blood agar unless with s aureus
38
What are the features of coxiella Burnetti
Gram negative obligate intracellular, aerobic, zoonotic, aerosol transmission *Q fever
39
What are the sx of valvular heart dz
Dyspnea on exertion (most common), angina, syncope, palpitations
40
What are the other terms used for stenosis
Sclerosis, fibrosis, calcification
41
What does stenosis lead to
Pressure overload an hypertrophy
42
What does regurgitation lead to
Volume overload; dilates
43
What is the jones minor criteria
Fever, arthralgia, increased sed rate or CRP, leukocytosis, prolonged PR interval, elevated ASO titer or anti DNAse B *need 2 major or one major and 2 minor criteria
44
What does mitral stenosis lead to
Left atrial enlargement (a fib) and RVH
45
What is ortner syndrome
Hoarseness - compression of left recurrent laryngeal n; seen with mitral stenosis
46
What are some things you may see on PE of someone with mitral stenosis
- Malar rash or blue facies (CO2 retention assoc with pulm HTN which vasodilates) - increased loud S1, increased S2 (P2 if PHT is present) - opening snap after S2 - diastolic low pitch decrescendo rumbling murmur best heart at apex in L lateral recumbent *use Bell
47
What is the treatment for mitral stenosis
Anticoagulation if in a fib; percutaneous balloon valvuloplasty (mitral commissotomy)
48
What are the causes of chronic vs acute mitral regurgitation
- chronic: MVP, mitral annular calcification (MAC) | - acute: rupture of chordal tendineae, rupture of papillary mm, ischemic papillary m dysfunction, IE
49
What is the pathophysiology of acute mitral regurgitation
Increases left atrial pressure abruptly causing pulm edema and LVF
50
What is the pathophysiology of chronic mitral regurgitation
Well compensated; left atrial enlargement, MAC
51
How can acute mitral regurgitation present
Cardiogenic shock
52
What are the PE findings of mitral regurgitation
- systolic murmur (blowing holosystolic) best heard at apex use diaphragm - radiates to left axilla - loudness of murmur correlate with severity - decreased S1 or normal; valsalva moves click and murmur closer to S1 - murmur increases with hand grip
53
What is the treatment for mitral regurgitation
- vasodilator to reduce afterload (nitroprusside) - decreases resistance to flow - ACEI for chronic MR - IABP - decreases afterload and helps perfuse coronary aa - surgery for acute severe MR
54
How do you treat the sx of MVP
If hyperadrenergic state - beta blocker | *valve repair favored over replacement
55
What arrhythmias can MVP cause
SVT, PVC, VT
56
What are the PE findings of aortic stenosis
- narrow pulse pressure (decreased systolic pressure) - delayed pulses: parvis (weak decreased amplitude due to decreased CO), tardus (late delayed carotid upstroke) - decreased A2, systolic murmur, harsh 2nd ICS RSB - radiates to Supra eternal notch/carotids - gallavardin phenomenon - murmur radiates to apex
57
What is the treatment for aortic stenosis
Balloon valvuloplasty (bridge therapy), surgery, TARV (transcatheter aortic valve replacement) - for sx, trileaflet, AoV sclerosis with high surgical risk
58
What are the causes of acute vs chronic aortic regurgitation
- acute: IE, aortic dissection, BAV, Chest trauma, balloon valvuloplasty - chronic: syphilis, ankylosing spondylitis, ascending aortic dilation, BAV, calcific degeneration, rheumatic, chest radiation
59
What are the PE findings of aortic regurgitation
Wide pulse pressure, De musset sign, corrigans pulse, quinckes pulse, traube’s sign, durozreys sign, hills sign, biserious pulse, diastolic decrescendo murmur 3rd ICS LSB, systolic murmur soft, Austin flint murmur - can mimic MS
60
What is the treatment for aortic regurgitation
- ARB - decreases afterload to decrease regurgitation volume | - surgery when symptomatic or EF <50-55%
61
What can tricupsid stenosis be associated with
Carcinoid, ergot agents (cabergoline)
62
What would you see in the JVP of someone with tricuspid stenosis
Prominent A wave
63
What PE findings would you see with tricuspid stenosis
ascites, hepatomegaly that may pulsate, diastolic low pitch decrescendo murmur LSB that increases with inspiration (carvallo’s sign) and decreases with expiration and valsalva
64
What is tricuspid regurgitation associated with
Pulmonary HTN, RV infarction, inferior MI, pacemaker,endocarditis
65
What would you see on JVP of someone with tricuspid regurgitation
V wave
66
What PE findings would you see with tricuspid regurgitation
Blowing holosystolic murmur LSB, 4th ICS increases with inspiration due to increased venous return; pulsating liver
67
What PE findings would you see with pulm stenosis
Systolic crescendo-decrescendo murmur ejection click 2nd-3rd ICS LSB radiates to left shoulder and increases on inspiration
68
What are most cases of pulm regurgitation due to
Pulmonary HTN; *diastolic decrescendo blowing murmur 2nd ICS LSB (graham steell); incrased P2 if PHT
69
What are the systolic murmurs
MR (MVP), TR, AS, PS, VSD
70
What are the diastolic murmurs
AR, PR, MS, TS
71
What are the continuous murmurs
PDA: machinery, AV fistula, ASD, coarctation
72
What are the class 1 anti arrhythmic drugs
Sodium channel blockers
73
What are the class 1A drugs
Quinidine, procainamide, disopyramide
74
What are the class 1B drugs
Lidocaine and mexiletine
75
What are the class 1C drugs
Flecainide and propafenone
76
What are the class 2 antiarrhtmic drugs
Beta blockers; esmolol and propranolol
77
What are the class 3 antiarrhythmic drugs
Potassium channel blockers; amiodrone, sotalol, dofetilide, ibutilide
78
What are the class 4 antiarrhythmic drugs
Caridioactive calcium channel blockers; verapamil and diltiazem
79
Which cells have fast action potential
Ventricular myocytes, atrial myocytes, purkinje fibers
80
Which cells have slow action potentials
SA node cells and AV node cells
81
What are the different stats of the sodium channels
- resting: channel is closed but ready to generate AP - activated: depolarization opens m-gates - inactivated: h gates are closed - not available for reactivation
82
What do most sodium channel blockers block
Channels in inactivated or activated state
83
What charge does the sodium channel blocker have to have to bind to the channel
Positive
84
What do class 1A drugs do
Block sodium channels - slow impulse conduction, reduce automatism of ectopic pacemakers; - state dependent block (open activated) - allows it to target ectopic pacemaker cells - intermediate dissociation - blocks potassium channels - prolong AP duration, prolongs QRS and QT
85
What is procinamide used to treat
``` Sustained V tach; has antimuscarinic activity and ganglion blocking properties (can cause hypotension) -pharmacokinetics: has class 3 activity; accumulates in renal dysfunction *measure parent drug and metabolite ```
86
What are the adverse effects of procainamide
- cardiac: QT prolongation, induction of torsade de pointes and syncope, excessive inhibition of conduction - extracardiac: SLE syndrome with arthritis, pleeuritis, pulm dz, hepatitis and fever, agranulocytosis
87
What is quinidine used for
Occasionally for a fib, sustained v arrhythmia; has antimuscarinic affects on the heart; beta blocking activity; can aus hypotension which leads to tach
88
What are the adverse effects of quinidine
- cardiac: QT prolongation, induction of torsades de pointes, slowing of conduction - extracardiac: tinnitus (cinhonism), thrombocytopenia, hepatitis
89
What is disoppyramide used to treat
Recurrent ventricular arrhythmia *potent muscarinic affect on heart
90
What are the adverse effects of disoppyramide
- cardiac: QT prolongation, torsades, negative inotropic effect -> heart failure - extracardiac: atropine like sx (urinary retention, dry mouth, blurred vision, constipation, exacerbation of glaucoma)
91
What do class 1B drugs do
Block inactivated sodium channels -> allows it to bind preferentially to a depolarized cell; dissociates fast -> no effect on normal tissue; shorten AP; DO NOT prolong QT
92
When is lidocaine used
Mono and polymorphic v tach; very effective in arrhythmia as result of acute MI
93
How is lidocaine aministered
Only IV
94
What are the adverse effects of lidocaine
Least toxic; can cause hypotension in patients with heart failure by inhibiting contractility; neuro: paresthesia, slurred speech, convulsions,
95
What are the features of mexiletine
Orally active; similar to lidocaine; used for v arrhythmias, relieve chronic pain (esp due to diabetic neuropathy and nerve injury); adverse effects:: tremor, blurred vision, lethargy
96
What do class 1 C drugs do
Block activated sodium channels; dissociate slowly; blocks certain potassium channels; do not prolong QT or AP but DOES prolong QRS
97
What are the features of flecainide
Blocks sodium and potassium channels; no antimuscarinic effects; used in patients with normal hearts; tx for supraventricular arrhythmias including AF, paroxysmal SVT (AVNRT AVRT) and life threatening ventricular arrhythmias such as sustained v tach
98
The adverse effects of flecainide
Can exacerbated ventricular arrhythmias when given to patients with preexisting ventricular tacharrhytmias, previous MI, or patients with ventricular ectopic rhythms
99
What are the characteristics of propafenone
Possesses weak beta blocking activity; used to prevent paroxysmal AF and SVT in patients without structural dz and in sustained ventricular arrhythmias
100
What are the adverse effects of propafenone
Exacerbation of ventricular arrhythmias, metallic taste, constipation, do not combine with CYP2D6 and CYP3A4 inhibitors -> increases risk of pro arrhythmias
101
What is the effect of beta blockers on sinoatrial nodal cells
Blocks formation of cAMP -> can’t activate funny channels or PKA which cant activate funny channels or T and L type calcium channels
102
What do beta blockers do the slope and threshold of the AP
decrease the slope due to effects on funny channels and T type calcium channels; incrase the threshold due to effect on L type calcium channels
103
What are the effects of beta blockers on the SA node and AV node
SA: decreases HR and increases RR interval AV: decreases conductance and increases PR interval
104
What are the indications for use of propranolol in arrhythmias
Those induced by stress, re-entrant arrhythmias that involve AV node (AVNRT and AVRT), a fib and flutter, arrhythmias associated with MI
105
What are the features of esmolol
Short acting; used as continuous IV infusion with rapid onset; use: supraventricular arrhythmias, arrhythmias assoc with thyrotoxicosis, MI with arrhythmias, adjunct in general anesthesia
106
What are the adverse effects of beta blockers
Reduced CO, bronchospasm, impaired liver glucose mobilization, unfavorable lipoprotein profile, sedation, depression, withdrawal
107
What are the contraindications to beta blockers
Asthma, PVD, raynauds, T1DM on insulin, Brady arrhythmias
108
What are the types of potassium channels
Calcium activated, inwardly rectifying, tandem pore domain, voltage gated
109
Which potassium channels are open in the resting state
Inwardly rectifying - no current occurs because resting state
110
What do class 3 drugs do
Block potassium channels; prolong AP, prolong QT, prolong refractory period
111
What does amiodarone do
Blocks potassium channels and inactivated sodium channels; prolongs QT and AP; adrenolytic activity; calcium blocking activity; causes bradycardia an peripheral vasodilation; use: ventricular arrhythmia and a fib
112
What are the pharmacokinetics of amiodarone
Metabolized by CYP3A4 (cimetidine inhibits an rifampin is inducer) long half life
113
What are the adverse effects of amiodarone
- cardiac: AV block and bradycardia, incidence of torsades is low - extracardiac: fatal pulmonary fibrosis, hepatitis, photodermatitis (blue grey color in sun exposed areas), deposits of drug in cornea - optic neuritis, blocks peripheral conversion of thyroxine to triiodothyronine (can cause hypo or hyperthyroidism)
114
What is the use of sotalol
Treatment of life threatening ventricular arrhythmias, maintenance of sinus rhythm in patients with a fib; side effects: torsade
115
What does dofetilide do
Blocks rapid component of delayed rectifier potassium current - effect is more pronounced at lower heart rates *eliminatd by kidneys, has very narrow therapeutic window; used to convert A fib to normal sinus rhythm and maintain rhythm after conversion
116
What are the side effects of dofetilide
QT prolongation an increased risk of ventricular arrhythmias
117
What does ibutilide do
Slows cardiac repolariztion by blocking rapid component of delayed rectifier potassium current; administered IV and cleared by liver; used to convert atrial flutter and fib to sinus rhythm
118
What are the adverse effects of ibutilide
QT prolongation and ventricular arrhythmias; patients require continuous ECG monitoring until QT returns to baseline
119
What do class 4 drugs do
Block activated and inactivated L type calcium channels; active in slow response cells - decrease slope of phase 0 depolarization, increase L type threshold potential, prolong refractory period in AV node
120
What are the clinical uses of class 4 drugs
Prevention of paroxysmal SVT; rate control in AF and flutter
121
What are the side effects of class 4 Drugs
- Cardiac: negative inotropic, av block, SA arrest, Brady arrhythmias, hypotension - extracardiac: constipation (verapamil)
122
What does adenosine do
Activates potassium current and inhibits calcium and funny currents causing marked hyperpolarization and suppression of AP in slow cells; inhibits AV conduction and increases nodal refractory period
123
What is adenosine used for
Conversation to sinus rhythm in paroxysmal SVT
124
What are the side effects of adenosine
Shortness of breath, bronchoconstriction, chest burning, av block, hypotension
125
Which leads shown atrial enlargement
I, II, III, V1
126
What does right atrial enlargement look like on EKG
Tall pointed taller in III p waves; P pulmonale; peaked p waves in leads II, III, AVF, V1 and 2
127
What does left atrial enlargement look like on EKG
Wide notched taller in I than III p waves; P mitrale; 2nd half of P wave negative in V1 or III
128
Can you distinguish between LVH and dilation on EKG
No; use term “enlargement”
129
How does right ventricular hypertrophy show on EKG
R waves assume prominence in right precordial leads and deep S waves in left leads; R:S ratio greater than 1
130
What are the causes of dominant R waves in V1
RVH, posterior or lateral MI, WPW, hypertrophic cardiomyopathy, muscular dystrophy, Normal variant
131
What is a hemiblock
Blockage of one of the 2 main divisions of the left bundle branch anterior (superior) and posterior (inferior)
132
Which hemiblock is more common
Left anterior
133
What kind of axis does a left anterior hemiblock have
Left
134
What kind of axis does a left posterior hemiblock have
Right
135
What is left anterior hemiblock associated with
MI from left anterior descending occlusion; small q in leads I and avL, small R in leads II, III and aVF
136
What is the criteria for a left posterior hemiblock
Right axis deviation, small R in leads I and avL, small q in leads II, III, aVF, no evidence of RVH
137
What is intrinsic deflection (intrinscoid)
Time lapse from beginning of QRS to peak of R wave
138
What are the features of BBB
Wide QRS complex (.12 sec or greater); T waves slope in opposite direction to QRS
139
What causes LBBB
Hypertension, ischemia, aortic stenosis, cardiomyopathy
140
What is LBBB with RAD indicative of
Congestive cardiomyopathy
141
If the T wave is in the same direction of the QRS in a BBB, what is this indicative of
Ischemia
142
What are some etiologies of 1st degree AV block
Atherosclerosis, HTN, DM, CHD (fibrosis), CAD, drugs (digitalis), hypothyroid, hyperthyroid, adrenal insufficiency, RF, SLE, amyloidosis, hemochromatosis, valvular calcifition
143
What are the 2 types of second degree AV block
Mobitz I (wenke bach) and mobitz II
144
What are the characteristics of wenckebach
Progressive PR interval with prolongation prior to dropped QRS; grouped beats
145
Where is the level of mobitz I
AV node; seen with inferior MI; narrow QRS
146
What can cause mobitz type II
Anterior MI, ischemic heart dz
147
What are the features of mobitz II on EKG
PR interval is uniform; dropped beat; block occurs at level of bundle of His, both bundle branches, or fascicles branches;; irreversible *may be seen with anterior MI because block is distal to AV node; worse prognosis
148
What are the features of 3rd degree heart block
Complete heart block; P waves never related to QRS; two independent rhythms (AV dissociation - no p waves conduct to the ventricle)
149
Where is the level of the block for 3rd degree heart block
Can occur above or below AV node - above: junctional rhythms; narrow QRS (rate 40-55) - below: ventricular pacemaker; wide QRS (rate 20-40)
150
How do you treat a 3rd degree AV block
Pacemaker
151
What is the empiric treatment for acute rheumatic fever
Penicillin G + gentamicin
152
What do you give to treat acute rheumatic fever to someone with a penicillin allergy
Erythromycin, azithromycin, clarithromycin, or clindamycin
153
What do you give to a patient who is likely to have recurrrent acute rheumatic fever that is allergic to beta lactam
Erythromycin, azithromycin, clarithromycin
154
What class of abx are erythromycin, azithromycin and clarithromycin
Macrolides
155
What is the empiric treatment for infective endocarditis
Vancomycin (IV) + ceftriaxone
156
What do you give to someone with IE from strep viridans with a strain that is highly penicillin susceptible
Penicillin G or ceftriaxone
157
What do you give to someone with IE from strep viridans that needs to be on a shorter drug course and does not have renal dz
- gentamicin + pen G | - gentamicin + ceftriaxone
158
What do you give to someone with IE from strep viridans who has a mild penicillin allergy
Ceftriaxone or gentamicin + ceftriaxone
159
What do you give to someone with IE from strep viridans that has a severe penicillin allergy
Vancomycin or pen desensitization
160
What do you give to someone with IE from staph aureus that has a methicillin susceptible strain
Nafcillin or oxacillin
161
What do you give to someone with IE caused from MRSA
Vancomycin; alternative: daptomycin
162
What do you give to someone with IE from staph aureus with a mild penicillin allergy
Cefazolin
163
What do you give to someone with IE from staph aureus that has a severe penicillin allergy
Daptomycin or vancomycin
164
What do you give to someone with IE from staph aureus that also has a brain abscess
Nafcillin
165
What organisms does daptomycin treat
Gram positive, including MRSA; binds to cell membrane via calcium dependent insertion off its tail leading to depolarization, potassium effux, and cell death
166
What do you give to treat IE from staph epidermidis and other coagulase negative staph
Vancomycin
167
What do you give to treat IE from HÁČEK
Ceftriaxone
168
What do you give to treat IE from enterococci (faecalis)
(Penicillin G or ampicillin or vancomycin) + gentamicin
169
What class is vancomycin
Glycopeptide
170
What class is cefazolin
1st gen cephalosporin
171
What class is nafcillin and oxacillin
Penicillinase resistant penicillin
172
What is the treatment for pericarditis in immunocompetent patients
NSAID + colchicine (important to order CRP to track treatment); corticosteroids used in severe or refractory cases (risks prolonging illness)
173
How does colchicine work
Binds to tubulin and prevents polymeriztion to microtubules -> leads to inhibition of leukocyte migration and phagocytosis
174
What are the adverse effects of colchicine
Hair loss, bone marrow depression, peripheral neuropathy, myopathy *SIDE EFFECTS ONLY WITH IV form
175
What are the duke major criteria
Positive blood cultures for: staph, viridans, bovis, HÁČEK, or community acquired enterococci in 2 cultures OR persistently positive in typical causes of IE OR single culture of coxiella burnetti; echo positive for IE; new valve regurgitation
176
What is the minor duke criteria
Predisposition, fever >38, vascular phenomena, glomerulonephritis, Osler nodes, Roth spots, or rheumatoid factor, micro vidence
177
What do you need for duke criteria to make dx of IE
2 major, 1 major with 3 minor, 5 minor
178
Which kind of patient usually have no pain with pericarditis
Uremic
179
What is the EKG progression of pericarditis
Diffuse ST elevation with PR depressions -> ST normalization -> inverted T waves -> return to baseline
180
How do you treat TB
Isoniazid + rifampin + ethambutol + pyrazinamide
181
What are the drugs used for heart failure
``` ACEI: -Prils ARBS: -Sartans Carvedilol Spironolactone Diuretics Direct vasodilators (nitroglycerin/isosorbide dinitrate, nitroprusside, hydralazine) Digoxin Dobutamine, dopamine Milrinone ```
182
What are causes of high output heart failure
Hyperthyroidism, pregnancy, anemia, wet beriberi, pagets dz
183
How do you calculate stroke volume
EDV-ESV
184
How do you calculate ejection fraction
SV/EDV
185
What are the features of diastolic heart failure
Normal ejection fraction with normal EDV; concentric remodeling HFpEF (preserved ejection fraction)
186
How is diastolic heart failure distinct from systolic heart failure
Diastolic has poor tolerance of a fib, poor tolerance of tach (shorter diastole), worsened by an increase in MAP, worsening by ischemia raises left atrial pressure -> angina with SOB*flash pulmonary edema
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What adaptive mechanisms occur in heart failure
Increase in renin, increase in aldosterone, sympathetic discharge, preload and afterload, ANP and BNP
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Which kind of remodeling has the worst outcome
Concentric hypertrophy
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What is ivabradine
Beta blocker
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What medications are used to prevent deterioration of cardiac function
ACEI, ARBs, beta blockers, spironolactone/eplerone
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What do ARBs do
Directly block angio II receptor
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What does less angiotensin II lead to
Less vasoconstriction (reduces afterload), less aldosterone secretion which reduces preload, less cell proliferation and remodeling
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What are the toxicities assoc with losartan
Hypotension, hypoglycemia, hyperkalemia, anemia, cough
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What is sacubitril
Prodrug that inhibits neprilysin (neutral endopeptidase) through active metabolite LBQ657; *cocrystallized with Valsartan
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How ones sacubitril/valsartan work
-neutral endopeptidase blockade leads to increased levels of natriuretic peptides -valsartan blocks angiotensin II responses Twice daily dosing
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What are the side effects of sacubitril/valsartan
Hypotension, hyperkalemia, increased serum Cr | Uncommon: decreased Hct and Hgb, angioedema, renal failure, cough
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What are the effects of ANP
Increased GFR, decreased renin
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Are ACEI or ARBs first choice for heart failure
ACEI
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What are the indications for ACEI and ARBs in heart failure
All patients with systolic failure or LV dysfunction without heart failure unless - not tolerated - pregnant - hypotension - serum Cr >3 mg/dL - hyperkalemia
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Which beta blocker works best for heart failure
Carvedilol
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What are the effects of carvedilol in CHF
Decrease pulm pressure, HR, MAP, right atrial pressure; increased stroke volume index
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What are the clinical applications of carvedilol
Recommended to any patient wit recent history of MI and reduced ejection fraction or reduced ejection fraction with no hx of MI
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Where is carvedilol metabolized
Liver
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What toxicities are associated with carvedilol
Hypotension, hypercholesterolemia, hyperTG, hyperkalemia, hyponatremia, hyperuricemia, anemia, thrombocytopenia, blurred vision, increased BUN and Cr
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How do beta blockers work to treat heart failure
Prevent down regulation of beta 1 receptors that occurs as a result of overactive sympathetic; keeps heart responsive to sympathetic drive, protects against dysthymia, reduces renin, reduces oxygen consumption, limits remodeling
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Who should carvedilol be given to
* stable patient with diastolic heart failure; symptomatic CHF with LVEF <40% unless contraindicated * give in combo with ACEI to all patients with left ventricular systolic dysfunction caused by MI
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What does ivabradine do
Selective inhibition of the hyperpolarization-activated cyclic nucleotide gated channels within SA node; disrupts funny current to prolong diastole and slow HR
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What are the clinical applications of ivabraine
Treatment of resting HR >70 in patients with stable symptomatic chronic heart failure with. Left ventricular ejection fraction <35% who are in sinus rhythm with maximally tolerated doses of beta blockers or contraindication to beta blocker use
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What is the effect of spironolactone post MI
Reduces fibrosis
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What are the effects of spironolactone on the heart
Decrease myocardial fibrosis, reduces early morning rise in heart rate, reduces mortality and morbidity in patients with severe heart failure
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How does furosemide treat pulmonary edema
Reduces preload
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What is metolazoe
Thiazide diuretic
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What is the order in which you use diuretics for heart failure
Loop first, add K sparing if needed, if still needed ad thiazide
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What are the causes of diuretic failure during treatment for heart failure
Excess dietary Na, decreased renal perfusion due to hypotension or worsening heart failure, NSAIDs, primary renal pathology, reduced absorption due to gut wall edema
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What are the vasodilators used to treat heart failure
``` Isosorbide dinitrate (dilate veins and decrease preload) plus hydralazine (dilate aa and decreases afterload) *especially useful in African Americans ```
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What are the uses of hydralazine in heart failure
Used in heart failure with reduced ejection fraction if intolerant to ACEI or ARB; AA heart failure; HTN emergency in pregnancy
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What toxicities are associated with hydralazine
Angina, flushing , peripheral edema, tachycardia, increased ICP, pruritus, paralytic ileus, drug induced lupus
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What is the MOA of digoxin
Inhibition of Na/K pump; increases IC sodium which promotes calcium influx via Na/Ca exchanger; direct suppression of AV node conduction - increases refractory period; positive inotropic effect, enhanced vagal tone, decreased ventricular rate
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What is digoxin used for
Control of ventricular response in those with chronic afib, treatment of mild to moderate heart failure in adults and pediatric patients to increase contractility
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What are the pharmacokinetics of digoxin
Long half life so needs a loading dose;; crosses the placenta but save use in pregnant women with supraventricular tach
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What toxicities are associated with digoxin
A lot of arrhythmias and blocks, PR prolongation, PVCs, ST depression, v tach or fib, blurred or yellow vision, laryngeal edem
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What causes digoxin toxicity
Too much calcium causes delayed contractions
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What does digoxin compete with to bind to Na/K pump
Potassium; *potassium levels must be kept within normal - too little K means too much block
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What are the hemodynamic benefits of digoxin
Increased CO which decreases symp tone, increases urine production, and decreases renin
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What electrical effects does digoxin have
Increases firing rate of Vagal fibers, increases responsiveness of SA node to Ach
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What are the effects of digoxin on the SA node
Decreases automaticity (but increases it after atropine)
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What are the effects of digoxin on the atrial myocardium
Decreases the duration of refractory period (increases after atropine), increases excitability (except at toxic doses), increases conduction velocity (except at toxic doses)
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What are the effects of digoxin on the av node
Increases duration of refractory period, decreases conduction velocity
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What are the effects of digoxin on purkinje fibers
Increases automaticity, increases duration of refractory period and excitability (except at toxic doses), decreases conduction velocity
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What are the effects of digoxin on ventricular myocardium
Decreases duration of refractory period, increases excitability and conduction velocity (except at toxic doses)
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What effects does digoxin have on EKGs
Depression of ST, longer PR interval (typical), AV dissociation (toxic), ectopic ventricular beats (toxic)
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What is the treatment for too much digoxin
KCl, lidocaine, phenytoin, antidigitalis abs (digibind)
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What drugs does digoxin interact with
Diuretics - cause hypokalemia which leads to increased digoxin binding -> toxicity - ACEI and ARBs: increase K and decrease digoxin effects - sympthomimetics - quinidine, spironolactone, verapamil, propafenone and alprazolam - interfere with clearance - cholesterol binding resins block absorption
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What are the treatments for diastolic heart failure
Treat associated conditions, exercise but avoid tachycardia, abrupt increase in BP, ischemia, a fib, use loop diuretics
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Which drugs have no benefit in diastolic heart failure
Nitrates, PDE5 inhibitors, digoxin
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How do you treat acute decompensated heart failure
Place in seated position, continuous pulse oximetry and supplemental oxygen and assisted ventilation, assess BP, place 2 IV lines, monitor urine output, *initiate diuretic therapy
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What does nitroprusside do
Dilates arteries and veins
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How do you treat hypertensive vs normotensive vs hypotensive patients in acute decompensated heart failure
- hypertensive: diuretic + nitroprusside or nitroglycerin - normotensive: diuretic + nitroglycerin - hypotensive: diuretic only
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How is nitroprusside administered
IV
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What is nasiritide
Synthetic B natriuretic peptide binds to guanlyate Cyclase receptor on vascular smooth m and endothelial surface to increase cGMP; treatment of ADHF with dyspnea at rest; toxicities: increased serum Cr
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What inotropic agents would you use to treat heart failure with hypotension and end organ dysfunction
- sympathomimetic: dobutamine and dopamine * discontinue carvedilol - PDE inhibitors (block degredation of cAMP in heart) - milrinone must be given IV
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How is dobutamine administered
IV
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How is dopamine administered
IV; causes widened QRS, local tissue necrosis
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Which drugs should you avoid in ADHF
Class I antiarrhythmics, calcium channel blockers, NSAIDs
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Which MI has increased symp vs parasympathetic activity
Symp: anterior; parasympathetic: inferior
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What can new LBBB be indicative of
STEMI
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Besides MI, what are the other cause of ST elevation
Pericarditis, LVH with J point elevation, normal variant
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What is persistent ST elevation > 2 weeks indicative off
Ventricular aneurysm
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What is normal QRS duration
.05-.1 sec
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Where are small q waves normal
Leads I, AVL, AVF, V5 V6
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What is ST depression indicative of
Subendocardial injury
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Where are t waves always upright
1,2,V3-6
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What is a normal T wave height
No greater than 5 boxes in standard leads; no greater than 10 in precordial leads
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What is the diff btw infarction, injury, and ischemia on EKG
Infarction - can’t depolarized Injury: unable to fully polarize Ischemia: impaired repolarization
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What leads to an anterior wall infarction show up on
V1-7
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What artery supplies the interior wall
RCA
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What artery supplies the lateral wall
Circumflex
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What can cause a false positive cTnT
Renal failure
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What are other causes of elevated troponin
PE, pulm HTN, resp failure, stroke, intracranial hemorrhage, shock
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What are deaths from MI most related to
V fib
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What is the ED standard of care for a STEMI
12 lead EKG with continuous monitoring; IV lines inserted, cardiac enzymes, CBC, CMP, PT, PTT - reperfusion: cath lab within 90 min - fibrinolytic: in ED within 30 min
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What is considered failure of fibrinolytic therapy
Failure of ST elevation to resolve by 50-70% within 1-2 hour
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What do you do if the hospital doesn’t have a cath lab
Transfer within 120 min
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What is the major risk of fibrinolytic therapy
Intracranial hemorrhage; not a risk with PCI
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What are the contraindications to fibrinolytic therapy
Active bleeding
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What is the initial medical management to someone having a STEMI
ASA PO given on presentation unless contraindicated; IV heparin or enoxaparin (adenosine diphosphate receptor inhibitor; anti platelet) use for one year after PC1 for STEMI; nitroglycerin; morphine; beta blocker; oxygen; stool softener; ACEEI if decreased EF nad increased BP
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What is the treatment for NSTEMI
Cath within 48 hours if high risk; anti thrombotic therapy, ASA, platelet receptor antagonist, anticoagulant (UFH, LMWH); if unstable - IV GP11b/111a antagonist; nitroglycerin
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What is dressler syndrome
Acute pericarditis after MI (2-10 weeks); hurts to breathe;; feels better when leaning forward; treat with ASA or NSAIDs
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What is accelerated idioventricular rhythm (AIVR)
Ventricular tach without the tach; seen after fibrinolytic therapy; benign
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What MI is associated with sinus Brady
Inferior MI
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What MI is associated with induction of 2nd degree AV block wenckebach
Inferior MI
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What are S3 and S4 indicative of
LV dysfunction
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Which MIs cause RV failure
inferior MI; decreased BP, clear lungs, increased JVP, kussmaul sign (distention of jugular on inspiration); treat with IV fluids
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How does mitral regurgitation occur as a result of MI
Papillary m rupture
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What MI is associated with a complication of a new holosystolic murmur
Inferior wall
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Which MI is associated with septum rupture
Anterior wall -> VSD; LV free wall rupture causes tamponade; LV aneurysms also assoc with anterior MI; rx: surgery
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What is a complication of LV aneurysm from MI
Arterial emboli
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What are the ddx for STEMI
Pericarditis, myocarditis, stress induced syndrome, early repolarization
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What is metabolic syndrome
Insulin resistant, HTN, high TG, low HDL, hyperuricemia, hypercoagulabl, obese BMI >30, overweight BMI 25-29
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How do you calculate BMI
Weight x 705/height (inches)^2
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What is the diff between supply and demand angina
Supply: decrease delivery to tissue; ex: vasoconstriction, stenosis, platelets release serotonin and thromboxane Demand:increased requirements; ex exercise, stress, emotion, fever, thyrotoxicosis; LVH due to AS; anemia
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What are the mechanical consequences of ischemia
Heart failure, necrosis, segmental akinesis, bulging (dyskinesia)
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What are the biochemical consequences of ischemia
Fatty acids cant be oxidized -> incrased lactate production -> acidosis
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What leads show a RV infarction
V3-6
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What is the pattern of pain of angina
Crescendo decrescendo lasting 15-20 min
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What is angina equivalent
Due to ischemia but described as dyspnea fatigue, faintness, and epigastric eructations (belching); pathogenesis: ischemia causing elevated LV filling pressure that leads to pulm edema; common in women, elderly, diabetic
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What are signs of risk factors for angina
Xanthelsma, Xanthomas, diabetic skin lesions, nicotine stains, pale, absent peripheral pulses
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What is a sytolic murmur of MR associated with in angina
RCA involvement - dysfunction of papillary m
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What can mimic angina in absence of CAD
AS, AI, pulm HTN, hypertrophy, heart failure
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What is the most common change seen on ECG with an anginal attack
ST depression
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What on the EKG correlates with prognosis of unstable angina/NSTE ACS
Magnitude of ST depression
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What ekg change would you see for stress cardiomyopathy
Deeply inverted T wave
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An increase in what is associated with increased mortality in NSTE ACS
BNP
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What are the functional and anatomical testing done for CAD
- functional: reveal presence of ischemia; exercise ECG, single photo emission CT (SPECT,PET), coronary flow, wall abnormality tests (echo, cardiac MRI) - anatomical: invasive angiography, coronary CT angio, coronary artery calcium scoring (CAC)
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What are the signs of high risk for coronary event after doing CAD testing
- positive stress test at low work load - ST depression > 5 min after completion of test - decrease in BP >10 during exercise - VT during exercise - reduced EF during exercise
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What are the contraindictions to exercise EKG
Recent MI, unstable arrhythmias, acute PE, aortic dissection, unstable angina, severe AS, decompensated HF, endocarditis, DVT
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What test do you do if patient cant exercise
Stress echo
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What is SPECT useful for
LBBB,LVH, digitalis effects
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What is a pharmacological stress test
Use when patient cant exercise/ab EKG; use vasodilator nuclear perfusion - adenosine/regadenosine/dipyridamole which increases HR; or can use dobutamine
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When is CABG performed
L main dz or 3 vessel dz
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Which drug is not shown to decrease mortality in CAD patients
CCBs
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What is given to prevent variant anginal attacks
Dihydropyridines CCB (amlodipine); BB, nitro, statin, antiplatelet, anticoagulant, cath if appropriate
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What are the lipid panel goals for people with 10 year risk of CHD
LDL < 70, HDL >60, TG <150, total chol <200
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What are the dietary recommendations for CAD
Low saturated fat and cholesterol, high fiber, fish oil, antioxidants; 2 gram Na, reduce alcohol
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What lead shows the best atrial enlargement
V1 - p wave
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What does the P wave look like in atrial enlargement
Diphasic (positive and negative)
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How do you tell the diff between right and left atrial enlargement
``` If initial (positive) part of P wave is bigger -> right If terminal (negative) part of P wave is larger -> left (caused by mitral stenosis or systemic HTN) *if P wave is bigger than 2.5 in ANY lead even if its not diphasic -> right atrial enlargement ```
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Where do you see right ventricular hypertophy on EKG
Large R wave in V1 and then gets progressively smaller from V2-4
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What do you see on EKG of LVH
Deep S wave in V1, very tall R wave in V5
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What happens to the T waves with LVH and in what leads
Have a long and gradual downward slope, inverted in leads V5 and 6
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Which arteries supply the anterior and posterior division of left bundle branch
Anterior: RCA Posterior: LCA
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What artery supplies the right bundle branch
LCA (LAD)
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What will you see on EKG for a left anterior hemiblock
Q wave in lead I and wide or deep S wave in III
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What do you see on EKG or a posterior hemiblock
Deep or wide S in lead I and q in III; caused by lateral infarction
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What is a fascicular block
Bundle branch block with a hemiblock
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What is seen on EKG of an intermittent block
Intermittent wide QRS patterns
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How many squares classifies a BBB
3 or more
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What are the right vs left chest leads
Right: V1 and 2 Left: V5 and 6
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What do you see on EKG with sinus block
Missed cycle with no p wave
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How can you distinguish between mobitz and wenckebach
Mobits has wide QRS; also if perform vagal maneuver wenckebach becomes more cycles; mobitz becomes 1:1
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What is the ventricular inherent rate with a complete AV block (ventricular focus)
20-40
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What is the ventricular rate with a junctional focus (block of upper AV node)
40-60
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What is stokes Adams syndrome
Complete AV block -> heart is beating so slow and can lose consciousness
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What is downward displacement of the pacemaker
No p waves, slow rate, wide QRS, indicates that there’s no supravenicular foci working; hyperkalemia can cause this tracing
325
Which drugs cause long QT Nd torsades
Antiarrhythmics group 1A an 3, antihistamines, abx,
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What do you give to a patient with long QT or torsades
Magnesium sulfate IV irrespective of whether the patient is hypomgnesemic or not
327
What do you give to someone with. Fib with no HF (LVEF >40%)
CCB or beta blocker -> then CCB and digoxin or beta blocker an digoxin -> then amiodarone
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What do you give to someone with a fib with HF (LVEF <40%)
Beta blocker -> then beta blocker and digoxin -> then amiodarone
329
What is CHADS2 score
CHF (1), HTN (1), age >75 (1), DM (1), stroke or TIA hx (2); if add up to 1 or higher need anticoagulant for afib (warfarin or DOAC)
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Which drugs can convert a fib to sinus rhythm vs maintain the rhythm
- convert: amiodarone, flecainide, dofetilide, ibutilide, propafenone - Maintain: dronedarone, flecainide propafenone sotalol, amiodarone dofetilide, catheter ablation
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What is the algorithm for choosing a drug for conversion of afib to sinus rhythm
- if no HF -> amiodarone, dofetilide, flecainide, ibutilide, propafenone - if HF: amiodarone dofetilide, ibutilide
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What do you give to prevent paroxysmal SVT
Verapamil, digoxin, catheter ablation
333
What do you give to treat active SVT
Adenosine, verapamil or dilitazm, beta blockers, digoxin, amiodarone
334
What is the algorithm for treating SVT
If adenosine doesn’t work and no HF: dilitazem or verapamil -> beta blocker -> digoxin If adenosine doesn’t work and HF: digoxin -> amiodarone -> dilitazem
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How do you treat acute high grade AV block that is symptomatic
Atropine -> if doesn’t work dopamine or epi
336
What does the u wave represent
Purkinje fiber repolarization
337
What is the rate of atrial escape rhythm
60-80
338
What can cause premature ventricular beats
Low O2, low K+, mitral valve prolapse, stretch, myocarditis
339
How many PVCs in a row classifies v tach
3 or more; if >30 sec - sustained v tach
340
What is R on T phenomenon
When a PVC falls on a T wave -> very vulnerable
341
Is sinus tach a paroxysmal tac
No- paroxysmal is sudden
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What is paroxysmal atrial tach
2 p waves for each QRS response -> assoc with digitalis toxicity
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What is AVNRT
AV nodal reentry tach
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Does v tach or SVT show fusion beats
Only v tach
345
What are people with WPW syndrome at risk for
SVT
346
What is lown ganong Levine syndrome
Bypasses AV node
347
What is brugada syndrome
RBBB with ST elevation in V1-3; susceptible to deadly arrhythmias
348
What is Wellens syndrome
Marked T wave inversion in V2 and 3; anterior descending coronary stenosis
349
What causes low voltage in all leads
COPD, hypothyroidism and chronic constrictive pericarditis
350
What do you see on EKG for a PE
Large S wave in lead I, ST depression in lead II, large q wave in III with T wave inversion; can also see T wave inversion in V1-4 Nd Right BBB *cor pulmonale
351
What does hyperkalemia cause on EKG
Flat p wave, QRS widens, T wave peaked
352
What does hypercalcemia cause on EKG
QT interval shortens
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What does hypocalcemia do to EKG
Prolonged QT
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What is the most common cause of heart failure
Ischemic heart dz
355
What are the ACC/AHA stages of heart failure
- A: risk for dz but do not demonstrate structural dz or symptoms; 5-10% mortality - B: asymptomatic; has LVH and/or impaired LV function, structural heart dz; 15-30% mortality - C:current or past sx of HF with structural heart dz; 15-30% - D: refractory HF; symptoms at rest; 50-50%
356
What are the NYHA stages
- class I: no limitation of physical activity; no sx with ordinary exertion; 5-10% - class II: slight limitation; ordinary activity causes sx; 15-30% - class III: marked limitation of activity; less than ordinary activity causes sx; asymptomatic at rest; 15-30% - class IV: inability to carry out physical activity; sx at rest; 50-60%
357
What are the characteristics of systolic heart failure
Decreased stroke volume, increased ventricular filling pressure; EF <40%; DOE, PND; assoc its CAD, VHD, HT, myocarditis
358
What are the characteristics of diastolic heart failure
Elevated diastolic pressure; SOB, DOE, pulmonary edema; ex: constrictive pericarditis, HTN/hypertrophic cardiomyopathy; myocardial fibrosis, amyloidosis; assoc with aging
359
What are causes of high output heart failure
Hyperthyroidism, anemia, pregnancy, AV fistula, beriberi, paget’s;; high CO but low EF
360
What are causes of low output heart failure
Ischemia heart dz, HTN; dilated cardiomyopathy, valvular and pericardial dz
361
What does RAAS do in heart failure
Activated as a result of decreased renal perfusion -> increases preload by increasing sodium and water reabsoption and increases afterload by increasing PVR
362
What is the effect of arginine vasopressin in heart failure
ADH: stimulates thirst and leads to dilutional hyponatremia; increases preload
363
What meds worsen heart failure
CCB, beta blockers, NSAIDs, antiarrhythmics
364
What can you see on chest XR of someone with heart failure
Cardiomegaly, pulm Edema, increased size of vessels in upper lungs, pleural effusions
365
What should you check in someone >65 with afib
Thyroid
366
The lower the _____ the higher the BNP
EF
367
What are indications for admission to the hospital for heart failure
Acute MI, severe resp distress, hypoxia, hypotension, cardiogenic shock, anasarca, syncope, heart failure refractory to oral meds
368
When is ACEI contraindicated
Angioedema pregnancy, bilateral renal artery stenosis
369
When should you NOT use a beta blocker in heart failure
Class IV heart failure
370
When is digitalis useful
HFrEF and a fib for ventricular rate control
371
When should you use spironolactone
Only in adjunct to other meds; class III and IV patients
372
What dos milrinone do
Inhibits PDE; inotropic vasodilator
373
What receptors do dobutamine vs dopamine stimulate
Dobutamine: beta 1 2 Dopamine: beta 1 and alpha at high concentrations; useful for short term tx
374
What drugs can you give in combo to reduce mortality, increase EF and increase exercise tolerance in heart failure patients
Hydralazine, nitrates and a diuretic
375
What patient population responds better to hydralazine and nitrates
African American
376
What is the definition of shock
Decreased O2 delivery or utilization, increased O2 consumption, hypotension (systolic <80 or 40 below baseline), MAP < 60-65
377
What do the extremities look like in different kinds of shock
- hypovolemic, cardiogenic, obstructive: cool, clammy, vasoconstriction, decreased skin turgor - distributive and dissociative shock: warm and pink assoc with vasodilation
378
What do the neck veins look like in hypovolemic shock
Flat
379
What are the metabolic manifestations of shock
Respiratory alkalosis (blowing off CO2) due to met acidosis; hyperglycemia or hypoglycemia, increased potassium, increased anion gap
380
What are examples of hypovolemic shock
Hemorrhagic, vomiting, diarrhea, burns, DKA, adrenal insufficiency, pancreatitis, bowel obstruction,systemic inflammation
381
What is the treatment for hypovolemic shock
Crystalloids; packed RBCs if hemorrhagic; O2
382
What happens to pulse pressure as loss of blood increases
Pulse pressure decreases
383
What is the most common cause of noncardiogenic shock
Distributive shock; high mortality rate
384
What are the signs of sepsis
Fever >38 or <36; tachycardia >90, tachypnea >20, increase WBC >12000 or <4000
385
What are the mediators of sepsis
IL-6, TNF alpha, NO
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What are the signs of distributive shock
Extremities warm, heart rate fast, BP low, neck veins flat, mental status changes, lungs dry, CI >4.2, mixed venous SVO2 >65%
387
What is the first line pressor in septic shock
NE
388
What is non septic distributive shock
Anaphylactic shock
389
What is the profile of cardiogenic shock
CI <22, increased PAOP, decreased EF, SVR (vasoconstriction), decreased perfusion (mixed venous oxyhemoglobin <65%)
390
What are the different classifications of cardiogenic shock
- cardiomyopathic: MI, severe septic shock, myocarditis, cardiomyopathy - arrhythogenic: tach (afib, flutter, re extrant tach), VT ,VF, Brady (complete heart block, 2nd degree mobitz II) - mechanical: severe aortic insufficiency or MR, acute valve rupture, critical AS, VSD, vent aneurysms, atrial myxoma
391
What are the clinical sings of cardiogenic shock
Decreased BP and UO, cool extremities, distended neck veins, pulm edema
392
What can cause acute MR
Pap rupture sen in inferior or posterior MI
393
What do you give with dobutamine for cardiogenic shock
Norepi
394
What should you avoid in cardiogenic shock
Nitrates
395
What do you give to decrease pulm edema in cardiogenic shock
Lasix
396
What are examples of extracardiac obstructive shock
Obstruction of RV output (massive PE air embolus), impaired diastolic filling of RV (SVC syndrome), cardiac tamponade, constrictive pericarditis, severe HTN
397
What are the classifications of obstructive shock
- pulmonary vascular | - mechanical: tension pneumothorax, pericardial tamponade, constrictive pericarditis
398
What are the characteristics of obstructive shock
Pleuritic chest pain and dyspnea, pulm HTN (increased P2), tracheal deviation (pneumothorax - unilateral breath sounds), distended neck veins with muffled heart sounds (cardiac tamponade)
399
How do you treat obstructive shock
14-16 gauge catheter in 2nd, 3rd ICS MCL followed by chest tube OR emergent tube thoracostomy in 5th ICS MCL
400
What is a sign of obstructive shock due to pericardial tamponade on echo
RA collapse; tx with echo/US to guide pericardilentesis
401
What is virchows triad
Stress, endothelial injury, hypercoagulability
402
What is the profile of obstructive shock
Increased HR, increased JVD without overload, extremities cool, lungs dry, SVR increased
403
What imaging would you use for obstructive shock
computer tomography pulm angiography (CTPA); permits visualization of thrombi in pulm aa
404
When is V/Q scan used
If patient is allergic to contrast, renal insufficiency, women <40 to decrease radiation exposure
405
What will show up on ECG for a PE
S1Q3T3
406
What is pulsus paradoxus
Systolic BP decreases > 10 with inspiration; seen in asthma, cardiac tamponade, and air embolus
407
What is shock index
Heart rate/systolic BP; normal is .5-.7