cardiac 2024 pt 2 Flashcards

1
Q

CAD usually due to what?

describe pathophysiology

r/f

ages gender

A

atherosclerosis.

inadequate tissue perfusion due to imbalance between increased demand and decreased coronary artery blood suppy.

DM is worse then smoking.

men >45 or women>55 with FH of CAD= male before 55 or female before 65.

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2
Q

virchow’s triad

A

think DVT risk factors:
intimal damage, stasis, hypercoagulability(protein S or C def, factor V leiden mutation, antithrombin III def, oral contraceptive, malignancy, PG, smoking

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3
Q

DVT
1. most specific sign
2. first line imaging
3. gold standard

A
  1. edema LE >3cm
  2. venous doppler ultrasound
  3. contrast venography, invasive
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4
Q

IVC filter for DVT when?

A

recurrent DVT/PE despite adequate anticoagulation OR stable pts in whom anticoagulation is contraindicated OR right ventricular dysfunction w/ an enlarged RV on echo

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5
Q

DVT tx in …
1. PG
2. malignancy

A
  1. LMWH as initial and long term therapy.
  2. same plus Warfarin or direct oral anticoagulants are alternatives to LMWH in these pts.
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6
Q

Common causes of right and left heart failure

A

left: CAD and HTN. Others include valvular disease and cardiomyopathyies.

right: left sided heart failure. Pulm disease(COPD and pulm HTN), mitral stenosis.

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7
Q

Rt sided heart failure pneumonic

A

S W E L L I N G

swelling in legs, feet, abdomen
wt gain (early sign, retaining fluid)
edema(pitting)
large neck veins
lethargic (low cardiac output)
irregular heart beat (careful to get afib)
nausea
girth of abdomen increased(hepatomegaly)

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8
Q

systolic heart failure.
describe EF,
___ ventricular systolic dysfunction,
___ ventricle cannot eject blood properly

A

reduced EF.
left, left

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9
Q

diastolic heart failure.
describe EF,
___ ventricular systolic dysfunction,
ventricle issue

A

preserved EF
left, ventricle too stiff to allow for filling of blood

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10
Q

left sided heart failure 5 S/S

A

SOB, crackles, orthopnea, difficulty breathing at night, pulm edema

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11
Q

gallop and LV chamber in systolic and diastolic heart failure

A

Systolic: S3, LV small with thick walls

Diastolic: S4, LV dilated with thin walls

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11
Q

left sided heart failure pneumonic for s/s

A

D R O W N I N G
difficulty breathing
rales/crackles
orthopnea
weakness
nocturnal paroxysmal dyspnea
increased hrt rate(fluid overload)
nagging cough(watch for frothy foam)
gaining wt

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12
Q

pathophysiology of heart failure: afterload, preload, contractility

A

initial insult leads to increased afterload, increased preload, and decreased contractility.

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13
Q

cheyne stokes breathing

A

deeper, faster breathing with gradual decrease and periods of apnea and cyanosis. think left sided heart failure.

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14
Q

3 ways to manage diastolic heart failure

A
  1. heart rate control
  2. BP control
  3. Relief of ischemia(BB, ACE, CCB, diuretics for volume overload).

No CCB in systolic heart failure.

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15
Q

4 ACE inh precautions

A

A A C E
avoid in PG
ANGIOEDEMA
Cough
Elevated potassium (watch for hyperkalemia)

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16
Q

high potassium on ecg

A

ST elevation (high pumps)
peaked T waves and ST elevations

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17
Q

No CCB in what d/s

A

SYSTOLIC heart failure

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18
Q

BB and CCB 3__ tropics

A

neg chronotropic(lower rate)
neg inotropic(less force)
neg dromotropic(less beats)

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19
Q

BB decreases what 3 things(not including HR and BP)

A

resistance, workload, cardiac output

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20
Q

avoid BB in what 2 conditions

A

COPD and asthma

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21
Q

avoid BB in 4 kinds of treatments (pneumonic)

A

B B B B
. bradycardia
2. breathing problems (wheezing, …)
3. bad for heart failure pts
4. blood sugar masking (70 or less)

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22
Q

Before giving CCB, count what

A

count HR and BP.

avoid in systolic below 100 and HR below 60

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23
Q

what is digoxin toxicity

A

Over 2.0

vision changes, anorexia, nausea, dizzy

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24
Q

creatinine levels

A

nml 0.6-1.2;

over 1.3 “no pee pee”

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25
Q

check what pulse and what lab in digoxin toxicity

A

apical pulse under 60

potassium below 3.5

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26
Q

digoxin, careful with what 2 pts

A

on diuretics or has renal problems

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27
Q

vasodilators do what 3 things.
what about preload and afterload

A

D- decrease BP
D- dilates vessels
D-decrease vascular resistance

decrease preload and afterload

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28
Q

top 5 vasodilators

A

nitro, nitroprusside, hydralazine, isosorbide, minoxidil

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29
Q

when to stop a vasodilator

A

on viagra, systolic below 100 or drops by 30 mmhg, lack of coordination, irritability, sweating, pallor

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30
Q

3 normal SE of vasodilator

A

HA, hypoTN, hot flushing(facial redness)

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31
Q

2 K++ wasting diuretics

caution in who

A

furosemide and HCTZ.

isosorbide not one.

caution in hypokalemia 3.5 or less

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32
Q

top 3 loops to give for worsening heart failure

A

furosemide, torsemide, bumnetanide

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33
Q

loops MOA

A

blocks reabsorption of Na into kidneys

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34
Q

what 3 drugs spare K++

A

lisinopril, losartan, spirolactone

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35
Q

what 3 things to check before giving a diuretic. pneumonic

A

B B P
BP, hold for systolic under 100
BUN & Cr
K++ imbalances

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36
Q

what is dilated CM

common cause

chamber

hallmarks

A

most common CM.
systolic dysfunction, leading to dilated, weak heart

idiopathic cause or viral(enterovirus, coxsackievirus B, echovirus)

usually left ventricle.

S3 gallop(due to filling of a dilated ventricle); displaced apical impulse

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37
Q

postviral myocarditis, HIV, lyme, parovirus B19, chagas d/s

A

poss etio for dilated CM

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38
Q

ETOH abuse, radiation, PG, autoimmune, thyroid d/o, vit B1 def(thiamine)

A

poss etio for dilated CM

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39
Q

Dilated CM demographics

A

2:1 male to female
african amer more then whites

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40
Q

dilated CM, remodeling of what? affects what valves, EF

A

left ventricle, thin wall, reduced EF, increased end systolic and diastolic volume leads to dilation. mitral insuff, tricuspid insuff

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41
Q

how to calculate cardiac output

A

HR x stroke volume

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42
Q

what is preload

A

end diastolic volume

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43
Q

describe frank starling law in dilated CM

A

increased stretch=increased contractility
relationship breaks down causing stroke volume to decrease and so does cardiac output

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44
Q

dilated CM tx

A

systolic heart failure: ACE, BB.
symptom control with diuretics

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45
Q

3 etio of hypercholesterolemia

A

hypothyroidism, PG, kidney failure

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46
Q

4 etio of hypertriglyceridemia,
may cause what organ issue

A

DM, ETOH, obesity, steroids, estrogen

pancreatitis

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47
Q

goals of lipid lowering agents

A

plaque stabilization
reversal of endothelial dysfunction
thrombogenicity reduction
atherosclerosis regression

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48
Q

FH guidelines to screen for hyperlipidemia

A

first degree male relative with CHD before age 55,
first degree female relative with CHD before age 65

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49
Q

plaque stabilization
reversal of endothelial dysfunction
thrombogenicity reduction
atherosclerosis regression

A

goals of lipid lowering agents

50
Q

AHA, describe screening in adults for hyperlipidemia

A

ages 20-39 who are free of CVD is reasonable to assess risk factors every 4-6 years to calculate their 10 year risk

51
Q

optimal age to screen for hyperlipidemia

A

higher risk: >1 risk factor(HTN, smoking, FH) or 1 severe risk factor. initiate screening at age 20-25 for males and age 30-35 for females

lower risk: initiate screening for age 35 for males, 45 for females

52
Q

lipid guidelines for initiation of statin therapy.

6 risk factors to look at

A

gender, age, smoking, BP, blood cholesterol level, DM, race

53
Q

lipid guidelines for initiation of statin therapy.

  • DM between ages what?
  • pts without CV disease ages what and ___% risk of having a MI or stroke within __ years
    *people age ____ 21 years of age with LDL > ____
    *anyone with clinical atherosclerotic CV disease
    Pts < ___ years old with familial hypercholesterolemia
A

DM ages 40-75 years old

CV ages 40-75 years old and 7.5% within 10 years

21 years old LDL >190

19 years old

54
Q

what are the best meds to lower elevated LDL

A

statins and then bile acid sequestrants

55
Q

what are the best meds to lower triglylcerides

A

fibrates then niacin

56
Q

what are the best meds to increase HDL

A

niacin then fibrates

57
Q

what are the best meds for DM for hyperlipidemia

A

statins and fibrates

58
Q

statins MOA

affect on LDL…

A

inhibit rate limiting step in hepatic chol synthesis via inhibition of enzyme HMG-COA reductase.

increase LDL receptors, promoting LDL clearance, reduce Tg

59
Q

niacin MOD

A

increase HDL(delays clearance), decreases hepatic prod of LDL and its precursor VLDL. Decreases Tg.

60
Q

best drug for
1. decrease LDL
2. increase HDL

A
  1. statin
  2. niacin
61
Q

contraindications: active hepatic d/s, persistant elevated LFTs, PG, breastfeeding

A

statin

62
Q

active PUD, active liver d/s, arterial bleeding

A

niacin

63
Q

fibrates MOA

A

inhibit triglyceride synthesis, increase activity of lipoprotein lipase(stim catabolism of Tg rich lipoproteins), increase HDL synthesis and decrease LDL synthesis

64
Q

only fibrate approved to use in combination with statin

A

fenofibric acid

65
Q

contraindications: active hepatobiliary ds, severe renal ds, breastfeeding, gemfibrozil+repaglinide

A

fibrates

66
Q

chol med..
1. risk of increased gallstone
2. taken in evening
3. can interact with drugs that inhibit CP450 systems
4. avoid with warfarin

A
  1. fibrates
  2. most statins (atorvastatin and rosuvastatin can be taking anytime)
  3. statins (erythromycin, diltiazem, -azoles)
  4. BAS
67
Q

name fibrates

A

fenofibrate and gemfibrozil

68
Q

name bile acid sequestrants

A

cholestyramine, colestipol, colesevelam

69
Q

cholestyramine, colestipol, colesevelam

A

bile acid sequestrants

70
Q

bile acid sequestrants affect what lipids

A

increase LDL receptors and decrease LDL levels

71
Q

lipid drug safe in PG

A

bile acid sequestrants

72
Q

bile acid sequestrants…
1. used in combo with what
2. adverse affect on tg
3. long term use
4. may impair absorption of what

A
  1. statin to reduce LDL, mild to mod increase in HDL
  2. increase Tg
  3. osteoporosis
  4. antibiotics, digoxin, warfarin, fat soluable vitamins… so take these meds 1 hour before BAS
73
Q

contraindications to BAS

A

severe hypertriglyceridemia, complete biliary obstruction

74
Q

cholestyramine used to treat what else

A

pruritus assoc with biliary obstruction

75
Q

ezetimibe MOA, indication, SE

A

inhibit intestinal chol absorption
often used in combo with statin to reduce LDL level
SE: HA, diarrhea, increased LFTs

76
Q

main effect on BP: ACE inh and ARBs

A

decrease SV and SVR

77
Q

main effect on BP: alpha blockers, BB, CCB

A

alpha: decrease SVR
BB: decrease HR and SVR
CCB: decrease SVR

78
Q

alpha receptors

A

think sympathetic system(fight or flight) and vasoconstriction of blood vessels

79
Q

beta receptors on heart

A

increase HR and SV, both leading to increase CO and increase BP

80
Q

BP equation

A

CO x SVR

81
Q

CCB work on what cells

A

vascular and muscle cells, block vasoconstriction

82
Q

diuretic MOA for HTN

A

decrease Na and H2O reabsorption therefor decrease BP

83
Q

HTN med for gout pt

A

CCB, losartan is the only ARB that doesn’t cause hyperuricemia

84
Q

HTN emergency

A

SBP > 180 and/or DBP >120 with evidence of end organ damage

85
Q

HTN emergency managment

A

IV BP agents. Mean arterial pressure should be reduced gradually by about 10-20% in 1st hour and additional 5-15% over the next 23 hours

86
Q

meds to treat HTN emergency

A

IV labetalol or Na nitroprusside infusion

87
Q

hypotension reading

affected by 3 things

A

90/60

CO
blood viscosity
total peripheral resistance

88
Q

4 kinds of shock

A

hypovolemic, cardiogenic, obstructive, distributive/impaired vasoconstriction

89
Q

pancreatitis, vomiting, bowel obstruction, DKA, renal loss, resp loss, severe burns

A

non haemorrhagic causes of hypovolemic shock

90
Q

S/S of hypovolemic shock

A

pale cool extremities/dry skin, slow capillary refill, decreased skin turgor, AMS, dry mucous membrane

no profound resp distress

91
Q

hallmark of hypovolemic shock

A

vasoconstriction, increased SVR, hypotension, decreased CO and decreased pulm capillary pressure

92
Q

class 1 and 2 of hypovolemic shock

A
  1. <15% blood loss: nml pulse, SBP nml
  2. 15-30% blood loss: pulse >100 (tachycardic), SBP >100
93
Q

class 3 and 4 of hypovolemic shock

A
  1. 30-40% loss: SBP <100, tachycardic, confusion, decreased urine output
  2. > 40%: lethargy, no urine output, …
94
Q

CBC in hypovolemic shock

A

increased hgb/hct due to dehydration(hemoconcentration.
decreased hgb/hct in late hemorrhagic shock

95
Q

Hallmark of distributive shock

A

decreased ALL
CO, SVR, PCWP

96
Q

most common form of distributive shock

A

septic shock.

early septic shock has increased CO and SVR due so warm extremities in these pts.

97
Q

pathophys of septic shock:

infective organism activate _____ system, then host produces ___ ___ ___ then ____ cause prompt peripheral ____then ___ in SVR. ____ capillary permeability (initiating ____), and end organ thrombosis.

A

infective organism activate immune system, then host produces systemic inflammatory response then cytokines cause prompt peripheral vasodilation then decrease in SVR. Increased capillary permeability (initiating shock), and end organ thrombosis.

98
Q

what is the only shock associated with increased CO (fast capillary refill time: warm, flushed extremities)

A

septic shock

99
Q

S/S of septic shock

A

hypotension with WIDE pulse pressure

bounding arterial peripheral pulses

100
Q

hypotension with WIDE pulse pressure

bounding arterial peripheral pulses

A

S/S of septic shock

101
Q

tx of septic shock

A

pan culture before initiating: zosyn + ceftriaxone or imipenem. gentamycin for pseudomonas. vanco for mrsa. clinda or flagyl for intra-abdominal infections, ceftriaxone in asplenic pts to cover N. Menigitidis & H. Influez

IV fluid resus with isotonic crystalloids (Normal saline , LR)

vasopressors: if no response to 2-3L of IV fluids with goal of MAP >60 +/- IV hydrocortisone.

102
Q

Septic shock organism tx

pseudomonas

mrsa

intra-abd infections

asplenic pts with cover what 2 organisms

A

gentamycin for pseudomonas. vanco for mrsa. clinda or flagyl for intra-abdominal infections, ceftriaxone in asplenic pts to cover N. Menigitidis & H. Influez

103
Q

anaphylactic shock

Ig _______________

tx med

cardio issue?

airway

observe pt for how long

A

IgEEEEEEEEEEEEEEEEEEEEEEEEEEEEE

epi 1st line (0.3 mg IM of 1:1,000 repeat q 5-10 min as needed).

if cardiovascular collapse, give epi 1mg 1:10,000

airway mgmt with benadryl 25-50mg IV blocks H1, ranitidine blocks H2

observe pt for 4-6 hours b/c 20% pts have a biphasic phenomenon (return of symptoms 3-4 hours before initial reaction)

104
Q

neuropathic shock

d/t what

pathophys

HR, SVR, pulse pressure

tx

A

due to acute spinal cord injury, regional anesthesia

pathophys: autonomic sympathetic blockade then unopposed increased vagal tone then BRADYCARDIA and HYPOTN. loss of sympathetic tone then warm, dry skin

decreased HR and SVR, hypovolemia, and WIDE pulse pressure

tx: fluids, pressors, +/- corticosteroids

105
Q

decreased HR and SVR, hypovolemia, and WIDE pulse pressure

A

neuropathic shock

106
Q

endocrine shock

A

for example: adrenal insuff (addisons)

tx hydrocortisone 100mg IV (often unresponsive to fluids and pressors)

107
Q

CO decreased, PCWP decreased, SVR increased

A

hypovolemic shock

108
Q

CO decreased, PCWP increased, SVR increased

A

cardiogenic and obstructive shock

109
Q

CO increased, PCWP could be up of down, SVR decreased

A

septic shock

110
Q

shocks with severe and no resp distress

A

hypovolemic has none. skin pale, mottled

cardiogenic and obstructive has severe. plus cool clammy skin

111
Q

HOCM definition

A

autosomal dominant d/o. diastolic dysfunction.

subaortic outflow obstruction due to asymmetrical septal hypertrophy and systolic anterior motion of the mitral valve

112
Q

obstruction in HOCM worsens with what 2 things

A

increased contractility and/or decreased LV volume

113
Q

HOCM murmur

A
  • harsh systolic murmur best heard at LSB
  • increased murmur intensity with decreased venous return(valsalva, standing) or decreased afterload
  • decreased murmur intensity with increased venous return(squatting, leg raise) or increased afterload(handgrip). increased LV volume preserves outflow.
    *possible loud S4, MR, pulsus bisferens
114
Q

harsh systolic murmur best heard at LSB

A

HOCM

115
Q

most common symptom in HOCM

A

diastolic dysfunction leading to increased left atrial pressure and left pulmonary vein pressure and therefore exertional dyspnea.

116
Q

other symptoms in HOCM

A

arrhythmia, angina, syncope

117
Q

HOCM tx

A

BB first line. CCB the alternative.

caution with digoxin(increased contractility), nitrates, diuretics(both decrease LV volume)

118
Q

AS vs HOCM

squatting and leg raise (increase LV volume)

A

this will decreased HOCM and increase AS

119
Q

dizziness, lightheadedness, palpitations, blurred vision, darkening of visual fields and/or syncope

A

cerebral hypoperfusion

orthostatic hypotension

120
Q

criteria for orthostatic hypotension

A

at least 20 drop in systolic or at least 10 drop in diastolic

121
Q
A
121
Q

med tx for orthostatic hypotension

A

fludrocortisone