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Cardio > First Aid > Flashcards

First Aid Flashcards

1
Q

Things that increase inotropy (4)

A

catecholamines
inc intracellular Ca
dec extracellular Na
digitalis

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2
Q

Things that decrease inotropy (5)

A 
Beta blockade
heart failure
acidosis
hypoxemia/hypercapnia
non-dihydropyridine CCBs
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3
Q

Things that increase SV (3)

A

anxiety
exercise
pregnancy

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4
Q

Hydralazine

A

VASOdilator, reduces afterload

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5
Q

Things that increase preload (3)

A

Exercise (slightly)
increased blood volume
sympathetics

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6
Q

Things that increase O2 demand (4)

A

increased afterload
inc contractility
inc heart rate
inc heart size (inc wall tension)

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7
Q

R =

A

(viscocity x length)/radius^4

x 8/pi

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8
Q

Things that increase viscosity (3)

A

polycythemia
hyperporteinemic states (eg multiple myeloma)
hereditary spherocytosis

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9
Q

Where is S1 loudest?

A

Mitral area

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10
Q

Where is S2 loudest?

A

Left sternal border

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11
Q

When is S3 normal?

A

children

pregnant

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12
Q

Causes of wide S2 split

A

RBBB

pulmonary stenosis

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13
Q

Causes of paradoxical S2 split

A

LBBB

aortic stenosis

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14
Q

What murmurs heard in aortic area?

A

Systolic murmur

  • AS
  • flow murmur
  • aortic valve sclerosis
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15
Q

What murmurs heard in pulmonic area?

A

Systolic ejection murmur

  • PS
  • flow murmur (ex. ASD)
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16
Q

What murmurs heard in tricuspid area?

A 
pansystolic 
-TR
-VSD
diastolic
-TS
-ASD
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17
Q

What murmurs heard in mitral area?

A

Sysolic
-MR
Diastolic
-MS

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18
Q

What murmurs heard in L sternal border?

A 
Diastolic
-AR
-PR
Systolic
-hypertrophic cardiomyopathy
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19
Q

What is the ASD murmur?

A

Flow across actual ASD doesn’t cause murmur

  • pulmonary flow murmur due to inc flow through pulmonary
  • diastolic rumble due to inc flow across tricuspid
  • progression –> louder diastolic murmur of pulm regurg from dilatation of PA
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20
Q

Dicrotic notch

A

Dip in aortic pressure at end of systole (right when aortic valve closes); due to blood flowing back into valve cusps

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21
Q

What does inspiration do to heart sounds?

A

increases intensity of R heart sounds

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22
Q

What does expiration do to heart sounds?

A

increases intensity of L heart sounds

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23
Q

What does hand grip do & what does this do to heart sounds?

A
  • inc systemic vascular resistance

- inc MR, VSD murmurs

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24
Q

What does valsava do & what does this do to heart sounds?

A
  • decreases venous return
  • most murmurs dec in intensity
  • MVP & hypertrophic cardiomyopathy murmurs increase
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25
Q

What does rapid squatting do & what does this do to heart sounds?

A
  • inc venous return, inc afterload

- dec MPV, hypertrophic cardiomyopathy murmurs

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26
Q

Where is MR murmur loudest & where does it radiate?

A

loudest at apex

radiates to axilla

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27
Q

Quality & timing of MR & TR murmurs

A

Holosystolic, high pitched, blowing

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28
Q

What increases MR murmur?

A

increased by increased TPR (squatting, handgrip)

or increased LA return (expiration)

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29
Q

Common causes for MR

A

ischemic heart disease
MVP
LV dilatation

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30
Q

Where is TR murmur loudest & where does it radiate?

A

Loudest at tricuspid area

radiates to R sternal border

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31
Q

What increases TR murmur

A

increased by increased RA return (inspiration)

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32
Q

Common causes for TR

A

RV dilatation or endocarditis

RF causes both

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33
Q

What extra sound does AS have?

A

ejection click at start of murmur (due to abrupt halting of valve leaflets)

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34
Q

What is “pulsus parvus et tardus”?

A

In aortic stenosis

= weak pulses compared to heart sounds

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35
Q

VSD murmur - where, and what?

A

Loudest at tricuspid

harsh holosystolic

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36
Q

MVP murmur - what?

A

midsystolic click followed by crescendo murmur, loudest at S2

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37
Q

What can MVP predispose to?

A

IE

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38
Q

Common causes of MVP

A

myxomatous degeneration
RF
chordae rupture

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39
Q

What worsens MVP

A

decreasing venous return (standing, valsalva)

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40
Q

AR murmur - quality and timing

A

Begins immediately at S2
high pitched
blowing

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41
Q

Clinical features of AR

A

wide pulse pressure when chronic

can have bounding pulses & head bobbing

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42
Q

Common causes of AR

A

aortic root dilatation
bicuspid aortic valve
RF

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43
Q

What decreases intensity of AR murmur?

A

vasodilators

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44
Q

What extra sound is heard with MS?

A

opening snap

-due to abrupt halt of leaflet motion after rapid opening due to fusion at leaflet tips

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45
Q

What does MS murmur sound like?

A

rumbling

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46
Q

What increases MS murmur?

A

increased LA return (ex expiration)

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47
Q

PDA murmur - timing and quality

A

continuous machine like murmur

loudest at S2

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48
Q

Common causes of PDA

A

congenital rubella

prematurity

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49
Q

Resting potential of ventricular myocyte

A

-85mV

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50
Q

ERP of ventricular myocyte

A

100msec

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51
Q

resting potential of nodal cells

A

-70mV

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52
Q

How does Ach/adenosine affect HR

A

dec rate of diastolic depolarization –> dec HR

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53
Q

How do catecholamines affect HR

A

inc depolarization –> inc HR

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54
Q

How does sympathetic stimulation affect HR?

A

increases the chance that If channels are open

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55
Q

Normal PR interval length

A

<200msec

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56
Q

Normal QRS duration

A

<120msec

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57
Q

What causes a U wave on ECG?

A

hypokalemia

bradycardia

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58
Q

Order of speed of conduction:

A

purkinje > atria > ventricles > AV node

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59
Q

How long is the delay through the AV node?

A

100msec

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60
Q

What can congenital long QT present with?

A

severe congenital sensorineural deafness

jervell + lange-nielsen syndrome

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61
Q

A-fib treatment

A

BB, CCB, or digoxin

prophylaxis against thromboemoblism w/ warfarin, aspirin

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62
Q

A-flutter treatment

A 
attempt to convert to sinus rhythm
use class IA, IC, or III antiarrhythmics, BBs
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63
Q

When and from where does ANP get released?

A

released from atria in response to increased blood volume & atrial pressure

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64
Q

Actions of ANP:

A

causes generalized vascular relaxation
constricts efferent & dilates afferent renal arterials (cGMP mediated), promoting diuresis & contributing to “escape from aldosterone”

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65
Q

What do peripheral chemoreceptors respond to?

A

dec PO2 (<60mmHg)
inc PCO2
dec pH of blood

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66
Q

What do central chemoreceptors respond to?

A

changes in pH and PCO2 of brain interstitial fluid, which are inflected by arterial CO2
(don’t respond directly to PO2)

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67
Q

Cushing reaction

A

Baroreceptors responsible
inc incracranial P constricts arterioles –> cerebral ischemia –> hypertension (sympathetic response) –> reflex bradycardia

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68
Q

Cushing triad

A

hypertension
bradycardia
respiratory depression

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69
Q

Normal RA pressure

A

<5

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70
Q

Normal RV pressure

A

25/5

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71
Q

Normal PA pressure

A

<25/5

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72
Q

Normal PCWP/LA pressure

A

<12

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73
Q

Normal LV pressure

A

130/10

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74
Q

Normal aortic pressure

A

130/90

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75
Q

Heart autoregulation is via:

A

local metabolites: CO2, adenosine, NO

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76
Q

Brain autoregulation is via:

A

local metabolites: CO2 (pH)

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77
Q

Kidney autoregulation is via:

A

myogenic & tubuloglomerular feedback

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78
Q

Lung autoregulation

A

hypoxia causes vasoconstriction (so only well ventilated areas are perfused)
(in other organs, hypoxia causes vasodilation)

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79
Q

Skeletal m. autoregulation is via:

A

local metabolites: lactage, adenosine, K+

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80
Q

Skin autoregulation

A

Sympathetic stimulation is most important (temp control)

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81
Q

Net fluid flow at a capillary =

A

(Pnet)x(Kf)
Kf is filtration constant (capillary permeability)
Pnet is from starling forces

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82
Q

Causes of edema:

A 
inc Pc (heart failure)
dec PIc (dec plasma proteins in nephrotic syndrome, liver failure)
inc Kf (inc cap perm due to toxins, infections, burns)
inc PIi (lymph blockage)
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83
Q

R –> L shunts

A

5 Ts:

tetralogy (most common), transposition, truncus, tricuspid atresia, total anomalous pulmonary venous retrun

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84
Q

Tricuspid atresia

A

absence of tricuspid valve
hypoplastic RV
requires both ASD & VSD for viability

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85
Q

Total anomalous pulmonary venous return

A

pulmonary veins drain into right heart circulation (SVC, coronary sinus, etc.)

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86
Q

What is the most common congenital cardiac anomaly?

A

VSD

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87
Q

How to close a PDA?

A

indomethacin

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88
Q

What improves tetralogy symptoms & why?

A

squatting

compressing the femoral aa. increases TPR –> directs less blood through the shunt and more through the lungs

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89
Q

What causes tetralogy?

A

anterosuperior displacement of the infundibular septum

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90
Q

Maternal diabetes associated defects

A

transposition

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91
Q

Marfan’s associated defects

A

aortic insufficiency (late complication)

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92
Q

Turner associated defects

A

preductal coarctation

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93
Q

rubella associated defects

A

septal defects, PDA, PA stenosis

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94
Q

Downs associated defects

A

ASD, VSD, AV septal defect (endocardial cushion defect)

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95
Q

22q11 associated defects

A

truncus, tetralogy

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96
Q

consequnces of PDA

A

RVH (rarely RH failure)

Unocrrected can lead to late cyanosis in lower extremities (differential cyanosis)

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97
Q

What keeps PDA open?

A

PGE synthesis & low O2 tension

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98
Q

Coarcation, info:

A

infantile type associated with turner syndrome
check femoral pulses
can result in AR
most commonly associated with bicuspid aortic valve

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99
Q

Transposition prognosis

A

not compatible with life unless a shunt is present (VSD, PDA, or PFO)
Die within first few months w/o surgery

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100
Q

Risk factors for HTN

A

inc age, obesity, diabetes, smoking, genetics

black > white > asian

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101
Q

malignant HTN =

A

severe & rapidly progressing

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102
Q

HTN predisposes to:

A

atherosclerosis, LVH, CHF, stroke, renal failure, retinopathy, and aortic dissection

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103
Q

Hyperlipidemia signs:

A

atheromas
xanthalasmas & xanthomas
corneal arcus

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104
Q

atheroma

A

plaque in vessel wall

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105
Q

xanthomas

A

plaque/nodule composed of lipid laden histiocytes, commonly in achilles tendon (tendonous xanthoma)

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106
Q

xanthelasma

A

plaque/nodule composed of lipid-laden histiocytes int eh skin, esp. eyelid

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107
Q

corneal arcus

A

lipid deposit in cornea, nonspecific (arcus senilis)

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108
Q

Monckeberg arteriosclerosis

A

calcification in media
esp radial or ulnar aa.
usually benign, not obstructive to blood flow, intima not involved
“pipestem aa”

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109
Q

ateriolosclerosis

A

hyaline thickening of small aa in primary htn or diabetes mellitus
hyperplasting “onion skinning’ in malignant htn

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110
Q

Atherosclerosis, about:

A

fibrous plaques & atheromas form in intima of ateries

disease of elastic aa and lg & med muscular aa

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111
Q

Atherosclerosis risk factors:

A

smoking, htn, DM, hyperlipidemia, FH

112
Q

Atherosclerosis pathogenesis:

A

endothelial cell dysfunction –> fatty streaks –> macrophage & LDL accumulation –> foam cell formation –> fatty streaks –> smooth muscle cell migration (involves PDGF + TGF-B) –> fibrous plaque –> complex atheroma (can see cholesterol crystals)

113
Q

Atherosclerosis complications:

A

aneurysms, ischemia, infarcts, peripheral vascular disease, thrombus, emboli

114
Q

Atherosclerosis locations:

A

abdominal aorta > coronary aa. > popliteal a. > carotid a.

115
Q

Atherosclerosis symptoms:

A

angina, claudication

can be asymptomatic

116
Q

What is abdominal aortic aneurysm associated with?

A

associated with atherosclerosis

117
Q

What is thoracic aortic aneurysm associated with?

A

associated with HTN, cystic medial necrosis (Marfan’s)

118
Q

Who is AAA most frequent in?

A

male smokers >50

119
Q

What is aortic dissection associated with?

A

htn, cystic medial necrosis (Marfan)

120
Q

What does aortic dissection feel like?

A

tearing chest pain radiating to the back

121
Q

Stable angina

A

mostly secondary to atherosclerosis
ST depression
retrosternal chest pain with exertion

122
Q

Prinzmetal’s variant angina

A

at rest
secondary to coronary a. spasm
ST elevation

123
Q

Unstable/crescendo angina

A

thrombus but no necrosis
ST depression
Worsening chest pain at rest or with minimal exertion

124
Q

What is an MI most often due to?

A

acute thrombosis due to coronary a. atherosclerosis –> myocyte necrosis

125
Q

Chronic ischemic heart disease

A

progressive onset of CHF over many years due to chronic ischemic myocardial damage

126
Q

MI artery frequency:

A

LAD > RCA > circumflex

127
Q

MI sxs

A

diaphoresis, n/v, severe retrosternal pain, radiating to L arm & jaw, SOB, fatigue, adrenergic sxs

128
Q

MI gross changes 4-24hrs

A

dark mottling

pale with tetrazolium stain

129
Q

MI gross changes 2-4 days

A

hyperemia

130
Q

MI gross changes 5-10 days

A

hyperemic border
central yellow-brown softening
Maximally yellow & soft by 10 days

131
Q

MI gross changes 7 wks

A

recanalized .

gray white

132
Q

MI LM changes 4-12 hrs

A

early coagulative necrosis, edema, hemorrhage, wavy fibers

133
Q

MI LM changes 12-24 hrs

A

contraction bands, release of necrotic cell content into blood, beg. of neutrophil emigration

134
Q

MI LM changes 2-4 days

A

extenive coagulative necrosis, tissue surrounding infarct shows acute inflammation, neutrophil emigration

135
Q

MI LM 5-10 days

A

granulation tissue appears at margins

136
Q

MI LM 7 wks

A

contracted scar complete

137
Q

MI risk from onset to 4 days

A

arrhythmia

138
Q

MI risk 5-10 days

A

free wall rupture, tamponade, papillary m. rupture, septal rupture due to macrophages that have degraded important structural components

139
Q

MI risk 7 wks

A

ventricular aneurysm

140
Q

MI dx in first 6 hours

A

ECG = gold standard in first 6 hrs

141
Q

Transmural MI ECG findings

A

ST elevation, pathologic Q waves

142
Q

Subendocardial MI ECG findings

A

ST depression

143
Q

Troponin I

A

rises after 4 hrs, elevated for 7-10 days

most specific

144
Q

CK-MB

A

can also be from skeletal m.

useful for reinfarction after acute MI

145
Q

AST

A

nonspecific

in cardiac, liver & skeletal muscle cells

146
Q

ECG MI locations:

A

LAD –> ant: V1-4, ant-sept: V1-2
LCX –> ant-lat: V4-6, lat: I, aVL
RCA –> inf: II, III, aVF

147
Q

MI complications:

A

arrhythmia, LV failure + pulmonary edema, cardiogenic shock, rupture, aneurysm, post infarction fibrinous pericarditis, Dressler’s syndrome

148
Q

Dressler’s syndrome

A

several weeks post MI

autoimmune phenomenon resulting in fibrinous pericarditis

149
Q

What is hypertrophic cardiomyopathy associated with?

A

Friedrich’s ataxia

150
Q

What to treat hypertrophic cardiomyopathy with?

A

BB or non-dihydropyradine CCB

151
Q

Causes of restrictive/obliterative cardiomyopathy:

A

sarcoidosis, amyloidosis, postradiation fibrosis, endocardial fibroelastosis (thick fibroelastic tissue in endocardium of young children), loffler’s syndrome (endomyocardial fibrosis w/ a prominent eosinophilic infiltrate), hemochromatosis (dilated cardiomyopathy can also occur)

152
Q

If isolated right heart CHF, usually due to what?

A

Cor pulmonale

153
Q

CHF drugs - which reduce mortality, which for symptom relief only?

A

ACE, ARB, BBs, Spironolactone reduce mortality

Nitrates & diuretics (thiazide or loop) for symptom relief

154
Q

What causes dyspnea on exertion?

A

Failure of CO to increase during exercise

155
Q

What are heart failure cells?

A

Seen with left sided heart failure

They’re hemosiderin-laden macrophages found in the lungs

156
Q

What causes orthopnea in heart failure?

A

increased venous return when supine –> exacerbates pulmonary vascular congestion

157
Q

Nutmeg liver

A

Can see with R sided heart failure
increased venous pressure –> inc resistance to portal flow
rarely leads to “cardiac cirrhosis”

158
Q

Bacterial endocarditis

A

FROM JANE
Fever, Roth spots, Osler’s nodes, new Murmur
Janeway lesions, Anemia, Nail-splinter hemorrhages, Emboli

159
Q

Roth spots

A

round white spots on retina surrounded by hemorrhage

in bacterial endocarditis

160
Q

Acute bacterial endocarditis

A

S. aureus (high virulence)
Large vegetations
Sudden onset

161
Q

Subacute bacterial endocarditis

A

Viridans strep (low virulence)
Small vegetations
Sequela of dental procedures
more insidious onset

162
Q

Causes of nonbacterial endocarditis:

A

malignancy, hypercoagulable sate, lupus

marantic/thrombotic endocarditis

163
Q

S. bovis

A

colon cancer

164
Q

S. epidermidis

A

prosthetic valves

165
Q

Most frequent valve affected in endocarditis

A

Mitral

166
Q

IV drug abusers - endocarditis –> which valve and which bugs?

A

Tricuspid valve

S. aureus, pseudomonas, candida

167
Q

Complications of endocarditis

A

chordae rupture, glomerulonephritis, suppurative pericarditis, emboli

168
Q

Rheumatic fever, cause of early deaths?

A

myocarditis

169
Q

Late sequalae of rheumatic fever

A

rheumatic heart disease

mitral > aortic&raquo_space; tricuspid

170
Q

Early rheumatic fever lesion

A

Mitral regurgitation

171
Q

Late rheumatic fever lesion

A

Mitral stenosis

172
Q

Rheumatic fever histology:

A 
Aschoff bodies (granuloma w/ giant cell)
Anitschkow's cells (activated histiocytes)
173
Q

Rheumatic fever, mechanism:

A

immune mediated
hypersensitivity type II raction
Antibodies to M protein
elevated ASO titers

174
Q

Rheumatic fever mnemonic

A

FEVERSS
Fever, Erythema marginatum, Valvular damage (vegetation & fibrosis), elevated ESR, Red hot joints (migratory polyarthritis), Subcutaneous nodules, St vitus dance (chorea)

175
Q

Acute pericarditis - clinical

A 
sharp pain (esp w/ inspiration)
relieved by sitting up & leaning forward
176
Q

Most common pericarditis

A

fibrinous pericarditis

177
Q

Causes of fibrinous pericarditis

A

Dressler’s syndrome, uremia, radiation

178
Q

Presentation of fibrinous pericarditis

A

loud friction rub

179
Q

Cause of serous pericarditis

A

noninfectious inflammatory diseases (ex. rheumatoid arthritis, SLE)

180
Q

Cause of suppurative/purulent pericarditis

A

infectious agents

181
Q

Tamponade - clinical features

A

dec CO, equilibrium of diastolic pressure in all 4 chambers, hypotension, elevated JVD, distant heart sounds, inc HR, pulsus paradoxus

182
Q

Syphilitic heart disease

A

tertiary syphilis
disrupts vasa vasorum of aorta
dilation of aorta & valve ring
calcification of aortic root & ascending arch
“tree bark” appearance of aorta
can result in aneurysm of ascending aorta or arch & valve incompetence

183
Q

Myxoma

A

most common primary tumor
90% in atria (mostly LA)
“ball-valve” obstruction in LA
associated w/ multiple syncopal episodes

184
Q

Rhabdomyomas

A

most common primary tumor in children

associated with tuberous sclerosis

185
Q

Metastasis

A

most common hear tumor

from melanoma, lymphoma

186
Q

Kussmaul’s sign

A

elevated JVP on inspiration

187
Q

Varicose veins

A

due to chronically elevated venous pressure
predisposes to poor wound healing, varicose ulcers
thromboemoblism is rare (compare with stasis of deep veins)

188
Q

Raynaud’s

A

arteriolar vasospasm in response to cold or emotional stress

189
Q

Raynaud’s phenomenon

A

raynaud’s when secondary to mixed CT disease, SLE, CREST syndrome

190
Q

Temporal (giant cell arteritis)

A

elderly women, associated w/ polymyalgia rheumatica, focal granulomatous inflammation
tx w/ high dose steroids

191
Q

Takayasu’s arteritis

A

<40, weak upper extremity pulses, fever, night sweats, arthritis, myalgias, skin nodules, occular disturbances
granulomatous thickening of aortic arch & proximal great vessels
Tx w/ corticosteroids

192
Q

Polyarteritis nodosa

A

young adults, fever, weight loss, malaise, headache, abd pain, melena, htn, neurologic dysfunction, cutaneous erruptions; typically renal & visceral vessels; transmural w/ fibrinoid necrosis; multiple aneurysms & constrictions on arteriogram
tx w/ corticosteroids, cyclophosphamide

193
Q

Kawasaki disease

A

fever, lymphadenitis, conjunctivitis, changes in lips/oral mucosa (“strawberry tongue”), hand foot erythema, desquamation, may develop coronary aneurysms
tx w/ IV immunoglobulin & aspirin

194
Q

Buerger’s disease (thromboangitis obliterans)

A

gangrene, autoamputation, superficial nodular phlebitis, segmental thrombosing vasculitis
tx w/ smoking cessation

195
Q

Microscopic polyangiitis

A

pauci-immune gn, palpable purpura, no granulomas

196
Q

Wegener granulomatosis

A

perforation of nasal septum, chronic sinusitis, otitis media, mastoiditis, hemoptysis, cough, dyspnea, hematuria, red cell casts, triad of focal necrotizing vasculitis, necrotizing granulomas in lung & upper airway, and necrotizing GN
CXR - large nodular densities
tx w/ cyclophosphamide, corticosteroids

197
Q

Churg-strauss syndrome

A

sinutitis, palpable purpura, peripheral neuropathy (eg wrist/foot drop), can also involve heart, GI, kidneys; pauci immune, granulomatous vasculitis w/ eosinophilia

198
Q

Henoch-Schonlein purpura

A

most common form of childhood systemic vasculitis, triad, abdominal painn, melena, multiple lesions of same age, association with IgA nephropathy

199
Q

Sturge-weber disease

A

congenital vascular disorder
affects capillary sized vessels
manifests with port wine stain (aka nevus flammeus) on face, ipsilateral leptomeningeal angiomatosis (intracerebral AVM), seizures, early onset glaucoma

200
Q

Strawberry hemangioma

A

benign capillary hemangioma of infancy, appears in 1st few weeks of life, 1/2000 births, grows rapidly & regresses spontaneously at 5-8 yrs

201
Q

Cherry hemangioma

A

benign capillary hemangioma of the elderly, does not regress, frequency increases with age

202
Q

Pyogenic granuloma

A

polypoid capilary hemangioma that can ulcerate & bleed; associated w/ trauma & pregnancy

203
Q

cystic hygroma

A

caverous lymphangioma of the neck

associated w/ turner syndrome

204
Q

glomus tumor

A

benign, painful, red-blue tumor under fingernails; arises from modified smooth muscle cells of glomus body

205
Q

bacillary angiomatosis

A

benign capillary skin papules found in AIDs pts; caused by bartonella henselae infections; freq mistaken for kaposi’s sarcoma

206
Q

angiosarcoma

A

highly lethal malignancy of liver; ass w/ vinyl chloride, arsenic, and ThO2 (thorotrast) exposure

207
Q

lymphangiosarcoma

A

lymphatic malignancy associated w/ persistent lymphedema (eg post radial mastectomy)

208
Q

kaposi’s sarcoma

A

endothelial malignancy of the skin ass w/ HHV-8 & HIV; freq mistaken for bacillary angiomatosis

209
Q

Essential HTN therapy:

A

diuretics, ACE, ARBs, CCBs

210
Q

CHF HTN therapy

A

diuretics, ACE/ARBs, BBs (compensated CHF), K sparing diuretics
BBs can be used cautiously in decompensated CHF; contraindicated in cardiogenic shock

211
Q

DM HTN therapy:

A

ACE/ARBs (protective against diabetic nephropathy), CCB, diuretics, BBs, alpha-blockers

212
Q

What does hydralazine do

A

inc cGMP –> smooth muscle relaxation
arterioles > veins
decrease afterload on heart

213
Q

What is hydralazine used for?

A

severe HTN, CHF, 1st line for HTN in pregancy (w/ methyl dopa), frequently given with BB to prevent reflex tachycardia

214
Q

Hydralazine toxicity:

A

compensatory tachycardia (contraindicated in angina/CAD), fluid retention, nausea, headache, angina, lupus-like syndrome

215
Q

What do CCBs do?

A

block L type Ca channels of cardiac and smooth muscle –> reduce muscle contractility

216
Q

Relative potency of the 3 CCBs on vessels:

A

nifedipine > diltiazem > verapamil

217
Q

Relative potency of the 3 CCBs on heart:

A

verapamil > diltiazem > nifedipine

Verapamil = Ventricle

218
Q

What are CCBs used for?

A

HTN, angina, arrhythmias (not nif.), prinzemetal’s angina, Raynaud’s

219
Q

CCB toxicity

A

cardiac depression, AV block, peripheral edema, flushing, dizziness, constipation

220
Q

Nitroprusside

A

Use to tx malignant HTN
short acting, inc cGMP via direct release of NO
can cause cyanide toxicity

221
Q

Fenoldepam

A

Used to tx malignant HTN
dopamine D1 receptor agonist
relaxes renal vascular smooth m.

222
Q

Diazoxide

A

Used to tx malignant HTN
K channel opener –> hyperpolarizes & relaxes vascular smooth m.
can cause hyperglycemia (reduces insulin release)

223
Q

What are nitroglycerin, isosorbite dinitrate used for?

A

angina, pulmonary edema

also aphrodisiac & erection enhancer

224
Q

Nitroglycerin, isosorbide dinitrate toxicity:

A

reflex tachy, hypotension, flushing, headache, “monday disease”

225
Q

“Monday disease”

A

With nitroglycerin & isosorbide dinitrate
development of tolerance to the vasodilating during the work week & loss of tolerance over the weekend –> resulting in tachycardia, dizziness, headache on reexposure

226
Q

Anti-anginal meds:

A

Nitrates (preload), BBs (afterload)

both dec O2 demand, so together they decrease an extra amount

227
Q

Pindolol & acebutolol

A

partial beta-agonists –> contraindicated in angina

228
Q

What do HMG CoA reductace inhibitors do?

A

**decrease LDL a lot, increase HDL a bit, dec TG a bit

inhibit cholesterol precursor –> mevalonate

229
Q

HMG CoA reductance inhibitors - side effects

A

hepatotoxicity (inc LFTs)

rhabdomyolysis

230
Q

What does niacin do?

A

dec LDL, **inc HDL, dec TG
inhibits lipolysis in adipose tissue
reduces hepatic VLDL secretion into circulation

231
Q

Niacin side effects:

A

red, flushed face (dec by aspirin or by long time use), hyperglycemia (acanthosis nigricans), hyperuricemia (exacerbates gout)

232
Q

Bile acid resins - which drugs?

A

cholestyramine
colestipol
colesevelam

233
Q

What do bile acid resins do?

A

dec LDL, slightly inc HDL and TGs

Liver uses cholesterol to make more bile acids

234
Q

Bile acid resins side effects:

A

pt hates it –> it tastes bad, GI discomfort
dec absorption of fat soluble vitamines
cholesterol gallstones

235
Q

Cholesterol absorption blocker - what drug?

A

ezetimibe

236
Q

What do cholesterol absorption blockers do?

A

dec LDL

237
Q

Cholesterol absorption blockers side effects:

A

rare inc LFTs

238
Q

What drugs are fibrates?

A

gemfibrozil, clofibrate, benzafibrate, fenofibrate

239
Q

What do fibrates do?

A

dec LDL, inc HDL, hugely dec TGs

upregulate LPL –> inc TG clearance

240
Q

Fibrates - side effects

A

myositis, hepatotoxicity (inc LFTs), cholesterol gallstones

241
Q

Digoxin

A 
= cardiac glycoside
75% bioavailable
20-40% protein bound
half life = 40 hours
urinary excretion
242
Q

How does digoxin work?

A

direct inhibition of Na/K ATPase (pos ino) & stimulates vagus

243
Q

Digoxin use

A

CHF (inc contractility), afib (dec conduction at AV node & depression of SA node)

244
Q

Digoxin toxicity

A

cholinergic (n/v/diarrhea, blurring yellow vision), ECG (inc PR, dec QT, scooping, T wave inversion, arrhythmia, hyperkalemia)

245
Q

What worsens digixon toxicity?

A

renal failure (dec excretion), hypokalemia (permissive for digoxin binding site on NaK ATPase), quinidine (dec dig clearance - displaces it from tissue binding sites)

246
Q

Antidote to Dig toxicity

A

slowly normalize K+, lidocaine, cardiac pacer, anti-dig Fab fragments, Mg2+

247
Q

Nesiritide

A

=recombinant B-type natriuretic peptide
causes inc cGMP & vasodilation
use for acute decompensated heart failure
toxicity –> hypotension

248
Q

class I antiarrhythmics

A

local anesthetics slow or block conduction (esp in depolarized cells), dec slope of phase 0 depol, inc threshold for firing in abnormal pacemaker cells; state dependant (selectively depress tissue that is frequently depolarized, eg fast tachycardia)

249
Q

What are the Class IA drugs?

A

quinidine, procainimide, disopyramide

250
Q

What do the class IA drugs do?

A

inc AP duration, inc ERP, inc QT interval, affect both atrial & ventricular arrhythmias, esp reentrant & ectopic supraventricular tachycardia

251
Q

Quinidine toxicity

A

cinchonism (headache, tinnitus), thrombocytopenia, torsade de pointes due to inc QT interval

252
Q

Procainamide toxicity

A

reversible SLE like syndrome

253
Q

What are the class IB drugs?

A

lidocaine, mexilitine, tocainide

phenytoin can fall into IB

254
Q

What do the class IB drugs do?

A

IB is Best post MI
dec AP duration, preferentially affect ischemic or depolarized purkinje & ventricular tissue
useful in acute ventricular arrhythmias (esp post MI) & in digitalis- induced arrhythmias

255
Q

Class IB toxicity

A

local anesthetic, CNS stim/depression, cardiovascular depression

256
Q

What are the class IC drugs?

A

flecainide, propafenone

257
Q

What do the IC drugs do?

A

no effect on AP duration, useful in Vtachs that progress to VF and in intractable SVT
usually used as a last resort in refractory tachyarrhythmias; for pts WITHOUT structural abnormalities
**IC is Contradindicated post-MI

258
Q

Class IC toxicities

A

proarrhythmic, esp Post-MI (contraindicated), significantly prolongs refractory period in AV node

259
Q

What can increase toxicity for Class I drugs?

A

hyperkalemia causes inc toxicity for all class I drugs

260
Q

Effect of different Class I’s on action potential duration

A

Class IA lengthens AP duration
Class IB shortens AP duration
Class IC doesn’t change AP duration

261
Q

What do class II (BBs) drugs do?

A

dec cAMP, dec Ca currents, suppress abnormal pacemaker by dec slope of phase 4
AV node particularly sensitive –> inc PR

262
Q

Which BB is very short acting?

A

esmolol

263
Q

What to use BBs for?

A

V-tach, SVT, slowing ventricular rate during afib & aflut

264
Q

BB toxicity

A

impotence, exacerbation of asthma, cardiovascular effects (brady, AV block, CHF), CNS effects (sedation, sleep alteration), may mask signs of hypoglycemia

265
Q

A metoprolol side effect

A

can cause dyslipidemia, treat overdose w/ glucagon

266
Q

What are the class III drugs?

A 
K IS BAD
ibutilide
sotolol
bretylium
amiodarone
dronedarone/dofetalide
267
Q

What do the class III drugs do?

A

inc AP duration, inc ERP, used when other antiarrhythmics fail, inc QT interval

268
Q

Sotolol toxicity

A

torsades, excessive Beta block

269
Q

Ibutilide tox

A

torsades

270
Q

Bretylium toxicity

A

new arrhythmias, hypotension

271
Q

Amiodarone toxicity

A

pulmonary fibrosis, hepatotoxicity, hypothyroidism/hyperthyroidism (40% iodine by weight), corenal deposits, skin deposits (blue/grey) resulting in photodermatitis, neurologic effects, constipation, cardiovascular effects (brady, heart block, CHF)
**Check PFTs, LFTs, and TFTs*

272
Q

What is special about amiodarone?

A

it has class I, II, III, IV effects bc it alters the lipid membrane

273
Q

What doe the Class IV (CCBs) do?

A

dec conduction vel, inc ERP, inc PR interval, used in prevention of nodal arrhythmias (eg SVT)

274
Q

Class IV toxicity:

A

constipation, flushing, edema, CV effects (CHF, AV block, SA node depression)

275
Q

Adenosine

A

inc K out of cells –> hyperpolarizes, dec Ca
drug of choice in diagnosing/abolishing SVT
Very short acting (~15sec)
effects blocked by theophylline

276
Q

Adenosine toxicity

A

flushing, hypotension, chest pain

277
Q

Mg2+

A

effective in torsades de points & digoxin toxicity

Cardio (7 decks)

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