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Flashcards in Firecracker 10/27 Deck (153):
1

STEMI - EKG

hyperacute T waves
T wave inversions
ST segement elevation
Q waves

2

ST segment elevation =

transmural ischemia

3

Leads II, III, aVF

inferior
posterior descending artery or marginal branch.

4

Leads I, aVL, V4-V6

Lateral infarct of the left anterior descending artery or circumflex.

5

Leads V1, V2, V3

septal infarct of LAD

6

Leads V4, V5, V6

anterior infarct of LAD

7

serum cardiac enzymes for STEMI

cardiac-specific troponin T (cTnT),
cardiac-specific troponin I (cTnI),
creatine kinase MB-isoenzyme (CKMB)

8

troponins for STEMI

more specific and sensitive
elevated for 7-10 days after

9

CKMB for STEMI

rises within 8 hours
returns to normal after 72

10

AV block

impaired conduction between the sinoatrial (SA) pacemaker and the ventricles.

11

First Degree AV Block

PR > 0.2
normal 1:1 P:QRS ratio

12

First Degree AV Block Cause

increased vagal tone
AV nodal dz
electrolyte disturbance
med side effect

13

Second Degree AV Block - Mobitz Type I

progressive PR lengething until QRS is dropped
Group Beating

14

Group Beating

lumping of P-QRS-T elements leading up to the dropped QRS complex.

15

Second Degree AV Block - Mobitz Type II

random dropped QRS
discernible ratio of P:QRS

16

Mobitz Type I Causes

intranodal or HIS bundle conduction defects that result from medications (e.g., beta blockers, digoxin, calcium channel blockers),
increased vagal tone, or
right coronary artery mediated ischemia.

17

Mobitz Type II Causes

infranodal conduction abnormality in either the bundle of His or Purkinje fibers.

18

Mobitz Type I Treatment

adjusting medications or pacing if associated with symptomatic bradycardia

19

Mobitz Type II Treatment

always treated with a pacemaker due to the increased risk of progressing to high grade or third degree AV block.

20

Third Degree AV BLock

P waves separate from QRS
supra-ventricular impulses completely fail to conduct impulses to the ventricles, and ventricular depolarization is initiated by pacemaker cells distal to the block

21

Third Degree AV Block causes

coronary ischemia
also congenital AV block, lupus, or Lyme disease

22

Third Degree AV Block symptoms

hypotension, dizziness, syncope

23

Third Degree AV Block treatment

pacemaker

24

VF most commonly associated with

coronary artery dz

25

VF risk factors

MI, decreased left EF, electrolyte disturbance
long QT syndrome, A fib

26

most common cause of mortality following MI

V fib

27

Patients with VF

sudden LOC or comatose
symptoms of MI prior to collapse

28

VF results in

insufficient forward cardiac output -->
CNS ischemic injury, MI, sudden cardiac death

29

initial therapy for VF

defibrillation followed by 2 minutes of CPR

30

VF - after 2 rounds of defibrillation

epinephrine (1mg bolus, then every 3-5 minutes) should be administered followed by another shock.

31

medicines to consider with VF refractory to defibrillation

magnesium and amiodarone

32

asystole or pulseless electrical activity

immediate high-quality chest compressions.
not shockable arrhythmias

33

mildly elevated LFTs

chronic hepatitis
alcohol induced hepatitis
NAFLD

34

LFTs 100s or 1000s

acute viral hepatitis

35

LFTs 10,000

toxin-related hepatitis
liver ischemia

36

location of AST

liver, cardiac muscle, skeletal muscle

37

hepatic pattern of liver disease

markedly elevated AST and ALt
minimal to no elevation in alk phos

38

half life of albumin

20 days

39

albumin in patients with advanced liver cirrhosis

low

40

severe liver damage labs

increased PT/INR

41

PHT value

greater/equal to 12
increased resistance to portal blood flow

42

Prehepatic PHT

portal vein thrombosis
schistosomiasis

43

Intrahepatic PHT

cirrhosis
hep B/c
PBC

44

posthepatic PHT

right sided heart failure
Budd-Chiari syndrome
severe TR

45

hepatic venous pressure gradient

balloon catheter to monitor gradient pressure btwn portal vein and IVC

46

PHT complications

variceal bleedings
SBP
ascites
pleural effusion

47

PHT management

screening for GE varices, beta blockers, diuretics, sodium restriction

48

transjugular intrahepatic portosystemic shunt

shunt between portal and hepatic vein (allowing portal vein to drain properly)

49

metabolic acidosis

ph <7.37
decrease in HCO3- levels

50

metabolic acidosis lab values

low pH, high H+
very low HCO3-
low pCO2
compensation - hyperventilation

51

normal anion gap values

10-15

52

causes of anion gap metabolic acidosis

methanol, uremia, DKA, paraldehyde, INH, lactic acidosis, ethylene glycol, salicylates

53

increased osmolol gap

suggesitive of toxic alcohol ingestion

54

OG =

Osm - (2Na + glucose/18 + BUN/2.6)

55

normal OG

<10

56

normal anion gap metabolic acidosis (hyperchloremic metabolic acidosis)

GI HCO3- loss
renal acidosis
drug induced hyperkalemia with renal insuff
other

57

metabolic acidosis/ GI HCO3 loss

diarrhea
external pancratic or small bowel drainage
jejunal and ileal loops

58

Normal anion gap hypokalemic renal acidosis

Type 1 and 2 RTA
acetazolamide, topiramate, amph b

59

normal anion gap hyperkalemic renal acidosis

Type 4 RTA (hypoaldosteronism)

60

Drug-induced hyperkalemia with renal insufficiency leading to normal anion gap metabolic acidosis is seen in

potassium sparing diuretics
trimethoprim
ACEI/ARB
NSAIDs, cyclosporine

61

other causes of normal anion gap metbaolic acidosis

acid loads (ammonium chloride)
expansion acidosis from rapid saline adminstration
hippurate

62

urine anion gap

Na(urine) + K - Cl

63

negative UAG

high levels of NH4 excretion
suggests normal renal function

64

positive UAG

low NH4 excretion
suggests renal tubular dysfunction

65

Compensation for metabolic acidosis

hyperventilation
cause reduction in pco2

66

expected PCO2 range with metabolic acidosis

Winter's formula
1.5 (measured HCO3) + 8 +/- 2

67

acute and severe metabolic acidosis treatment

administration of NaHCo3

68

absolute iron def

decreased iron levels in body stores
- poor nutriion
- impaired absorption
- blood loss

69

Functional iron def

insuff availability of iron to incorporate into precursors
- anemia of chronic dz
-treatment with erythropoiesis-stimulating agents

70

anemia of chornic dz

hepcidin-induced block on iron release from stores

71

etiology of iron def anemia

menorrhagia
gi bleed (colon polyp or cancer)
meckel's diverticulum in child

72

breast milk contains low

iron

73

iron absorbed in

duodenum

74

stages of iron def

loss of iron stores -> decreased ferritin --> decreased serum iron --> increased TIBC --> decreased iron sat --> normocytic anemia -- > microcytic anemia

75

symptoms of iron def anemia

pallor, fatigue
exertional dyspnea, orthostatic hypotension
tachycardia
koilonychia (spoon nails)

76

plummer-vinson syndrome

anemia + glossitis + esophageal webs

77

ferritin

intracellular protein that stores iron

78

transferrin

decreased in total iron --> upregulation of transferritin synthesis

79

iron def anemia gold standard

bone marrow biopsy - hardly ever performed

80

treatment of iron def anemia

trial or oral iron to menstruating women
work up

81

oral iron, don't take with

tea, coffee, calcium (decreased absorption)
acidity (increase absorption)

82

oral iron side effects

n/v, constipation, black stool

83

dextran

parenteral iron
can cause life-threatening anaphylaxis

84

blood transfusion for iron anemia

unstable patients (hypotensive, hypoxic)
hemoglobin of 7 for healthy patients, 10 for patients with CAD

85

acute mesenteric ischemia causes

arterial thrombus (atherosclerosis)
venous thrombus (hypercoaguable)
arterial occlusion from emboli
hypoperfusion - blood loss, CHF

86

CMI cause

ischemia due to long standing atherosclerotic dz or 2 or more mesenteric vessels
also, vasculitidies

87

CMI - age

over 60
females > males

88

CMI - vessels

celiac trunk
superior mesenteric artery
inferior mesenteric artery

89

AMI symptoms

diffuse non localized pain
N/v
bloody diarrhea

90

CMI symptoms

postprandial pain
weight loss
n,v,diarrhea

91

AMI pe findings

hyperactive/absent bowel sounds
positive occult blood
tachycardia

92

CMI PE findings

malnutrition
abdominal bruit
signs of peripheral vascular dz

93

diagnosis of mesenteric ischemia

CT angiography

94

mesenteric ischemia - plan films

can be used to exclude perforated viscus and free air under diaphragm

95

AMI complications

bowel necrosis, perforation, peritonitis, sepsis, death

96

CMI complications

acute thrombosis/embolism
prolonged hospitalization due to chronic malnutrition

97

AMI treatment

fluid resuscitation, ng tube, IV antibodies
embolectomy + thrombolytic influsion via angiography catheter

98

CMI treatment

open or endovascular revasc
warfarin

99

CMI with bowel necrosis

laparotmy to remove tissue

100

systolic dysfunction due to

decreased ventricular contraction

101

diastolic dysfunction due to

noncompliant ventricle

102

causes of systolic dysfuncton

ischemia/CAD
anemia, myocarditis, dilated CM, fluid overload

103

causes of diastolic dysfunction

HTN
increased afterload (Aortic stenosis)
restrictive processes

104

LSHF symptoms

pulmonary congestion - DOE, orthopnea, paroxysmal noctural dyspnea

105

LSHF - DOE

caused by interstitial fluid in lung stimulating juxtacapillary receptors

106

LSHF - orthopnea

because of increased venous return to right side of heart, worsen pulmonary congestion

107

paroxysmal nocturnal dyspnea

gradual reabsorption of fluid from interstitium into vascular compartment that leads to increase in venous return, worses PCongestion

108

LSHF - fluid overload

decreased CO
activates RAAS
retention of salt, water

109

hemoptysis in LSHF

rupture of engored bronchial veins

110

brick red sputum in LSHF

increased pressure in alevolar capillareis --> alevolar macrophages inget RBC --> hemosiderin laden macrophages

111

systolic HF ausculation

S3 gallop - kentucky

112

diastolic HF ausculation

S4 gallop - tennessee

113

BNP cutoff

400

114

Chest x ray findings HF

Kerley B lines – thin pulmonary opacities caused by fluid in the interstitium of the lung
Enlarged cardiac silhouette
Peribronchial cuffing – excess fluid in the small airway passages of the lung causes localized patches of atelectasis.
Cephalization of the pulmonary vasculature – antigravitational redistribution of the pulmonary blood flow due in part to increased pulmonary vascular resistance and pulmonary HTN.

115

LSHF acute treatment

Lasix (furosemide)
morphine
nitroglycerin
oxygen
positioning

116

LSHF morphine

decreases anxiety and preload through venodilation

117

Nitroglycern in LSHF

titrate IV SBP no less than 80

118

long term treatment of LSHF

beta blockers
spironolactone
ACE inhibitors

119

CCB and LSHF

not recommended

120

physical findings of atypical pneumonia

slower onset, insidious
no signs of consolidation

121

maintaining K balance

excreted in distal nephron
excretion enhanced with reabsorption of Na+
secretion increased by aldosterone
GI tract absorbs 90%

122

pleurisy

any condition that causes an irritation of the parietal pleura.

123

diastolic HF - echo

normal/high EF
decreased EDV
increased EDP

124

digoxin in HF

symptoms relief, reduce hospitalization
no effect on mortality

125

tetanus management

benzos
immune globulin
metronidzale or penicllin g

126

lifestyle modifications for CHF

exercise, sodium restriction

127

Mobitz Type I pathophysiology

intranodal or HIS bundle conduction defects that result from medications (e.g., beta blockers, digoxin, calcium channel blockers), increased vagal tone, or right coronary artery mediated ischemi

128

Mobitz Type II pathophysiology

infranodal conduction abnormality in either the bundle of His or Purkinje fibers.

129

LS CHF x ray findings

cardiomegaly
kerley b lines
peribronchial cuffing
cephalization of pulm vasculature

130

clinical features of pleurisy

sharp knife like pain worse on inspiration
after preceded by URI symptoms

131

emphysema

lung condition highlighted by pathological enlargement of distal airways due to airway destruction.

132

chronic bronchitis

productive cough of at least 3 months per year for 2 consecutive years.

133

COPD risk factors

smoking!!
pulmonary irritants, alpha-1 antitrypase, asthma

134

protease-antiprotease hypothesis

Nicotine and smoke derived free radicals cause accumulation of PMNs and macrophages in the alveoli.
Activated PMNs → release proteases which result in tissue damage.
Smoking also enhances macrophage elastase activity, which is not susceptible to cleavage by α1-antitrypsin.

135

functional alpha1-antritrypsin def

smoking derived free radicals can disrupt the balance between proteases and anti-proteases by inactivating α1-antitrypsin → "functional" α1-antitrypsin deficiency.

136

COPD patient presents with

combination of cough (productive or non-productive) and dyspnea of insidious onset and chronic duration.

137

COPD PE findings

Hyperinflation or “barrel chest” (increased AP diameter)
Diminished breath sounds
Hyperresonance to percussion
Prolonged expiration with “pursed lips” breathing → sudden expiration may cause atelectasis due to rapidly decreased alveolar pressure.

138

obstructive pattern COPD symtpoms

tachypnea, tachycardia, and cyanosis.

139

wheezes

expiratory, obstruction

140

crackles

inspiratory, opening of collapsed alveoli

141

COPD diagnosis

hyperinflation with an obstructive pattern, and systemic findings of hypoxemia and hypercapnia

142

COPD PFTS

Decreased FEV1
Decreased FEV1/FVC ratio
Decreased VC
Decreased DLCO
Increased TLC, RV, FRC (from trapped air)

143

COPD ABGs

Chronic respiratory acidosis, leading to chronic metabolic alkalosis → elevated PCO2 and bicarbonate.
Polycythemia may occur in response to chronic hypoxemia.

144

COPD CXR

hyperlucent lung fields. Air trapping can lead to flattening of the diaphragm. In severe disease the heart can also become elongated and tubular shaped as a result of the increased air in the thorax.

145

COPD death

Respiratory acidosis and hypercapnic respiratory failure
Cor pulmonale (rare)
Massive spontaneous secondary pneumothorax

146

cor pulmonale occurs as result of

hypoxia

147

increased afterload can cause

RV failure

148

COPD treatment goals

reduce obstruction by dilating the airways and reducing mucus secretion, and prevention of disease progression.

149

COPD treatment

1) smoking cessation 2) antitussives/expectoants 3) inhaled b2 agonists 4) anticholinergics 5) inhaled corticosteroids

150

antitussives

dextromethophran
codeine-guaifenesin

151

inhaled b2 agonists

bronchodilators
salmeterol

152

inhaled anticholinergics

bronchodilator
ipratropium bromide
slower onset, longer duration

153

inhaled corticosteroids

budesonide, fluticasone