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CCRN > CCRN > Flashcards

CCRN Flashcards

1
Q

ADH release

A

in reponse to increased serum osmolality; made in hypothalamus, stored in PP

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2
Q

ADH function

A

makes kidneys retain water

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3
Q

s/s SIADH

A

decreased Na, decreased serum Osmo, dec UOP

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4
Q

cardinal sign of SIADH

A

dilutional hyponatremia

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5
Q

Complication of SIADH

A

seizures

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6
Q

3 etiologies of SIADH

A

Oat Cell Ca
Viral PNA
Head Problems

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7
Q

Tx SIADH

A

Fluid Restriction
Treat Cause
Hypertonic Solutions

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8
Q

Contraindicated for use in SIADH

A

hypotonic solutions, D5W

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9
Q

s/s DI

A

increased Na level; Increased UOP; Increased serum Osmo; urine sg 1.001-1.005

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10
Q

etiology DI

A

Head problems/trauma

Dilantin

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11
Q

Complication of DI

A

hypovolemic shock

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12
Q

Tx DI and two things to monitor

A

Give ADH ; IVF

Monitor EKG for ischemia r/t vasopressin therapy and monitor urine sg

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13
Q

CV s/s of hypoglycemia and what causes them

A

tachycardia, palpitations, diaphoresis, irritability, restlessness; adrenal medulla releases adrenalin to get liver to release glucose

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14
Q

can mask CV s/s of hypoglycemia

A

beta blockers

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15
Q

CNS s/s of hypoglycemia

A

confusion, lethargy, slurred speech, seizures, coma

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16
Q

s/s DKA

A

bg 400-900; dehydration, acidosis, Kussmaul’s respirations

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17
Q

Tx DKA

A

Primarily-insulin gtt; also IVF (NS to hydrate IV, then 1/2NS to hydrate tissues, then D51/2NS to avoid hypoglycemia r/t insulin gtt)

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18
Q

HHNK

A

hyperglycemia hyperosmolar non-ketotic coma

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19
Q

risk factors of HHNK

A 
elderly (pancreas ages)
TPN (pancreatic fatigue)
diet-controlled DM
pancreatitis
thiazide use (makes body retain glucose)
steroid use (induces insulin resistance)
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20
Q

s/s HHNK

A

BG 1000-2000; severe dehydration; no acidosis; LTBB; make small amt insulin but doesn’t dec bg, just prevents fat b-d/ketosis

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21
Q

Tx HHNK

A

IVF; small amt insulin

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22
Q

In acidosis, potassium ions move

A

out of cell, as H+ ions move into cell; change in pH 0.1 should increase K level by 0.6

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23
Q

HA + nuchal rigidity + pos Kernig’s sign

A

SAH

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24
Q

TIA

A

reversible, s/s last

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25
Q

RIND

A

reversible ischemia neurological deficit; s/s last

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26
Q

CI

A

cerebral infarct-stroke

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27
Q

basilar vertebral artery cerebral infarct stroke

A

supplies brainstem, problem will be there

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28
Q

loss (opposite side of infarct)of 1/2 of both visual fields in CI

A

homonymous hemianopsia

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29
Q

eyes deviate toward here in CI

A

toward side of infarct

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30
Q

most important indicator of neurological status

A

LOC

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31
Q

goal of stroke TX

A

decrease cerebral edema

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32
Q

first sign of uncal herniation

A

pupil change

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33
Q

turn head side to side, eyes return to midline

A

Oculocephalic Reflex/Doll’s Eyes Reflex–indicates brainstem integrity.

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34
Q

2 holes in head

A

tentorial notch and foramen magnum

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35
Q

arms up and to center

A

decorticate posturing–problem with cortex

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36
Q

arms down and point out

A

decerebrate posturing–problem with brainstem

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37
Q

brain tracts that go from brain, cross at medulla, and go down opposite sides of SC

A

pyrimidal tracts–control movement

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38
Q

Pupil in ennervated by (3)

A 
3rd CN (Optic)
SNS (dilates)
Pns (constricts)
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39
Q

uncal herniation

A

lateral shift (midline shift) of brain tissue

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40
Q

epidural bleed would cause this type of herniation

A

uncal herniation

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41
Q

ipsalateral dilated pupil is first sign of

A

uncal herniation; often happens with no change in LOC yet

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42
Q

CI in epidural bleed/uncal herniation

A

mannitol–only works on good tissue; would shrink brain and allow more room for bleed

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43
Q

respiratory patter in upper brainstem (midbrain) lesion is

A

hyperventilation

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44
Q

Pontine infarct s/s (2)

A 
apneustic breathing (long pause b/t inspiration and expiration); 
bilateral pinpoint pupils
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45
Q

pressure on a pyrimidal tract will cause

A

positive Babinski on foot of opposite side

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46
Q

herniation through foramen magnum

A

supratentorial herniation

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47
Q

1st, 2nd, and 3rd and 4th signs of supratentorial herniation

A
  1. change in LOC (lethargy, stupor); measure with GCS
  2. pupils dilate bilaterally
  3. hyperventilation (body tries to induce alkalosis to dec ICP)
  4. Cushing’s Triad (inc SBP, widening pulse pressure, dec HR and dec RR)
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48
Q

Avoid with Increased ICP (5)

A

Acidosis; hypotonic IVF; hyperextension/flexion of neck; wrist restraints; decreased PRO intake

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49
Q

Normal CPP

A

70-95 mmHg

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50
Q

CPP formula

A

MAP-ICP= CPP

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51
Q

MAP formula

A

DBP + 1/3(pulse pressure)

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52
Q

Normal Ventricular Fluid pressure (most sensitive indicator of increased ICP)

A

0-10 mmHg

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53
Q

Basilar Skull Fx, presenting s/s (4)

A

Raccoon Eyes
Battle’s Sign (bruising over mastoid bone)
CSF leak (otorrhea and rhinorrhea)
Anosmia (Lose CN #1)

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54
Q

CSF leak: how to test otorrhea and rhinorrhea

A

otorrhea is bloody, look for Halo sign with clot in the middle.
rhinorrhea is clear–check for glucose (CSF is 60% glucose)

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55
Q

s/s bacterial meningitis

A

usually Staph

CSF has elevated PRO and decreased glucose, is purulent with positive leukocytes.

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56
Q

s/s viral meningitis

A

enterovirus and herpes virus usually;

CSF has elevated PRO (not as much as bacterial), normal glucose, and positive lymphocytes

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57
Q

bacterial vs. viral meningitis

A

bacterial: Low glucose, leukocytes
viral: normal glucose, lymphocytesauto

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58
Q

in a seizure this can point to the problem

A

eye deviation

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59
Q

autoimmune destruction of ACh receptors at NMJ; post-synaptic defect; chronic d/o with abnormal fatiguability brought on by activity.

A

myasthenia gravis

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60
Q

hallmark of MG

A

symptoms improve with rest

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61
Q

initial findings in MG

A 
ocular muscle weakness,
diplopia
dysphagia
hoarseness
limb weakness
...........respiratory difficulty/failure
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62
Q

precipitating factor of MG crisis

A

inadequate meds
flu/menses/pregnancy
stress/ surgery

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63
Q

Tx MG

A

Mestinon (pyridostigmine), Steroids, Respiratory management

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64
Q

Dx Mg

A

Symptomatic improvement with Tensilon 2 mg IV

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65
Q

medications that interact with Mestinon

A

aminoglycosides, procainamide, quinidine

*careful use with narcs and barbiturates

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66
Q

acute d/o in which antibodies attack peripheral nerves causing demyelination and loss of nerve conduction

A

Guillian-Barre Syndrome

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67
Q

Hallmark of Guillian-Barre

A

bilateral and symmetrical ascending paralysis

improvement is descending

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68
Q

Causes of GB

A

Viral infections- URI, Epstein-Barr, HIV, Hep A,B,C
Campylobacter jejuni infection
Vaccines

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69
Q

Tx GB

A

High PRO levels in CSF

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70
Q

Kernig’s Sign

A

Severe stiffness of the hamstrings causes an inability to straighten the leg when the hip is flexed to 90 degrees; indicates meningeal irritation

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71
Q

Brudzinski’s sign

A

Severe neck stiffness causes a patient’s hips and knees to flex when the neck is flexed.

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72
Q

trousseau’s sign

A

sign of latent tetany that occurs in hypocalcemia; spasm of hand after arm compressed by bp cuff for several minutes

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73
Q

etiology of pancreatitis

A

obstruction of pancreatic ducts secondary to gallstones or infection, causes autodigestion of fatty pancreas (less common causes- EtOH, trauma, drug toxicity from cyclosporine, steroids, thiazides, or tetracyclines.)

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74
Q

These problems develop with pancreatitis (4)

A
  1. hypocalcemia (Ca used to digest fats)
  2. HHNK
  3. Left pleural effusion and Left sided atelectasis (pancrease swells and lifts diaphragm
  4. Bilateral rales (right are sympathetic rales)
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75
Q

how pancreatitis can lead to ARDS

A

phospholipase A released during pancreatic autodigestion, which kills Type II alveolar cells that make surfactant

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76
Q

s/s pancreatitis (3)

A

+ Cullen’s sing-bruising around belly button d/t pancreatic bv b-d
+ Turner’s sign-bruising in flank/groin
Elevated Amylase

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77
Q

order of abdominal assessment

A

IAPP; inspect, Auscultat, Percuss, Palpate

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78
Q

Assessment of bowel infarction

A

Hypoactive bowel sounds
Leukocytosis
Hyperresonance and abd tenderness
Tympanic note/absence of dullness in liver area (last two d/t air)

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79
Q

LBO vs. SBO

A

LBO: large distention, no v/d
SO: small distention, n/v/d

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80
Q

LIver disease causes problems with: (3)

A

Coagulopathy, blood glucose control, and excretion of ammonia

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81
Q

Avoid these with liver disease (4) because they increase NH3

A
  1. Hypokalemia (kidney will retain NH3 with K)
  2. dehydration (inc BUN)
  3. increased protein intake (can happen with GIB)
  4. Acidosis, hypotension; LR
    (Lactate converted to bicarb by liver; dec liver function with LR can lead to Lactic Acidosis)
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82
Q

LR used in OR to

A

counteract hypotension induced acidosis

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83
Q

Neomycin treatment in liver disease-use and complication

A

reduces gut bacteria that make NH3; complication is vitamin deficiency since gut bacteria also produce riboflavin, folate, and vitamin K

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84
Q

jaundice + increased indirect bilirubin indicates problem in

A

liver. Indirect is unconjugated, liver conjugates bilirubin (attaches to an albumin)

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85
Q

jaundice + increased direct bilirubin indicates problem in

A

gallbladder, which stores direct (conjugated) bilirubin

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86
Q

+Kehr’s sign (left shoulder pain) indicates

A

Ruptured Spleen

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87
Q

Acute renal failure is characterized by decreased UOP of

A
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88
Q

prerenal RF cause and treatment

A

decreased UOP d/t renal hypoperfusion (CHF, HoTN); Tx IVF, inotropes

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89
Q

renal RF cause and Tx

A

decreased UOP d/t kidney damage (tissue or tubules) caused by ischemia or nephrotoxicity

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90
Q

damage to kidney tubules

A

acute tubular necrosis; caused by ischemia or nephrotoxicity; 50% MR, 25% recover 1 year, 25% need lifetime HD

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91
Q

causes of ischemic ATN

A

prolonged HoTN (hemmorrhage, burns, sepsis, HF), transfusion reactions

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92
Q

causes of nephrotoxic ATN

A

heavy metals, medications, street drugs, rhabdomyolysis, radiocontrast (esp to dehydrated pt)

93
Q

do not treat nephrotoxic ATN with

A

Lasix; will worsen toxicity

94
Q

oliguric stage of ATN recovery

A

10-17d; increased BUn/cr, hyperkalemia, FVO, CHF, dialysis Tx

95
Q

Polyuric stage of ATN recovery

A

proximal tubule is necrotic, fluid and lytes are leaking out, cannot concentrate urine; 2 wks-3 mos; increased BUN,cr, hypokalemia, pt is fluid depleted

96
Q

recovery stage of ATN recovery

A

3 mos to 1 yr; pray

97
Q

wt gain of 1 Kg in 24 h is fluid retention of

A

1000 mL

98
Q

ischemia to kidneys begins when MAP is

A
99
Q

Best measurement of GFR is

A

creatinine clearance

100
Q

prerenal vs renal (oliguric) ATN: Urine sodium

A

prerenal:

101
Q

normal urine sodium

A

20-200

102
Q

prerenal vs. renal ATN: BUN/creatinine ratio

A

prerenal: 20:1
renal: 10:1

103
Q

prerenal vs. renal ATN: Lasix/fluid challenge

A

prerenal: +urine
renal: - urine

104
Q

4 stages of chronic renal failure

A 
Diminished renal reserve (50% nephron loss)
Renal Insufficiency (75% loss)
ESRD (90%)
Uremic syndrome (100%)
(creatinine increases as you progress)
105
Q

EKG change not caused by hyperkalemia

A

ventricular irritability

106
Q

progression of EKG changes in hyperkalemia (5)

A
  1. peaked T wave
  2. prolonged pri, flattened p wave
  3. lose p wave
  4. qrs widens
  5. qrs biphasic–sine wave
107
Q

s/s hyperkalemia

A

muscle weakness and ekg changes

108
Q

CaCl treatment for hyperkalemia

A

doesn’t decrease K level; cardioprotective to allow normal conduction at higher K level; effective in one minute

109
Q

hyperkalemia treatment (4)

A

CaCl, insulin/D50, NaHCO3 (pushes K into cell), kayexelate (removes K from cell and puts in bowel)

110
Q

ekg changes with hypokalemia (3)

A

u wave, ST depressions, ventricular irritability

111
Q

s/s hypercalcemia

A

muscle weakness, apathy

112
Q

s/s hypocalcemia

A

+Chvostek’s, +Trousseau’s, twitching, seizures

113
Q

renal pts tend to have low Ca and high Phos because

A

kidneys activate Vitamin D, less kidney function, less Vitamin D, less Ca absorbed from gut

114
Q

vented pts can have decreased Phos because

A

only source is leafy greens; need TPN or phos infusion

115
Q

cryoprecipitate

A

contains Factors 8,13, and fibrinogen; used to treat hemophilia and DIC

116
Q

DIC patho

A

overstimulation of clotting cascade–>bleeding once clotting factors used up—>clots breakdown into anticoagulant split productis—>further bleeding

117
Q

DIC most often caused by

A

OB emergency (placenta high in tissue thromboplastin)

118
Q

labs in DIC

A

**decreased fibrinogen level
increased PT/PTT, FSPs, D-Dimer
decreased plts

119
Q

intrinsic clotting cascade is stimulated by

A

endothelial injury

seen in ARDS, septic shock

120
Q

extrinsic clotting cascade is stimulated by

A

tissue injury, which releases tissue thromboplastin

121
Q

DIC treatment

A 
(in OB emergency, just deliver baby)
Heparin
FFP
cryoprecipitate
remove trigger
122
Q

Functions of heparin

A

neutralizes thrombin which inhibits fibrin formation

123
Q

HIT patho

A

if pt doesn’t have antithrombin III heparin will cause clotting instead, plts get used up

124
Q

HIT treatment

A

Argatroban (ACOVA)–direct thrombin inhibitor, doesn’t use antithrombin III

125
Q

TPN causes decreased

A

Phos, because builds muscles

126
Q

antibodies form and destroy platelets (

A

Idiopathic (Immune) Thrombocytopenic Purpura

127
Q

ITP vs. DIC (present similarly)

A

ITP–no increase in FSPs

128
Q

plt transfusion for ITP

A

usually unneeded since problem is not with production of plts

129
Q

massive blood transfusion cause decreased

A

calcium

130
Q

medication to decrease Phos

A

amphogel-phosphate binder

131
Q

Accelerated HTN

A

DBP>120, associated with retinal hemmorrhages

132
Q

Malignant HTN

A

DBP>140, associated with retinal hemmorhages and papilledema (optic disc swelling)

133
Q

Tx hypertensive crisis

A

vasodilators and sympathetic blockers

134
Q

Dilated CM responds to

A

digoxin

135
Q

Hypertrophic CM, AKA and definition

A

Hypertrophic Obstructive CM (HOCM)
Idiopathic Hypertrophic Subaortic Stenosis (IHSS)
“Fat Septum” Thickening of heart muscle at expense of LV chamber. Decreased filling, SV and CO, pools blood in periphery

136
Q

HCM treatment

A

Beta Blockers and CCBs (negative inotropes) Decreased contractility and HR to increase filling

137
Q

Contraindicated in treatment of HCM

A

positive inotropes, dig, dopa

nitrates, morphine

138
Q

S1

A

Tricuspid and Mitral valves close

139
Q

S2

A

Aortic and Pulmonic valves close

140
Q

systolic murmur

A 
S1 lub (murmur) S2 dub
AS and MI
141
Q

diastolic murmur

A

S1 lub S2 dub (murmur)

MS and AI

142
Q

aortic area

A

right 2nd ICS

143
Q

pulmonic area

A

left 2nd ICS

144
Q

mitral area

A

5th ICS MCL

145
Q

tricuspid area

A

4th ICS left sternal border

146
Q

holosystolic (heard through entire systole), rough radiating murmur, “washing machine,” increases with holding breath

A

aortic stenosis

147
Q

blowing murmur, causes giant V waves on PA waveform

A

mitral insufficiency

148
Q

pt teaching re: stents

A

ASA and plavix after

149
Q

nursing post op cath

A

manual pressure 20-30 minutes after until bleeding controlled; VS, distal pulses, CSTM, assess site for bleeding/hematoma

150
Q

most common complication of heart cath

A

local vascular problem at insertion site: hematoma, RP bleed, thrombosis, distal embolism

151
Q

complications of heart cath (4)

A

death, MI, CVA, renal dysfunction r/t contrast

152
Q

prevent contrast-induced nephropathy by

A

lowest dose possible; IVF; acetylcysteine day before and day of cath (antioxidant and vasodilating effects)

153
Q

hold these nephrotoxic meds 24 hours before a heart cath (4)

A

some antibiotics, cyclosporine, NSAIDS, metformin

154
Q

IABP assessments

A

HOB 15-no higher
pulses
monitor bleeding

155
Q

s/s cardiogenic shock

A

confusion/restlessness, increased RR, rales, rapid thready pulse, JVD, narrow pulse pressure, S3S4, Hypotension, dec UOP, dec CO, increased CVP, SVR, and PAWP d/t vasoconstriction

156
Q

functions of IABP

A

perfuse coronary arteries during diastole, decreased afterload, increased suction out of LV, increased CO

157
Q

contraindication to IABP

A

aortic insufficiency (balloon would put blood back into LV), PVD

158
Q

IAPB used in treatment of

A

cardiogenic shock post MI, post CABG and heart caths

159
Q

complications of IABP

A

limb ischemia, aortic dissection, infection

160
Q

causes increased PAP but normal PAWP

A

Pulmonary HTN

161
Q

oxygen deprivation to heart begins to cause irreversible injury after

A

20 minutes

162
Q

RCA supplies

A

Inferior wall; half SA node, most of AV node, RA and RV, mitral valve

163
Q

complications of RCA occlusion

A

SB, CHB/AV dissociation, RV infarct, mitral insufficiency

164
Q

LAD supplies

A

Anterior and Septal Walls; Bundle of His; Bundle Branches; ventricular septum

165
Q

Complications of LAD occlusion

A

Mobitz II HB, RBBB( if these develop post-MI, 94% mortality rate, need PPM); VSD

166
Q

EKG sign of myocardial contusion

A

STE in injured leads

167
Q

EKG sign in pericarditis

A

STE in all leads

168
Q

1 COD in surgical/trauma patients

A

MSOF/MODS

169
Q

Assess with trauma: AMPLE

A 
A=Allergies
M=Meds
P=Past Illness
L=Last meal
E=Events preceding injury
170
Q

Tx Tylenol poisoning

A

acetylcysteine: 140 mg/Kg loading dose, 70 mg/Kg q4h for 17 doses; activated charcoal if

171
Q

3 grades of Tylenol poisoning

A

Grade 1: n/v
Grade 2: RUQ pain
Grade 3: increase in LFTs

172
Q

danger of ASA poisoning

A

ASA-induced renal tubular acidosis, kidney damage

173
Q

Tx ASA poisoning

A

lavage/induced emesis; activated charcoal; urinary alkalinization with NA HCO3 to increase speed of excretion and counteract renal tubular acidosis; HD

174
Q

watch for this lyte imbalance with ASA poisoning

A

hypokalemia

175
Q

s/s compensatory stage of shock

A

anxiety, irritability, cool & pale (vasoconsriction), inc HR, dec UOP

176
Q

s/s progressive stage of shock

A

lactic acidosis–>vasodilation–>hypotension
dec CO, CVP, PAWP
inc SVR

177
Q

septic shock causative organisms

A

Gm - bacteria: E. coli, Klebsiella, Enterobacter, Pseudomonas, Serratia

178
Q

1 COD in ICU

A

septic shock, 40-60% mortality rate

179
Q

normal HCO3`

A

23-27

180
Q

Causes of Metabolic Alkalosis

A

Multiple blood transfusion (sodium citrate in banked blood to dec clotting is converted by liver into bicarb); hypokalemia, vomiting, contraction alkalosis

181
Q

causes of respiratory alkalosis

A

hypoxemia (body tries to blow off CO2); CNS d/o (body tries to dec ICP by inducing alkalosis); ASA OD; sepsis

182
Q

causes of respiratory acidosis

A

OD, cardiac/respiratory arrest, COPD, d/o’s that cause dec ventilation (MG, ALS, GB)

183
Q

causes of metabolic acidosis

A

DKA, starvation ketoacidosis, diarrhea, renal failure

184
Q

breath sounds are louder than normal in

A

pneumonia; bronchial bs on expiration and not over trachea d/t inc noise conduction in semisolid tissue

185
Q

breath sounds are quieter than normal in

A

atelectic tissue

186
Q

bronchial bs

A

over trachea, harsh, heard on expiration

187
Q

bronchvesicular bs

A

over mainstem bronchi; heard equally insp and expir

188
Q

vesicular bs

A

heard over lung lobes on inspiration

189
Q

pulmonary consolidation/lobar PNA causes these signs

A

dull percussion note, dec tactile fremitus, bronchial bs

190
Q

hallmark of ARDS

A

refractory hypoxemia

191
Q

ARDS treatment

A

PEEP to distend alveoli and inc gas exchange and preven hyaline membrane from absorbing fluid

192
Q

danger of high O2 over 24 h

A

destruction of Type II alveolar cells which make surfactant

193
Q

initial vent setting for adult in respiratory failure

A

10 ml/Kg (2x normal volume)

194
Q

massive PE can cause

A

right sided HF; JVD, inc CVP, liver engorgement

195
Q

elevates within 3 h of AMI; high sensitivity

A

myoglobin

196
Q

blown pupil indicates

A

increased pressure on CNIII

197
Q

bilateral pinpoint pupils can indicate

A

pons infarct

198
Q

opioids cause bilateral pupil

A

constriction

199
Q

these murmurs are low pitched and best heard with bell

A

AV valve stenosis

200
Q

nursing care post pneumonectomy

A

no CT, just regular drain; position on operative side to facilitate drainage and prevent mediastinal shift; TCDB; avoid unneeded suction and fluids

201
Q

anxiety vs. fear

A

anxiety-can’t identify cause

fear-can identify cause

202
Q

IMV

A

intermittent manditory ventilation (vent mode)

203
Q

ARDS + this lab increase is poor prognosis, multisystem involvement

A

lactate dehydrogenase

204
Q

synthesis of best evidence r/t a clinical question

A

systematic review

205
Q

derived from systematic reviews to use clinically

A

clinical practice guidelines

206
Q

hypovolemic shock-PA readings

A

dec PAWP, inc CO and SVR

207
Q

PAWP is an indicator of

A

preload

208
Q

cardiogenic shock-PA readings

A

dec CO, inc PAWP and SVR

209
Q

distributive shock-PA readings

A

Dec SVR, and PAWP

inc CO

210
Q

this invalidates PAWP readings

A

PEEP

211
Q

inferior wall MI 12 lead changes

A

STE in leads II, III, aVF

212
Q

anterior wall MI 12 lead changes

A

STE in v1-v6

213
Q

posterior wall MI 12 lead changes

A

STE in lead I and aVL and ST dep in v1-v3

214
Q

lateral wall MI 12 lead changes

A

STE in I, aVL, v5-v6

215
Q

PAD correlates with

A

PAWP and LVEDP

216
Q

PAWP vs. PAD

A

PAWP should be less than PAD by 1-4 mm Hg (blood flows hi to low pressure)

217
Q

if PAWP > PAD

A

overwedged cath or cath in wrong zone or PEEP>10

218
Q

take wedge reading when

A

end of exhalation-fluctuates with breathing

219
Q

a wave of PA waveform

A

atrial contraction; falls just after QRS

220
Q

c wave of PA waveform

A

mitral valve closing (can be inside a wave)

221
Q

v wave of PA waveform

A

atrial filling (falls just after t wave)

222
Q

normal PAWP

A

4-12 mmHg

223
Q

PAWP elevated in

A

MV d/o, tamponade, pericarditis, LV failure, FVO

224
Q

PAWP decreased in

A

IV depletion/shock

225
Q

to find PAWP

A

take mean of a wave

226
Q

normal PAS

A

20-30 mm Hg; when RV is pushing blood into PA

227
Q

PAS is elevated in

A

lung d/o, pulmonary vascular resistance and pulmonary vasoconstriction

228
Q

PAD reflects

A

LVEDP-pulmonic valve is closed during diastole

229
Q

normal PAD

A

6-12 mmHg

CCRN (1 decks)

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