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SNRAObPedGer > Complications of Pregnancy > Flashcards

Complications of Pregnancy Flashcards

1
Q

3rd leading cause of maternal death

A

Pre-eclampsia

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2
Q

1st and 2nd cause of maternal death

A

Hemorrhage/ Thromboembolism

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3
Q

Pre-Eclampsia is a

A

Hypertensive disorders in pregnancy

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4
Q

Hypertensive disorders of pregnancy

A

In pregnancy there is decreased sensitivity to vasopressors, Does not happen in pre-eclampsia

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5
Q

Gestational HTN

A

Defined: HTN without proteinuria developing after 20
wks gestation with subsequent resolution postpartum
• 25% will develop preeclampsia

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6
Q

Preeclampsia

A

HTN and proteinuria after 20 wks gestation

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7
Q

Term Eclampsia only when

A

CNS involvements lead to seizures

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8
Q

Creatinine should be

A

Lower

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9
Q

Inflammatory mediators are

A

Hurtful

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10
Q

HELLP stands for

A

Hemolytic Elevated LFT, Low Platelets

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11
Q

Typically absent in less than 20 weeks gestation

A

Hemoconcentraton, Thrombocytopenia, Proteinuria

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12
Q

Typically rare in less than 20 weeks gestation

A

Serum uric acid 5.5mg/dl

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13
Q

Present in ALMOST ALL CASES in >20 weeks of gestation

A

Serum uric acid 5.5mg/dl

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14
Q

Typically absent in third trimester

A

Proteinuria, Serum uric acid 5.5, hemoconcentration and thrombocytopenia

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15
Q

Both present in SEVERE disease at >20 weeks of gestation

A

Hemoconcentration

Thrombocytopenia

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16
Q

Typically present in >20 weeks gestation

A

Proteinuria

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17
Q

Mild or severe HTN during those two times

A

<20 weeks gestation or >20 weeks gestation

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18
Q

Define Gestational HTN

A

HTN without proteinuria developing after 20 weeks gestation with subsequent resolution postpartum
25% develop preeclampsia

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19
Q

Define Pre-eclampsia

A

HTN and Proteinuria that develops AFTER 20 WEEKS of gestation

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20
Q

When is the term eclampsia useed?

A

When there is HTN with CNS involvement resulting in seizures

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21
Q

Diagnostic Criteria for Preeclampsia : Preeclampsia WITHOUT severe features (BPP 1)

A 
BP ≥ 140/90mmHg after 20 weeks gestation
Proteinuria ≥ 300mg/24h
Protein-Creatinine ratio ≥0.3
1+ on urine dipstick specimen
EDEMA
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22
Q

Diagnostic Criteria for Preeclampsia : SEVERE Pre-eclampsia (BTSPNI)

A 
BP ≥ 160/110 mmHg
Thrombocytopenia (plt count < 100,000)
Serum Cr > 1.1mg/dl OR 2 times the baseline Cr.
Pulmonary Edema
New onset CEREBRAL+ Visual disturbances
Impaired liver function (HELLP)
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23
Q

Serum Cr in the pregnant woman should be much _______why?

A

lower because of GFR which is much higher

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24
Q

Most cases of preeclampsia is with

A

Nulliparous (first pregnancy)

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25
Q

Risk Factors of Preeclampsia: Demographic factors (ABH)

A

Advanced maternal age > 35 years
Black race
Hispanic ethnicity

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26
Q

Risk Factors of Preeclampsia: Genetic Factors (HFHP)

A

History of Preeclampsia in previous pregnancy
Family Hx of Preeclampsia
History of Placental Abruption, Fetal growth restriction, or fetal death (PFD)
Partner who fathered a preeclamptic pregnancy pregnancy in another woman (through fetal genes)

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27
Q

Risk Factors of Preeclampsia: Medical Conditions (CODCAS)

A 
Chronic HTN
Obesity
Diabetes Mellitus
Chronic Renal Disease
Antiphospholipid antibody syndrome
Systemic Lupus Erythematus
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28
Q

Risk Factors of Preeclampsia:Obstetric conditions

A

Multiple Gestation

Hydatidiform mole

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29
Q

Risk Factors of Preeclampsia: Behavioral factor

A

Cigarette smoking (risk reduction)

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30
Q

Risk Factors of Preeclampsia: Partner related risk factors

A

Nulliparity

LIMITED PRE-CONCEPTIONAL EXPOSURE TO PATERNAL SPERM

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31
Q

Preeclampsia Pathophysiology : Related to which factorts

A

NO exact pathogenic mechanism defined but probably related to maternal, paternal, fetal and placental factors

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32
Q

Preeclampsia Pathophysiology

DDEEHHPPS

A 
Defective spiral artery/remodeling
Placental Hypoperfusion
Systemic Vasoconstriction
ENDOTHELIAL DYSFUNCTION
Disease PLACENTA releases PRO-INFLAMMATORY PROTEINS into MATERNAL CIRCULATION
Hypertension 
END ORGAN DAMAGE
Proteinuria
HELLP
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33
Q

Blood flow in normally

A

Low resistance / High Flow

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34
Q

In preeclampsia , blood flow is , which leads to

A

High resistance / low flow leading to Placental ischemia and hypoxia

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35
Q

Familial tendency of PIH is

A

Recessive genetic inheritance

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36
Q

Endothelial Factors (VADA)

A 
Vascular endothelial damage/dysfunction (in placenta and renal vessels) 
Arterial vasospasm ( liver, heart , brain) 
Decreased NO and prostaglandins (vasodilators), Increase ENDOTHELIN (vasoconstriction)
Abnormal stimulation of RASS (increase snsitivy to angiotensin 2 and NE)
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37
Q

My note : imbalance betwwen

A

Thromboxane –> Vasoconstriction

Prostacyclin –> Vasodilation

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38
Q

Platelet factors in preeclampsia

A

Damaged endothelium –> platelet activation, aggregation and adhesion

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39
Q

What do platelets release that causes vasoconstriction?

A

Thomboxane

Serotonin

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40
Q

What is the role of serotonin in MILD preeclampsia?

A

It will increase Prostaglandin and NO , but ACTIVATES RAAS via positive feedback loop –> Increase uteroplacental perfusion

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41
Q

Mild preeclampsia activate RAAS doing what to placental flow?

A

Improves uteroplacental perfusion

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42
Q

What happens in SEVERE PREECLAMPSIA?

A

Too much endothelial damage leads to serotonin-induced GREATER platelet aggregation via feedback loop

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43
Q

Coagulation factors leads to ________risk

A

Thromboembolic risk

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44
Q

Increase thromboembolic risk due to

A

Endothelial damage –> release of vWF factor VIII

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45
Q

PRE-ECLAMPSIA CAUSES AN

A

Exaggerated risk of thromboembolism

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46
Q

What is the role of von Willebrand with platelet

A

Tell platelet where to go

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47
Q

Both a direct and indirect cause of HTN

A

Endothelin and Calcium

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48
Q

Pre-Eclampsia and Hepatic factors

A

Increase uptake of free fatty acids–>hypertriglyceremia and increased risk for fatty liver.

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49
Q

What does the increase in triglycerides cause

A

Inhibit release of PROSTACYCLIN by damaged endothelium (vasodilator) and contributes to Liver dysfunction

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50
Q

CV hallmark of Pre-eclampsia

A

Increase BP

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51
Q

Cardiovascular changes in Pre-Eclampsia include

A

Increase BP

Increase sensitivity to cathecholamines and overactive SNS

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52
Q

CV changes normalize

A

shortly after delivery

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53
Q

Hemodynamics changes in preeclampsia

CO, SVR , PCWP/CVP

A

High CO
Normal to elevated SVR
Slighly low PCWP /CVP

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54
Q

Hemodynamics Preload , contractility and SVR

A

Decrease preload
Increase contractility
SVR normal or increase

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55
Q

Normal CVP /PCWP in severe preeclampsia

A

vasoconstriction

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56
Q

For example, In normal patient, if you give fluid with CVP of 8 itll go up to 14, with pre-eclampsia it will go up to

A

20

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57
Q

Greater than 1L bolus can lead to

A

Pulmonary edema

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58
Q

Normal pregnancy Colloid oncotic pressure usually-________but there is an ____________ in preeclampsia

A

Decrease due to decrease albumin: exaggerated decreased.

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59
Q

______-COP and _____ lead to Pulmonary Edema

A

Decreased; Increase Vascular permeability.

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60
Q

What helps lung issue from water

A

Surfactant

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61
Q

Hypercoagubility in pregnancy due to

A

Accelerated (shorter) prothrombin Time
Increase activation of factors II, V, X
Decrease Fibrinogen

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62
Q

Hypercoagubility in pregnancy due to

A

Decreased antithrombin III levels

normally inhibit factors IX, X, XI, XII

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63
Q

Severe pre-eclamptic patients may need this concentrate

A

Antithrombin

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64
Q

Pre-eclampsia renal effects are

A

Glomerular enlargement –> ischemia –> Glomerulopathy –> proteinuria and 25% decrease in GFR

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65
Q

A decrease in UOP of _________requires assessment of Intravascular volume

A

<400ml/24 h

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66
Q

Endocrine and metabolic changes in preeclampsia include

A

Disruption of balance between vasodilators and vasoconstrictors

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67
Q

Vasodilators are

A

Nitrous

PGI2

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68
Q

Vasoconstrictors are

A

Endothelin
Angiotensin II
Thromboxane A2
Serotonin

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69
Q

Serum Cr. should not be

A

1.1

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70
Q

Edema –> increase

A

Risk airway narrowing

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71
Q

What is an OMINOUS sign with Pre-eclampsia

A

EPIGASTRIC /SUBCOSTAL PAIN
Indicate hemorrhage /bleeding
SUBCAPSULAR HEMORRHAGE and INTRAPERITONEAL Bleeding

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72
Q

There can be epigastric subcostal pain because

A

Liver capsule can be distended by edema and hemorrhage

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73
Q

What is subcapsular hemorrhage and intraperitoneal bleeding confirmed by

A

US/CT scan

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74
Q

Classic findings in preeclampsia include

A

Severe Headaches
Visual Changes
Hyperreflexia

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75
Q

Unknown etiology of seizures may be HTN (HEVEHI)

A 
Encephalopathy
Vasospasm
Edema
Hemorrhage
Infaction
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76
Q

Severe eclampsia asssociated wtih (2) in uterine

A

Intrauterine Growth retardation

Oligohydramnios

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77
Q

What is the effect of Magnesium at the NMJ

A

Decrease uptake , binding and distribution of Ca2+ in vascular smooth muscle which prevents the interraction of myosin with actin

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78
Q

Central anticonvulsant effect of magnesium by

A

Decreased cerebra vasoconstriction/ischemia

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79
Q

Other effects of Magnesium

A

decrease vascular response to catecholamines
decrease ACE levels
Increase PGI2 production by endothelium

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80
Q

Magnesium effect on NMB

A

Potentiate the NMB

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81
Q

Placental relief of vasoconstriction by

A

Inhibiting TXA2 synthesis
Calcium channel blockade
Increase UBF

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82
Q

Magnesium Sulfate: therapeutic levels: 1.7-2.4

A

Normal , untreated patient

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83
Q

Magnesium Sulfate: therapeutic levels: 5-9

A

Therapeutic

84
Q

Magnesium Sulfate: therapeutic levels: 12

A

Loss of DTRs

85
Q

Magnesium Sulfate: therapeutic levels: 15-20

A

RESPIRATORY ARREST

86
Q

Magnesium Sulfate: therapeutic levels: >25

A

ASYSTOLE

87
Q

How do you treat Mg toxicity

A

Stop infusion
IV Calcium
Bircarbonate for acidemia
Intubation/Ventialtion for resp impairment

88
Q

Magnesium antagonizes

A

Calcium, giving more calcium help

89
Q

No clear benefit of those

A

AntiHTN

90
Q

What can be used to minimize maternal morbidity associated with

A

Encephalopathy
CVA
Placental abruption
End organ damage

91
Q

Treatment goals BP

A

DBP 90-105mmHg

MAP 105-125 mmHg

92
Q

Most common used antihypertensive

A

Hydralazine

93
Q

Hydralazine effects

A

Relaxes arterioles
Decrease SVR, BP and may Increase HR
NO effect on UP/FP BF

94
Q

2nd most common use antihypertensive (LADA)

A

Labetalol
Alpha:beta 1:7
Decrease SVR with Increase HR
AVoid in asthmatic /liver dysfunction , crosses the placenta

95
Q

Characteristics of Nitroglycerin VDVU

A

Venous>arterial relaxation
Decrease preload> afterload
Very rapid onset (hypotension)
UBBF preserved but crosses UP/FP

96
Q

Nitroprusside characteristics

A 
Powerful Vadodilator arterial>venous
Decrease Afterload 
Crosses Placenta (worry about cyanide toxicity)
97
Q

Nifedipine characteristics

A

Arterial dilator with little cardiodepresion

Can exaggerate HoTN if receiving MgSO4

98
Q

ESMOLOL characteristics

A

IV bolus for sympathetic block during intubation.

99
Q

4 complications of Pre-eclampsia PPOH

A

Oliguria
HELLP
Pulmonary Edema
Placenta abruption with preeclampsia

100
Q

Oliguria best diagnosted with

A

Decrease in UOP w/ serial measurements over time

101
Q

Refractory oliguria is

A

<30ml for 3 hours responding to IVF bolus

Can be pre-renal, intra-renal, or post-renal

102
Q

What is the hallmark of HELLP?

A

Hemolysis

103
Q

HELLP is secondary to

A

Severe form of Pre-eclampsia

104
Q

HELLP is due to unknown insult but most likely

A

Intravascular platelet activation

Microvascular endothelial damage

105
Q

Hallmark for Pre-eclampsia is

A

Increase BP

106
Q

Hemolysis indicators are (ALIT)

A

Abnormal peripheral blood smear + Increase bilirubin level >1.2mg/dl
Increase liver enzymes AST (SGOT) >70
LDH >600
Thrombocytopenia < 100,000

107
Q

Many HELLP patients have

A

Pre-eclampsia first

108
Q

What does RUQ/neck? shoulder pain indicate?

A

50% chance of hepatic subscapular hematoma/bleeding

109
Q

AST vs ALT which is more specific to the liver

A

ALT

110
Q

Maternal complications with HELLP include: (CCDPA)

Which one occurs more with HELLP than preeclampsia

A 
CVA
CV
DIC
Placental abruption 
ARF (occurs more frequently with HELLP than preeclampsia)
111
Q

All HELLP patients show some evidence of

A

compensated DIC

112
Q

Treatment of HELLP and preEclampsia

A

Delivery of fetus

113
Q

HELLP patients have better outcomes with this medication

A

Dexamethason

114
Q

HELLP postpartum check for

A

Retained produces of placental or fetus with Ultrasound.

115
Q

Etiology of Pulmonary placenta with severe eclampsia (DIIL)

A

Decrease colloid oncotic pressure
Increase pulmonary capillary permeability
Increase intravascular hydrostatic pressure
LVF (SVR increase)

116
Q

A respiratory complication of severe pre-eclampsia is

A

ARDS

117
Q

In Placental Abruption, if fetal death occurs with abruption will have

A

50% maternal blood loss

118
Q

Severe abruption can be complicated by

A

DIC

119
Q

Treat severe abruption by (DFPP)

A

Delivery baby
PRBCs
FFPs
Platelets

120
Q

When to avoid regional

A

Clinical bleeding + Thrombocytopenia

121
Q

If there is a short interval

A

Clinical judgement call of risk vs benefit

122
Q

DIC development mostly with (ASA)

A

Abruption
Amniotic fluid embolism
Sepsis

123
Q

For PT/PTT

A

Trach platelet count and Fibrin degradation products

124
Q

MAG sulfate and anesthesia: Combined with epidural

A

AT risk for hypotension due to sympathectomy

Titrate epidural slowly and treat with EPHEDRINE PRN

125
Q

Action of magnesium on vasoconstrictors

A

Mg blunts contractile response to vasoconstrictions

Also inhibits catecholamines release after SNS stimulation (like intubation)

126
Q

Magnesium action on calcium release

A

Magnesium inhibits Ca2+ facilitate presynaptic transmitter release (no depolarization for you )

127
Q

MG act like a NMB at

A

> 12mg/dl

128
Q

Hypermagnesemia enhances sensitivity to __________ what is not affected_____

A

All NDNMBs ; Succinylcholine

129
Q

What happens at mag level > 12mg/dl

A

Loss of DTRs

130
Q

Consider use of CVP and PCWP

A

Severe preeclampsia with persistent oliguria and renal failure
A-LINE

131
Q

Absolute contraindications to anesthesia is

A

Patient’s refusal (can be charged with battery)

132
Q

AT this level in thoracic spine, may vomit and have hypotension

A

T6

133
Q

Epidural vs General Endotracheal anesthesia advantage

A

Epidural @ T4 blunts hemodynmaic and neuroendocrine responses better than GETA

134
Q

With coagulopathy and decreased platelet which anesthesia is better?

A

Spinal preferred over epidural

135
Q

Spinal considerations advantage and risk

A

reliable dense block with rapid onset but can lead to profound HoTN and fetal compromise (treat with Ephedrine 50mg IM )

136
Q

How do you know HOw high Epidural has reached

A

T4 hypotension
C3 stop breathing
ASK if they feel anything

137
Q

Long epidural needle for women with

A

BMI> 50

138
Q

C-section with GETA INDICATIONS

A

Coagulopathy
Placental abruption
Severe fetal distress

139
Q

Causes the highest mortality in preeclamptic women

A

Intracranial hemorrhage (intubation leads to increase ICP and risk of hemorrhagic veins)

140
Q

Postpartum management”: Severe preeclampsia;

Magnesium infusion

A

Continue Mag 24 hours after delivery or until diuresis begins

141
Q

Why monitoring bed for 24 hours unless complications arise?

A

Possible pulmonary edema and HELLP

142
Q

Persistent eclampsia

A

HTN oliguria, higher risk of M&M

143
Q

What is eclampsia

A

Convulsion and or coma occuring during pregnancy in a woman who ALSO MEETS diagnostic criteria for preeclampsia (Proteinuria, HTN, edema)

144
Q

Until proven otherwise

A

Seizures during pregnancy = Eclampsia

145
Q

What terminates the seizure during eclamptic seizures?

A

Pt stop breathing

Increased CO2 levels in the brain terminate seizures

146
Q

Pt can go from Normal to Full eclamsia skipping

A

Pre-eclampsia

147
Q

Risk factors of Eclampsia (FMMN-PPRST)

A 
First pregnancy 
Multiple Gestation
Molar Pregnancy
Triploidy
Preexisting HTN
Renal diseas
Non-immune hydrops fetalis
SLE
Previous hx of preeclampsia/eclampsia
148
Q

Maternal complications of Eclampsia

DAHN-PPCA

A 
Abruption
HELLP
DIC
Neurological deficit
Pulmonary aspiration
Pulmonary Edema
CP arrest
Acute renal failure
149
Q

Describe seizures with Eclampsia

A

Begins with facial twitching f/b 20 second tonic phase with a generalized clonic seizure and apnea lasting an additional 60 sec–> Postictal stage with variable coma follows.

150
Q

Things complicating seizures include

A

Aspiration of stomach contents

CR arrest

151
Q

Goals of anesthetic management during seizures: Primary

SPE

A

Stop the convulsions
Establish clear airway
Prevent major complications

152
Q

Other Goals of anesthetic management during seizures: Primary ADIG

A

Antihypertensive
Induce/augment labor
Delivery should be expedited (UBF goes down, fetal bradycardia)
Give magsulfate

153
Q

Increase ICP not a concern if a patient is

A

Conscious

Alert and seizure free

154
Q

Indicate possible major intracranial pathology

A

Persistent coma

neurologic deficits

155
Q

BP control for anesthesia

A

Do not let get DBP get to >110

156
Q

Epidural ok if

A

Alert, awake and seizure controlled

157
Q

Neurosurgical anesthetic with opioids , relaxants, ___________ and mild _____

A

VA, hyperventilation (CO2 decrease-> ICP decrease)

158
Q

Major contraindications to Spinal

A

Increased ICP –> Herniation

159
Q

Meds use in spinal that can lead to seizures

A

Lidocaine

Bupivacaine

160
Q

Decreases DVT incidence

A

Early ambulation

161
Q

3 possible origins of DVT

A

Superficial vein
Pelvic vein
Ovarian vein

162
Q

DVT pathophysiology

A

A blood clot or thrombus that forms in a deep vein of the leg or pelvis either partially or totally blocking the flow of blood

163
Q

PE pathophysiology

A

1 . A DVT or parts of it breaks off from the vein
2. the break away clot travels through the bloodstream
to the heart and migrates toward the lung
3. The clot blocks a vessel to the lung interrupting blood supply.

164
Q

If DVT untreated

A

24% risk of PE –> 15% whe PE occurs

165
Q

if DVT treated

A

4.5%risk of pE

166
Q

2/3 of pregnancy related PEs occur

A

Postpartum monitor >4 hours PP

167
Q

4 risk of thromboembolism MECS

A

Smoking
Malignancy
Contraceptive
Endothelial injury

168
Q

Why is there venous stasis?

A

Gravid uterus makes blood harder to go black

169
Q

Pulmonary Embolism HTN

A

from embolus –> RV overload –> RV failure-> Rsided CHF

170
Q

S/S of PE PAD-C

A

Dyspnea (JVD)
Palpitations
Angina
Cough with hemoptysis

171
Q

ECG S/S of PE

A

RV strain
ST-T wave changes
SVT

172
Q

CXR evidence of PE

A

25-40% of PE have normal CXR

173
Q

Better works

A

V/Q scan, pulmonary angiography, spiral CT

174
Q

For PE spiral CT scan shows

A

Pulmonary dead space

175
Q

Anesthesia Focus with PE (VASA)

A 
Adequate maternal/fetal oxygenation
Support maternal circulation
Anticoagulation
Venous interruption
Surgical embolectomy for rapidly deteriorating patients.
176
Q

Clinical presentation depends on

A 
Size and number
Rate of clot
Preexisting
Recurrence
Resp failure from extensive or pulmonary edema
177
Q

Treatment of DVT goal

A

Prevent PE

178
Q

IV heparin should be d’c’d

A

when active labor begins

179
Q

Warfarin post pastrum

A

Continue for 3 months ( if no AC can be used, greenfield filter)

180
Q

Does warfarin cross breastmilk

A

NO

181
Q

Avoid

A

Esophageal temp probe

Gastric tube

182
Q

Diagnosis of exclusion after autopsy usually

A

Amniotic Fluid Embolism

183
Q

Amniotic fluid embolism

A

Amniotic entering fluid vein

184
Q

Etiology unclear but studies suggesting metabolites of

A

Arachidonic acid (leukotrienes) and meconium responsible

185
Q

Early phase of AFE about____Mins

A

30 min

186
Q

AFE Early phase symptoms

PPRDVHH

A 
Pulmonary Vasopasm
Pulmonary HTN
RVF
Decrease CO
V/Q mismatch
Hypoxemia
Hypotension
187
Q

V/Q mismatch is a

A

Deadspace problems

188
Q

Ventilation is a

A

Shunt problem

189
Q

AFE 2nd phase symptoms (LPD)

A

LVF
Pulmonary Edema
DIC

190
Q

Presentation of AFE

A

3rd trimester after abdominal trauma and postpartu

191
Q

Differential diagnosis of AFE (ONA)

A

OB complications (abruption, eclampsia)
NonOB complication (PE, VAE, sepsis, MI, anaphylaxis)
Anesthesia (High neuraxial block, LA systemic Tox, med
error)

192
Q

When does amniotic Fluid embolism occur?

A

After maternal exposure to fetal issue

193
Q

Amniotic fluid embolism is

A

anaphylactoid syndrome of pregnancy –> HELPFUL MEDICATION Is EPI

194
Q

AFE presentation similar to

A

Shock and anaphylaxis

195
Q

FHR during AFE

A

severe decelerations but FHR variability is present

196
Q

Management of AFE: airway

A

100% oxygen

Intubate the trachea and support ventilation as needed

197
Q

Management of AFE: CV support (SEAL)

A

Start CPR if needed
Ensure LEFT UTERINE DISPLACEMENT to RELIEVE AORTOCAVAL COMPRESSION if appropriate
AMINISTER FLUIDS and VASOPRESSORS
Large bore IV access, invasive pressure monitoring

198
Q

Management of AFE: FETUS (ME)

A

Monitor fetal well being

Expedite delivery for nonreassuring status in VIABLE EVENT or in the event of maternal CPR in the 2nd half of pregnancy

199
Q

Management of AFE: Hemostatic support (MES)

A

Massive transfusion protocol
Ensure normothemia
Send blood owrk

200
Q

Venous Air Embolism most common with

A

General Anesthesia

Less with regional because they are spontaneously breathing

201
Q

Venous Air embolism pathophysiology

A

pressure gradient as small as -5cm2 between surgical field and heart allows venous air entrapment

202
Q

2 things associated with the development of Venous Air Embolis

A

Steep Trendeleburg position

Uterine Exterioriation during C-section

203
Q

Fatal volume

A

> 3mg/kg are fatal RV air lock

204
Q

Small air volumes leads to (VAHH)

A

V/Q mismatch
Hypoxemia
Arrythmia
Hypotension

205
Q

Venous Air embolism with patent FO

A

paradoxical air embolism

CV/neuro complications

206
Q

Venous Air embolism presentation

A

50% angina
25% Decrease SaO2
>20% drop in BP (2%)

207
Q

Resuscitation of patient with massive venous air embolism

PDS -CEIP

A 
Prevent air entrapment (change position, flood surgical 
       field)
Discontinue Nitrous give 100% oxygen
Support ventilation and circulation
Central venous catheter to aspirate air
Expedite delivery
Imaging to rule out intercerebral air. 
Paradoxical cerebral artery gas may benefit from 
     Hyperbaric oxygen therapy

SNRAObPedGer (25 decks)

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