Ex1 OB 3 Flashcards
1
Q
PIH
A
Encompasses a range of disorders collectively
Formerly known as “toxemia of pregnancy”, which includes:
- isolated systemic hypertension (nonproteinuric hypertension)
- preeclampsia (proteinuric hypertension)
- eclampsia
2
Q
HTN during pregnancy
A
Common, ~ 10% of pregnancies
Associated with a higher incidence of maternal, fetal, and neonatal mortality and morbidity
3
Q
PIH Etiologies
A
- Vasospasm caused by abnormal sensitivity of vascular smooth muscle to catecholamines
- -Antigen-antibody reactions between fetal and maternal tissues during first trimester that initiates placental vasculitis
- An imbalance of vasoactive prostaglandins (thromboxane A and prostacyclin) leading to vasoconstriction of small arteries and aggregation of platelets
4
Q
Hypertensive States
A
- Gestational hypertension
- Preeclampsia, eclampsia
- Chronic essential hypertension
- Chronic hypertension (secondary to renal disease, endocrine disease, coarctation of the aorta)
- Chronic hypertension with superimposed preeclampsia
5
Q
Gestational HTN
A
Characterized by onset of systemic HTN, without proteinuria or edema
Usually mild with minimal impact on pregnancy
Resolves before 12 weeks postpartum
-BP normalizes during first few weeks postpartum but systemic HTN often recurs with subsequent pregnancies
-Risk of developing essential HTN later in life increased in women with gestational HTN
6
Q
Preeclampsia
A
Occurs in 5 – 8% of pregnancies in US
Incidence varies with geographical location (up to 18% in parts of Africa)
Disease is mild in 75% of patients
7
Q
Preeclampsia is primarily a disease of
A
Primigravidas
8
Q
Preeclampsia is associated with
A
High rates of neonatal mortality
-d/t decreased placental blood flow, decreased oxygen delivery to fetus, etc.
9
Q
Preeclampsia maternal mortality
A
Cerebral hemorrhage (30 – 40%) Pulmonary edema (30 – 38%) Renal failure (10%) Cerebral edema (9%) DIC (9%) Airway obstruction (6%)
10
Q
Preeclampsia risk factors
A
Predisposing factors: Nulliparity Black race Maternal age < 20 years or > 35 years Low socioeconomic status Multiple gestation Hydatidiform mole Polyhydramnios Obesity Chronic hypertension Diabetes Underlying renal disease
11
Q
Preeclampsia diagnosis
A
development of HTN + proteinuria after 20 weeks of gestation
-2 categories
12
Q
“classic” preeclampsia
A
Classic triad:
HTN, generalized edema, proteinuria
13
Q
Mild Preeclampsia
A
HTN with SBP > 140 mmHg or DBP > 90 mmHg in patient who had normal BP prior to pregnancy
Proteinuria > 300 mg over 24 hours
14
Q
Severe Preeclampsia
A
-SBP > 160 mmHg or DBP > 110 mmHg on two occasions < 6h apart
- Proteinuria > 2g in a 24h period or 2-4+ on urine dipstick testing
- Increased serum creatinine (>1.2 mg/dL)
- Oliguria = 500 mL/24h
15
Q
Preeclampsia with severe features
A
Visual or other cerebral disturbances Epigastric pain Retinal hemorrhages, exudates, or papilledema Pulmonary edema *difficult IV access d/t pitting edema
16
Q
Pathophysiology of preeclampsia
A
“A disease of theories”
The current concepts recognize that its a multisystem disorder characterized by vasoconstriction, metabolic changes, endothelial dysfunction, and activation of the coagulation cascade in conjunction with an inflammatory response
2-stage model has been proposed:
- failure of placental vascular remodeling results in reduced placental perfusion
- ischemic placenta may then produce circulating anti-angiogenic factors that promote generalized maternal vascular endothelium dysfunction, leading to systemic manifestations of preeclampsia
17
Q
Normal Placentation
A
involves transformation of branches of maternal uterine arteries, spiral arteries, from thick-walled muscular arteries into sac-like flaccid vessels that permit delivery of greater volumes to uteroplacental unit
In an uncomplicated pregnancy: normal placenta connection to uterine wall.
18
Q
Normal placentation involves the invasion of spiral arterial walls with
A
endovascular trophoblastic cells
19
Q
In preeclampsia, what does not occur (pathogenesis)?
A
transformation of spiral arteries does not occur bc the placental trophoblastic cells do not invade the spiral arteries, resulting in…
Narrow vessels –> placental hypoperfusion –> ischemia
20
Q
Preeclampsia is associated with what abnormalities
A
Elevated levels of circulating renin, angiotensin, aldosterone, catecholamines
–> resulting in generalized vasoconstriction + endothelial damage; edema, hypoxemia, hemoconcentration
–> decreased renal blood flow, GFR, urine output
*puffy, swollen, but dehydrated
21
Q
Preeclampsia: coagulation findings
A
thrombocytopenia, increased fibrin split products, + prolonged PT may occur
DIC rare but possible
22
Q
Preeclampsia creates an imbalance in ________ ratio due to _______
A
imbalance in thromboxane to prostacyclin ratio
due to decreased prostacyclin production
23
Q
Clinical effects of prostacyclin
A
decreased vasoconstriction, platelet aggregation, uterine activity
Increased uteroplacental blood flow
24
Q
Clinical effects of thromboxane
A
Increased vasoconstriction, platelet aggregation, uterine activity
Decreased uteroplacental blood flow
25
One of the most serious forms of preeclampsia
HELLP Syndrom
26
HELLP Syndrome
Hemolysis, Elevated Liver Enzymes, and Low Platelets
| *only in this if mom has all - otherwise pre-eclampsia with severe features
27
HELLP Syndrome: Labs
-hemolysis: indicated by abnormal peripheral blood smear + an increased bilirubin level
- Elevated liver enzymes:
* aspartate aminotransferase (AST) >70 U/L
* lactate dehydrogenase (LDH) >600 U/L
- Platelet count < 100,000/mm3
28
HELLP syndrome: clinical indications
Assuming no other coagulopathy, hemostasis not problematic unless platelet count < 40,000 /mm3
*rate of fall* is of clinical significance:
Regional anesthesia C/I if platelets drop dramatically over short period
-Platelet count usually returns to normal within 72h of delivery, but thrombocytopenia may persist for longer periods
29
HELLP syndrome: most important factor relating to anesthesia
Platelet count dropping precipitiously --> catch mom in time (normal platelets:: 90 to 70) to place epidural, but cannot remove until plt count resolves
30
Medical Management:Mild Preeclampsia
Tx for preeclampsia: Bedrest + delivery of infant
Hospitalization diminishes chances of convulsions + enhances fetal survival
Outpatient management includes bedrest, daily urine dip for protein, and BP measurement
Antihypertensives for DBP > 100 mmHg and gestation > 30 weeks
31
Medical management: Severe Preeclampsia
Goals include prevention of convulsions, control of maternal blood pressure, and initiation of delivery
Antihypertensives for control of blood pressure and corticosteroids used to accelerate fetal lung maturity
32
Preeclampsia: Indications for Delivery
- DBP consistently > 100 mmHg in a 24-hour period or confirmed > 110 mmHg
- Rising serum creatinine
- Persistent or severe headache
- Epigastric pain (liver distension)
- Abnormal LFTs
- Thrombocytopenia
- HELLP syndrome
- Eclampsia
- Pulmonary edema
- Abnormal FHR
- SGA fetus
33
Delivery -- preeclampsia
- Vaginal delivery is preferable to C/S and labor induction is generally *aggressive*
- A clear endpoint for delivery should be determined, usually w/in 24h
- If delivery is not achieved within the set time frame, then a cesarean is warranted
34
Why is vaginal delivery preferred over C/S in preeclampsia?
thrombocytopenia + coagulopathy from preeclampsia increases risk of bleeding
35
Eclampsia
Preeclampsia + generalized seizures
Most seizures occur before delivery
-PP seizures occur most often w/in 48h after delivery
36
Pathophysiology of eclampsia
seizures attributed to platelet thrombi, hypoxia due to local vasoconstriction, and foci of hemorrhage in the cortex
37
Relationship between eclampsia + HTN
poor correlation with severity of HTN
| 25 – 40% of patients will have normal BP at time of their first eclamptic seizure
38
hallmarks of hypertensive encephalopathy
retinal hemorrhages, exudates, and papilledema
| *very infrequent in eclampsia
39
Severe Preeclampsia: HTN Tx
*Hydralazine
-longer onset time, not good for urgent situations
*Labetalol
-quick onset
-doses up to 1mg/kg do not effect baby blood flow
*Nifedipine
-CCB + increases UBF
***assoc. with: lowering moms bp, prolonging pregnancy, improving fetal O2
*Sodium Nitroprusside
-risk of fetal cyanide toxicity
Nitroglycerin
40
Severe Preeclampsia: Fluid management
* Significant hypovolemia d/t shift of fluid/proteins to extravascular compartment
- inverse relationship between intravascular volume + severity of HTN has been demonstrated
41
Severe preeclampsia: pts with very elevated DBP expected to have
negative CVP readings
42
Severe Preeclampsia: Coagulation Abnormalities
- assess coag status
| - administration of platelets, FFP, pRBCs may be necessary
43
Agent of choice for seizure prevention + control in preeclampsia/eclampsia
Magnesium Sulfate
44
Magnesium sulfate - outcomes
- can reduce seizures by 50% w/o any serious maternal morbidity
- beneficial effect may be vasodilation + increase in CO (by a reduction of SVR)
45
Magnesium Sulfate: MOA
- Anticonvulsant effect likely from acting as an N-methyl-D-aspartate (NMDA) receptor antagonist
- Increased production of endothelial vasodilator, prostacyclin
- Protects against ischemic damage of cells by substitution of calcium
46
Magnesium Sulfate Dosing
- Initial dose: 4–6g IV over 10–20 min, followed by maintenance infusion 1–2g/h
- In presence of renal failure, rate of infusion should be modified by evaluating serum magnesium levels
47
Magnesium Therapeutic Index
- Narrow therapeutic index
- therapeutic range: serum levels 4 to 8 mEq/L
- normal serum magnesium level is 1.5 – 2.0 mEq/L
48
Magnesium Toxicity: Plasma Mag Level 5-10
Effects: EKG changes
- PR prolonged
- widened QRS
49
Magnesium Toxicity: Plasma Mag Level 10
Loss of DTRs
50
Magnesium Toxicity: Plasma Mag Level < 15
SA + AV Block
51
Magnesium Toxicity: Plasma Mag Level > 15
Respiratory paralysis
52
Magnesium Toxicity: Plasma Mag Level 25
Cardiac arrest
53
Tx: Magnesium Toxicity
10 mL of 10% calcium gluconate slow IV push to counteract effects
54
Why calcium gluconate and not chloride for mag toxicity tx?
Chloride is 3x as potent, but extremely irritating to vessels when given IV push
55
Magnesium: pros
```
Anticonvulsant
Vasodilation
Increased uterine blood flow
Increased renal blood flow
AntiHTN
Increased prostacyclin release by endothelial cells
Decreased plasma renin activity
Decreased ACE
Attenuation of vascular responses to pressor substances
Reduced platelet aggregation
Bronchodilation
Tocolysis (improves uterine blood flow and antagonizes uterine hyperactivity)
```
56
Magnesium: cons
Tocolysis with prolonged labor + increased postpartum hemorrhage
Decreased FHR variability
Generalize muscle weakness
Increased sensitivity to muscle relaxants
Neonatal effects: lower APGAR scores + decreased muscle tone
*mag can relax mom = can relax uterus + baby too
57
Anesthetic options for Severe preeclampsia: Technique of choice
- Epidural anesthesia recommended for C/S delivery in severe preeclamptic pt as technique of choice
- Epidural analgesia early in labor may help to reduce circulating levels of maternal catecholamines, thus improving uteroplacental perfusion
58
Anesthetic options for Severe preeclampsia: Spinal
Spinal anesthesia in context of severe preeclampsia has not been recommended in the past, bc concern rapid onset of sympathectomy would precipitate HOTN
- But single-shot spinal for C/S can be safely used in pt with severe preeclampsia
- HOTN avoided w/ meticulous attention to technique + volume expansion
59
Anesthetic options: Neuraxial C/I
Coagulopathy or C/I's
| = GETA
60
Risks -- GETA for C/S d/t preeclampsia
- Periglottic edema (difficult airway)
| - HD response to intubation: HTN
61
In patients receiving mag sulfate who undergo GETA, what may occur?
activity of Sux + NDMR enhanced
62
GETA for C/S in pt with preeclampsia: induction risk + Tx
Risk of HTN --> stroke + pulmEdema
Prophylaxis: Labetolol 10mg IV
Tx: SNP or NTG
63
Most common medical complication of pregnancy
Diabetes Mellitus
64
any degree of glucose intolerance with first recognition during pregnancy
Gestation Diabetes (GDM)
65
Midline defect
occurs on the anterior (front) portion of body, usually in middle or center of body.
Like cleft palate or imperforate anus
66
Hyperglycemia around _____ results in 6x increase in ______
Hyperglycemia around conception or early organogenesis results in a 6-fold increase in midline birth defects
67
Ketoacidosis
- immediate threat to life
- leading cause of perinatal morbidity
- 40% of perinatal mortality
68
GDM Complications
```
Pregnancy:
Placental insufficiency
Superimposed preeclampsia
Diabetic nephropathy
Diabetic ketoacidosis
```
Fetal macrosomia:
assoc. with operative delivery, shoulder dystocia, birth trauma
Neonatal complications: respiratory distress syndrome, hypocalcemia, hyperbilirubinemia, hypoglycemia
69
GDM effect on placenta
Associated with placental abnormalities
| -uteroplacental blood flow index lower by 35-40% in diabetic parturients
70
GDM: poorly regulated + higher HbA1c effect at tissue level
2,3-DPG levels lower = blood oxygen release at tissue level impaired
71
Most common cause of 3rd trimester bleeding
placenta previa
abruptio placentae
uterine rupture
72
Postpartum hemorrhage is most often due to
uterine atony (soft)
retained placenta
placenta accreta (grew thru uterus)
uterine inversion
73
Obstetrical Hemorrhage
```
Blood loss assoc. w/ pregnancy or parturition
and 1 or + :
-Causes maternal or perinatal death
-Requires blood transfusion
-Decreases hematocrit by 10 points
-Triggers emergency therapeutic response
```
74
Abruptio placenta
placental abruption
a partial or complete separation of the placenta before delivery of the fetus
75
Most common cause of OB hemorrhage + maternal death
Abruptio placenta
76
Placenta Previa
Occurs when placenta is implanted low in uterus, either overlying or encroaching cervical opening (cervical os)
77
Types of placenta previa
Low implantation: small portion of placenta covers cervical os. Possibility to deliver vaginally
Partial: can cause just as much bleeding as total.
Total: overlying cervical os
78
Placenta Previa is more common
- in multiparous women
| - previous C/S or uterine myomectomy
79
Placenta Previa is characterized by
painless vaginal bleeding in 3rd trimester
80
Bleeding d/t placenta previa
may stop spontaneously, risk of severe bleeding can occur at any time
81
Placenta Previa: Tx
< 37 weeks, mild to moderate bleeding: bedrest + observation
> 37 weeks: C/S
82
Abruptio Placenta Risk Factors
chronic HTN, PIH, preeclampsia, maternal cocaine use, excessive alcohol intake, smoking, + previous history of abruption
83
Abruptio Placenta manifestations
vaginal bleeding + uterine tenderness
Categorized based on severity (degree of placental separation)
Blood loss can be underestimated d/t potential for substantial hemorrhage concealed behind placenta
84
Abruptio Placenta Risks
DIC (30%, high risk)
d/t open venous sinuses in uterine wall = amniotic fluid enters maternal circulation
Severe abruption: fetal mortality 50%, maternal mortality 1-3%
85
Placenta Accreta
Abnormally firm attachment of placenta to uterine wall
placenta becomes difficult or impossible to separate from uterus + produce life-threatening maternal hemorrhage
86
Placenta Accreta - increased risk if
history of placenta previa or C/S
87
Placenta increta
placenta invades the myometrium
88
Placenta percreta
placenta has invaded the myometrium and serosa, sometimes into adjacent organs, such as the bladder
89
Uterine rupture
- potentially life threatening complication
- May occur in a previously scarred uterus or result from uterine manipulation, trauma, or overly aggressive use of oxytocin (or VBAC)
90
What must be available for TOLAC?
Trial of Labor after C/S
-ACOG recommends physician capable of performing C/S + anesthesia provider be immediately available (< 30 minutes away if in rural area)
91
Uterine rupture S/S
- non-specific
- fetal bradycardia almost always occurs
- Maternal hypotension along with loss of function of uterine pressure monitors often evident
92
Tx Uterine Rupture
emergency laparotomy
| GA indicated
93
Vasa Previa
fetal umbilical cord passes in front of the presenting part of fetus
-vessels of umbilical cord are vulnerable to trauma during vaginal exam or aROM
94
Vasa Previa risks
bleeding from fetal circulation = fetus at risk
95
Vasa Previa Tx
immediate delivery
96
PPH
postpartum hemorrhage
| causes: uterine + non-uterine
97
Uterine causes - PPH
most frequent: uterine atony + retained placental products
| others: uterine rupture + uterine inversion
98
Non-uterine causes - PPH
vaginal tears, perineal hematoma, maternal coagulopathy
99
Uterine Atony: risk factors
```
Prolonged labor
Overdistended uterus (macrosomia or multiple births)
Infection
Grand multiparity
Administrations of drugs that relax uterus:
-Halogenated anesthetics
-β-sympathomimetic agonists
-Magnesium sulfate
```
100
Uterine Atony Tx
-oxytocin
Doses can precipitate HOTN (continuous infusions preferable)
-Hemabate + ergot alkaloids (Methergin) are potent uterotonic agents used to treat atony
101
Retained Placenta Tx
~ 1% of vaginal deliveries
Usually reqs manual exploration of uterus + facilitated by epidural/spinal
Additional uterine relaxation achieved w/ nitroglycerine 50–100mcg IV
Ketamine can be used if regional not in place
If bleeding excessive + hypovolemia present, regional may be C/I d/t HOTN
GA + RSI may be necessary
As soon as uterus is relaxed sufficiently to allow extraction, volatile should be d/c'ed to prevent uterine atony + further bleeding
102
Amniotic fluid embolism
Mortality ~ 80%
Survival uncommon, survivors often have neurological dysfxn
Most occur during or immediately after labor
103
AFE Pathogenesis
initiating event poorly understood
Usually during labor or other procedure, amniotic fluid + debris enters maternal circulation
-may trigger a massive anaphylactic rxn, activation of complement system, or both
104
AFE presentation
Acute SOB, +/- cough, followed by severe HOTN
Fetal distress evidenced by fetal bradycardia from hypoxic insult
Cyanosis
Asystole
105
Phases of AFE
Early phase:
Pulm vasospasm
Acute RHF
Often fatal early (50% die w/in 1h)
Second phase: LVF + pulmEdema
106
AFE Tx
*supportive*
Administer O2 + intubate
Aggressive CPR if arrests
Treat HOTN w/ crystalloid + blood products
Use vasopressors
*early delivery of fetus = may improve survival of mom + may result in survival of fetus
*HD, plasmapheresis, ECMO w/ IABP ?
107
Leading cause of maternal death globally
hemorrhage
108
Maternal hemorrhage usually occurs
immediately after delivery (35%)
109
Abnormal OB blood loss
> 500 mL vaginal delivery
| > 1L C/S
110
Major hemorrhage
Blood loss 2,500 mL or +
Transfusion of 5 or + units blood
Treatment for coagulopathy
111
Causes of maternal hemorrhage: antepartum
Placenta previa
Placental abruption
Uterine rupture
Vasa previa
112
Causes of maternal hemorrhage: postpartum
```
Uterine atony
Genital trauma
Retained placenta
Placenta accreta
Uterine inversion
```
113
PPH risk factors
```
Multiple gestation
Macrosomia
Polyhydramnios
High parity
Prolonged labor
Chorioamnionitis
Augmented labor
Tocolytics
Maternal blood disorders
> 35 years
HTN disorders
High concentrations of volatile anesthetic agents
```
114
strong predictor for subsequent development of severe postpartum hemorrhage
Fibrinogen levels of < 2 g/dL in early stage of postpartum bleeding
115
Accounts for 80% of PPH
uterine atony
116
uterine atony is the loss of tone in uterine musculature following delivery as a result of failure to respond to ________
normal endogenous oxytocic substances, oxytocin, and prostaglandin
117
No vaginal bleeding, can mom have uterine atony?
Yes - can be atonic, engorged uterus with > 1L blood
118
Prevention of uterine atony is facilitated how?
Administration of oxytocin immediately after delivery
119
s/s hypovolemia
may not be present until > 1200-1500mL blood loss
120
Circulating blood volume expands from ____
20-100%
121
RBC volume increases by
30%
122
CO increases by
50%
123
Risks of hypovolemia or hypovolemic shock in pregnancy
Masked s/s d/t normal increases in pregnancy:
HR increases 15-20 bpm
Peripheral vasodilation
Widened pulse pressure
124
Hypovolemic shock: moms SBP may not drop until ____
2-3L blood have been lost
125
Surgical management of maternal hemorrhage
```
Bimanual compression of uterus
Uterine balloon tamponade
Uterine compression sutures
Arterial ligation
Peripartum hysterectomy
Angiographic arterial embolism
```
126
Crystalloids are distributed between intravascular and extravascular space by a ratio of
1:3
127
Exsanguinating hemorrhage tx
immediate resuscitation with any fluid; blood products = saving
**O negative should be considered
128
Transfusion of red blood cells is usually unnecessary in patients with
Hgb = 10 g/dL or +
129
Transfusion of pRBCs should be administered if
Hgb < 6 g/dL
130
Transfusion Guidelines
Once > 10 units pRBCs given:
1:3 FFP:pRBC
+ 6u platelets
(avoid dilutional coagulopathies)
*ongoing measurement of Hgb, coags, + platelets guide therapy
131
Key strategy to avoid coagulopathy during MTP
Administer FFP before abnormal PTT values occur
132
Resuscitative goals
Avoidance of hypothermia
Early support of coagulation system (1: 1: 1)
Cell salvage: autologous transfusion using suction + washing systems
Administration of antifibrinolytic therapy (tranexamic acid)
Recombinant factor VIIa
133
External Bimanual uterine compression
- Emergency maneuver to reduce PPH + permit time for resuscitation + control of bleeding
- Aorta compressed with closed fist just above umbilicus to temporarily halt uterine blood flow
- 'External aortic abdominal pressure'
134
Complications of resuscitation and transfusion include:
```
Accidental admin of ABO incompatible blood
Dilutional coagulopathies
Transfusion reactions
Hypothermia
Hyperkalemia + hypocalcemia
```
135
Principle duties of anesthesia providers (during maternal hemorrhage)
Maintain vital functions
Replace blood loss
Provide the conditions under which hemorrhage can be controlled
136
Advent of ultrasonography has also allowed providers to
anticipate patients at high risk for hemorrhage, such as those with placental abnormalities, thus guiding planning for care + predicting blood loss
137
Initial responsibilities of anesthesia provider in unexpected hemorrhage:
Assess VS, BP, O2 sat, HR, capillary refill, peripheral + core temp, + LOC
Obtain abbreviated history
Assess airway, anticipated difficulty with intubation
Achieve proper venous access (2x18g min)
Call for help early, especially in cases of brisk bleeding
138
Non-initial responsibilities of anesthesia provider in unexpected hemorrhage:
Ensure adequate pain control
Indwelling epidural catheter for analgesia can be used for procedures with minor -moderate hemorrhage
Early transfer to OR should be considered at beginning of hemorrhage management in order to provide appropriate neuraxial or GA
Compare VS to stated EBL
Communicate discrepancies to OB team
Review ongoing fluid resuscitation + pharmacotherapy + assume responsibility for management
Send initial laboratory assays (Hgb/Hct, coags)
Order blood + blood products as needed
139
In the event of massive uncontrollable hemorrhage, anesthesia provider should be prepared for
emergency hysterectomy
Patient under regional may have to be converted to GA
140
Anticipated Hemorrhage
- Early consultation w/ anesthesia staff = essential in pts w/ known elevated risk of severe hemorrhage
- Transfer to another facility (if inadequate resources for MTP not available)
- Assemble anesthesia team: do not attempt to do cases of anticipated hemorrhage alone
141
After team assembled, Anesthetic management: Anticipated Hemorrhage
Ensure/have the following:
- all uterotonic Rx in OR
- immediate availability of vasopressors
- Procure a supply of calcium chloride (Tx: low ionized calcium d/t rapid transfusion)
- Order blood products for immediate availability: 10 units PRBC, 10 units FFP, 10 units of platelets
- Prepare transfusion lines, assemble rapid infusion devices, or pressure bags
- Set up fluid warmer/blanket
- Establish communication lines w/ central lab + blood bank
- Have POC devices for hemoglobin, electrolytes available
- Plan for GA
- Establish min 2 large IVs
- Place CVC w/ 7+ Fr cordis
- Utilize invasive ABP monitoring (beat-to-beat pressure measurement + frequent blood sampling)
