• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/168

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

168 Cards in this Set

  • Front
  • Back
What is the space of Retzius?
Peritoneal space btwn pubis bone and bladder.
How many parathyroid glands are there?
Usually 4: 2 superiorly and 2 inferiorly.
Nerve between the carotid artery and jugular vein?
Vagus
Name of node in left axilla associated w/ gastric cancer?
Irish's node
MCC fever < 48 hrs postop?
Atelectasis d/t inflammation
MC organ injured in penetrating abd trauma?
Small bowel
MCC hypertension in post op setting?
Pain
What is Trosseau's sign?
Migratory thrombophlebitis seen commonly in advanced intra-abdominal malignancy.
What is Curling's ulcer?
Stress ulcer that occurs in stomach in response to severe burns.
What is Saint's Triad?
Chronic cholecystitis (d/t GB stones), diverticulitis and hiatal hernia in presence of dyspepsia.
Definition of shock?
Inadequate tissue PERFUSION leading to cellular hypofunction.
Oxygen delivery does not equal metabolic demands.
-One way or another the tissue does not receive enough oxygen!

Reversible in early states, but if left untreated, --> death!
Many things cause it.
What is a LATE sign of shock?**
HYPOTENSION!!
3 components of perfusion?
Pump: heart

Pipes: vessels

Fluid: blood volume
What is cardiac output?
Volume of blood pumped by heart per minute.

CO maintains arterial BP and O2 delivery

CO = SV x HR
What is the average adult cardiac output?
5L/min
What is the cardiac index?
Correction for cardiac output relating cardiac output to body surface area.
(2.5-4.2 l/min/m2
Normal strove volume?
60-70 mL
3 things that determine stroke volume?**
Preload,

Afterload,

Myocardial contractility
Relation of cardiac output to end diastolic volume?
As end diastolic volume increases, SV increases, and in turn, cardiac output increases.
Relation of stroke volume to myocardial contractility and afterload?
SV increases as myocardial contractility increases and afterload decreases.
Aberrations in preload, afterload or myocardial function lead to....?
Shock
What is Frank Starling Law (simplified)?
The more the ventricle stretches, the harder it is going to contract

The greater the volume of blood entering the heart during diastole, the greater the volume of blood ejected during systolic contraction and vice versa.
Allows CO to be synced w/ venus return, arterial blood supply and other forces w/out depending upon external regulations to make alteration.
What is preload?
Volume in ventricle at the end of diastole.
Ventricular end diastolic volume (VEDV).

Influenced amt of end diastolic stretch on myocardial muscle fibers.
What is Starling's Law?
The force of ventricular ejections is related to:
- Volume in ventricle at end diastolic (preload). and
- Amt of myocardial stretch on ventricle.
What is ejection fraction?
End diastolic volume - end systolic volume / end diastolic volume.
What is normal ejection fraction?
60-75%
8 causes of decreased cardiac output?
MI,
Bradycardia,
Decreased SV and hypovolemia,
Neg inotropes,
High PEEP (pos end expiratory pressure),
Tamponade,
Valvular heart dz (ex aortic stenosis),
Increased systemic vasc resistance.
What is PEEP?
Positive End Expiratory Pressure.

If you don't have much blood coming back to heart --> decreased preload --> decreased CO.
What is afterload?
The resistance that the heart has to pump against.

Vasoconstriction increases afterload, aortic stenosis increases afterload.
5 causes of increased cardiac output?
HTN,
Decreased systemic vasc resistance,
Positive inotropes,
Hypermetabolic state,
Sepsis
What are vasopressors used for hemodynamically?
Causes constriction of blood vessels leading to increase in blood pressure.
What is a chronotrope?
Something that affects the heart RATE.
What is an inotrope?
Agent that affects myocardial contractility.
Primary location of alpha 1 receptors? Response when stimulated?
Arteries, arterioles, veins.

Constriction.
Primary location of alpha 2 receptors? Response when stimulated?
GI tract.

Decreased tone, motility and secretions.
Primary locations of beta 1 receptors? Response when stimulated?
Heart

Increased rate and force of contraction.
Primary location of beta 2 receptors? Response when stimulated?
Skeletal muscle blood vessels, coronary arteries, bronchial smooth muscle.

Dilation and relaxation.
What receptors does Norepinephrine stimulate?
alpha 1 & 2, beta 1
What receptors does epinephrine stimulate?
all: alpha 1 & 2, beta 1 & 2
What receptors does dopamine stimulate?
dopaminergic, alpha 1, beta 1
What receptors does phenylephrine stimulate?
alpha 1 & 2
What receptors does metaraminol stimulate?
alpha 1, beta 1
What receptors does ephedrine stimulate?
alpha 1, beta 1, beta 2
What receptors does vasopressin stimulate?
V 1, V2
What receptors does dobutamine stimulate?
alpha 1, beta 1, beta 2

Inotrope. A lot of beta 1 activity.
What is phenylephrine used for?
Intense vasoconstriction. Used for nosebleeds.
What is also known as the "filling pressure"?
Preload
What can increase preload?
Vasopressors

Volume expanders.
What can decrease preload?
Vasodilators

Diuretics
What is central venous pressure (CVP)?
An indirect measurement of volume status.

Measurement of pressure in the inferior vena cava
What is a more accurate measurement of volume status?
Pulmonary artery catheter (Swan Ganz)
How is afterload estimated?
By the systemic vascular resistance (SVR). - can also be measured with swn ganz catheter.

In certain shock states, reducing SVR and therefore afterload, can improve myocardial contractility (in cardiogenic shock).
What is systemic vascular resistance?
Resistance to blood flow offered by all of the systemic vasculature EXCLUDING pulmonary system.

Determined by factors that influence vasc resistance like vasoconstriction and vasodilation.
Determined by change in blood vessel diamtere as well as blood viscosity.
What is the equation for SVR?
(MAP - CVP) / CO

CVP: central venous pressure.
Changes in SVR in hypovolemic shock?
High SVR secondary to compensatory vasoconstriction.

SVR decreases when volume is restored.
Change in SVR in neurogenic shock?
Low SVR secondary to loss of vasomotor tone.
Change in SVR in septic shock?
Low SVR secondary to mediators.
2 afterload reducing agents: vasodilators?
Nitroprusside: reduces resistance on arterial side.

Nitroglycerine: increases venous capacitance.
What is the equation for BP?
BP = Co x SVR
What is the function of vasopressors?

3 most common agents?
Agents that augment vascular tone. Increased SVR results in increase in BP.

Norepinephrine, Phenylephrine, Dopamine
What is the hallmark of cardiogenic shock?
Decreased contractility
What types of agents are used to treat cardiogenic shock?
3 examples?
Inotoropic agents are used to increase myocardial function:

Dopamine, Dobutamine, Epinephrine
5 drugs that are positive inotropes?
Dobutamine,
Epi,
Dopamine,
Milrinone (phosphodiesterase inhib),
Digoxin (oral)
4 drugs that are negative inotropes?
Amiodarone,
Diltiazem,
Verapamil,
Lopressor (b-blocker)
What is pulmonary capillary wedge pressure?
Swan Ganz cath is inserted into right atrium and balloon inflated while catheter is further advanced while monitoring wave forms.
Cath is moved through right atrium, right ventricle into pulm artery.
The cath tip gets wedged into small branch of pulm artery causing waveform to flatten.
How is the Left ventricular end diastolic pressure determined? And what is it used for?
It is approximated with a Swan Ganz Cath which approximates the left atrial pressure (which should be equal to left vent diastolic pressure).

Used to figure preload and myocardial contractility.
3 types of shock states?
Hypovolemic,

Obstructive,

Distributive
What constitutes hypovolemic shock? Etiology of hypovolemic shock?
Loss of >20% circulating volume.
Loss of blood, plasma, extracellular, extravascular, water.

Common causes: hemorrhage, dehydration, burns, 3rd space losses.
Pathology/ physiology of hypovolemic shock?
Loss of volume --> compensatory increased heart rate with low cardiac output.
High peripheral resistance d/t catecholamine surge , low CVP.
BP decreases if losses not replaced (late sign!!)
How do the kidneys try to compensate for hypovolemic shock?
Renin released --> angiotensin --> peripheral vasoconstriction and aldosterone release.
This helps to raise SBP and increase intravascular volume.
How do hormones try to compensate for hypovolemic shock?
ADH is secreted from pit. and stimulates the thirst center in brain.

GH, TH and corticosteroids secreted to protect the heart and brain.
What do you see in a class I hemorrhage?
<750 mL,"", <15% blood loss.
Pulse <100.
Normal BP.
Resp: 14-20 bpm.
Urine output >30 ml/hr.
No CNS sx.
What do you see in a class II hemorrhage?
Main thing: tachycardia!!

750-1500 ml, 15-30% loss.
pulse >100!!
Narrow pulse pressure.
Resp: 20-30.
Urine output: 20-30 ml/hr.
CNS: anxious.
What do you see in a class III hemorrhage?
Main thing: hypotension!!

1500-2000, 30-40% loss.
Pulse >120.
Hypotension!
Resp: 30-40.
Urine 5-15 ml/hr.
CNS: confused.
What do you see in class IV hemorrhage?
>2000, >40% loss.
Pulse >140.
Hypotension.
Resp: >35.
Urine: negligible.
CNS: lethargic!!
What would be considered sx of mild hypovolemic shock?
<15% blood volume loss.
Cool extremities,
Delayed cap refill,
Thirst.
What would be considered sx of moderate hypovolemic shock?
15-40% volume loss.
Low urine output secondary to effects of aldosterone and vasopressin, tachycardia, tachypnea.
What would be considered severe hypovolemic shock?
>40% volume loss.
Decreased urine output,
Decreased bp,
ischemia,
severe mental status changes
In general, clinical features of hypovolemic shock?
Pale, cool, clammy skin.
Apprehensive, restless.
Mental status changes: earliest sign.
Hypotension, tachycardia.
ORTHOSTATIC HYPOTENSION*,
OLIGURIA, ANURIA*,
NARROW PULSE PRESSURE
Dx of hypovolemic shock?
History, physical.

CBC; decrease H&H: a late sign in ACUTE hemorrhage.
May see increased H&H in dehydration d/t hemoconcentration.
Management of hypovolemic shock?
RESTORE CIRCULATING VOLUME!!!
Istotonic solutions initially.
RBCs when indicated.
ID and control source of hemorrhage.
Prevent hypothermia!
Aggressively treat coagulopathy.
What is obstructive shock?
When the heart can't pump.
What is obstructive shock of intrinsic origin?
Decreased myocardial contractility due to direct damage?
2 Causes of obstructive shock of intrinsic origin?
AMI,
Blunt myocardial injury (BMI) - formerly myocardial contusion.
What is obstructive shock of extrinsic origin?
Increased external pressure on heart or mediastinal contents.
3 causes of obstructive shock of extrinisic origin?
Tamponade,

Tension pneumo,

Massive PE
First Treatment for AMI?**
MONA!!!***

Morphine,
Oxygen,
Nitro,
Aspirin
Treatment for AMI after mona?
Get 12 lead ekg,
Start adjunctive tx: beta b, nitro IV, heparin, IV, GIIb/IIIa.
Reperfusion?: fibrinolytics, angioplasty/ PCI and stent.
Hemodynamic support.
What is cardiogenic shock?
Result of acute or decompensated heart failure.

Heart has poor contractility:
- low ejection fraction
- kidneys are blind,
- heart doesn't communicate,
What is the MCC of blunt myocardial injury --> obstructive shock?
MVA
What would you see on EKG in blunt myocardial injury?

What would you see clinically?
EKG: PACs, PVCs, new RBBB, afib, ST seg changes.

Friction rubs, rales, hemodynamic instability, arrhythmias.

High level suscpicion important!!
Treatment for blunt myocardial injury?
Supportive!! No gold standard for dx. Observe for at least 24 hrs for risk of dysrhythmias. Give hemodynamic support.

Follow by ECG, serial cardiac enzymes, troponin

Can do echo: TRANSTHORACIC > TEE.
MUGA: MUltiple Gated Acquisition scan - nuc med non invsaive test to eval cardiac function.
What are some signs/ symptoms of tension pneumothorax, causing obstructive shock?
Tracheal deviation AWAY form ptx.
Decreased breath sounds on injured side.
JVD,
SOB,
Decreased BP/ hemodynamic instability.
How should a tension pneumothorax be dx?
Can be seen on xray, but the time it takes to get an x-ray can be considered malpractice!!

Dx based on phys exam.
Treatment for a tension pneumothorax?
Needle decompression

Chest thorocostomy
What is Beck's triad?
Triad seen in cardiac tamponade.

- Narrow pulse pressure.
- JVD.
- Muffled heart sounds.
Besides Beck's triad, what else might you see in presentation of cardiac tamponade?
Low voltage on ECG,
Elevated CVP,
Maybe pulsus paradoxus (breathing so hard that on inspiration, you see a fall of systolic bp > 10mmhg).
2 treatments for cardiac tamponade?
Sub-xiphoid window to drain the pericardium.

Pericardiocentesis.
What are the s/s of massive PE causing obstructive shock?
Dyspneua,
Hemoptysis,
Pleuritic chest pain,
ECG changes,
Hypoxia,
Resp alk w/ hypoxia on ABG,
Hemodynamic instability.
Most have tachycardia.
Diagnosis of a massive PE?
VQ scan.
**CONTRAST ENHANCED SPIRAL CT (CTA).
Pulm angiogram: "gold standard"

D-dimer: useful in outpts (breakdown product of fibrin mesh that has been stabilized by Factor XIII - final step in thrombus formation.) *Won't be useful if any trauma!!
Treatment of PE?
Supportive care.
Anticoagulation.
Greenfield filter.
Thrombolytics
Surgery.

**PREVENTION IS KEY!!!
In general, management of obstructive shock?
OXYGEN!!!**
Adequate volume.
Inotropic support.
Treat underlying prob: release tamponade, fill tension pneumo, find PE!!!
What is distributive shock?
Shock caused by vasodilation.
3 types of distributive shock?
Neurogenic shock,

Septic shock

Anaphylactic shock
2 major causes of neurogenic shock?
Spinal cord disruption

Spinal cord compression/ contusion
What occurs in neurogenic shock?
Loss of vasomotor control: NO SYMPATHETIC TONE!!

Blockade of periph autonomic regulation.

Increase in vascular space d/t expansion of venous capacitance bed and venous pooling.
Signs/ symptoms of neurogenic shock?
Warm skin,
Hypotension,
Paralysis,
BRADYCARDIA (instead of tachy) b/c of autonomic dysregulation.
Cardiac output normal, SVR low, PCWP low to norm.
Management of neurogenic shock?
IV fluid,
Vasopressors,
Maintain body temp,
Pacemaker?
What is the progression of sepsis?
SIRS -->
Sepsis -->
Severe sepsis -->
Septic shock
What is SIRS?
Systemic Inflammatory Response Syndrome.

Pro-inflammatory state marked by:
** tachycardia, tachypnea, leukocytosis, fever (need 2 of the 4).
**Does NOT have anything to do with infection!!
What constitutes sepsis?
2 or more of the SIRS criteria.

AND:

Known or presumed source of INFECTION!
What is severe sepsis?
Sepsis

AND

1 or more organ dysfunction.
What are some acute organ dysfunctions that could be a marker of severe sepsis?
CNS: altered consciousness, confusion, psychosis.
Lungs: Tachypnea, PO2 < 70, O2sat <90%.
Liver: Jaundice, Increased enzymes, decreased albumin, increased PT.
Heart: Tachycardia, hypotension, altered CVP, Altered PAOP.
Kidneys: Oliguria, anuria, increased creat.
Circulation: Decreased plts, Increased PT/PTT, Decreased protein C, Increased D-dimer.
What is septic shock?
Severe sepsis AND refractory hypotension requiring VASOPRESSORS!!

OVERWHELMING response to infection.
Reaction btwn bacterial products and normal host defenses.
Release of endotoxin that produces adverse biochem, immunologic and neural mechanisms.
What is MODS: "Multiple Organ Dysfunction Syndrome"?
A syndrome of progressive but potentially reversible dysfunction involving two or more organs or organ systems that arises after resuscitation from an acute disruption of normal homeostasis.
What is the MCC mortality on the SICU?
MODS: results from prolonged shock state.

Usual progression is: pulm, hepatic, renal.
Mortality rate proportional to # of organ systems involved: 80-100% w/ 3 or more systems.
What is the pathophysiology of septic shock?
Decreased PVR secondary to release of activated cytokines in sepsis or histamines in anaphylaxis.
Mediators in sepsis like bacterial products like lipopolysaccharides and inflam mediators.
Early on, increased cardiac output w/ decreased SVR.
Capillaries leak.
Massive inflammation cause a reduction in tissue O2 extraction --> hypoxia.
Physical exam finding in Septic shock?
Hypotension: wide pulse pressure.
Warm skin.
Rash.
Low CVP.
Low SVR.
High CO.
Management of septic shock?
- EARLY RECOGNITION!!!!!
- panculture before abx.
- Source control: abx/surg w/in 1 hr!!!
- IV FLUIDS!!
- EARLY HEMODYNAMIC RESUSCITATION!!
- Vasopressors.
- tight glycemic control.
- Corticosteroids (refractory vasopressor dependent shock).
- Proper vent mgmt w/ low tidal volume in pts w/ ARDS.
What is anaphylactic shock?
Acute, life threatening reaction caused by:
- Stimulation of membrane bound IgE.
- Rlease of inflam mediators (histamines, Plt activating factor) from mast cells and basos.

Early on, Increased cardiac output w/ decrease SVR.
Capillary leak.
9 causes of anaphylaxis?
Foods.
Venoms.
Meds.
Latex.
Blood/ blood products.
Contrast media.
Seminal fluid.
Physical factors.
Idiopathic.
What are the 5 MCC of food anaphylaxis?
Cow's milk.
Egg whites.
Fish.
Millet seeds.
Shellfish.
What is the MCC of venom anaphylaxis?
Hymenoptera (bees, etc).
2 major causes of drug anaphyalxis?
Penicillins.

Aspirin and nonsteroidal anti-inflammatory drugs.
Physical exam findings in anaphylactic shock? (7)
Urticaria/ pruritis,
Vasodilation,
Bronchoconstriction,
Angioedema,
Increased vascular permeability,
Resp distress,
Stridor.
Management of anaphyalctic shock?
AIRWAY AIRWAY AIRWAY!!!
Epinephrine,
Antihistamines,
IV fluids
How much epinephrine should you give for anaphylactic shock?
0.3-0.5 mL of a 1:1000 solution given IM.
How much benadryl should you give for anaphylactic shock?
25-50 mg IV for adults.
3 other meds (besides epi and benadryl) that can be given for anaphylactic shock?
H2 blockers (Tagamet, Zantac).

Corticosteroids.

Glucagon (induces endogenous catecholamine release)
7 major things that should be asked about in a bleeding disorders history?
Family history of bleeding.
Hematuria.
Menorrhagia.
Excessive bleeding w/ dental procedures.
Med hx.
Spontaneous mucosal bleeding (ex nosebleeds).
Previous bleeding needing transfusion.
What is step 1 of the coag cascade (simplified)?
Platelet aggregation and activation of the factors which leads to Prothrombin being converted to Thrombin.
What is step 2 of the coag cascade?
Thrombin causes conversion of Fibringoen to Fibrin.
What is step 3 of the coag cascade?
Factor XIII causes loose fibrin to cross link and form a clot.
What are most acquired bleeding disorders associated with?
Medications.

But, may also be a sign of intrinsic disease.
8 causes of acquired bleeding disorders (including meds)?
Heparin,
Vit K deficiency,
Warfarin (II, VII, IX, X),
Chronic liver dz,
Renal failure,
ASA,
Hypothermia,
Platelet disorders
2 congenital autosomal dominant bleeding disorders?
VWD,

Factor IX deficiency
Autosomal recessive congenital bleeding disoders?
Factor I, V VII, X deficiency
Sex linked congenital bleeding disorders?
Hemophilia A (factor VIII)

Hemophilia B (factor IX): 15-20% of all hemophilias.
What is the #1 cause of bleeding in the post op period?
INADEQUATE HEMOSTASIS!!!
What is DIC?
Disseminated INtravascular Coagulation.

Diffuse intravascular coagulation and thrombosis.
Deposition of platelet thrombin microemboli causing tissue injury.
Massive consumption of clotting factors --> diffuse bleeding!
Causes of DIC? (4)
Tissue debris released into bloodstream (ex: placenta) induces platelet aggregation.

Endothelial damage stimulates tissue factor.

Hypotension --> stasis.

Massive trauma to lungs, brain.
What would you see on labs in DIC?
Decreased fibrinogen,
Thrombocytopenia,
Increased FDP,
Prolonged PT & PTT,
Prolonged thrombin time.
Treatment for DIC?
**TREAT UNDERLYING OR PRECIPITATING EVENT!!
- ID bleeding source.

Repleat factors, platelets, fibrinogen.
Heparin?
What should you always use first when repleating volume?
Crystalloids! : Normal saline, Lactated Ringer's
What should you use second when repleating volume?
Colloids: 1/3 less volume than crystalloids.

RBCs,
FFP, platelets,
Cryo,
Hespan (hetastarch),
Albumin.
What is the 3:1 rule when it comes to fluid replacement?
Approx 300 cc of crystalloid req to compensate for q 100 cc of blood loss.
Crystalloid rapidly equilibrates across intravascular space.
Q liter of blood loss needs 3 liters of fluid replacement.
What should you think of giving if hemodynamic stability is not achieved w/ 2 liters of crystalloid?
Think give blood cells!
Complications of giving RBCs?
Sepsis, Infectious disease,
Immunologic transfusion reaction,
Thrombophlebitis,
Pulmonary edema
Metabolic (hypocalcemia, alkalosis, acidosis, K+),
Emoblism (air, particulate)
Hypothermia
What is the risk of contracting HIV from a blood transfusion?**
1 in 2.3 million transfusions.
What is the risk of contracting Hep C from a blood transfusion?**
1 in 2 million transfusions.
6 manifestations of an immunologic transfusion reaction?
Hemolytic transfusion reaction,
GVHD,
Febrile reactions,
Thrombocytopenia,
Urticaria,
Anaphylactic shock.
What does FFP contain?
Albumin,
Fibrinogen,
Globulins,
Coagulation factors.

Also: minerals (Na, K) critical to proper cell function.
Indications for giving FFP?
Replacement therapy in pts w/ mltpl coag factor deficiencies who are actively bleeding (liver dz, DIC, dilutional coagulopathy from massive blood loss). This i smost common use.

As replacement therapy in hereditary bleeding disorders if concentrated factor isn't available.

Reversla of Warfarin effect if IMMEDIATE hemostasis needed.
Dosing of FFP?
Dosed by wt: 10-20 ml/kg
Usual adult dose: 4-6 units.

*No cross matching required.
Complications of FFP therapy?
Allergic reaction (1% ppl).
Citrate toxicity w/ large volumes.
Viral transmission similar to plts and PRBCs, but not assoc w/ white cell assoc viruses like CMV or HTLV since plasma is acellular.
What is cryo?
What is it used for?
Obtained from FFP.
Rich in factor VIII, fibrinogen, vWF, factor XIII and fibronectin.
Increased dz risk (pooled).
Repleats fibrinogen lost in DIC.
Used in decreased fibrinogen states, VWD, hemophilia A.
How much factor VIII is in cryo?
Each units cryo contains at least 80 units factor VIII.
At what fibrinogen levels might you give cryo?
Dose?
Fibrinogen level < 100 mg/dL.

Dose: 6-10 units
What is fibrin glue?
Source of fibrinogen and thrombin used as a hemostatic agent to decrease microvascular bleeding during surgery.
Risks of cryo?
Blood-borne pathogens.

Hemolysis w/ large volumes.
How many platelets does one unit of random donor platelets contain?
How much can it raise the pts plt count?
5.5 x 10^10 suspended in 50 mL plasma.

Can raise plt count 5-7,000.
How many platelets does one unit of single donor platelets contain?
3.0 x 10^11 plts suspended in 200-600 mL plasma.
What does leukoreduction do?
Removes white blood cells from platelets. The white cells are responsible for alloimmunization and CMV transmission.
At what platelet count in a stable patient would you give a platelet transufison?
<10,000
At what platelet count in a patient with minor bleeding, fever or splenomegaly would you give a platelet transufsion?
<20,000
At what platelet count in a pt w/ significant bleeding or undergoing an invasive procedure, would you give plt transfusion?
<50,000
What do you want to get the platelet count to in a pre-op pt?
100,000
What are some other reasons you would give a platelet transplant?
Pts w/ documented plt function abnormalities,
Pts actively bleeding d/t thrombocytopenia,
To decrease risk of spontaneous bleeding.