H476 Exam 1 (Modules 1&2)

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Last updated 6:34 PM on 9/8/26
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101 Terms

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hemodynamics

blood flow and pressure needed to deliver oxygen to tissues and support organ perfusion

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MAP

average arterial pressure driving systemic organ perfusion; 70-100 mmHg (initial goal is >65)

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CVP/RAP

central venous pressure/right atrial pressure; one clue to venous congestion and right heart-preload (about 2-6 mmHg)

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PAP

pulmonary artery pressure; reflects right ventricular output and pulmonary vascular load (systolic 15-30, diastolic 4-12, mean 10-20 mmHg)

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POAP/PCWP

estimates left-arterial and left-sided filling pressures; important in CV patients (6-12 mmHg)

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CO/CI

cardiac output/cardiac index; blood pumped each minute; CI adjusts cardiac output for body surface area (CO: 4-8 L/min, CI 2.5-4.0 L/min/m2 (less than 2.2 being low output in shock))

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SV/SVI

stroke volume/stroke volume index; blood ejected with each beat; influenced by preload, afterload, and contractility (SV: 60-100 mL/beat)

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SVR

systemic vascular resistance; resistance against left-ventricular ejection; an estimate of systemic afterload (800-1200 dyn s/cm5)

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SvO2/ScvO2

balance between oxygen delivery and tissue oxygen consumption (SvO2: 60-80%, ScvO2 70-75%)

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PVR?

estimates right-ventricular afterload

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SVR?

estimates left-ventricular afterload

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WBC

4.0-11.0 x10^3; reflects circulating leukocytes; care about infection/inflammation, immune suppression, marrow failure, and the differential/trend

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Hemoglobin

12-17.5; reflects O2 carrying capacity; care about bleeding, anemia, hemodilution, hypoxemia, ischemia, and transfusion context

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Hematocrit

36-53%; proportion of blood volume made of RBCs; care about blood loss, hemoconcentration, dilution, and trend with hemoglobin

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Platelets

150-400x10^3; central to primary hemostasis; care about bleeding, DIC, HIT, sepsis, procedures, and antiplatelet therapy

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Sodium

134-145 - water balance and neurologic function; rapid changes can cause seizures, cerebral edema, or osmotic injury

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Potassium

3.5-5 - cardiac conduction and muscle function; severe high or low values can produce lethal dysrhythmias

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Chloride

98-106 - fluid and acid-base balance; trends may help explain metabolic acidosis/alkalosis and effects of IV fluids

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Bicarbonate/ total CO2

22-29 - metabolic component of acid-base balance; interpret with pH and PaCO2 when the patient is unstable

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Magnesium

1.7-2.2 - myocardial stability and neuromuscular function; low levels can worsen dysrhytmias and make potassium difficult to correct (muscles)

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Phosphorus

2.5-4.5 - ATP, diaphragm function, and cellular metabolism; severe depletion can contribute to weakness and ventilator weaning failure

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Total calcium

8.5-10.5 - contraction, conduction, and coagulation; ionized calcium is often more useful in critically ill patients

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BUN

7-20 - affected by renal function, hydration, catabolism, GI bleeding, and protein intake; interpret with creatinine and volume status

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Creatinine

0.6-1.3 - marker used to estimate kidney filtration; a rising trend may signal AKI even before dramatic absolute elevation

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Serum osmolarity

275-295 - reflects concentration of circulating solutes; useful with sodium disorders, toxic alcohols, DKA/HHS, and osmolar therapy

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Urine specific gravity

1.005-1.030 - reflects urine concentration; interpret with renal function, fluid balance, diuretics, and endocrine disorders

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Adult urine output

0.5ml/kg/hr is a common perfusion/AKI surveillance threshold; trend output rather than relying on one our alone

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pH

7.35-7.45 - overall acid-base status; severe acidemia or alkalemia can impair cardiovascular and neurologic function

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PaCO2

35-45 - respiratory component; rises with hypoventilation and falls with hyperventilation

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HCO3

22-26 - metabolic component; low values suggest metabolic acidosis and high values suggest metabolic alkalosis in the appropriate context

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PaO2

80-100 on room air at sea level - arterial oxygen tension; interpret with age, FiO2, PEEP, lung disease, and oxygenation goal

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base excess

-2 to +2 - helps estimate the metabolic contribution to an acid-base disturbance

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rising or elevated lactate

can signal inadequate perfusion or unresolved disease even when blood pressure appears acceptable

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PT

11-13.5 - evaluates the extrinsic/common pathway; affected by warfarin, liver dysfunction, factor deficiency, and DIC

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INR

0.8-1.1 without anticoagulation; standardized PT; therapeutic targets are indication-specific

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aPTT

25-35- evaluates the intrinsic/common pathway; may be used with unfractionated heparin

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Fibrinogen

200-400 - substrate for clot formation; low or rapidly falling levels are concerning in DIC and major hemorrhage

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D-dimer

reflects fibrin breakdown but is nonspecific in ICU patients

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Troponin

indicated myocardial injury but not necessarily type 1 MI

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BNP/NT-proBNP

elevation supports cardiac wall stress but is not specific for acute heart failure

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AST and ALt

10-40 and 7-56 - markers of hepatocellular injury; very rapid elevations can occur with ischemic hepatitis after shock

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Alkaline phosphatase and total bilirubin

44-147 and 0.1-1.2 - useful when cholestasis or biliary obstruction is suspected

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INR usefulness

can provide more immediate information about hepatic synthetic dysfunction than albumin when liver failure is acute

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Norepinephrine

vasoconstrictor with some inotropy; common first-line support for vasodilatory/septic shock; titrate to MAP and end-organ perfusion

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Epinephrine

strong adrenergic vasopressor/inotrope; used in refractory shock, anaphylaxis requiring infusion support, bradycardic/low-output states, and post-arrest instability

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Vasopressin

non-adrenergic vasoconstrictor; commonly added for vasodilatory shock; many adult protocols used a fixed dose rather than bedside titration; can cause a squeeze on vasculature thus long-term use causing loss of fingers or toes

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Phenylphrine

predominately alpha-1 vasoconstrictor; may be selected when vasodilation is prominent and tachyarrythmia limits beta-adrenergic stimulation

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Dobutamine

beta-1 predominant inotrope; used for low cardiac output with adequate blood pressure, cardiogenic shock, and selected sepsis-related myocardial dysfunction

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Milrinone

inodilator; common in advanced heart failure, right-ventricular dysfunction, pulmonary hypertension, and pediatric cardiac critical care; watch hypertension and renal clearance

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Dopamine

adrenergic/dopaminergic agent; now less favored as first-line septic-shock therapy because of arrhytmia risk

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Propofol

sedative-hypnotic for ventilated adults and procedures; rapid onset/offset; monitor hypotension, triglycerides, and risk for propofol infusion syndrome with high/prolonged exposure

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Dexomedetomidate

alpha-2 agonist sedation that can preserve arousability; common for ventilator/light sedation and agitation; monitor bradycardia and hypotension

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Midazolam

benzodiazepine sedation and seizure therapy; can accumulate with prolonged infusion and contribute to hypotension and delirium risk

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Fentanyl

opioid analgesic frequently used for severe pain and ventilator tolerance; monitor respiratory depression, chest-wall rigidity with rapid/high exposure, ileus, and tolerance

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Ketamine

dissociative anesthetic/analgesic; used for procedures, analgesia, sedation, and selected refractory broncospasm or status epilepticus; some ICU uses are off-label

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neuromuscular blockers such as cisatracurium, rocuronium, and vecuronium

used for selected severe ventilator dyssynchrony, procedures, or refractory hypoxemia; paralysis never replaces analgesia and sedation

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Unfractionated heparin

anticoagulation for VTE, ACS, mechanical support, and selected devices; monitor the protocol-defined assay, bleeding, platelets, and HIT risk

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Bivalirudin

direct thrombin inhibitor used in PCI and increasingly selected ECMO/VAD or HIT situation; monitor bleeding and the institution-specific assay

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IV insulin

hyperglycemic emergencies and selected critically ill patients; frequent glucose and potassium surveillance are essential because errors can cause rapid severe harm

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Hypertonic NaCl

used for severe symptomatic hyponatremia and intercranial hypertension; sodium correction and neurologic response must be closely monitored

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IV potassium and phosphate replacement

concentrated electrolytes are high alert; use standarized concentrations/rates and monitor renal function, ECG when indicated, and repeat levels

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Amiodarone

IV antiarrhytmic for selected atrial and ventricular dysrhytmias; monitor rhythm, OT, blood pressure, and bradycardia

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Lidocaine

IV antiarrythmic for selected ventricular dysrhythmias; neurologic toxicity can occur with accumulation

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Nitroprusside

potent arterial/venous vasodilator for selected hypertensive emergencies or afterload reduction; requires close blood-pressure monitoring and attention to toxicity with prolonged/high exposure

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Nitroglycerin

venodilator/coronary vasodilator used for ischemia, acute pulmonary edema, and selected hypertensive cardiac emergencies; titrate to symptoms/hemodynamics

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Nicardipine or clevidipine

titratable arterial vasodilators frequently used for controlled BP reduction, including neurologic critical care; monitor for overshoot hypotension

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Epoprostenol

prostacyclin infusion for pulmonary arterial hypertension and selected severe right-heart/pulmonary vascular disease; interruption can cause rapid clinical deterioration

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shock

inadequate oxygen delivery or utilization that threatens cellular and organ function

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early cues of shock

tachycardia, narrowed pulse pressure, delayed capillary refill, anxiety, cool skin, or declining urine output

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worsening cues of shock

hypotension, AMS, weak pulses, oliguria/anuria, rising lactatr, and metabolic acidosis

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hypovolemic shock

inadequare circulating volume reduces preload and cardiac output

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hypovolemic shock causes

hemorrhage, GI losses, dehydration, burns/capillary loss, and significant third spacing

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recognizing hypovolemic shock (NCLEX)

unexplained tachycardia plus cool skin and decreasing urine output after trauma

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infusions with hypovolemic shock

use blood products and a massive-transfusion pathway when clinically indicated rather than relying on large volumes of crystalloid for major hemorrhage if large volumes of crystalloid used - correct the underlying fluid/electrolyte cause

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cardiogenic shock

pump failure reduces forward flow despite adequate or elevated filling pressures

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cardiogenic shock causes

acute MI, decompensated HF, myocarditis/cardiomyopathy, mechanical complications, and severe dysrhytmias

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cues of congestion (with cardiogenic shock)

crackles, pulmonary edema, JVD, peripheral edema, or elevated filling pressures

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cardiogenic shock NCLEX clue

a large fluid bolus can worsen pulmonary congestion when the primary problem is pump failure rather than volume loss; avoid an automatic large fluid bolus

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cues of cardiogenic shock

hypotension plus pulmonary congestion and oliguria

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anaphylaxis

can cause vasodilation, capillary leak, bronchoconstriction, and airway edema

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airway cues (anaphylaxis)

hoarseness, stridor, tongue/lip swelling, dysphagia, and rapidly progressive edema

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breathing cues (anaphylaxis)

wheezing, broncospasm, increased WOB, and hypoxemia

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circulatory cues (anaphylaxis)

hypotension, syncope, tachycardia, and poor perfusion; skin may be warm or flushed early

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anaphylaxis NCLEX

do not wait for a rash before treating a patient with sudden airway or circulatory compromise after an exposure

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neurogenic shock

loss of sympathetic vascular tone, most often after high cervical or thoracic spinal cord injury

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cues of neurogenic shock

hypotesnion with inappropriate bradycardia, warm dry skin, vasodilation, and impaired temperature regulation

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spinal shock

neurologic loss of reflexes and motor/sensory function below the injurt

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priorities with neurogenic shock

maintain spinal alignment, airway, and ventilation while rapidly evaluating for hemorrhage and other causes of hypotension

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obstructive shock

mechanical barrier prevents adequate cardiac filling or forward blood flow

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causes of obstructive shock

tension pneumothorax, cardiac tamponade, and high-risk pulmonary embolism with cardiopulmonary failure

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priority in obstructive shock

relief of the obstruction

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septic shock

sepsis with severe circulatory and metabolic dysfunction that threatens organ perfusion

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common sources of septic shock

pulmonary, urinary, abdominal, skin/soft tissue, vascular-line, and other device-related infection

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complications of septic shock

AKI, ARDS, DIC, encephalopathy, hepatic dysfunction, and multiple-organ dysfunction

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possible cues of septic shock

fever or hypothermia, tachycardia, tachypnea, hypotension, AMS, oliguria, hypoxemia, or mottled skin

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infusions with septic shock

give antimicrobials ideally within one hour, and at least 30mL/kg crystalloid in the first 3 hours

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DIC

disseminated intravascular coagulation; systemic pathologic coagulation activation that can produce both microvascular thrombosis and consumption-related bleeding

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common triggers of DIC

sepsis, major trauma, obstetric catastrophes, malignancy, and other severe inflammatory states

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DIC cues

oozing from lines/wounds, petechiae, ecchymosis, GI/GU bleeding, ischemic digits, organ dysfunction, or unexpected thrombosis

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DIC lab values

falling platelets, prolonged coagulation times, low fibrinogen, elevated D-dimer/fibrin degradation products, and falling hemoglobin