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Summary University of Texas, Rio Grande Valley NURS 3312; NURS3312 Adult health EXAM 4 Blueprint | Completed 100% updated Fall 2025/26.

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University of Texas, Rio Grande Valley NURS 3312; NURS3312 Adult health EXAM 4 Blueprint | Completed 100% updated Fall 2025/26.











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Subido en
1 de octubre de 2025
Número de páginas
22
Escrito en
2025/2026
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Shock: Diagnostics

Hypovolemic Shock

• Theres a reduction of intravascular volume by 15-30% = 750-1500 mL of blood in a
70 kg person




• Decrease volume causes decr venous return of blood to heart → decr stroke volume
and CO → drop In BP and tissues cannot be perfused
• Interventions
o Correct the underlying cause
▪ Ex: if the pt is hemorrhaging → stop the bleeding by applying pressure
▪ Ex: if the pt has diarrhea and vomiting → meds for that
o Fluid and blood replacement
▪ 2 large-gauge IV lines or intraosseous catheter if IV can't be quickly
inserted (in the sternum, tibia, humerus)
▪ Crystalloids: LR and 0.9% NaCl; Give 3 mL for each mL of EBL; (can
cause hypernatremia, hypokalemia, pulmonary edema, abdominal
compartment syndrome)
▪ Colloids: Albumin 5-25% (can cause HF) FOR HEMORRHAGE; if pt
needs hgb for O2 transport and to correct coagulopathy; pt responds
better if given in 1:1:1 ratio
▪ Blood products: needs are based on pt’s O2 needs and coagulation
status (so look for the VS, ABGs, aPTT/PT, and clinical appearance)
o Redistribution of fluid
▪ Trendelenburg is NOT indicated
o Pharmacology
▪ Vasoactive meds if fluid adm fails

, ▪ Meds to treat underlying cause of dehydration (Ex: insulin if
dehydration is 2ndary to hyperglycemia, desmopressin for DI,
antidiarrheals for diarrhea, etc)
• Nursing management
o MONITOR for pt who are at risk for fluid deficits to prevent hypovolemia
o MONITOR for blood transfusion reactions (obtain VS, CBC, and type and
crossmatch before)
o MONITOR for fluid replacement complications (dyspnea, overload)
o MONITOR for transfusion-related ALI (pulmonary edema, hypoxemia, resp
distress, and pulm infiltrates)
o MONITOR for ACS (dyspnea and decr UO)
o MONITOR hemodynamic pressure, VS, ABGs, lactate lvls, hgb, hct, bladder
pressure, and I&O)
o MONITOR temp (rapid resuscitation → hypothermia)
o ASSESS the jugular venous pressure (it is low in HS)
o Report changes in BP, pulse pressure, CVP, HR, rhythm, and LS

Stages of Shock

1. Compensatory
• Normal BP, vasoconstriction, ^ HR, and ^ contractility → adequate CO
• Fight-or-flight
• Body shunts blood from organs to the brain and heart → skin may be cool
and pale, bowel sounds are hypoactive, and decr. UO
• S/S: ^ lactic acid → metabolic acidosis → ^RR → ^ pH → resp alkalosis,
anxious, or confused
• Interventions
o Correct the underlying cause
o Adm IV fluids, O2, and obtain lab tests to rule out and treat metabolic
imbalances or infection
o Monitoring tissue perfusion: LOC, VS, UO, skin, capillary refill, signs of
mottling, RR, lactic acid lvl; sodium and glucose are elevated.
o Reduce anxiety: provide brief explanations, support, and provide info
about their outcomes. Speak in a calm, reassuring voice and use
gentle touch.
o Clarifying advance directives
o Promoting safety: close monitoring, frequent reorientation, hourly
rounding, and implementing interventions to prevent falls.
2. Progressive

, • Hypotensive (systolic <100 or decr of 40 from baseline, decr/ MAP, declining
mental status
• Hypoperfusion begins in all body systems causing ischemia → HF
• S/S: RR are rapid and shallow, crackles, decr pulmonary blood flow causes
arterial O2 lvls to decr and CO2 lvls increase, hypoxemia, pulmonary
vasoconstriction, decr surfactant, ARDS; arrhythmias and ischemia, ^HR
and sometimes exceeding 150 bpm, chest pain, MI,^ troponin I; changes in
behavior, become agitated, confused, or demonstrate signs of delirium,
lethargy increases, and pt begins to lose consciousness; ^BUN and
creatinine, fluid and electrolyte shifts, acid-base imbalances, and loss of
renal-hormonal regulation of BP, UO decr to <30; pt is less able to metabolize
meds and metabolic wastes such as ammonia and lactic acid,
gluconeogenesis and glycogenolysis are impaired, more susceptible to
infection bc liver fails to filter bacteria from blood, liver enzymes and bilirubin
lvls are elevated, pt develops jaundice; stress ulcers in the stomach, in the
small intestine the mucosa can become necrotic and slough off → bloody
diarrhea; the clotting cascade → DIC, bruises and petechiae may appear in
skin, PTT and aPTT are prolonged,
• Interventions
o Hemodynamic monitoring, ECG, ABGs, serum electrolyte levels,
physical and mental changes
o Rapid and frequent adm of prescribed meds and fluids
o Mechanical ventilation, dialysis ad intra-aortic ballon if needed
o Early nutritional support, targets hyperglycemic control w/ IV insulin
(<180 mg/dL) and of antacids, histamine-w blockers, or antipeptic
meds to reduce GI ulceration and bleeding
o Preventing complications: monitoring blood lvl of meds, observing for
signs of infections because of the lines and catheters used, aseptic
technique, reduce the incidence of VAP (frequent oral care w/
toothbrush, aseptic suction, turning, ^HOB to prevent aspiration, and
daily stop of sedation). Asses for acute delirium
o Promoting rest and comfort: reduce pt physical activity and treat pain
and anxiety. Perform care in blocks of time. Protect pt from temp
extremes which ^ metabolic rate and O2 consumption
o Supporting family members
3. Irreversible
• Pt does not respond to treatment and cannot survive
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