NURS 644 Exam 1 Questions & Answers | 100%
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Intravascular hypovolemia (hemmorhagic shock, renal
loss, GI loss, Third spacing)
Venodilation: anaphylaxis, neurogenic shock, drugs
DDX Hypovolemic Shock
Impaired Cardiac Filling: Cardiac Tamponade, High
pleural pressure (PEEP, TPX) other obstruction (tumor,
thrombus)
Arrhythmia, Systolic RV or LV dysfunction (Ischemia,
CM, metabolic derangement, CCB, BB, sepsis,
myocardial contusion, toxins)
Diastolic Dysfunction: Ischemia, Hypertrophy,
Restrictive CM, Tamponade
DDX Cardiogenic Shock
Excessive afterload: PE, AS, Hypertrophic Obstructive
CM, ARDS, Malignant HTN
Valve dysfunction: AI, Papillary muscle rupture,
Endocarditis, MS
Device malfunction: ECMO, VAD, IABP
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Sepsis
Hepatic Failure
Adrenal Insufficiency
Thiamine Deficiency
DDX Distributive Shock
Toxins (ASA, CO, Cyanide)
Thyroid Storm
AV shunts
Cellular dysoxia (prolonged shock states)
Recovery of underlying condition
PaO2/FiO2 of >200
PEEP <8
Prerequisites for weaning FiO2 < 50%
pH >7.25
Hemodynamic stability
Spontaneous breathing effort
Less complications: barotrauma, cardiac arrhythmias,
Benefits of NIPPV
hypotension, volutrauma, VAP
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Acute hypercapnic RF in COPD
Cardiogenic Pulmonary Edema
Indications for NIPPV
Immunosuppressed patients with pulmonary
infiltrates, fever and ARespFX
Ventilator management of Manipulation of FiO2 or PEEP
O2
Manipulation of tidal volume and rate
Ventilator Management of
CO2 To retain Co2--> Lower rate/less Vt
To blow off CO2--.> increase rate/Vt
Push: blood in lung space displaces lung to the other
side. Tracheal deviation. Hemothorax
PUSH/PULL SIGN
Pull sign: Air vacuum pulls to affected side.
Pneumothorax
Types of Acute Resp Hypoxemia vs Hypercabia
Failure
Most common cause
PNA, PE, ARDS, Alveolar Collapse, Pulm AV
communication
Increased A-a gradient
Hypoxemic RF V/Q
Mismatch pulmonary vasoconstriction (reduce perfusion) to the
area of the lung with reduced ventilation
hypoxic pulmonary vasoconstriction- unique to pulm
vasculature
responsive to O2 therapy
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