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NURS 3552 UWORLD NCLEX RATIONALES
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NURS 3552 UWORLD NCLEXRATIONALES
1
, UWORLD NCLEX RATIONALES/INFORMATION TO
KNOW
CARDIAC RATIONALES:
Hypovolemic shock most commonly occurs from blood loss but can occur in any condition that reduces
intravascular volume. Hypovolemia is classified as either an absolute (ex. hemorrhage, surgery,
gastrointestinal bleeding, vomiting, diarrhea) or a relative (ex. pancreatitis, sepsis) fluid loss. Reduced
intravascular volume results in decreased venous return, decreased stroke volume and cardiac output,
inadequate tissue perfusion, and impaired cellular metabolism.
Clinical manifestations of hypovolemic shock are associated with inadequate tissue perfusion and
include:
• Change in mental status
• Tachycardia with thready pulse
• Cool, clammy skin
• Oliguria
• Tachypnea
Decreased urine output (<0.5 mL/kg/hr) despite fluid replacement indicates inadequate tissue perfusion
to the kidneys and is a manifestation of hypovolemic shock in a client with normal renal function
Heparin is an anticoagulant that helps prevent further clot formation. It is titrated based on a partial
thromboplastin time (PTT). The therapeutic PTT target is 1.5-2.0 times the normal reference range of
25-35 seconds. A PTT value >100 seconds would be considered critical and could result in life-
threatening side effects. Common sentinel events that result from heparin drips include epistaxis,
hematuria, and gastrointestinal bleeds.
A normal hematocrit for a female is 35%-47% (0.35-0.47). In a client with a history of chronic anemia, a
hematocrit of 30% (0.30) may be an expected finding.
A normal platelet count is 150,000-400,000/mm 3 (150-400 x 109/L). In a client with a history of liver
cirrhosis, a platelet count of 80,000/mm 3 (80 x 109/L) would be anticipated. An episode of bleeding
rarely occurs with a platelet count >50,000 mm3 (50 x 109/L).
A normal prothrombin time is 11-16 seconds, and so a level of 11 seconds would not be concerning.
Heparin infusions require close monitoring by the nurse. The partial thromboplastin time is the
laboratory value required to accurately monitor the therapeutic effects of heparin.
2
,Ventricular paced rhythms are seen in clients with ventricular pacemakers. Ventricular pacemakers
typically have one lead placed in the right ventricle. The pacer spike just before the QRS complex
signals electrical stimulation of the ventricle by the pacemaker lead (Option 3). The pacemaker lead
depolarizes the right ventricle first, and electricity travels across the heart to depolarize the left
ventricle. This atypical electrical pathway distorts and widens the QRS complex. The T wave can be seen
immediately after the wide QRS complex.
Implanted permanent pacemakers are often placed in clients with symptomatic bradycardia or heart
block. Demand pacemakers are the most common type of implanted permanent pacemaker.
The demand pacemaker sends an electrical impulse (pacer spike) only if the pacemaker does
not sense an intrinsic heartbeat occurring at the programmed threshold rate (eg, 40/min).
Ventricular paced rhythms have a pacer spike just before the QRS complex, which is usually distorted
and wide. Implanted permanent pacemakers are often placed in clients with symptomatic bradycardia
or heart block.
Electrical cardioversion is a treatment modality considered for A. Fib that has been unresponsive to
drug therapy. A Fib (rapid, irregular atrial contractions) results in ineffective atrial kick and predisposes
to thrombus formation (blood clots) in the left atrium. If a client is in A. Fib for more than 48 hours,
anticoagulation therapy is needed for 3-4 weeks before cardioversion. Anticoagulation therapy is
necessary as cardioversion may dislodge an atrial thrombus, putting the client at risk for a stroke or
other sequelae of thromboembolism. If 4 weeks of anticoagulation is not an option, TEE must be
performed prior to cardioversion.
A TEE (Transesophageal Echocardiogram) is indicated prior to cardioversion for a client who has been in
AF for more than 48 hours, as cardioversion is contraindicated in the presence of an atrial thrombus.
3
, In peripheral artery disease (PAD), the arteries of the extremities become atherosclerotic (progressive
thickening and hardening due to chronic vascular damage). PAD reduces tissue perfusion and can
cause ischemic pain of the lower extremities with movement or exercise (intermittent claudication).
Pain with PAD can also occur at rest and manifests in the lower extremities as burning, aching, or
numbness. Factors that cause chronic vascular changes and increase risk for PAD include:
• Hypertension: Vessel damage from chronically elevated vascular resistance
• Diabetes mellitus: Inflammatory vascular changes from hyperglycemia
• Hyperlipidemia: Increased plaque formation (ex. atherosclerosis)
• Smoking: Chronic vasoconstriction from nicotine inhalation
Elevated estrogen levels (ex. oral contraceptive use, pregnancy, hormone replacement therapy) make
blood hypercoagulable. However, elevated estrogen levels are more likely to form thrombi in veins than
in arteries due to lower venous pressure and slower blood flow (ex. venous stasis).
Unlike chronic venous insufficiency, in which vessels ineffectively return blood from the feet to the
central circulation, standing is not a risk factor for PAD, as standing facilitates blood flow by gravity to
the lower extremities.
In peripheral artery disease, arteries in the extremities become atherosclerotic (progressive thickening
and hardening due to chronic damage). Peripheral tissue perfusion is impaired, causing pain with
exercise (ex. intermittent claudication) and at rest. Risk factors include hypertension, diabetes mellitus,
hyperlipidemia, and smoking.
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