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Comp 1 - Comp topics for 283 class
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11/15/23, 11:04 AM Comp 1 - Comp topics for 283 classComp 1 Topics
GCS: A quick, practical standardized system for assessing the degree of consciousness in the
critically ill and for predicting the duration and ultimate outcome of coma, primarily in patients
with head injuries. The system involves eye opening, verbal response, and motor response, all of
which are evaluated independently according to a rank order that indicates the LOC and degree
of dysfunction. A score of 15 indicates no impairment, 3 is compatible with brain death, and
score lower than 8 is usually accepted as a state of coma.
Stroke (brain attack) a. In clients with hemorrhagic strokes, the head of the bed is usually
elevated to 30 degrees to reduce intracranial pressure and to facilitate venous drainage. For
clients with ischemic strokes, the head of the bed is usually kept flat. Maintain the head in a
midline, neutral position to facilitate venous drainage from the head. Avoid extreme hip and neck
flexion; extreme hip flexion may increase intrathoracic pressure, whereas extreme neck flexion
prohibits venous drainage from the brain.
Thrombotic Stroke ▪ Typically, there is no decreased level of consciousness within the first 24
hours. ▪ Symptoms get progressively worse as the infarction and edema increase. Embolic Stroke
▪ Sudden, severe symptoms ▪ Warning signs are less common. ▪ Client remains conscious and
may have a headache. Hemorrhagic Stroke ▪ Sudden onset of symptoms ▪ Symptoms progress
over minutes to hours due to ongoing bleeding.
Monitor for increased ICP, because the client is most at risk during the first 72 hours following
the stroke. 6. Position the client on the side to prevent aspiration, with the head of the bed
elevated 15 to 30 degrees as prescribed. 7. Monitor level of consciousness, pupillary response,
motor and sensory response, cranial nerve function, and reflexes. 8. Maintain a quiet
environment. Prepare to administer anticoagulants, antiplatelets, diuretics, antihypertensives, and
antiseizure medications as prescribed depending on the type of stroke that has been diagnosed.
Anticoagulants: Anticoagulants prevent the extension and formation of clots by inhibiting
factors in the clotting cascade and decreasing blood coagulability. 2. Anticoagulants are
administered when there is evidence of or likelihood of clot formation— myocardial infarction,
unstable angina, atrial fibrillation, deep vein thrombosis, pulmonary embolism, and the presence
of mechanical heart valves. 3. Anticoagulants are contraindicated with active bleeding (except
for disseminated intravascular coagulation), bleeding disorders or blood dyscrasias, ulcers, liver
and kidney disease, and hemorrhagic brain injuries.
Thrombolytic Medications: Thrombolytic medications activate plasminogen; plasminogen
generates plasmin (the enzyme that dissolves clots). 2. Thrombolytic medications are used early
in the course of myocardial infarction (within 4 to 6 hours of the onset of the infarct) to restore
blood flow, limit myocardial damage, preserve left ventricular function, and prevent death. 3.
Thrombolytics are also used in arterial thrombosis, deep vein thrombosis, occluded shunts or
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catheters, and pulmonary emboli. B. Contraindications 1. Active internal bleeding 2. History of
hemorrhagic stroke 3. Intracranial problems, including trauma.
Cardiac Glycosides A. Digoxin 1. Description a. Cardiac glycosides inhibit the sodium
potassium pump, thus increasing intracellular calcium, which causes the heart muscle fibers to
contract more efficiently. b. Cardiac glycosides produce a positive inotropic action, which
increases the force of myocardial contractions. Cardiac glycosides are used second-line for heart
failure (medications affecting the renin-angiotensin-aldosterone system are used more often) and
cardiogenic shock, atrial tachycardia, atrial fibrillation, and atrial flutter; they are used less
frequently for rate control in atrial dysrhythmias (beta blockers and calcium channel blockers are
used more often). Side and adverse effects a. Anorexia, nausea, vomiting, diarrhea b.
Bradycardia c. Visual disturbances: Diplopia, blurred vision, yellow vision, photophobia d.
Headache e. Fatigue, weakness f. Drowsiness. The optimal therapeutic range for digoxin is 0.5 to
2.0 ng/dL (0.63 to 2.56 nmol/L). Advise the client to eat foods high in potassium, such as fresh
and dried fruits, fruit juices, vegetables, and potatoes. Antidote: Digoxin immune Fab is used in
extreme toxicity.
Angiotensin-Converting Enzyme (ACE) Inhibitors: ACE inhibitors prevent
peripheral vasoconstriction by blocking conversion of angiotensin I to angiotensin II. These
medications are used to treat hypertension and heart failure; also, ACE inhibitors are
administered for their cardioprotective effect after myocardial infarction. Side and adverse
effects 1. Nausea, vomiting, diarrhea 2. Persistent dry cough (ACE inhibitors) 3. Hypotension 4.
Hyperkalemia 5. Tachycardia 6. Headache 7. Dizziness, fatigue 8. Insomnia 9. Hypoglycemic
reaction in the client with diabetes mellitus 10. Bruising, petechiae, bleeding 11. Diminished
taste (ACE inhibitors). A persistent dry cough is a common complaint for those taking an ACE
inhibitor, but this often subsides after a few weeks. Instruct the client to contact the PHCP if this
occurs and persists.
Pericarditis is an acute or chronic inflammation of the pericardium. b. Chronic pericarditis, a
chronic inflammatory thickening of the pericardium, constricts the heart, causing compression. c.
The pericardial sac becomes inflamed. d. Pericarditis can result in loss of pericardial elasticity or
an accumulation of fluid within the sac. e. Heart failure or cardiac tamponade may result. 2.
Assessment a. Pain in the anterior chest that radiates to the left side of the neck, shoulder, or back
b. Pain is grating and is aggravated by breathing (particularly inspiration), coughing, and
swallowing c. Pain is worse when in the supine 1706 position and may be relieved by leaning
forward. d. Pericardial friction rub (scratchy, high-pitched sound) is heard on auscultation and is
produced by the rubbing of the inflamed pericardial layers. e. Fever and chills f. Fatigue and
malaise g. Elevated white blood cell count h. Electrocardiographic changes with acute
pericarditis; ST-segment elevation with the onset of inflammation; atrial fibrillation is common.
i. Signs of right ventricular failure in clients with chronic constrictive pericarditis. Interventions
a. Assess the nature of the pain. b. Place the client in a high Fowler's position, or upright and
leaning forward. c. Administer oxygen. d. Administer analgesics, nonsteroidal anti-inflammatory
drugs (NSAIDs), or corticosteroids for pain as prescribed. e. Auscultate for a pericardial friction
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rub. f. Check results of blood culture to identify the causative organism. g. Administer antibiotics
for bacterial infection as prescribed.
Administer diuretics and digoxin as prescribed to the client with chronic constrictive pericarditis;
surgical incision of the pericardium (pericardial window) or pericardiectomy may be necessary. i.
Monitor for signs of cardiac tamponade. j. Notify the PHCP if signs of cardiac tamponade occur.
Pacemakers A. Description: Temporary or permanent device that provides electrical
stimulation and maintains the heart rate when the client’s intrinsic pacemaker fails to provide an
adequate rate B. Settings 1. A synchronous (demand) pacemaker senses the client’s rhythm and
paces only if the client’s intrinsic rate falls below the set pacemaker rate for stimulating
depolarization. 2. An asynchronous (fixed rate) pacemaker paces at a preset rate regardless of the
client’s intrinsic rhythm 1692 and is used when the client is asystolic or profoundly bradycardic.
Spikes 1. When a pacing stimulus is delivered to the heart, a spike (straight vertical line) is seen
on the monitor or ECG strip. 2. Spikes precede the chamber being paced; a spike preceding a P
wave indicates that the atrium is paced, and a spike preceding the QRS complex indicates that
the ventricle is being paced. 3. An atrial spike followed by a P wave indicates atrial
depolarization, and a ventricular spike followed by a QRS complex represents ventricular
depolarization; this is referred to as capture.
Respiratory Acidosis: Description: The total concentration of buffer base is lower than
normal, with a relative increase in hydrogen ion concentration; thus, a greater number of
hydrogen ions is circulating in the blood than can be absorbed by the buffer system.
Interventions 1. Monitor for signs of respiratory distress. 2. Administer O2 as prescribed. 3.
Place the client in a semi-Fowler’s position. 4. Encourage and assist the client to turn, cough, and
deep breathe. 5. Encourage hydration to thin secretions. 6. Reduce restlessness by improving
ventilation rather than by administering tranquilizers, sedatives, or opioids, because these
medications further depress respirations. 7. Prepare to administer respiratory treatments as
prescribed; suction the client’s airway, if necessary. 8. Prepare for endotracheal intubation and
mechanical ventilation if CO2 levels rise above 50 mm Hg and signs of acute respiratory distress
are present.
Respiratory Alkalosis A. Description: A deficit of carbonic acid and a decrease in hydrogen
ion concentration that results from the accumulation of base or from a loss of acid without a
comparable loss of base in the body fluids. B. Causes: Respiratory alkalosis results from
conditions that cause overstimulation of the respiratory system. Assessment. Interventions 1.
Monitor for signs of respiratory distress. 2. Provide emotional support and reassurance to the
client. 3. Encourage appropriate breathing patterns. 4. Assist with breathing techniques and
breathing aids if needed and as prescribed (voluntary holding of breath, using a rebreathing
mask, CO2 breaths with rebreathing into a paper bag). 5. Provide cautious care with ventilator
clients so that they are not forced to take breaths too deeply or rapidly. 6. Prepare to administer
calcium gluconate for tetany as prescribed.
Metabolic Acidosis: A total concentration of buffer base that is lower than normal, with a
relative increase in the hydrogen ion concentration, resulting from loss of too much base and/or
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