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Exam 4: PNR 206/ PNR206 (Latest 2024/ 2025 Updates
STUDY BUNDLE WITH COMPLETE SOLUTIONS) Medical-
Surgical Nursing II | Questions and Verified Answers|
100% Correct| Grade A- Fortis
Normal Body pH - ANSWER7.35-7. Normal pCO2 range - ANSWER35- Normal pHCO3 range - ANSWER22- Ratio of bicarbonate to carbonic acid - ANSWER20: acids - ANSWERcompounds that form hydrogen ions when dissolved in water bases - ANSWERcompounds that reduce the concentration of hydrogen ions in a solution buffers - ANSWERA substance that consists of acid and base forms in a solution and that minimizes changes in pH when extraneous acids or bases are added to the solution. acid sources - ANSWERincomplete glucose breakdown cell destruction bicarbonate ( main buffer of ECF) 1st line of defense against changes in the amount of free hydrogen ions - ANSWERbuffers chemical buffers - ANSWERpaired mistures usually a weak base and acid salt two most common are bicarbonate and phosphate protien buffers - ANSWERthe most common buffer albumin and hemoglobin are examples when hydrogen increases in the blood some excess hydrogen binds to the hemoglobin in the RBCs the second line of defense in acid base imbalance - ANSWERrespiratory system ways the respiratory system reacts in acid base imbalance - ANSWERhyperventilation hypo-ventilation breathing controls the amount of CO2 in the lungs and arterial blood
what does hypo-ventilation do - ANSWERit increases the CO2 in the respiratory tract and the arterial blood creating an acidic state what does hyperventilation do - ANSWERit decreases the CO2 in the respiratory tract and the arterial blood creating an alkaline state the third line of defense in acid base imbalances - ANSWERthe renal system ways the renal system reacts in acid base imbalance - ANSWERmovement of bicarbonate formation of acids formation of ammonium compensation - ANSWERbody attempts to correct blood pH changes fatal blood pH - ANSWER>6.9 or <7. faster of the compensatory mechanisms - ANSWERrespiratory, but it is also easily overwhelmed more powerful of the compensatory mechanisms - ANSWERrenal, but can take hours to days to start working respiratory compensation - ANSWERchanges in pulmonary ventilation correct the pH of the body fluids by expelling or retaining CO2. if there is a co2 excess, pulmonary ventilation increases to expel co2 and bring the blood pH back up to normal. if there is a co2 deficiency, ventilation is reduced to allow co2 to accumulate in the blood and lower the pH to normal renal compensation - ANSWERan adjustment of pH by changing the rate of H+ secretion by the renal tubules. the kidneys are slower to respond to pH imbalances but better at restoring a fully normal pH. in acidosis, the rate of H+ secretions increase as well as additional ammonia to buffer the added H+. In alkalosis, the bicarbonate concentration and pH of the urine are elevated. This is partly because there is so much HCO3- and not enough H+ in the tubular fluid to neutralize all the HCO3- in the filtrate respiratory compensation for acidosis - ANSWERhyperventilate decrease H+ blow off CO Inhibits chemo-receptors Metabolic Compensation for acidosis - ANSWERhold HCO3 in blood bind HCO3 to H+ strong and long lasting excrete H+ Respiratory Compensation for alkalosis - ANSWERhypo-ventilation
no change in Ca increased Cl electrolyte values in metabolic alkalosis - ANSWERhypokalemia hypocalcemia decreased Cl electrolyte values in respiratory alkalosis - ANSWERhypokalemia hypocalcemia increased Cl electrolyte values in combined alkalosis - ANSWERhypokalemia hypocalcemia decreased Cl interventions for metabolic acidosis - ANSWERhydration and drugs or treatments to control the problem causing acidosis interventions for respiratory acidosis - ANSWERmaintain patent airway and enhance gas exchange emergent phase of a burn - ANSWERduring the first 72 hours, fluids shift into the interstitial space increasing risk for hypovolemic shock resuscitation phase of burn injury - ANSWERbegins at onset and continues about 48 hours priority goals of the emergent phase of burns - ANSWERsecure airway support circulation by fluid replacement keep pt comfortable with analgesics prevent infection with careful wound care maintain body temp provide emotional support dry weight - ANSWERis the patient's weight without excess fluid. When dry weight is reached , there are no signs of fluid overload or dehydration ; breathing is normal, with no signs of fluid in the lungs ; and blood pressure is normal for the patient ( not too high or too low ) " Target weight " is the goal weight for a given treatment, and is usually determined by the dry weight. It is used to calculate fluid rates, energy requirements, and drug dosages in burn victims. direct airway burn injury - ANSWERburns of the face, lips, ears, neck, eyelids, eyebrows, and eyelashes, are indicators of an airway injury change in respiratory pattern upper airway edema
changes in respiratory pattern for pts with an airway burn injury - ANSWERprogressively hoarse brassy cough drool or have difficulty swallowing may wheeze, crow, or have stridor apply O2 and notify RT carbon monoxide poisoning - ANSWER-carbon monoxide binds with hemoglobin and reduces oxygen supply to tissues -cannot be seen. smelled, or tasted -s/s include: nausea, vomiting, headache, weakness, and unconsciousness -death may occur with prolonged exposure -prevention by ensuring proper ventilation when using fuel-burning devices -gas-burning devices should be inspected annually -flues and chimneys should be unobstructed -carbon monoxide detectors should be installed and inspected regularly thermal (heat) injury - ANSWERexcept for rare events like steam inhalation, aspiration of scalding liquid, or explosion of flammable gases under pressure, thermal burns to respiratory tract usually limited in upper airway above the glottis (nasopharynx, oropharynx, and larynx) Respiratory tract down to major bronchioles can be damaged by steam Ulcerations, redness, and edema of mouth and epiglottis are first manifestations, with rapid swelling, leading to upper airway obst; stridor, hoarseness, and SOA result Smoke Poisoning - ANSWERa localized inflammatory reaction occurs causing a decrease in bronchial ciliary action and a decrease in surfactant, caused by the inhalation of the by products of combustion, Headache, Dizziness, Dyspnea, Nausea, Characteristic "cherry-red" color to the skin, Confusion, Visual disturbances, Irritability, Hallucinations, Hypotension, Seizures, Coma pulmonary fluid overload - ANSWERrelated to capillary leak, fluid resuscitation, can occur even when lung tissues have not been directly damaged the pt will be SOA, and have dyspena in the supine position, crackles can be heard, elevate the head at least 45 degrees and apply humidified O2 and notify burn team as well as RT external factors effecting burn pts - ANSWERMay also have breathing problems from external factors Most common is tight eschar from deep circumferential chest burns—eschar either restricts movement or compresses structures in neck and throat that air flow is impaired Inspect pts chest hourly for ease of resp, amount of chest movement, rate, and effort Use continuous pulse ox to ax breathing effectiveness in maintaining blood O2 levels
purpose of pressure garments for burn patients - ANSWERapplied p the graft heals to help prevent contractures and tight hypertrophic scars (inhibit mobility) Also inhibit venous stasis and edema formation in areas w/ decreased lymphatic outflow May be elastic wraps or specially designed, custom-fitted, elasticized clothing that provides continuous pressure over burned areas Must be worn at least 23h/day, q day, til scar tissue is mature (12-24 mos) Can be uncomfortable w/ itchiness and increased warmth Reinforce that its very beneficial insaving mobility and reducing scarring potential complications for patients with burn injuries - ANSWERrisk for infection airway obstruction fluid overload hypovolemic shock kidney damage ARDS imbalanced nutrition- less than the body requires impaired physical mobility disturbed body image PTSD sexual dysfunction severe depression atrial fibrillation - ANSWERMultiple rapid impulses from many foci depolarize in the atria in a totally disorganized manner at the rate of 350-600 times per minutes. Atria quivers can lead to the formation of thrombi., Rate: Atrial 400-650; Ventricular usually 120 - 180 P wave: Not present; often wavy baseline QRS: Normal Conduction: Variable AV conduction Rhythm: Irregularly Irregular
- chaotic, unpredictable depolarizations w/i atrium, no atrial kick
- CAD, HTN, COPD, etc. Carotid massage: may slow ventricular rate treatment of atrial fibrillation - ANSWERAF; HTN is mcc. Also MI, HF, alcohol and hyperthyroidism and valvular diz. digoxin IV push or oral or Cardizem IV to slow AV conduction rate Therapy: IF HDUS (low BP, AMS)-->cardiovert IF stable then check duration; if <48hrs then cardiovert with drugs or electrical. > 48 hrs there is a high risk of thromboembolism with cardioversion, so treat with rate control with BBs and CCBs + 3-4 wks of antiocoagulation before cardioversion is attempted. anticoag. based on CHADS2 score. sinus rhythm with 1st degree atrioventricular block - ANSWERUsually benign (may never progress and live w/ 1st degree AVB forever)
P waves present, normal QRS normal PRI >.20 (5 little boxes) (I have .36 written for some reason) Exactly like NSR EXCEPT the longer PRI MOST COMMON CONDUCTION DISTURBANCE—occurs in both healthy and diseased hearts First degree AVB can be due to: Inferior MI Digitalis toxicity (hallmark of block conduction issues! Means dig >2. Watch for VISUAL DISTURBANCES!! [halo]) Hyperkalemia (K>5) Increased vagal tone Myocarditis Interventions include tx'ing underlying cz and observing for progression to a more advanced AVB Not reason to run to room, many pts have this—just check and make sure pt okay ANYTIME if chng from baseline—check pt, how tolerating? Anything different? Check VS! wenckebach - ANSWERother name for Second degree AV block- Type 1 (Mobitz 1), PR interval increases until p followed by no Qrs, -Impulse conduction through AV node becomes progressively longer until it fails and a P wave is not conducted and a QRS is dropped -Ischemia to AV node is usually secondary to inferior myocardial infarction, Causes: usually result of myocardial ischemia or MI, digitalis, beta blockers, calcium- channel blockers, excessive vagal tone, may be a normal variant especially in athletes. Can progress. Treatment: if no symptoms, usually no treatment necessary. If the heart rate is brady and the client becomes symptomatic, then follow ACLS protocol for bradycardia: atropine, temporary pacemaker if atropine ineffective, dopamine or epinephrine. third degree heart block - ANSWERForm of AV dissociation which no impulses from atria are conducted to ventricles Atria are stimulated & contract independently of ventricles. Ventricular rhythm is an escape rhythm. Ectopic pacemaker may be above or below bifurcation of bundle of His. Clinical associations - Severe heart dx: CAD, MI, myocarditis, cardiomyopathy Systemic diseases: Amyloidosis, scleroderma Drugs: Digoxin, B-, Ca channel blockers Clinical significance - ↓CO with subsequent ischemia, HF, & shock Tx - Permanent pacemaker ASAP, If symptomatic, transcutaneous pacemaker until a temporary transvenous pacemaker can be inserted Drugs (e.g., atropine, epinephrine): Temp to ↑ HR & support BP until temp pacing is initiated Syncope possible from severe bradycardia or even periods of asystole.
Tx: Call RRT, Racemic epinephrine ( a areosol vasoconstrictor), and possible intubation ARDS - ANSWERacute respiratory distress syndrome , acute lung injury characterized by coughing and rales, Respiratory failure due to increased capillary permeability edema. Associated with increased lung stiffness (noncompliance)., Treatment for ARDS is to find & manage cause/symptoms, steroids, diuretics, bronchodialators, and give Pavulon (paralyzes muscles, for intubation.) superficial burns - ANSWERdamage the epidermis and may involve the upper dermis. They usually appear red and painful but heal readily without scar tissue. Examples include sunburn or a mild scald. superficial partial thickness burns - ANSWERepidermis and superficial dermis are injured. Usually caused by hot water. Blistering occurs, painful to the touch, good perfusion of the dermis. Heals in 14-21 days with minimal scarring and return of function deep partial thickness burns - ANSWERepidermis and deep dermal layer, blotchy in color with white, painful with diminished light touch, slow healing 3 to 5 weeks, chance of converting to a full thickness burns full thickness burns - ANSWERBurns that affects all skin layers and may affect the subcutaneous layers, muscle, bone, and internal organs, leaving the area dry, leathery, and white, dark brown, or charred. deep full thickness burns - ANSWERDestroys all skin layers and possibly fat, muscle, bone and nerves; Appear brown or charred and underlying tissues maybe white, life- threatening, leathery, waxy skin. Healing time is months and grafts are required. angina pectoris - ANSWERTransient (short-lived) chest discomfort caused by partial or temporary blockage of blood flow to the heart muscle. chronic stable angina - ANSWERchest pain that has as its primary cause atherosclerosis, which results in a long term but relatively stable level of obstruction in one or more coronary arteries acute coronary syndrome - ANSWERcondition that develops when the oxygen supply is prolonged and not immediately reversible; encompasses the spectrum of unstable angina, non-ST-segment-elevation myocardial infarction (NSTEMI), and ST-segment- elevation myocardial infarction (STEMI). unstable angina pectoris - ANSWERdiscomfort lasts longe than 15-20 minutes and occurs without cause becomes more frequent and severe
caused by unstable plaque that are prone to rupture vessel becomes blocked with blood clots, but dissolves within 20 minutes does not respond well to nitrates increased risk for heart attack new onset angina - ANSWERFirst angina symtoms, usually after exertion or other increased demands on the heart. Prinzmetal's angina - ANSWERvariant angina; occurs at rest, usually in response to reversible, severe spasm of a major coronary artery. myocardial infarction - ANSWERNecrosis (death) of the myocardium caused by an obstruction in a coronary artery; commonly known as heart attack, Symptoms of this: WOMEN: atypical discomfort, shortness of breath & fatigue. MEN & OLDER CLIENTS: shortness of breath, pulmonary edema, dizziness, altered mental status or dysrhythmia. OTHER SYMPTOMS: Pain, nausea & vomiting, diaphoresis, dyspnea, dysrhythmias, fear & anxiety, pallor, cyanosis & coolness of extremities, crackles or wheezes in respiration. O2 nasal cannula @4L Nitro q 5 min until pain subsides chew 325mg of ASA or 75 mg of Plavix if can not take ASA Morphine for additional pain and to reduce O2 needs wandering atrial pacemaker - ANSWERthis dysrhthmias may occur in normal hearts as a result of flunctuations in vagal tone. It may also be seen in patients with heart disease or COPD. Wandering atrial pacemaker may also be a precursor to multifocal atrial tachycardia. There is usually no treatment required., Rate: Atrial & Ventricular 45 - 100 (slow MAT) P wave: ≥ 3 different 'P' waves QRS: Normal Conduction: P-R intervals vary Rhythm: Irregularly irregular Carotid massage: no effect sinus rhythm with premature atrial contraction - ANSWERPACs don't get us worried, as a rule UNLESS—start getting too frequent, may mean a-fib is coming MAIN THING—how does pt handle it?!?! When atrial tissue becomes irritable premature P wave may not always be visible (hidden in preceding T wave)—examine T wave shape changes...PAC usually followed by a pause Causes of atrial irritability: Stress Fatigue Anxiety Inflammation Infection
PRI: Can only be measured if P wave precedes the QRS complex; if measurable, will be less than 0.12 seconds QRS: Less than 0.10 seconds (may be wide if from low junction), the most common cause of this rhythm in healthy individuals is sinus bradycardia.it may also be seen in the presence of a high degree or complete av block.if the ventricular rate si slow, hemodynamic compromise may occur.treament depends upon the underlying cause and the baseline dysrhythmias. atropine or a pacemaker may be used to increase the ventricular rate ventricular arrhythmias - ANSWERAbnormal rhythms originating in the ventricle→ premature ventricular contractions (PVC) → Bizarre and wide QRS complexes: T wave pointing in opposite direction of QRS complexes, QRS randomly related to P waves, if present; myocarditis or myocardial injury are possible causes, In adults, sudden death from an acute myocardial infarction is usually caused by premature ventricular contraction - ANSWER-coming from an area below the AV Junction from somewhere in ventricles. -Occurs earlier than normal beat -QRS wide and bizzare -Compensatory pause after PVC -pause allows rhythm to return to normal -unifocal PVC originates from a specific site -multifocal PVC originates from many sites -begeminy normal beat: abnormal beat: normal beat: abnormal beat, etc etc -SIX PVCs or more per minute equals trouble. -couplet two PVCs in a row -multifocal couplet and two different PVCs in a row -Run of VT more than three PVCs CX: -caffeine -nicotine -stress -hypoxia -hypokalemia -hypomagnesia -CAD -heart failure -anterior wall MI TX: -if stable: watch -oxygen -anterior wall MI lidocaine couplets - ANSWERtwo PVCs in a row not an emergency is K or Mg low is pt acidotic
bigeminy - ANSWERcardiac arrhythmia in which every second heartbeat is a PVC trigeminy - ANSWERcardiac arrhythmia in which every third heartbeat is a PVC quadrigeminy - ANSWERPVC that occurs every fourth beat paroxysmal ventricular tachycardia - ANSWERan ectopic rhythm in excess of 100 bpm and usually faster than 170 bpm that begins abruptly with a pre-mature atrial or junctional beat and is supported by an atrioventricular nodal reentry mechanism or by an atrioventricular reentry involving an accessory pathway. If deteriorates into vfib=death ventricular ectopy - ANSWERA ventricular ectopic beat (VEB) is an extra heart-beat originating in the lower chamber of the heart. This beat, also called a premature ventricular contraction (PVC), occurs before the beat triggered by the heart's normal function ventricular tachycardia - ANSWERRate: 120 - 200 usually P wave: Usually absent (unrelated to the QRS) QRS: Wide & bizarre shape (PVCs) Conduction: No correlation between 'P' if present and QRS Rhythm: Regular or Irregular Cannon A waves may be present Carotid massage: no effect Tx: immediate defirillation within 4-6 minutes torsades des pointes - ANSWER-polymorphic VT -prolonged QT or prominent U wave ---delayed ventricular repolarization Due to: ---decreased K or Mg ---drug induced (Ia, III, antipsychotics, Abx, antihistamines) Treatment: DCC, bolus MgSO4, pacing or drugs (epi, isoproterenol) to increase the HR Idioventricular - ANSWER1. Rate: 20-40bpm (ventricular!)
- Rhythm: Normal
- P waves: None
- PR interval: None
- QRS duration: >0.10 seconds Wide and bizarre
- Clinical Significance: Give atropine and pacemaker ventricular fibrillation - ANSWERwhen ventricular musculature of the heart is quivering. Med emergency char by rapid and disorganized ventricle pulsation.
SIRS + BLOOD CULTURES = SEPSIS
SEPSIS + HYPOTENSION = SHOCK
MODS - ANSWERMultiorgan dysfunction syndrome; functional abnormalities in one or more vital organ system in patients with SIRS; once occurs mortality is greater than 50% septic shock - ANSWERHigh-output failure; high mixed venous pressure. Findings: hot pt, dilated arterioles, decr TPR., Shock syndrome that is frequently fatal, caused by the systemic release of the cytokine TNF-α after bacterial infection of the bloodstream, usually with Gram- negative bacteria., Endotoxin mediated shock, massive peripheral vasodilation (dec. resistance), peripheral pooling of blood, compensatory increase in heart rate coumadin - ANSWERWarfarin Anticoagulant BLEEDING, FEVER, nausea pulmonary embolism - ANSWERthis develops when a blood-borne substance lodges in a branch of a pulmonary artery & obstructs flow. Common sources are deep vein thrombosis, air from IV infusions, fat from long-bone fractures & amniotic fluid. Emboli interfere with gas exchange to pulmonary circulation distal to the emboli, resulting in hypoxemia. Place client in high fowler's position., S/S: difficulty breathing, chest pain on inspiration, and palpitations. risk is increased with flying and prolonged bed rest Tx: O2, heparin, alteplase, lovenox shock - ANSWER(pathology) bodily collapse or near collapse caused by inadequate oxygen delivery to the cells hypovolemic shock - ANSWERan emergency condition in which severe blood and fluid loss makes the heart unable to pump enough blood to the body. This type of shock can cause many organs to stop working. The body tries to adapt by increasing the HR and peripheral vasoconstriction to increase the volume of blood returned to the heart and increase cardiac output cardiogenic shock - ANSWERShock, or lack of perfusion, brought on not by blood loss, but by inadequate pumping action of the heart. It is often the result of a heart attack or congestive heart failure. distributive shock - ANSWERless distribution of blood to areas = venous pooling, most common in general anesthesia and spinal cord injuries and septic shock (bacterial infection where toxins in blood). cause: general anesthesia and spinal cord injuries and septic shock obstructive shock - ANSWERThis shock is due to inadequate circulating blood volume, due to obstruction or compression of great veins, aorta, pulmonary artery, or of the heart itself.
early shock - ANSWER-arterial pressure falls due to vasodilation -NE and DA used to increase vasoconstriction (alpha receptors), Pallor,increased heart rate and respiration's and restlessness or confusion compensatory stage of shock - ANSWERMAP decreases 10-15 mmHg from baseline, release of RAAS system, ADH, epi, norepi keeps volume in central blood vessels. Hypoxia in non vital organs and kidneys. Mild acidosis and hyperkalemia. Cellular effects still reversible. Widespread vasoconstriction. Increase in NA and water resorption, decrease in urine output. Respiratory alkalosis from hyperventilation. Vasopressin excretion is increased leading to fluid retention progressive stage of shock - ANSWERMAP decrease more than 20mmHg, Compensory mechanisms start to fail, altered capillary permeability resulting in edema, wet lungs and poor gas exchange, myocardial ischemia/infarction, dysrhytmias, renal failure resulting in metabolic acidosis, continued translocation of bacteria- life can still be saved with quick action refractory stage of shock - ANSWERPeriph Constriction: ↓Perfusion, ↑Lactic Acid, blood pools in cap bed, Hypotension, Hypoxemia, organ failure from lactate, urea, ammonia, CO2, No recovery. Care of a patient with HIV - ANSWERstandard precautions private room do not reuse supplies
