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A patient has a BP of 90/54 mmHg. Calculate the MAP using (SBP + 2 × DBP) ÷ 3. Is the result concerning?
MAP = (90 + 108) ÷ 3 = 66 mmHg. This is close to the commonly used minimum perfusion target of 65 mmHg. Assess symptoms, perfusion, and trends.
CO = HR × SV = 110 × 50 = 5,500 mL/min, or 5.5 L/min.
Afterload. The left ventricle must pump against greater vascular resistance.
Preload. Increased ventricular filling and volume can worsen pulmonary congestion in a failing heart.
Hyperkalemia. ACE inhibitors decrease aldosterone activity, reducing potassium excretion.
Suspect angioedema. Hold the medication and obtain emergency airway evaluation.
Accumulation of bradykinin associated with ACE inhibition.
Hyperkalemia. ARBs can decrease aldosterone-mediated potassium excretion.
Check the prescribed hold parameters; withhold if indicated and notify the prescriber. Beta blockers can worsen bradycardia.
Propranolol blocks beta-2 receptors and can cause bronchoconstriction.
Peripheral edema from dilation of arterioles and increased capillary hydrostatic pressure.
Excessive slowing of SA/AV nodal activity. Assess the rhythm and BP, hold according to parameters, and notify the prescriber.
Take the first dose at bedtime as directed and rise slowly because of first-dose orthostatic hypotension.
Hypokalemia, which increases the risk of cardiac dysrhythmias. Assess the ECG and notify the prescriber.
Potassium. Both medications can increase potassium and cause hyperkalemia.
Chronic hypertension damages blood vessels and organs, increasing the risk of stroke, kidney disease, LVH, and heart failure.
Fluid retention. A rapid increase in daily weight can occur before obvious edema or worsening shortness of breath.
Fluid backs up into the pulmonary circulation, causing pulmonary congestion and impaired gas exchange.
Systemic venous congestion from impaired right ventricular pumping.
Heart failure or increased ventricular stretch. BNP is released in response to increased cardiac wall stress.
Echocardiogram. It evaluates cardiac function, chamber size, valves, and ejection fraction.
Reduced ejection fraction and impaired systolic pumping.
Digoxin toxicity. Visual changes and GI symptoms are classic warning findings.
Hypokalemia increases the risk of digoxin toxicity because potassium and digoxin compete for binding at the sodium-potassium ATPase.
Hold the dose according to prescribed parameters and notify the prescriber. Digoxin can slow heart rate and AV conduction.
Reduced edema, improved breathing, decreased lung crackles, and reduced excess weight from fluid loss.
Albuterol. It is a short-acting beta-2 agonist used for quick relief of bronchospasm.
Beta-2 agonists can cause tremors and stimulate cardiovascular activity, resulting in tachycardia and palpitations.
Poor asthma control. Frequent rescue inhaler use requires reassessment of the treatment plan.
Possible severe airflow obstruction or impending respiratory failure. A silent chest is not necessarily improvement.
Red zone. This indicates severe airflow limitation and requires following the emergency asthma action plan.
Green zone. It generally indicates good asthma control.
Yellow zone. The patient should follow the asthma action plan and reassess symptoms.
Rinse the mouth and spit after each dose to reduce the risk of oral candidiasis.
Albuterol first to open the airways, followed by the inhaled corticosteroid.
Report the symptoms promptly. Montelukast has a serious neuropsychiatric warning.
No. Montelukast is a maintenance/prevention medication, not an immediate rescue bronchodilator.
LABA monotherapy is not appropriate for asthma. A LABA must be used with inhaled corticosteroid therapy.
It blocks muscarinic receptors, reducing acetylcholine-mediated bronchoconstriction.
Long-acting maintenance bronchodilation. It is not intended for immediate relief of an acute attack.
An acute COPD exacerbation. Assess respiratory status, oxygenation, sputum changes, and mental status.
Assess airway, breathing, oxygenation, and mental status; administer prescribed oxygen and escalate care. Do not withhold oxygen because of COPD.
88–92% when prescribed for patients at risk of hypercapnic respiratory failure, with individualization based on clinical status and blood gases.
Air trapping and chronic hyperinflation due to loss of elastic recoil.
Chronic airway inflammation and enlargement of mucus-producing glands and goblet cells.
Destruction of alveolar walls decreases the surface area available for oxygen and carbon dioxide exchange.
Cor pulmonale, or right-sided heart dysfunction caused by pulmonary hypertension.
Hypercapnia and worsening respiratory failure. Assess ventilation and obtain further evaluation.
Bronchospasm, airway inflammation/edema, and increased mucus production.
Cold air can trigger airway hyperresponsiveness and bronchoconstriction.
Stable angina. It is predictable with exertion and improves with rest or prescribed nitroglycerin.
Unstable angina or acute coronary syndrome. Rest pain is an emergency finding requiring prompt evaluation.
Variant (Prinzmetal) angina, caused by coronary artery spasm.
Blood pressure and medication history, especially recent use of PDE-5 inhibitors such as sildenafil.
Headache is a common effect caused by vasodilation. Monitor BP and prevent falls from dizziness.
The combination can cause profound hypotension.
Obtain a 12-lead ECG promptly and initiate the acute coronary syndrome evaluation.
Myocardial injury. Interpret it with symptoms, ECG findings, and serial results to determine the cause.
STEMI, an acute coronary occlusion pattern requiring urgent reperfusion evaluation.
NSTEMI, assuming the clinical findings support acute myocardial ischemia.
Peripheral arterial disease. An ABI of 0.90 or lower is abnormal.
No. It may indicate noncompressible calcified arteries; further vascular assessment is needed.
PAD with intermittent claudication, caused by inadequate arterial blood flow during activity.
Arterial insufficiency from PAD.
Deep vein thrombosis (DVT). Avoid massaging the leg and arrange prompt evaluation.
Pulmonary embolism. This requires emergency assessment and intervention.
Venous stasis. Immobility slows venous blood flow and increases clot risk.
Dependent edema, aching, warmth, and possible venous ulcers near the medial ankle.
Severe hyperkalemia with risk of life-threatening dysrhythmias. Notify the provider and initiate urgent management.
Dysrhythmias caused by hypokalemia. Assess ECG and replace potassium as prescribed.
Negative chronotropic effect: reduced heart rate due to beta-1 blockade.
Verapamil slows AV nodal conduction through calcium-channel blockade.
Possible digoxin toxicity or dysrhythmia. Check apical pulse, ECG, potassium, renal function, and digoxin level as ordered.
The AV junction, which has an intrinsic rate of approximately 40–60 bpm.
The ventricles or Purkinje system may be acting as the backup pacemaker; this rate is approximately 20–40 bpm.
AV nodal slowing or AV block. Assess ECG, heart rate, BP, and symptoms.
Diphenhydramine can cause drowsiness and impair driving; avoid driving while affected.
The medication may cause drowsiness and impair reaction time; avoid driving while taking it.
Rebound nasal congestion, also called rhinitis medicamentosa, from prolonged topical decongestant use.
Pseudoephedrine can increase heart rate and blood pressure; assess cardiovascular status and notify the prescriber.
Urinalysis and urine culture to identify infection and the causative organism.
Bacterial UTI. Nitrites support certain gram-negative bacteria, and WBCs indicate inflammation.
Sulfa allergy. The medication contains sulfamethoxazole.
Possible medication-associated hyperkalemia. Monitor potassium and renal function and notify the prescriber.
Pulmonary sensitivity or toxicity. The patient needs prompt evaluation.
Stop strenuous activity and promptly contact the prescriber because fluoroquinolones can cause tendon injury or rupture.
This is an expected medication effect. Phenazopyridine relieves urinary pain but does not treat the infection.
Enlargement of the prostate compresses the urethra and obstructs urine flow.
Finasteride reduces DHT and gradually shrinks the prostate; symptom improvement is not immediate.
Tamsulosin relaxes smooth muscle and can cause orthostatic hypotension. Rise slowly and use fall precautions.
A kidney stone moving through the urinary tract and irritating the lining.
Hydration as appropriate, pain control, and monitoring for passage. Small stones may pass spontaneously.
Thiazides reduce urinary calcium excretion and can help prevent certain calcium stones.
Prerenal AKI caused by hypovolemia and reduced kidney perfusion.
Intrarenal AKI, potentially acute tubular necrosis from ischemic or nephrotoxic injury.
Postrenal AKI caused by obstruction of urine outflow.
Recognize life-threatening hyperkalemia, initiate urgent escalation, and prepare for prescribed treatment.
Reduced erythropoietin production by damaged kidneys, resulting in decreased red blood cell production.
Fluid retention due to reduced kidney function, potentially causing pulmonary congestion.
Stage 5 CKD or end-stage renal disease. Dialysis or kidney transplant may be needed depending on the patient's condition.