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NSG210 Week 02 Summary: Chronic Illness, Older Adult Care, Oxygenation, Cardiac Assessment, Heart Failure

Week 02 runs August 31 through September 4, 2026, and carries most of the Exam 1 med-surg content: the September 2 lecture (chronic illness overview, older adult management, alterations in oxygenation) and the September 3 lecture (cardiac assessment and early perfusion, dominated by heart failure). This is the densest single week for Exam 1 - budget the most review time here.

Chronic Illness Overview

A chronic condition is a health problem lasting 3 months or longer that does not resolve spontaneously and is rarely fully curable. Chronic illness differs from acute illness in almost every dimension: no single onset pattern versus sudden onset, permanent versus temporary, a focus on “illness” (living with it) rather than “disease” (curing it), and modified rather than resumed responsibilities.

Some numbers worth remembering: chronic conditions are the leading cause of death and disability in the United States (7 of 10 deaths), affect about 125 million people, and account for 78 percent of healthcare costs. Contributing causes include declining infectious disease mortality, longer lifespans, modern lifestyle factors, and better screening that catches more disease earlier.

Chronic illness affects the whole family, not just the patient - it is expensive, raises ethical issues, and requires “living with uncertainty.” Challenges patients face include managing symptoms, adjusting psychologically to disability, preventing and managing crises, validating self-worth, normalizing daily life, building support networks, and eventually facing death with dignity. The illness course is often described as a trajectory rather than a fixed path.

Health disparities and social determinants of health (SDOH): disparities arise from social factors including age, education, disability, economic instability, income inequality, limited English proficiency, limited social support, mental illness, race, and social isolation, compounded by implicit and explicit bias. The SDOH model organizes these into five connected domains around health outcomes: neighborhood and built environment, health and healthcare, social and community context, education, and economic stability.

Nursing care of chronic illness balances direct care and supportive care, takes a holistic approach, treats quality of life as a patient-defined outcome, and respects the patient’s right to care without judgment. Care has been shifting from acute settings into the community: nurses may function as case managers, occupational health nurses, school nurses, visiting nurses, or parish nurses, with self-care, preventive care, continuity, and collaboration as the core concepts. Home and community teaching focuses on what the patient specifically needs to manage at home, given time for the patient to grasp the significance of the diagnosis before loading on information.

Key exam point: the desired outcome of chronic illness management is not cure - it is acceptance of the condition and its limitations, paired with a realistic appraisal of remaining strengths.

Management of the Older Adult

Demographics and leading causes of death: heart disease is the leading cause of death in older adults, followed by cancer, unintentional injury, chronic lower respiratory disease, stroke, and Alzheimer’s disease. Falls are the leading cause of injury and preventable morbidity/mortality in this population.

Age-related physiologic changes by system, since these set up why older adults present differently and are covered heavily on exams:

Nutrition and sleep: older adults need fewer total calories but more nutrient-dense food (protein, vitamins, minerals, fiber), often complicated by budget and physical limits on shopping/cooking. Sleep quality is disrupted by respiratory problems, restless leg syndrome, nocturia, pain, and dementia; poor sleep drives cognitive decline, fall risk, daytime fatigue, and poor ICU outcomes.

Geriatric syndromes and screening tools:

The “geriatric triad” is cognitive changes, falls, and incontinence. The SPICES tool is the standard rapid nursing screen for this population, used within 24 hours of hospital admission and validated as predictive of adverse events:

SPICES is an alert/screening system, not a substitute for a full nursing assessment - a “yes” on any item triggers a more complete workup. A complementary framework is the American Geriatrics Society’s 5 Ms: Mind (cognition/mood), Mobility, Medications, Multicomplexity, and Matters Most (the patient’s own goals) - SPICES is a checklist for inpatient screening, the 5 Ms is a broader outpatient/primary-care conceptual model.

Urinary incontinence types, since this is both a SPICES item and a standalone geriatric topic:

Type Mechanism Management
Stress Physical pressure (cough, sneeze, lifting) on a weak pelvic floor/sphincter Kegel exercises, avoid heavy lifting, pessaries, sling surgery
Urge Sudden intense urge then leakage, overactive bladder Bladder training, limit caffeine/alcohol, anticholinergics or beta-3 agonists
Overflow Bladder does not empty fully, dribbling Timed voiding, treat cause, intermittent catheterization
Mixed Combination of stress and urge Combine pelvic floor exercises and bladder training
Functional Normal bladder control but a physical or cognitive barrier prevents reaching the toilet Improve access, scheduled toileting, mobility aids

Incontinence is common in older adults but is not a normal, inevitable part of aging. For acute incontinence specifically, the mnemonic DIAPPERS covers reversible causes: Delirium, Infection, Atrophic vaginitis, Pharmaceuticals, Psychological factors, Excess urine output, Restricted mobility, Stool impaction.

Mental health: depression is the most common affective disorder in older adults (not Alzheimer’s - a common exam distractor), with elevated suicide risk. Delirium is an acute, reversible confused state that can progress to permanent brain damage or death if not treated promptly - distinguish it from dementia, which has a slow, progressive onset (Alzheimer’s accounts for about 70 percent of dementia cases and is not a normal part of aging).

Pharmacologic considerations: polypharmacy (multiple concurrent medications) is common given multiple chronic conditions, and aging changes drug absorption, metabolism, distribution, and excretion. The guiding principle is “start low, go slow” - lower starting doses, slower titration, simplified regimens, and ongoing review of whether each medication is still needed.

Ethical and legal: the Patient Self-Determination Act (1990) requires informing patients of their right to make advance directives - a living will (instructions for care) or durable power of attorney for healthcare (naming a proxy decision maker).

Alterations in Oxygenation: Asthma and COPD

Asthma is a chronic inflammatory airway disorder causing hyperresponsiveness, mucosal edema, and mucus production, typically reversible spontaneously or with treatment - the most common chronic disease of childhood. The strongest risk factor is allergy, followed by family history and chronic exposure to irritants/allergens. Pathophysiology: sensitized mast cells trigger bronchoconstriction, increased capillary permeability, mucosal edema, and mucus production; the attack is prolonged by inflammatory cells (basophils, eosinophils). Increased airway resistance and air trapping drive tachypnea and respiratory alkalosis early on; severe, prolonged asthma unresponsive to treatment is status asthmaticus, a medical emergency. A dangerous sign is inaudible breath sounds with reduced wheezing - this can mean the patient is too obstructed to move enough air to wheeze, not that they are improving.

Diagnostics: pulmonary function tests (FEV1, PEFR) evaluate obstruction severity and reversibility; ABGs show early hypoxemia with mild respiratory alkalosis, progressing to hypoxemia with respiratory acidosis if severe; skin testing identifies allergens.

The asthma exacerbation treatment mnemonic (A-S-T-H-M-A) covers the acute management bundle:

Beta-2 agonist side effects worth knowing cold: beta-2 receptors exist on skeletal muscle and liver as well as airway smooth muscle. Stimulating them activates the Na+/K+-ATPase pump, driving potassium from serum into cells - this produces hypokalemia on labs (total body potassium is unchanged, it has just shifted), which raises arrhythmia risk, especially stacked with albuterol’s own tachycardia effect. Beta-2 stimulation in the liver and muscle also triggers glycogenolysis and gluconeogenesis while blunting insulin release, producing transient hyperglycemia. Both effects are usually mild and self-limited after a single dose but become clinically relevant with frequent or continuous nebulized dosing during a severe, prolonged exacerbation - watch potassium and glucose trends in that situation.

COPD is an umbrella term for progressive, largely irreversible airflow obstruction, defined functionally by a reduced FEV1/FVC ratio that does not fully reverse with bronchodilators. Smoking causes 80-90 percent of COPD deaths; other causes include occupational dust/chemicals, air pollution, secondhand smoke, and alpha-1 antitrypsin (AAT) deficiency (under 5 percent of cases). Most COPD patients have a mix of the two classic patterns:

  Chronic bronchitis Emphysema
Where Airways Alveoli (air sacs)
Definition Clinical: productive cough 3+ months/year for 2+ consecutive years Structural: destruction of alveolar walls, elastin breakdown
Classic picture “Blue bloater” - overweight, cyanotic, chronic cough, less breathless at rest “Pink puffer” - thin, barrel chest, pursed-lip breathing, breathless on exertion
Key symptom Chronic productive cough Progressive dyspnea

Alpha-1 antitrypsin deficiency deserves special attention because it changes management. AAT is a liver-made protein that normally protects lung elastin from neutrophil elastase; without enough of it, elastin is destroyed over time, causing early-onset emphysema (often in the 30s-50s) even in non-smokers, and it can also cause liver cirrhosis since the misfolded protein accumulates in liver cells. Suspect it with early-onset COPD, minimal smoking history, a family history of COPD or liver disease, or emphysema affecting the lower lung zones (the reverse of the usual smoking pattern, which is upper-zone predominant). Diagnosis is a blood AAT level, followed by genotyping. Beyond standard COPD therapy, eligible patients can receive augmentation therapy - IV infusions of pooled human AAT protein to slow decline.

Cor pulmonale is right-sided heart failure caused specifically by lung disease: chronic hypoxia from lung disease (most often COPD) causes pulmonary vasoconstriction, which over time produces pulmonary hypertension, forcing the right ventricle to pump against higher resistance until it hypertrophies, dilates, and fails. Signs include peripheral edema, JVD, hepatomegaly/ascites, and worsening dyspnea beyond the patient’s baseline lung disease. Management prioritizes treating the underlying lung disease and correcting hypoxia (long-term oxygen therapy is one of the few interventions shown to reduce mortality here); diuretics are used cautiously since the right ventricle is preload-dependent.

COPD complications: respiratory insufficiency/failure, pneumonia, pneumothorax, atelectasis, cor pulmonale, and dysrhythmias. Diagnostics: CBC (secondary polycythemia from chronic hypoxia), serum AAT level, ABGs, pulse oximetry, chest x-ray (flattened diaphragm in emphysema), and pulmonary function tests (increased residual volume, decreased FEV1).

COPD pharmacology: anticholinergics (ipratropium short-acting, tiotropium long-acting), beta-2 agonists (albuterol short-acting, salmeterol long-acting for nocturnal symptoms), corticosteroids for frequent exacerbations or bronchodilator-refractory symptoms, and AAT replacement for the genetic deficiency subgroup. During an acute exacerbation, treatment order is typically oxygen first, then rapid assessment plus short-acting bronchodilators, then corticosteroids and antibiotics as needed - identify and treat the underlying trigger (most often a respiratory infection or air pollution exposure).

CPAP versus BiPAP: both are non-invasive positive pressure ventilation, but CPAP delivers one constant pressure (splints the airway open, used for obstructive sleep apnea, the patient does all the work of breathing), while BiPAP delivers two pressures - higher on inhalation, lower on exhalation - giving actual ventilatory assistance. BiPAP is the go-to for acute COPD exacerbations with respiratory failure because the inspiratory support helps blow off CO2 and reduces work of breathing, often avoiding intubation; CPAP alone does not provide that assist.

Home care teaching for COPD: pursed-lip breathing and diaphragmatic breathing to conserve energy and keep airways open; teach early signs of infection or exacerbation (fever, increased or purulent sputum, upper respiratory infection, increased SOB, decreased activity tolerance, increased oxygen need) for prompt reporting; wear a medical ID and carry a medication list; referral to pulmonary rehab and smoking cessation programs; discuss end-of-life care as appropriate.

Cardiac Assessment in the Older Adult

Age-related cardiac changes: left ventricular wall thickening (mild hypertrophy), stiffening and calcification of the heart muscle and valves (especially aortic and mitral), increased left atrial size, and arterial stiffening that raises systolic blood pressure and widens pulse pressure - this last one is a hallmark aging change that occurs even without disease. Loss of SA node pacemaker cells raises arrhythmia risk (especially atrial fibrillation) and lowers maximum achievable heart rate. Reduced beta-adrenergic responsiveness means heart rate does not rise briskly with exertion, so older adults rely more on the Frank-Starling mechanism (increased preload) to raise cardiac output. Diastolic function declines faster than systolic function with age, which is exactly why HFpEF (heart failure with preserved ejection fraction) is so common in this population.

The single most tested clinical pearl in this section: older adults often do not present with classic cardiac symptoms. Chest pain can be absent even during an MI (“silent ischemia”). Confusion, dizziness, fatigue, falls, or a vague “not doing well” can be the only presenting sign of a cardiac event.

Cardiac assessment components in aging: history should account for atypical presentation; vital signs should expect a widened pulse pressure and be screened for orthostatic hypotension (a fall risk); inspection/palpation should check JVD, peripheral edema, and PMI location/character; auscultation should note that S4 is common and often benign in older adults (a stiff ventricle) while any new murmur warrants workup (aortic stenosis from valve calcification is common with age); ECG commonly shows baseline changes like first-degree AV block or bundle branch block, but a new atrial fibrillation is not baseline and needs attention.

Heart Sounds and Auscultation

Only S1 and S2 occur in a normal heart. S1 (“lub”) is the closure of the mitral and tricuspid (AV) valves at the start of systole, loudest at the apex. S2 (“dub”) is the closure of the aortic and pulmonic (semilunar) valves at the start of diastole, loudest at the base, and normally splits slightly wider on inspiration. Only valve closures produce sound - normal valve opening is silent, so a murmur heard during systole or diastole (rather than at S1/S2 themselves) usually indicates stenosis (valve does not open fully) or regurgitation (valve does not close fully).

Auscultation sequence (“APE To Man”): Aortic area (2nd right intercostal space) leads to Pulmonic area (2nd left intercostal space) leads to Erb’s point (3rd left intercostal space) leads to Tricuspid area (4th-5th left intercostal space) leads to Mitral/apex area (5th intercostal space, midclavicular line).

Site Location Best for Common older-adult finding
Aortic 2nd right ICS S2 (A2), aortic murmurs Aortic stenosis from valve calcification
Pulmonic 2nd left ICS S2 (P2), physiologic splitting Pulmonic flow murmurs
Erb’s point 3rd left ICS S1/S2 timing, aortic/pulmonic regurgitation Aortic regurgitation
Tricuspid 4th-5th left ICS Tricuspid murmurs Tricuspid regurgitation (louder with inspiration - Carvallo’s sign)
Mitral/apex 5th ICS, midclavicular line S1, S3, S4, mitral murmurs S3 (heart failure), S4 (stiff ventricle), mitral regurgitation

Use the diaphragm for high-pitched sounds (S1, S2, most murmurs) and switch to the bell with the patient in left lateral decubitus for low-pitched sounds (S3, S4, mitral stenosis).

PMI (point of maximal impulse): normally at the 5th intercostal space, midclavicular line, about 1-2 cm and brief/tapping. Displacement laterally or downward suggests LV enlargement, relevant in older adults with longstanding hypertension.

S3 versus S4 is one of the most frequently tested distinctions in this unit:

Feature S3 (ventricular gallop) S4 (atrial gallop)
Timing Early diastole, right after S2 Late diastole, right before S1
Cause Rapid filling into a volume-overloaded or poorly contractile ventricle Atrial contraction forcing blood into a stiff, non-compliant ventricle
Cadence mnemonic “Ken-tuc-ky” “Ten-nes-see”
Requires Adequate volume/flow Normal sinus rhythm - absent in atrial fibrillation
Significance in young/healthy people Can be normal (children, young adults, pregnancy, athletes) Always abnormal
Significance in older adults Usually pathologic - a classic bedside sign of decompensated heart failure Common, often reflects expected age-related ventricular stiffening, but still correlate with other findings
Associated with Systolic dysfunction (HFrEF) Diastolic dysfunction (HFpEF), LVH, hypertension, aortic stenosis

If both S3 and S4 are heard together, it is called a summation gallop, typically with tachycardia shortening diastole enough that the two sounds merge - it signals significant cardiac dysfunction.

Pulmonary circuit pressures are much lower than systemic pressures, since the right ventricle only pumps the short distance to the lungs: pulmonary artery pressure runs about 15-25/8-15 mmHg (mean 10-20) compared to a systemic 90-140/60-90 (mean 70-100). Pulmonary hypertension is defined as a mean pulmonary artery pressure over 20 mmHg at rest, and becomes more common with age, often secondary to left heart disease, COPD, or chronic hypoxia.

Heart Failure

Heart failure (HF) is a clinical syndrome from structural or functional cardiac disorders in which the heart cannot pump enough blood to meet the body’s metabolic demands (or can only do so at elevated filling pressures). It is the most common reason for hospitalization in people over 65, affects roughly 6 million Americans, and prevalence is projected to rise 46 percent by 2030.

Classification

A normal EF does not rule out heart failure - HFpEF patients can have textbook HF symptoms with an EF of 55 percent, because the problem is the ventricle’s ability to fill, not to squeeze. Distinguishing systolic from diastolic failure by symptoms alone is not reliable; an echocardiogram measuring EF is what actually differentiates them, which is why echo is central to the diagnostic workup.

Pathophysiology: Neurohormonal Compensation

When cardiac output drops, baroreceptors sense reduced flow and trigger the sympathetic nervous system, while reduced renal perfusion triggers the renin-angiotensin-aldosterone system (RAAS): the kidneys release renin, which converts angiotensinogen to angiotensin I, which ACE (mostly in the lungs) converts to angiotensin II. Angiotensin II causes vasoconstriction (raising afterload), stimulates aldosterone release (sodium and water retention, raising preload), stimulates ADH release (more water retention), and drives pathologic cardiac remodeling (hypertrophy, fibrosis). Natriuretic peptides (ANP, BNP), released from overdistended cardiac chambers, counter this with vasodilation and diuresis, but are usually not strong enough to overcome the RAAS/SNS effects.

This is a compensatory mechanism that becomes maladaptive: in the short term it helps maintain blood pressure and organ perfusion, but chronically it becomes a vicious cycle - more afterload makes the weak heart work harder, more preload worsens congestion, and chronic angiotensin II/aldosterone exposure drives fibrosis and remodeling that lowers EF further, which triggers even more RAAS activation. Nearly every major HFrEF medication class exists specifically to interrupt some point in this cycle.

Manifestations

Left-sided HF Right-sided HF
Pulmonary congestion (cannot pump into systemic circulation) Peripheral/visceral congestion (cannot pump into pulmonary circulation)
Dyspnea, cough, crackles, low SpO2, orthopnea, paroxysmal nocturnal dyspnea Jugular venous distention, dependent edema, hepatomegaly, ascites, weight gain

Acute HF is a rapid progression of symptoms requiring urgent intervention and hospitalization.

Staging and Diagnosis

The ACC/AHA staging system (Stages A through D) tracks disease progression, with early stages (“at risk for HF” and “pre-HF”) targeting risk-factor modification. The NYHA classification grades severity by symptoms and is used once a patient is in Stage C or D. Diagnostic workup includes echocardiogram (the key test - measures EF and identifies structural abnormalities), chest x-ray, 12-lead ECG, and labs including electrolytes, BUN, creatinine, liver function tests, TSH, CBC, and BNP.

The Four Pillars of Guideline-Directed Medical Therapy (GDMT) for HFrEF

Current guidelines call for starting all four classes together at low doses rather than adding them sequentially, since RAAS and SNS overactivation are both driving damage simultaneously.

  1. SGLT2 inhibitors (dapagliflozin, empagliflozin) - originally a diabetes drug class, now shown to have independent cardiac benefit. Cause mild osmotic diuresis (reduces preload) and improve myocardial metabolism, reducing hospitalization risk even in non-diabetics. Watch for volume depletion/hypotension, genital fungal infections, and rare euglycemic diabetic ketoacidosis; hold before major surgery.

  2. Diuretics - loop diuretics (furosemide) are the most potent, first-line for volume overload; thiazides (metolazone) are often added for synergy in resistant edema; mineralocorticoid receptor antagonists/MRAs (spironolactone) block aldosterone directly, sparing potassium and providing a mortality benefit beyond symptom relief, not just fluid removal. Loop and thiazide diuretics can cause hypokalemia; MRAs can cause hyperkalemia, especially combined with an ACE inhibitor or ARB. Monitor daily weight, I&O, electrolytes, and orthostatic blood pressure.

  3. RAAS blockers - ACE inhibitors (lisinopril, side effect of dry cough from bradykinin), ARBs (valsartan, used when ACE-I is not tolerated), and ARNIs (sacubitril-valsartan, which combines ARB action with neprilysin inhibition to boost natriuretic peptides, now preferred over ACE-I/ARB alone for stronger mortality benefit). Never combine an ACE inhibitor with an ARB, and never combine an ACE inhibitor with an ARNI - both combinations risk angioedema; switching from an ACE inhibitor to an ARNI requires a 36 hour washout. Contraindicated in pregnancy. Monitor blood pressure, renal function, and potassium.

  4. Beta-blockers (carvedilol, metoprolol succinate extended-release) - block sympathetic stimulation of the heart, are negative inotropes initially but improve long-term contractility and significantly reduce mortality with sustained use. Start at low doses and titrate slowly, since the initial negative inotropic effect can transiently worsen symptoms; never stop abruptly (rebound tachycardia and ischemia risk); avoid starting during active, unstabilized fluid overload.

Hydralazine plus isosorbide dinitrate is a notable combination therapy that pairs a pure arterial vasodilator (hydralazine, no venous/preload effect) with a venodilator (isosorbide dinitrate, reduces preload) to cover both sides of the loading equation - used especially in Black patients with HFrEF per the BiDil/A-HeFT trial data, or when ACE-I/ARB/ARNI cannot be tolerated (e.g. renal impairment).

Preload, Afterload, and How Drugs Target Each

Preload is the venous side - the volume/stretch in the ventricle at end-diastole, tied to the Frank-Starling mechanism (“how stretched is it before it squeezes”). Afterload is the arterial side - the resistance the ventricle must overcome to eject blood (“what it pushes against”). In heart failure, RAAS/ADH-driven fluid retention raises preload while RAAS/SNS-driven vasoconstriction raises afterload simultaneously, which is exactly why GDMT stacks drug classes that hit both sides at once: diuretics and nitrates reduce preload; ACE-I/ARB/ARNI and hydralazine reduce afterload.

Chronotrope, Inotrope, Dromotrope

These describe which cardiac property a drug changes: chronotropic affects heart rate, inotropic affects contractility (force of squeeze), dromotropic affects conduction velocity through the AV node. Each can be positive (increases the function) or negative (decreases it). Beta-blockers are negative on all three. Digoxin is the classic exam trap: it is a negative chronotrope and negative dromotrope (slows the heart and slows AV conduction, useful for rate control in atrial fibrillation) but a positive inotrope (strengthens contraction) - a combination worth memorizing since it is unusual. Digoxin has a narrow therapeutic index and toxicity (nausea, visual changes, arrhythmias) is a major nursing concern, especially since hypokalemia from diuretic therapy potentiates digoxin toxicity.

Nursing Assessment, Diagnoses, and Interventions

Nursing assessment focuses on treatment effectiveness and the patient’s ability to self-manage: health history covers dyspnea, fatigue, edema, and sleep disturbance; physical exam covers restlessness/anxiety/level of consciousness, respiratory rate and effort, lung auscultation (crackles, wheezes), heart sounds, JVD, peripheral pulses, edema, hepatomegaly, and daily weight/I&O.

Major nursing diagnoses: activity intolerance from decreased cardiac output, hypervolemia, anxiety, powerlessness related to chronic illness, and impaired ability to manage the treatment regimen. Potential complications to monitor for: pulmonary edema, hypotension/poor perfusion/cardiogenic shock, arrhythmias, thromboembolism, and pericardial effusion.

Interventions: promote activity tolerance by alternating activity with rest rather than prolonged bed rest; manage fluid volume with daily weights, low-sodium diet adherence, and positioning that facilitates breathing and reduces venous return; control anxiety with comfort measures and psychological support; reduce powerlessness by involving the patient in treatment decisions and screening for depression; and build a comprehensive education/discharge plan using the teach-back technique. For pulmonary edema specifically, recognize early signs and intervene to reduce preload; home care referral, HF disease-management clinics, and telehealth can reduce hospitalizations and cost. End-of-life discussions and palliative/hospice referral are appropriate for advanced disease.

Applying It: The Henry Winston Case Study

A 92-year-old man, 2 days post-admission for an HF exacerbation, non-adherent with fluid/sodium restriction (family bringing in soda, not eating due to anorexia), demonstrates both sides of HF at once: left-sided signs (worsening SOB, cough, bilateral wheeze, SpO2 94 percent) and right-sided signs (2+ peripheral edema, 9 lb weight gain, distended abdomen with hypoactive bowel sounds, anorexia). His vitals - HR 92 with a “slightly irregular” rhythm, BP 154/80, SpO2 94 percent - suggest a possible new arrhythmia (atrial fibrillation is common in HF) and mild hypoxemia trending toward his reported symptoms, even though he is above the 90 percent SpO2 threshold in his orders.

His medication list is a working example of the four-pillar approach in the context of a real patient: furosemide (loop diuretic, but wastes potassium), digoxin (positive inotrope, requires checking apical pulse and holding for HR under 60), enalapril (ACE inhibitor, retains potassium - creating an interaction to watch with both the potassium chloride supplement and the diuretic’s own potassium loss), metoprolol (beta-blocker, hold for bradycardia/hypotension), and potassium chloride replacement. The clinical judgment point: before giving this medication set, the nurse needs current vitals (apical pulse, BP) and a current potassium level, because furosemide and potassium chloride push potassium in opposite directions from enalapril, and hypokalemia would potentiate digoxin toxicity. Given his active, worsening respiratory symptoms and that he has been off supplemental oxygen since the prior night, the first action is reassessing his respiratory status and reapplying oxygen per protocol - addressing the acute oxygenation problem before proceeding to routine scheduled medications.