STAT Stitch Deep Dive Podcast Beyond The Bedside

STAT Stitch Deep Dive Podcast Beyond The Bedside

di Regular Guy

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Stagione 7

CC Pharm Milrinone

Core Profile & Mechanism Milrinone is a parenteral positive inotrope and vasodilator with selective phosphodiesterase III (PDE3) inhibitor activity. By preventing cyclic adenosine monophosphate (cAMP) breakdown in cardiac and vascular muscle cells, it increases myocardial contractility, causes vasodilation, and improves diastolic relaxation (lusitropy). This dual action reduces preload, afterload, and systemic vascular resistance with little to no chronotropic activity. Therapeutic effects occur at plasma levels of 100 to 300 ng/mL. Primary Indications Milrinone is used for the short-term treatment of acute heart failure and other low cardiac output states like cardiogenic shock or post-cardiac surgery low cardiac output syndrome (LCOS). It can provide long-term palliative support in stage D heart failure patients awaiting transplant or mechanical circulatory support. Off-label uses include pediatric septic shock or postresuscitation stabilization, cerebral vasospasm after aneurysmal subarachnoid hemorrhage, and persistent pulmonary hypertension of the newborn (PPHN) with poor nitric oxide response. Dosing & Administration Adult HF Dosing: A 50 mcg/kg IV loading dose over 10–60 minutes (though heart failure guidelines do not recommend a bolus), followed by 0.125 to 0.75 mcg/kg/minute continuous infusion. Renal Adjustments: Elimination is primarily renal (83% excreted unchanged in urine, half-life of 2.4 hours). For CrCl ≤ 50 mL/min, the adult continuous infusion rate must be adjusted down sequentially from 0.43 mcg/kg/min (CrCl 41–50) down to 0.2 mcg/kg/min (CrCl ≤ 5). Pediatric rates also require reductions for CrCl < 50 mL/min. Administration Safety: Standard infusion is 200 mcg/mL, diluted in 0.45% or 0.9% NaCl or 5% Dextrose, run via a controlled device. It is not FDA-approved for intraosseous use, but the same doses can be given IO if IV access is unavailable. Critical Safety & Adverse Reactions Incompatibilities: Milrinone must never be co-administered with furosemide, as precipitation occurs immediately in the same line. It also cannot be given simultaneously with blood. Arrhythmias & Monitoring: Continuous ECG monitoring is mandatory. Milrinone carries a substantial risk of serious ventricular arrhythmias (VT up to 12%, VF 0.2%), atrial flutter/fibrillation (up to 8%), supraventricular tachycardia, and premature ventricular contractions. Hypotension & Other Risks: Hypotension occurs in 2.9% to 10.7% of patients. To reduce this risk, clinicians often avoid the loading dose in septic shock and neonatal PPHN. Thrombocytopenia is a delayed reaction occurring in up to 58% of patients.

CC | PRIMER Assessment of the Resp System

Gas Exchange: Primary goal: O2/CO2 exchange across alveolar-capillary membrane. Anatomy: Upper tract warms/humidifies/filters air; epiglottis covers larynx to prevent aspiration. Carina is highly sensitive, triggering vigorous cough on stimulation. Aspiration: Right mainstem bronchus is shorter, wider, straighter than left; aspiration is far more common in right lung. Dead Space: Normal tidal volume (VT) is ~500 mL (~150 mL is anatomical dead space [VD] without gas exchange). Alveoli & Surfactant: 300M+ alveoli connect via pores of Kohn. Surfactant lowers surface tension, preventing collapse (atelectasis). Pleural Biology: Visceral pleura lacks pain fibers; parietal pleura has pain fibers, causing sharp pleuritic pain during inflammation. Ventilation: Inspiration is active (diaphragm contracts, drawing air in); expiration is passive via elastic recoil. Compliance & Resistance: Compliance decreases in edema, ARDS, fibrosis, and increases in COPD. Resistance is driven by airway diameter. Control: Central chemoreceptors (medulla) respond to CSF pH/H+ changes; peripheral receptors respond to low PaO2, low pH, high PaCO2. COPD may rely on hypoxic drive. Defense: Alveolar macrophages provide primary defense below bronchioles. Smoking impairs their phagocytic activity. Gerontologic & Assessment Key Concepts Aging: Stiffened chest walls, decreased muscle strength, and fewer elastic alveoli cause early airway closure in lung bases (lower PaO2). Decreased cilia, cough force, and pharyngeal sensation raise infection/aspiration risks. Hypoxia Findings: Early signs: restlessness, apprehension, tachycardia, mild hypertension, tachypnea. Late signs: cyanosis, coma, hypotension, accessory muscle use. Physical Exam:Fremitus: High in pneumonia/edema (dense); low in COPD, pleural effusion. Percussion: Normal resonance; hyperresonance in air trapping (COPD, pneumothorax); dullness in fluid/consolidation (effusion, pneumonia). Sounds: Bronchial (trachea, 2:3 ratio), Bronchovesicular (scapulae, 1:1), Vesicular (periphery, 3:1). High-Yield Diagnostics & Procedures Oximetry: Arterial SpO2 (normal >95%) is inaccurate if <70%, or with cold, hypoperfusion, vasopressors. Venous SvO2/ScvO2 (normal 60-80%) tracks O2 supply/demand balance. Low values show anemia, low cardiac output, high demand. High values (sepsis) signal poor tissue extraction. Procedures:Bronchoscopy: Signed consent, NPO 6-12h before, keep NPO after until gag reflex returns. Thoracentesis: Done sitting upright leaning on table; post-procedure chest X-ray checks for pneumothorax.

CC | PRIMER Supporting Resp System

I. Oxygen Therapy & Delivery Systems Target: Maintain SpO2 >92% (or >88% in chronic COPD) or PaO2 >60 mmHg. Supplementing FiO2 >60% for >24 hours risks oxygen toxicity, causing severe pulmonary edema and inflammatory alveolar damage. Low-Flow Systems: Nasal Cannula (1–6 L/min, 24%-44% FiO2), Simple Mask (6–12 L/min, 35%-50% FiO2, requires >=6 L/min), Non-Rebreather (10–15 L/min, 60%-90% FiO2, keep reservoir bag inflated). High-Flow Systems: Venturi Mask (delivers precise, fixed FiO2 for COPD), High-Flow Nasal Cannula (up to 60 L/min, 100% FiO2, heated humidification). CO2 Narcosis: Some COPD patients lose sensitivity to high CO2, relying on a hypoxic drive to breathe. However, never withhold oxygen during severe, life-threatening hypoxemia. II. Artificial Airways & Ventilation Modes Airways: NPA (used in conscious or unconscious patients) vs. OPA (strictly unconscious patients to avoid vomiting/aspiration). Verify ET tube placement immediately via bilateral breath sounds, symmetric chest movement, and EtCO2 capnography; confirm via chest X-ray (2–3 cm above carina). Cuff Management: Keep cuff pressure at 20–30 cm H2O to prevent aspiration and protect tracheal capillary perfusion. Ventilation Modes:AC (Assist-Control): Preset rate/VT. Spontaneous breaths get full VT; risks hyperventilation and respiratory alkalosis. PC (Pressure Control): Preset pressure; VT varies. Prevents barotrauma in "stiff" or noncompliant lungs. SIMV: Preset rate/VT; spontaneous breaths vary in volume. PSV (Pressure Support): Preset pressure assisting spontaneous breaths; patient controls rate/VT to facilitate weaning. PEEP: Splints open alveoli. High PEEP risks decreased venous return, preload, and cardiac output due to increased thoracic pressure. III. Nursing Interventions & Complications Suctioning: Only PRN (not routinely). Hyperoxygenate with 100% FiO2 before/after; limit passes to <10 seconds. Stop insertion when meeting resistance (carina) to avoid mucosal damage. VAP Prevention: Elevate HOB 30–45 degrees, perform daily SAT/SBT trials, provide oral care with Chlorhexidine, and initiate early mobility. Unplanned Extubation: Stay with the patient, call for help, and manually ventilate with BVM and 100% O2. Accidental Decannulation (Trach <7 days): Spread stoma with hemostat, insert tube with obturator, then remove obturator; if impossible, cover stoma and use BVM over mouth/nose. IV. Chest Tubes & Drainage Systems Water-Seal Chamber: Shows tidaling (water rises on inspiration, falls on expiration). Cessation means lung re-expansion or tube occlusion. Continuous bubbling indicates an air leak. Disconnection: Submerge the distal end in sterile water to re-establish a water seal. Never routinely clamp or strip chest tubes.

CC | PRIMER Obstructive Resp Complications

1. Bronchiectasis: Mucus Stasis Pathophysiology & Presentation: Inflammation destroys elastic and muscular wall structures, causing permanent dilation and impaired mucus clearance. It presents as a persistent cough with thick, purulent sputum. Massive hemoptysis is a life-threatening complication. Care: CT scan is the gold standard. Care involves antibiotics (minimum 14 days), bronchodilators, and ACTs with hydration (2-3 L/day). 2. Cystic Fibrosis (CF): Ion Transport Defect Pathophysiology & Presentation: An autosomal recessive CFTR mutation disrupts sodium and chloride transport, producing thick, dehydrated mucus that plugs respiratory, GI, and reproductive ducts. This causes progressive organ scarring, pancreatic insufficiency, and malabsorption. Care: Sweat chloride testing is the gold standard. Management relies on aggressive ACTs and mucus-liquefying medications (dornase alfa), combined with pancreatic enzyme replacement before meals and mutation-specific CFTR modulators. 3. Asthma: Reversible Airflow Hyperreactivity Pathophysiology & Presentation: Inflammation involves mast cells and eosinophils. Triggers cause an early IgE-mediated bronchospasm, often followed by a late-phase response 4-6 hours later. Signs include wheezing, dyspnea, and cough. A sudden absence of wheezing ("silent chest") is an emergency. Care: Spirometry confirms reversibility (>12% and >200 mL FEV1 improvement post-bronchodilator). Inhaled corticosteroids (ICS) are first-line anti-inflammatories, often paired with LABAs. SABAs provide rescue relief, and patients follow an Asthma Action Plan based on peak flow zones. 4. COPD: Progressive Airflow Limitation Pathophysiology & Presentation: Non-reversible airflow limitation is driven by chronic exposure to toxins, mainly smoking. Inflammation causes alveolar destruction (emphysema), goblet cell hyperplasia, and loss of elastic recoil. It presents with progressive exertional dyspnea, chronic cough, and a "barrel chest". Care: Diagnosed when post-bronchodilator FEV1/FVC is <70%. Key care includes smoking cessation and stepwise inhaled drugs (LAMAs, LABAs, ICS). Calorie-dense nutrition combats cachexia, while pursed-lip breathing reduces air trapping.

CC | PRIMER Lower Resp. Complications

1. Lower Respiratory Infections: Pneumonia & Tuberculosis (TB) Pneumonia: Acute lung parenchymal infection where pathogens invade via aspiration, inhalation, or blood. Inflammation increases vascular permeability, causing capillary leakage and alveolar fluid consolidation, impairing gas exchange. Clinical Rule: Initiate empiric antibiotic therapy immediately upon suspicion to reduce mortality; adjust only after culture results. Prevent aspiration pneumonia by elevating the head of the bed to ≥30° and checking the gag reflexes. Tuberculosis (TB): Airborne disease caused by M. tuberculosis. LTBI vs. Active TB: Latent TB (LTBI) is asymptomatic, non-infectious, has normal chest x-rays, and requires single-drug therapy (e.g., isoniazid). Active TB is infectious, symptomatic, and treated with a 4-drug regimen (isoniazid, rifampin, pyrazinamide, ethambutol). Clinical Priority: Due to the rise of multidrug-resistant strains (MDR-TB), Directly Observed Therapy (DOT) is the standard of care for non-adherent patients. 2. Acute Pleural & Trauma Emergencies Tension Pneumothorax: A life-threatening emergency where air enters the pleural space on inspiration but cannot escape, causing positive pressure, lung collapse, and mediastinal shift that compresses the heart and unaffected lung. Manifestations: Severe dyspnea, tachycardia, and tracheal deviation. Requires immediate needle decompression and chest tube insertion. Flail Chest: Fracture of ≥3 consecutive ribs in ≥2 places, causing paradoxical chest wall movement (moves inward during inspiration, outward during expiration). Treat with oxygen, analgesics, and positive pressure ventilation to stabilize the segment. 3. Vascular & Blockage Emergencies: Pulmonary Embolism (PE) Pathophysiology: Blockage of pulmonary arteries by a thrombus (usually from lower-limb DVT), obstructing alveolar perfusion. Diagnosis & Management: Dyspnea is the most common symptom. A spiral CT scan is the gold standard for diagnosis (or V/Q scan if contrast is contraindicated). Key Care: Administer immediate anticoagulation (LMWH or IV heparin) to prevent clot extension; long-term therapy (e.g., warfarin) continues for ≥3 months. 4. Oncologic Malignancies: Lung Cancer NSCLC vs. SCLC: Non-Small Cell (84%) grows moderately and is treated surgically if diagnosed in early stages (I–IIIA). Small Cell (SCLC, 13%) is highly aggressive, spreads early via blood and lymph (frequently to the brain), and is treated primarily with systemic chemotherapy and prophylactic cranial irradiation.

CC | PRIMER ARDS/ ARF

Acute Respiratory Failure (ARF) and Acute Respiratory Distress Syndrome (ARDS) are critical pulmonary conditions where gas exchange is insufficient to support systemic organs. The 80/20 Core: Pathophysiology & Clinical Care 1. Classification of ARF ARF is a symptom of inadequate lung function, categorized into two types: Hypoxemic (Oxygenation Failure): PaO2<60 mm Hg on room air. The core defect is inadequate O2 exchange, caused by V/Q mismatch, shunt, diffusion impairment, or alveolar hypoventilation. Shunt is an extreme mismatch where alveoli fill with fluid, making O2 therapy alone ineffective. Hypercapnic (Ventilatory Failure): PaCO2>50 mm Hg with pH<7.35. It represents insufficient CO2 removal. Primary causes include CNS depression, neuromuscular disease, chest wall abnormalities, or airway obstruction (COPD, severe asthma). 2. ARDS Pathophysiology & Phases ARDS is a progressive form of ARF triggered by direct or indirect lung injury. Its hallmark is refractory hypoxemia—unresponsive to supplemental oxygen. It progresses in three phases: Injury/Exudative (24–72 hours): Inflammatory mediators damage the membrane, causing edema. Alveolar type II cells are damaged, reducing surfactant, which causes collapse (atelectasis) and stiff lungs. Reparative/Proliferative (1–2 weeks): Fibroblasts and inflammatory cells infiltrate, increasing resistance, causing pulmonary hypertension and decreased compliance. Fibrotic/Late Phase: Diffuse scarring and remodeling further reduce gas exchange surface area, correlating with a poor prognosis. 3. Interprofessional Management Treatment focuses on treating causes, optimizing gas exchange, and avoiding complications: Ventilation Support: BiPAP decreases the work of breathing (WOB) in mild ARF. Severe ARDS requires low tidal volume (VT) ventilation (4–8 mL/kg) to prevent barotrauma/volutrauma. This causes permissive hypercapnia (allowing PaCO2 up to 60 mm Hg if pH≥7.30). High PEEP is applied to recruit collapsed alveoli. Prone Positioning: For severe ARDS with refractory hypoxemia; turning patients prone recruits dorsal alveoli, improving V/Q matching. Supportive Care: Corticosteroids reduce airway inflammation. Fluid management keeps patients "on the dry side" to minimize pulmonary edema. Enteral nutrition should begin within 24–48 hours to preserve respiratory muscle mass.

CC | PRIMER Fluid and e- Balance

Fluid Compartments & Homeostasis Distribution: Water is 50%–60% of adult weight (varies with fat). ICF holds 2/3 of water; ECF holds 1/3 (interstitial fluid/plasma). Weight change is the best fluid shift indicator (1 kg = 1 L). Capillary Exchange: Governed by hydrostatic (pushes out) and plasma oncotic (albumin pulls in) pressures. Edema occurs if hydrostatic pressure rises, oncotic falls, or lymphatics are blocked. Third-spacing traps nonfunctional fluid. Regulatory Mechanisms Hormones: Dehydration triggers thirst and pituitary ADH, raising renal water reabsorption. Aldosterone promotes sodium retention and potassium excretion. Atrial stretch releases natriuretic peptides (ANP/BNP) to excrete sodium/water. Electrolytes & Clinical Imbalances Sodium (136–145 mEq/L): Governs ECF osmolality (280–295 mOsm/kg) and impacts CNS. Hypernatremia (>145 mEq/L) causes cell shrinkage; rapid correction risks cerebral edema. Hyponatremia (<136 mEq/L) causes cell swelling; rapid correction risks osmotic demyelination. Potassium (3.5–5.0 mEq/L): Dictates membrane potentials. Hyperkalemia (>5.0 mEq/L) causes peaked T waves, wide QRS, and arrest. Treatment: stop intake, diuretics/binders, shift K+ with insulin/beta-agonists, and stabilize heart with IV calcium. Hypokalemia (<3.5 mEq/L) causes flat T waves, U waves, and weakness. IV KCl must be diluted, infused slowly (<10 mEq/hr), and never pushed. Divalent Cations: Calcium (9.0–10.5 mg/dL) is regulated by PTH and calcitonin. Hypercalcemia sedates nerves/muscles; hypocalcemia causes tetany with positive Chvostek/Trousseau signs. Magnesium (1.3–2.1 mEq/L) is vital for ATP. Hypomagnesemia (<1.3 mEq/L) resembles hypocalcemia, causing hyperactive reflexes and torsades. Acid-Base Balance (pH 7.35–7.45) Regulated by buffers, lung CO2 excretion, and renal bicarbonate/H+ control: Respiratory Acidosis: Carbonic acid excess from hypoventilation (CO2 retention). Respiratory Alkalosis: Carbonic acid deficit from hyperventilation (CO2 depletion). Metabolic Acidosis: Bicarbonate deficit or acid buildup; anion gap is 8–12 mmol/L. Metabolic Alkalosis: Bicarbonate excess or acid loss (vomiting/NG suction). Crystalloid Solutions Tonicity Effects: Hypotonic (e.g., 0.45% NaCl) dilutes ECF, swelling cells to treat hypernatremia. Isotonic (e.g., 0.9% NaCl, Lactated Ringer's) expands ECF volume without shifts. Hypertonic (e.g., 3.0% NaCl) draws water out of cells to treat hyponatremia.

CC | PRIMER Cards Assessment

1. Anatomy, Perfusion & Conduction Layers & Chambers: Heart layers: endocardium, myocardium, epicardium. Pericardium contains 10-15 mL of fluid. LV is 2-3x thicker than RV to pump into systemic circulation. Coronary Flow: Perfusion occurs primarily during diastole. LCA (branches into LAD, circumflex) supplies LV/LA/septum. RCA supplies RA/RV/posterior LV. In 90% of people, RCA supplies the AV node/bundle of His; blockages cause conduction defects. Electrical System: SA Node → AV Node → Bundle of His → Bundle Branches → Purkinje fibers (impulse in 0.12s).P wave: Atrial depolarization. QRS: Ventricular depolarization. T wave: Ventricular repolarization. U wave: Purkinje repolarization; prominent in hypokalemia. 2. Hemodynamics & Autonomic Control Metrics: CO=HR×SV (4-8 L/min). CI adjusts CO for BSA (2.8-4.2 L/min/m²). SV Determinants:Preload: End-diastolic stretch (CVP/RV: 2-8 mmHg; PAWP/LV: 6-12 mmHg). Afterload: Force opposing ejection (SVR: 800-1200). Contractility: Contraction force; increased by positive inotropes, decreased by ischemia/acidosis. Perfusion: BP=CO×SVR. MAP=3SBP+2DBP; must be >60 mmHg to prevent vital organ ischemia. Regulation: Sympathetic (β-adrenergic) increases HR/contractility; α1 receptors vasoconstrict. Parasympathetic (vagus) slows HR. Baroreceptors inhibit sympathetic tone under pressure overload, causing vasodilation and bradycardia. 3. Monitoring, Diagnostics & Care Invasive Lines: Reference arterial lines to the phlebostatic axis (4th ICS, mid-chest). Too low produces falsely high BP; too high produces falsely low BP. Monitor distal extremity hourly for neurovascular compromise. PA Catheter: Hypokalemia, hypomagnesemia, and hypoxia increase cardiac irritability, raising ventricular dysrhythmia risk during insertion. Biomarkers:Troponin (cTnT/cTnI): Choice for ACS; rises in 4-6 hrs, peaks 10-24 hrs, persists 10-14 days. BNP / NT-pro-BNP: Distinguishes cardiac vs. respiratory causes of dyspnea. Procedures:Cardiac Cath: Pre-op: NPO 6 hrs, check dye allergy, assess distal pulses. Post-op: monitor bleeding, maintain bedrest, assess perfusion, push fluids. TEE: NPO 6 hrs; post-op: withhold oral intake until gag reflex returns.

CC | PRIMER HTN

Hemodynamic Pathophysiology: Blood pressure (BP) is determined by cardiac output (CO) multiplied by systemic vascular resistance (SVR). Hypertension occurs when regulatory mechanisms (sympathetic nervous, vascular endothelium, renal, and endocrine) fail. The hallmark is persistently increased SVR, leading to vessel remodeling, atherosclerosis, and ischemia. Diagnostic Classification: Based on two or more accurate readings on separate occasions, BP is categorized as:Normal: <120 SBP and <80 DBP mmHg Elevated: 120–129 SBP and <80 DBP mmHg Stage 1: 130–139 SBP or 80–89 DBP mmHg Stage 2: >=140 SBP or >=90 DBP mmHg Target Organ Damage: Often asymptomatic ("silent killer") until severe. Complications include cardiovascular(LVH, CAD, heart failure), cerebrovascular (stroke, encephalopathy), renal (nephrosclerosis, CKD), retinal (vision loss), and peripheral vascular disease. Hypertensive Crisis: Occurs at SBP >180 and/or DBP >120 mmHg.Hypertensive Emergency: Active target organ damage exists. Requires immediate hospitalization and IV drug titration (e.g., sodium nitroprusside). The goal is to reduce Mean Arterial Pressure (MAP) by 20% to 25% to prevent ischemia. Hypertensive Urgency: No active target organ damage; managed with oral drugs (e.g., captopril, labetalol, clonidine). High-Yield Clinical Management & Interventions First-Line Pharmacotherapy: Preferred agents for Stage 1 include thiazide diuretics, calcium channel blockers (CCBs), and ACE inhibitors or ARBs. Loop or potassium-sparing diuretics may also be utilized. Orthostatic hypotension and sexual dysfunction are common side effects that hinder adherence. Actionable Lifestyle Modifications: Mandated for all elevated or hypertensive patients:Diet & Sodium: Adopt the DASH diet; restrict sodium to <=2300 mg/day (ideally <=1500 mg/day). Exercise & Weight: Minimum 150 minutes of moderate exercise per week. Weight loss reduces BP by 1 mmHg per kg lost. Substances: Avoid nicotine; limit alcohol (males: <=2 drinks/day; females: <=1 drink/day). Nursing Best Practices: Use correct cuff size (falsely high if too small). Assess for orthostatic changes (SBP drop >=20, DBP >=10, or HR increase >=20 bpm upon standing). Teach proper home BP monitoring (legs uncrossed, arm at heart level, rest 5 mins).

CC | PRIMER Heart Failure

1. Core Typology & Risk Factors HFrEF (Systolic): EF < 40%. LV is dilated/hypertrophied, unable to eject blood effectively, reducing CO. HFpEF (Diastolic): EF ≥ 50%. LV is stiff, noncompliant, causing high filling pressures and decreased filling volume. Causes: HTN and CAD are primary. Long-term HTN control reduces HF incidence by 50%. 2. Pathophysiology: The Compensation Trap Trigger: Myocardial injury -> decreased CO. Cascade:RAAS: Renal hypoperfusion triggers renin release, converting angiotensinogen to Angiotensin I, then Angiotensin II (vasoconstrictor). This stimulates water/sodium retention (via aldosterone/ADH) and myocardial fibrosis. SNS: Baroreceptors sense low BP, releasing catecholamines to increase HR and contractility, raising myocardial O2 demand. Remodeling: Chronic SNS/RAAS activation forces ventricular dilation/hypertrophy, making the heart more spherical and less effective, further declining LVEF. Counter-Regulation: Natriuretic peptides (ANP/BNP) promote vasodilation and diuresis, opposing RAAS/SNS. 3. Left vs. Right HF Left-Sided (Pulmonary Congestion): LV failure backs fluid into the left atrium/pulmonary bed. Signs: Dyspnea, orthopnea, paroxysmal nocturnal dyspnea (PND), bilateral crackles, displaced PMI, and pink, frothy sputum. Right-Sided (Systemic Congestion): RV failure backs fluid into systemic veins. Signs: JVD, peripheral pitting edema, abdominal ascites, and hepatomegaly. Left HF is the primary cause of Right HF. 4. ADHF & Diagnostics Profiles: Congestion (Wet/Dry) and perfusion (Warm/Cold). Wet-Warm (congested but perfused) is most common. Wet-Cold (fluid overload + hypoperfusion: cool extremities, low urine output, altered mentation) is critical, risking cardiogenic shock. Diagnostics: Echocardiogram is the gold standard for LVEF/structure. BNP/NT-proBNP levels correlate with LV failure severity and fluid retention. 5. Pharmacotherapy & Interventions HFrEF Survival Drugs: ACEi/ARBs/ARNIs (Sacubitril/Valsartan) and Beta-blockers (Metoprolol succinate, carvedilol) block neurohormonal activation and reverse remodeling. Aldosterone antagonists (spironolactone) and SGLT-2 inhibitors (dapagliflozin) reduce mortality. ADHF Management: Loop diuretics (furosemide) reduce preload/congestion (monitor K+/Mg++). Vasodilators (Nitroglycerin, Nitroprusside) decrease preload/afterload. Short-term IV Inotropes (Dobutamine, Dopamine) support low CO. Nursing Priorities: High-Fowler's position reduces venous return. Monitor daily weights (same scale/clothes before breakfast); notify provider of weight gain >3 lbs in 2 days or 5 lbs in a week.

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