STAT Stitch Deep Dive Podcast Beyond The Bedside
Temporada 7
CC | Heart Failure
CC | Coronary Artery Disease and ACS
CC | Dysrhythmia
CC | Sepsis, SIRS, MODS, Shock
CC | GU
CC | Blood Disorders
CC | CKD & AKI (GU)
CC | Neuro Assessment
CC | ICP
por Regular Guy
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.
Atherosclerosis is the foundational pathology of coronary artery disease (CAD). It is a progressive inflammatory disease characterized by lipid deposition within the intima of the arterial wall, triggered by chronic endothelial injury from factors like tobacco smoking, hypertension, hyperlipidemia, and diabetes. The disease progresses through three key developmental stages over several decades: Fatty Streak: The earliest lesions, consisting of lipid-filled smooth muscle cells that appear yellow, starting in coronary arteries by age 20. Fibrous Plaque: Appearing by age 30, lipoproteins transport lipids into the intima, where collagen covers them to form a grayish-white plaque. This narrows the vessel lumen and reduces distal blood flow. Complicated Lesion: The most dangerous stage. Continued inflammation leads to plaque instability and rupture. This triggers massive platelet aggregation and thrombus formation on the exposed arterial wall, which can cause partial or total vessel occlusion. Collateral circulation—arterial anastomoses that bypass blockages—can develop in response to chronic, slow-developing ischemia, allowing the heart to receive adequate oxygen. However, with acute coronary occlusion or severe spasms, collateral vessels lack the time to develop, resulting in severe ischemia or myocardial infarction (MI). The 80/20 Core of CAD: Risk Factors and Clinical Variations CAD is driven by a combination of nonmodifiable and major, modifiable risk factors: Lipid Profiles: High low-density lipoprotein (LDL > 130 mg/dL) and total cholesterol (>200 mg/dL) accelerate plaque formation, whereas high-density lipoprotein (HDL, often called 'good cholesterol') protects arteries by transporting lipids back to the liver. Hypertension & Diabetes: Shearing stress from high blood pressure (>120/80 mm Hg) directly injures the endothelium. Diabetes increases CAD risk two to four times by altering lipid metabolism and promoting endothelial dysfunction. Tobacco & Lifestyle: Nicotine triggers catecholamine release (increasing heart rate and blood pressure), while carbon monoxide injures the endothelium and reduces oxygen transport. Physical inactivity and obesity further exacerbate these risks. Demographic & Sex Disparities: CAD risk increases for men over 45 and women over 55. Men typically present with typical MI symptoms and have larger coronary arteries. Women experience onset about 10 years later (partly due to loss of estrogen's cardioprotective effects post-menopause), more often present with atypical symptoms like fatigue or shortness of breath, and suffer from higher post-MI mortality and undertreatment. Genetics contribute 40% to 60% of CAD risk, primarily influencing lipid metabolism.
Cell Properties & Conduction** Heart cells have four properties: automaticity, excitability, conductivity, contractility [1, 2]. Conduction travels from the SA node (60–100 bpm) through the AV node (40–60 bpm), bundle of His, bundle branches, to Purkinje fibers (20–40 bpm) [1, 3]. Vagal tone slows heart rate (HR); sympathetic activity increases HR and contractility [1]. Resting potential features high internal K+, external Na+; depolarization (Phase 0) is rapid Na+ influx [1, 4]. ECG Basics & Waveforms Leads II and V1 are used for monitoring [2]. Grid: horizontally, small square = 0.04s, large = 0.20s; vertically, small = 0.1 mV, large = 0.5 mV [5]. * P Wave (0.06–0.12s): Atrial depolarization [6]. * PR Interval (0.12–0.20s): Atrial-ventricular conduction [6]. * QRS Complex (<0.12s): Ventricular depolarization; pathologic Q (>=0.03s) suggests MI [6]. * ST Segment (0.12s): Isoelectric line; elevation or depression indicates ischemia or MI [6]. * T Wave (0.16s): Ventricular repolarization [6]. * QT Interval (0.34–0.43s): Total ventricular depolarization/repolarization [6]. Dysrhythmias & Treatment * Sinus Bradycardia (<60 bpm): Regular. Symptomatic bradycardia is treated with atropine, transcutaneous pacing (TCP), or dopamine/epinephrine [7, 8]. * Sinus Tachycardia (101–180 bpm): Due to stress, fever, pain; treat the cause [8, 9]. * PSVT (151–220 bpm): Reentrant. Vagal maneuvers, rapid IV adenosine (causes brief asystole), BBs, CCBs, or cardioversion [8, 10]. * Atrial Flutter: Sawtooth F-waves (200–350 bpm). Rate controllers, cardioversion, or catheter ablation [8, 11]. * Atrial Fibrillation: Chaotic f-waves (350–600 bpm); irregular. Lost atrial kick drops CO; stasis risks thrombi/stroke [11, 12]. Rate control: metoprolol, diltiazem, digoxin. Stroke prevention: warfarin, apixaban [12]. * AV Blocks: 1st-degree: constant PR >0.20s [8, 13]. Type I (Wenckebach): progressive PR lengthening until QRS drops [8, 13]. Type II (Mobitz II): constant PR, random dropped QRS; requires pacemaker [8, 14]. 3rd-degree (complete): complete AV dissociation; needs TCP, dopamine/epinephrine, pacemaker [8, 14]. * PVCs: Early, wide (>0.12s) distorted QRS. R-on-T can trigger lethal VT/VF [14, 15]. * VT (150–250 bpm): Stable VT uses amiodarone/procainamide; pulseless VT needs CPR/defibrillation [15, 16]. * VF: Chaotic quivering; zero CO. Lethal. Needs CPR, rapid defibrillation, epinephrine, amiodarone [16-18]. * Asystole / PEA: No pulse. Needs CPR, epinephrine, and intubation [18]. Key Interventions * Defibrillation: Unsynchronized shock (Biphasic 120–200J, Monophasic 360J) for VF/pulseless VT [17, 19]. * Cardioversion: Synchronized shock on R-wave for unstable tachycardias [20, 21]. * Pacemakers: Demand pacing. Malfunctions: failure to sense (inappropriate firing), capture (no contraction), or pace (no spike) [22, 23]. Limit arm activity post-insertion to avoid lead displacement [24].
1. The Continuum: Perfusion Failures Shock: Decreased tissue perfusion causing a life-threatening cellular O2 supply/demand imbalance. SIRS: Systemic inflammation from infection, trauma, or ischemia, causing capillary leak and endothelial damage. Sepsis & Septic Shock: Sepsis is infection + dysregulated host response + organ dysfunction (altered mentation, SBP ≤100, RR ≥22, lactate >1 mmol/L). Septic shock is a subset with persistent hypotension requiring vasopressors to maintain MAP ≥65 mmHg despite aggressive fluid resuscitation. MODS: Failure of ≥2 organ systems. Lungs (ARDS) are usually the first to fail. 2. The 4 Main Shock Types Cardiogenic: Pump failure (commonly MI). Low CO (<4 L/min), high preload (PAWP, CVP), and high afterload (SVR). Shows pulmonary crackles, cool/clammy skin. Hypovolemic: Volume deficit (absolute: hemorrhage, GI loss; relative: burns, third-spacing). Low preload (CVP, PAWP), low CO, high compensatory SVR. Distributive: Vasodilation & relative hypovolemia.Neurogenic: Spinal injury ≥T5; loss of SNS tone causes massive vasodilation. Sign: hypotension with bradycardia, dry/warm skin. Anaphylactic: Allergic reaction causing bronchospasm, laryngeal edema, and capillary leak. First line: Epinephrine (IM/IV). Septic: Cytokine-mediated endothelial damage, microthrombi (DIC risk), and hypermetabolism. Early phase: high CO, low SVR (warm, flushed skin). Obstructive: Physical block to flow (PE, tamponade, tension pneumothorax). Shows JVD, pulsus paradoxus, low CO, high SVR. 3. Stages of Shock Initial: Cellular anaerobic metabolism, lactic acid buildup; clinically silent. Compensatory: SNS activation shunts blood to heart/brain. Tachypnea, tachycardia, cool skin (except early sepsis), activated RAAS, decreased bowel sounds. Progressive: Compensatory failure. Capillary leak (anasarca), profound hypotension (MAP <60), dysrhythmias, ARDS, ischemic gut, AKI (high creatinine, oliguria), and DIC. Refractory: Multi-organ failure, profound hypoxia, unresponsive to therapy. 4. Priority Nursing & Intensivist Actions Hour-1 Sepsis Bundle: 1) Measure/remeasure lactate if >2; 2) Blood cultures before antibiotics; 3) Broad-spectrum antibiotics; 4) 30 mL/kg crystalloid for hypotension/lactate ≥2; 5) Vasopressors (Norepinephrine is 1st choice) for MAP ≥65. Evaluation: Passive leg raise (PLR) challenge checks fluid responsiveness. Monitor urine output (goal >0.5 mL/kg/hr). Nutrition: Start trophic enteral nutrition (10 mL/hr) within 24h to protect gut mucosa.
1. Anatomy & Blood Supply The upper urinary tract has two retroperitoneal, bean-shaped kidneys (T12–L3) and 2 ureters. The lower tract comprises the bladder and urethra. Each kidney is shielded by a fibrous capsule and cushioned by fat. The functional unit is the nephron (~1 million), consisting of a glomerulus, Bowman's capsule, and tubule system (PCT, loop of Henle, DCT, and collecting ducts). Blood flow is ~1200 mL/min (20-25% of cardiac output) via the renal artery, which divides into afferent arterioles. 2. Physiology of Urine Formation Urine is formed through filtration, reabsorption, secretion, and excretion. Glomerular Filtration: Hydrostatic pressure filters blood across a porous, semipermeable membrane into Bowman’s capsule, yielding a filtrate lacking cells and large proteins. Normal Glomerular Filtration Rate (GFR) is ~125 mL/min; only ~1 mL/min is excreted as urine. Tubular Function:PCT: Reabsorbs 80% of electrolytes and water, all glucose, amino acids, and bicarbonate; secretes H+ and creatinine. Loop of Henle: Conserves water and concentrates filtrate. Descending loop is water-permeable; ascending limb actively reabsorbs Cl- and Na+ (25% of sodium load) and is water-impermeable. DCT & Collecting Ducts: Finalize regulation of water (controlled by ADH, which increases permeability) and acid-base balance (reabsorbing HCO3- and secreting H+). Aldosterone promotes Na+ and water reabsorption in exchange for K+ excretion. Atrial Natriuretic Peptide (ANP) opposes this by increasing Na+ excretion and GFR. 3. Hormonal & Regulatory Functions Erythropoietin: Released during hypoxia or hypoperfusion, stimulating RBC production (deficient in renal failure, causing anemia). RAAS: Juxtaglomerular cells release renin during hypoperfusion, low BP, or hyponatremia. Renin converts angiotensinogen to angiotensin I, which ACE converts to angiotensin II—causing vasoconstriction and aldosterone release. Prostaglandins (PGE2, PGI2): Medullary vasodilators that maintain renal blood flow and counteract vasoconstrictors. Vitamin D: Kidneys perform the final activation step of vitamin D, essential for calcium absorption. 4. Diagnostics & Assessment Key Labs: Serum creatinine is the most reliable renal function index (released at a constant rate from muscle). Creatinine clearance (24-hr urine) approximates GFR. BUN rises with dysfunction but is altered by protein intake, tissue breakdown, and hydration. Physical Exam: Involves palpation of the right kidney and indirect fist percussion of the costovertebral angle (CVA) to elicit pain in infection or obstruction. Nephrotoxic Risks: Drugs like aminoglycosides, NSAIDs, and contrast media are highly nephrotoxic. Dehydration increases the risk of contrast-induced nephropathy.
Core Clinical Concepts Blood disorders disrupt homeostasis. Key pathological threads include: Fatigue: Secondary to tissue hypoxia (anemia, cancer). Infection Risk: Compromised immunity and risk for infection is a major concern in hematologic cancers and a common side effect of therapy. Pain: Common and classic in sickle cell disease (SCD) and oncology. Perfusion & Clotting: Excessive clotting impairs perfusion; inadequate clotting causes blood loss and fluid volume deficit. Anemia: Definition & Pathophysiology Anemia is not a disease but a manifestation of an underlying pathologic process. It is defined as a deficit in red blood cell (RBC) count, hemoglobin (Hgb) quantity/quality, and/or volume of packed red blood cells (hematocrit). Tissue hypoxia drives all clinical findings. The body compensates via cardiopulmonary escalation, increasing heart rate (HR) and stroke volume to maintain cardiac output (CO). Low blood viscosity contributes to systolic murmurs and bruits. If O2 demand exceeds supply, angina or MI occurs. Chronic overwork leads to heart failure (HF), cardiomegaly, congestion, and peripheral edema. Diagnostics & Classification Diagnostics rely on CBC, reticulocyte count, and peripheral smear. Anemia is classified by: Morphology (RBC size/color): Most accurate framework.Normocytic, Normochromic (MCV 80–95 fL, MCH 27–31 pg): Caused by acute blood loss, hemolysis, CKD, cancers, or SCD. Microcytic, Hypochromic (MCV <80 fL, MCH <27 pg): Caused by iron deficiency, thalassemia, lead poisoning, B6/copper deficiency. Macrocytic, Normochromic (MCV >95 fL, MCH >31 pg): Caused by B12 (cobalamin) deficiency, folic acid deficiency, or liver disease. Etiology (Cause): Best for structuring care. Divided into decreased RBC production, blood loss, or increased RBC destruction (hereditary like SCD/G6PD vs. acquired like DIC, HELLP, prosthetic valves, or bypass). Severity & Clinical Manifestations Symptoms depend on onset speed, severity, and Hgb level: Mild (Hgb 10–12 g/dL): Often asymptomatic. Heavy exercise triggers compensatory palpitations, mild fatigue, and dyspnea. Moderate (Hgb 6–10 g/dL): Cardiopulmonary symptoms (dyspnea, palpitations) occur both during activity and at rest. Severe (Hgb <6 g/dL): Multi-system decompensation occurs.Integumentary: Pallor (shunted blood flow), jaundice (bilirubin from RBC hemolysis), and severe itching (accumulation of skin bile). Cardiopulmonary: Marked tachycardia, angina, murmurs, and congestive failure.
1. Pathophysiology AKI: Sudden, potentially reversible decline in GFR.Prerenal: Decreased perfusion (hypovolemia, shock, HF). Oliguria occurs without tissue damage; reversible with fluids. Intrarenal: Direct tissue damage, 90% from Acute Tubular Necrosis (ATN) (ischemia, sepsis, nephrotoxins). Postrenal: Mechanical obstruction (BPH, calculi) causing urine reflux. CKD: Gradual, irreversible nephron loss (GFR <60 for >3 months). Primary causes: Diabetes (50%), Hypertension (25%). Stage 5 (ESRD) GFR <15. 2. Clinical Phases & Manifestations AKI Phases:Oliguric (<400 mL/d): Fluid overload (edema, hypertension, pulmonary edema), acidosis, hyperkalemia (ECG: peaked T, wide QRS), and uremia. Diuretic (1–5+ L/d): Osmotic diuresis (high urea). Risk of hypovolemia, hypotension, hyponatremia, and hypokalemia. Recovery: GFR increases, BUN/Creatinine stabilize (takes up to 12 months). CKD Manifestations (Uremia):Cardiovascular: Leading cause of death; due to vascular calcification, volume overload, and hypertension. Hematologic: Anemia from decreased erythropoietin. CKD-MBD: Low active Vitamin D reduces calcium absorption. Hypocalcemia triggers PTH release, causing bone demineralization (osteomalacia, osteitis fibrosa) and calcifications. 3. Diagnostics & Priority Interventions Metrics: GFR is the best indicator of kidney function. Creatinine is the best AKI marker. Proteinuria is first sign of CKD. Hyperkalemia Emergency Care:Cardioprotection: IV Calcium Gluconate (stabilizes myocardium). Shift K+ Intracellularly: IV Regular Insulin + Glucose, or IV Sodium Bicarbonate. Definitive Removal: Hemodialysis or Kayexalate (avoid in paralytic ileus due to bowel necrosis). Fluid Limits: Oliguric AKI: previous 24-hr loss + 600 mL. Anemia: Exogenous EPO. Monitor for hypertension, clots; supplement iron. 4. RRT & Post-Op Care HD: Rapid fluid/solute shifts. Assess AV Fistula for thrill and bruit. Safety: No BP/blood draws/IVs in access arm. Complication: Hypotension, cramps. PD: Uses peritoneal membrane. Core complication: Peritonitis (abdominal pain, rebound tenderness, cloudy effluent). CRRT: Slow, continuous solute/fluid removal for hemodynamically unstable AKI. Transplantation: Post-op priority is fluid/electrolyte balance. Watch for massive diuresis (replace mL-for-mL) or ATN. CVD is the leading cause of death post-transplant.
1. Structure & Cellular Biology Organization: The CNS consists of the brain, spinal cord, and CN I-II. The PNS contains CN III-XII, spinal nerves, and the ANS. Cells & Myelin: Neurons conduct action potentials via saltatory conduction across nodes of Ranvier, accelerated by myelin. Astrocytes form the blood-brain barrier and create scar tissue (gliosis) upon injury. Oligodendrocytes myelinate CNS axons; Schwann cells myelinate PNS axons. Synapses: Neurotransmitters cross synapses to alter impulse transmission, using excitatory (glutamate) or inhibitory (GABA) pathways. 2. Pathways, Lobes & Perfusion Tracts: Ascending tracts carry sensory input (spinothalamic for pain/temp; dorsal columns for touch, vibration, position). Descending tracts (corticospinal) carry motor output. Motor Lesions: UMN lesions cause spasticity, hyperreflexia, and weakness. LMN lesions cause flaccidity, hyporeflexia, and muscle atrophy. Cerebral Lobes: Frontal lobe controls cognition and motor speech (Broca's). Parietal lobe senses sensory data. Temporal lobe handles hearing/language (Wernicke's); occipital processes vision. Perfusion: Anterior circulation stems from carotids; posterior from vertebral-basilar systems, joining at the circle of Willis. 3. Bedside Assessment Mental Status: Ongoing check of consciousness, orientation, cognition, and mood/affect. Cranial Nerves: CN III, IV, VI coordinate eye movements. Pupil non-constriction (CN III) is an early sign of brain herniation. Corneal reflex tests CN V/VII. Gag reflex tests CN IX/X; a weak gag risks aspiration. Midline tongue protrusion checks CN XII. Sensory & Proprioception: Test touch, pain, vibration, and digit position. A positive Romberg test indicates posterior column dysfunction. Reflexes: Deep tendon reflexes are graded 0–5. An extensor plantar response (toes up) signals an abnormal UMN lesion. 4. Diagnostics & Nursing Interventions CSF Analysis: Normal CSF is clear/colorless, with pressure of 60–150 mm H2O, protein of 15–45 mg/dL, and glucose of 40–70 mg/dL. Lumbar Puncture (LP) Care: LP is contraindicated in increased ICP due to risk of herniation. Pre-procedure, check coagulation and place the patient in a sitting/side-lying flexed position. Post-procedure, keep flat, monitor for headache, and push fluids. Aging: Aging causes cerebral atrophy, wider ventricles, reduced blood flow, and demyelination. This leads to orthostatic hypotension, poor thermoregulation, and high fall risks.
Intracranial Regulation & Monro-Kellie Doctrine The skull contains brain tissue (78%), blood (12%), and CSF (10%). Under Monro-Kellie, because this volume is constant, an increase in any one component must be offset by displacing another; otherwise, intracranial pressure (ICP) rises. Compensations include displacing CSF, collapsing cerebral veins, and compressing tissue. Decompensation causes ischemia. Normal ICP is 5 to 15 mm Hg; sustained pressure >20 mm Hg is abnormal. Cerebral Perfusion Pressure (CPP) & Blood Flow CBF requires constant O2 and glucose. Autoregulation maintains constant CBF when MAP is between 70 and 150 mm Hg. CPP = MAP - ICP. Normal CPP is 60 to 100 mm Hg; <50 mm Hg causes ischemia and neuron death, while <30 mm Hg is incompatible with life. Hypercapnia (high PaCO2) and acidosis dilate cerebral vessels, increasing CBF and ICP. Pathophysiology of Worsening ICP Insult triggers edema, compressing ventricles and vessels. This decreases CBF, causing hypoxia and brain cell death. The resulting acidosis and hypercapnia trigger vasodilation, raising blood volume and worsening ICP in a lethal feedback loop. Unrelieved pressure causes brainstem compression and downward herniation through the foramen magnum, causing respiratory arrest and death. Assessment & Clinical Findings LOC: The most sensitive indicator of neurologic status. Cushing’s Triad: Systolic hypertension with widening pulse pressure, bradycardia, and irregular respirations—an emergency indicating impending herniation. Ocular: Compression of CN III causes an ipsilateral fixed, dilated pupil, indicating herniation. Motor: Rising ICP leads to decorticate flexion (cortical interruption) or decerebrate extension (midbrain/brainstem damage; arms stiff, hyperpronated). CSF Leak: Rhinorrhea/otorrhea from basilar fractures poses a high meningitis risk. Confirm CSF via glucose testing or the halo sign (yellow ring around blood) on gauze. Interventions & Management Airway first: Intubate if GCS ≤ 8. Limit suction to <10s and 2 passes, pre-oxygenating with 100% O2. Positioning: Elevate HOB to 30 degrees midline to promote venous drainage, avoiding extreme hip/neck flexion. Osmotherapy: Give IV Mannitol (25%) or Hypertonic Saline to shift fluid from cells into vessels. Monitor sodium and osmolality. Diagnostics: Head CT is the gold standard. Lumbar puncture is contraindicated due to herniation risk. Ventriculostomy: Gold standard for monitoring ICP. Level the transducer with the tragus of the ear. If P2 wave is higher than P1, compliance is compromised.
Core Concepts & Emergency Recognition A stroke is an emergency where cell death occurs due to ischemia (inadequate blood flow, 87% of cases) or hemorrhage (bleeding, 13%). Interruption of blood flow alters brain metabolism in 30 seconds, stops it in 2 minutes, and causes cell death in 5 minutes. The FAST protocol is critical for rapid recognition: Face drooping, Arm weakness/drift, Speech difficulties, and Time of symptom onset (critical for determining treatment eligibility). Pathophysiology & Classification Ischemic Stroke: Divided into Thrombotic (60% of cases; associated with hypertension, diabetes, and atherosclerosis; symptoms develop slowly/stepwise) and Embolic (clot from the heart, often due to atrial fibrillation, travels and occludes a cerebral artery; onset is sudden with severe deficits). Hemorrhagic Stroke: Includes Intracerebral (bleeding into brain tissue, mostly caused by hypertension) and Subarachnoid (SAH) (bleeding into CSF-filled space, often from ruptured aneurysms). SAH can trigger severe vasospasms, peaking 6–10 days post-bleed. Key Diagnostics & Triage Immediate noncontrast head CT or MRI is mandatory to rapidly differentiate ischemic from hemorrhage. The NIH Stroke Scale (NIHSS) (scores 0–42) is the primary clinical tool to document baseline severity and track neurologic changes. Acute Interventions & Hemodynamic Targets Ischemic: IV tPA must be given within 3 to 4.5 hours of symptom onset after screening out hemorrhage, active bleeding, or recent trauma. Endovascular therapy with stent retrievers is highly effective. Keep BP <185/110 mmHg before tPA, and <180/105 mmHg for 24 hours after. If ineligible for tPA, lower BP only if SBP >220 or DBP >120 mmHg. Hemorrhagic: Anticoagulants and antiplatelets are strictly contraindicated. Manage hypertension to maintain SBP <160 mmHg. For SAH, administer the calcium channel blocker nimodipine to prevent vasospasm. High-Priority Nursing ADPIE Actions Airway & Aspiration: Keep the patient NPO until a formal swallowing screen is completed within 24 hours to prevent aspiration pneumonia. ICP Management: Elevate the head of bed 30°, keep head/neck in midline, and avoid hip flexion to maximize venous drainage and reduce intracranial pressure. Safety & Pattern Recognition: Left-brain stroke causes right hemiplegia, aphasia, slow/cautious behavior, and depression. Right-brain stroke causes left hemiplegia, spatial-perceptual neglect, and highly impulsive, safety-compromising behavior. Protect from injury and address one-sided neglect. VTE Prophylaxis: Implement passive/active range of motion, sequential compression devices, and low-molecular-weight heparin.