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  • Diabetic Emergencies: Mastering DKA and HHS Crisis Management

    Diabetic Emergencies: Mastering DKA and HHS Crisis Management
    2025/11/23

    Check out ThinkLikeANurse.org

    COMPREHENSIVE NOTES

    1. Core Difference: DKA vs HHS
      DKA (Type 1 diabetic, absolute insulin deficiency)

    No insulin → body burns fat → ketones formed → metabolic acidosis

    Deep, rapid Kussmaul respirations

    Total body potassium depleted though serum may appear high

    State of starvation + dehydration

    HHS (Type 2 diabetic, relative insulin deficiency)

    Some insulin remains → prevents ketones → no significant acidosis

    Extreme hyperglycemia (often 600–1200+)

    Severe dehydration + high serum osmolality

    Slow onset, often in older adults

    1. Diagnostic Markers
      DKA Diagnostic Triad

    Hyperglycemia > 250

    Metabolic acidosis

    pH < 7.30

    Bicarb < 18

    Anion gap elevated

    Ketones moderate to large (blood or urine)

    HHS Diagnostic Markers

    Extreme hyperglycemia > 600 (often > 1000)

    Serum osmolality > 320

    Minimal or no ketones, pH > 7.3

    1. DKA Treatment Priorities (FIK Sequence)

    This is a major NCLEX priority sequence.

    F – Fluids first

    Severe dehydration: 4–6 liters lost

    Start aggressive normal saline

    About 1 liter in the first hour

    Goal: restore perfusion and blood pressure quickly

    I – Insulin second

    Only after fluids have begun

    Regular insulin IV bolus → insulin infusion

    Critical NCLEX rule: Check potassium FIRST

    K – Potassium last

    Insulin drives potassium into cells → serum potassium drops fast

    If potassium < 3.3 → HOLD insulin and replace potassium immediately

    Begin potassium replacement once potassium < 5.2 AND urine output is present

    When glucose reaches 200–250

    Switch to D5 ½ NS

    Purpose: prevent hypoglycemia while continuing insulin to clear ketones and acidosis

    1. HHS Treatment Priorities
    2. Fluids (most critical)

    Fluid loss often 9–12 liters

    More aggressive initial resuscitation than DKA

    Start 0.9% normal saline, often 1–2 liters in the first hour

    1. Slow, careful insulin

    Lower dose: ~0.05–0.1 units/kg/hr

    Begin only after fluid resuscitation

    Target glucose drop: 50–70 per hour

    Purpose: prevent cerebral edema, caused by rapid osmotic shifts

    1. Prevent thrombosis (HHS-specific)

    Hyperosmolar blood → massive thrombosis risk

    Early low molecular weight heparin unless contraindicated

    Fluid transition

    Switch fluids when glucose reaches 250–300

    Use 0.45% sodium chloride

    1. High-Yield Scenarios
      Scenario 1: DKA with potassium 3.0

    Priority:

    Start normal saline

    Hold insulin

    Immediate aggressive potassium replacement

    Once potassium rises above 3.3 → start insulin infusion

    NCLEX trap: Giving insulin first.

    Scenario 2: HHS elderly patient, glucose 1250, osmolality 400

    Priority:

    Aggressive normal saline

    Insert Foley catheter for hourly urine output

    Start LMWH for clot prevention

    Delay insulin until hydration improves

    Then start low-dose insulin infusion slowly

    1. Prevention and Patient Education
      Who is high risk for DKA?

    Type 1 diabetics

    Young adults

    Those experiencing diabetes burnout

    Patients omitting insulin doses

    Any illness that increases metabolic demand

    Discharge teaching essentials

    Sick-day rules: Never skip insulin

    Check blood glucose 4–10 times/day

    Check ketones when glucose > 250

    1. Evolving Role of Technology

    Continuous glucose monitors (e.g., Eversense 365)

    Automated insulin delivery systems

    Omnipod 5

    iLet / Twist system

    These systems significantly reduce DKA admissions (40–60%)

    Nurses increasingly become educators and system managers rather than crisis responders

    Need to reach out? Send an email to Brooke at ThinkLikeaNursePodcast@gmail.com
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    15 分
  • SIADH vs DI: Clear, Simple, & Finally Understandable

    SIADH vs DI: Clear, Simple, & Finally Understandable
    2025/11/22

    Check out thinklikeanurse.org

    Comprehensive Notes

    1. Core Concept

    Both conditions revolve around one hormone: ADH, the body’s water-saving signal.

    SIADH: Too much ADH → body holds water (soaked inside)

    DI: Not enough ADH or kidneys ignore ADH → body loses water (dry inside)

    The blood and urine move in opposite directions in each disorder.

    1. SIADH — “Soaked Inside, All Diluted”
      What Happens

    ADH is high → kidneys save water

    Blood becomes diluted

    Urine becomes concentrated

    Classic Causes

    Small cell lung cancer (ectopic ADH)

    Head trauma

    Pituitary surgery

    SSRIs

    Carbamazepine, vincristine

    Severe pneumonia, meningitis

    Severe pain or nausea

    Hallmark Labs

    Low sodium

    Low serum osmo

    High urine specific gravity

    High urine osmo

    Typical Patient Picture

    Confusion, headache, lethargy

    Weight gain (one kilogram equals one liter held)

    High blood pressure

    Puffy face or eyes

    Not thirsty

    Very low urine output, dark concentrated urine

    Priority Interventions

    Strict fluid restriction

    Daily weights

    Neuro checks every few hours

    Seizure precautions (especially when sodium drops below one twenty)

    Critical Medication

    Hypertonic saline (three percent) for seizures or very low sodium

    Must use a central line

    Must correct sodium slowly (no more than eight to twelve points in twenty-four hours)

    Major Warning

    Correcting sodium too fast risks central pontine myelinolysis, an irreversible brainstem injury.

    Never Do

    Never give hypotonic fluids

    Never give normal saline

    Never increase free water

    1. Diabetes Insipidus — “Dry Inside, All High”
      What Happens

    Little or no ADH signal

    Kidneys dump water

    Blood becomes concentrated

    Urine becomes extremely dilute

    Two Types

    Central DI

    Pituitary does not make ADH

    Causes: head trauma, brain tumors, pituitary surgery

    Nephrogenic DI

    Kidneys ignore ADH

    Causes: lithium, some antibiotics, chronic high calcium

    Hallmark Labs

    High sodium

    High serum osmo

    Very low urine osmo

    Very low specific gravity

    Typical Patient Picture

    Intense thirst

    Clear water-like urine

    Ten to twenty liters of urine per day

    Rapid weight loss

    Tachycardia, low blood pressure

    Signs of hypovolemic shock

    Priority Interventions

    Aggressive fluid replacement (D5W or free water)

    Hourly intake and output

    Daily weights

    Watch closely for shock

    Stopping the Water Loss

    Central DI: Give desmopressin (DDAVP)

    Nephrogenic DI:

    Stop lithium or offending drug

    Give a thiazide diuretic (paradox: triggers earlier sodium and water reabsorption)

    Major Warning

    Never fluid restrict DI — causes immediate circulatory collapse.

    1. SIADH vs DI: The Instant EN-KLEX Pattern
      Think Like a Nurse Bow-Tie Pattern

    Low sodium + high urine osmo → SIADH

    Action: fluid restrict

    Safety: neuro checks, seizure precautions

    High sodium + low urine osmo → DI

    Action: free water, D5W, desmopressin

    Safety: hourly intake and output, watch for shock

    1. Bedside Pearl

    If a post-pituitary surgery patient suddenly puts out large amounts of clear urine and their sodium is rising past one forty-five:
    → Stop what you’re doing and call the provider immediately.
    This is a DI crisis until proven otherwise.

    Need to reach out? Send an email to Brooke at ThinkLikeaNursePodcast@gmail.com
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    15 分
  • Respiratory Emergencies: ARDS, Pulmonary Edema & Tension Pneumothorax

    Respiratory Emergencies: ARDS, Pulmonary Edema & Tension Pneumothorax
    2025/11/22
    This episode breaks down three of the most dangerous respiratory emergencies nurses face: ARDS, cardiogenic pulmonary edema, and tension pneumothorax. Using clear bedside cues and rapid-action frameworks, you learn how to spot these crises early, understand the physiology driving them, and take the immediate steps that prevent collapse. From pink frothy sputum to tracheal deviation to refractory hypoxia, this conversation turns complex pathology into a simple action plan rooted in airway-first priorities, lung-protective strategies, and critical “never delay” rules. By the end, you’ll know exactly how to differentiate a mechanical problem, a cardiac overload problem, and an inflammatory lung problem—and what to do the moment each one appears. Need to reach out? Send an email to Brooke at ThinkLikeaNursePodcast@gmail.com
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    15 分
  • Electrolyte Emergencies: Lifesaving Moves Every Nurse Must Know for NCLEX

    Electrolyte Emergencies: Lifesaving Moves Every Nurse Must Know for NCLEX
    2025/11/22
    Check out thinklikeanurse.org for more#Comprehensive Notes##I. OverviewFocus: 6 electrolytes + 4 acid–base disordersGoal: Know one classic sign + one lifesaving intervention for eachNCLEX weight: High (8–16 questions across categories)Foundational rule: Always assess volume status first — dry vs overloaded guides almost every interventionII. SodiumA. HyponatremiaClassic sign: seizures (especially when levels plunge)Why: water shifts into brain → swelling → seizure riskLifesaving action: 3% hypertonic saline, rapid bolus for active seizureAdditional pearls:Chronic hyponatremia (e.g., “tea and toast” elderly patient): correct slowly to prevent osmotic demyelination syndromeLimit correction to 6–8 points in 24 hours once stableB. HypernatremiaClassic sign: intense thirst + confusionWhy: brain cells shrink from dehydrationLifesaving action: give free water (D5W IV, oral, or tube)Rule: correct slowly to prevent cerebral edemaIII. PotassiumA. HypokalemiaClassic sign: U-waves on ECGLifesaving action: potassium replacementSafety rules:Never exceed 10–20 per hour through a peripheral lineOral preferredReplace magnesium first—low magnesium prevents potassium correctionB. HyperkalemiaThe most urgent electrolyte emergencyClassic sign: tall peaked T-waves → wide QRS → sine-wave → cardiac arrestThree-step lifesaver sequence:Stabilize: calcium gluconate protects myocardiumShift: insulin + dextrose (or high-dose albuterol) moves potassium into cellsRemove: kayexalate, loop diuretics, or dialysisIV. Calcium & MagnesiumA. HypocalcemiaClassic signs:Chvostek sign (facial twitch with cheek tap)Trousseau sign (carpal spasm with BP cuff)Lifesaving action: slow IV calcium gluconateRisk of fast push: bradycardia, severe hypotensionB. HypermagnesemiaOften renal failure or magnesium infusionsClassic signs:Profound hypotensionLoss of deep tendon reflexes (areflexia)Lifesaving action:Stop magnesiumGive calcium gluconate to counteract cardiac depressionV. Acid–Base DisordersInterpretation Rule:pH + bicarbonate same direction → metabolicpH + CO₂ opposite directions → respiratoryClinical principle:Treat the patient before the numberVolume status affects everything.A. Respiratory AcidosisCause: CO₂ retention from hypoventilation (opioids, COPD flare)Signs: sleepiness, poor arousalLifesaving action: improve ventilation — stimulate, bilevel support, or intubateB. Respiratory AlkalosisCause: hyperventilation (pain, anxiety, early sepsis, PE)Signs: tingling around mouth and fingers, lightheadedLifesaving action: treat cause — calm anxiety, treat PE, manage painC. Metabolic AcidosisClassic sign: Kussmaul respirations (deep, rapid breathing)DKA clue: fruity acetone breathMnemonic for causes: MUDPILESMethanolUremiaDKAPropylene glycolIronLactic acidosisEthylene glycolSalicylatesLifesaving action: treat underlying causeDKA → insulinLactic acidosis → fix shockGive bicarbonate only when pH < 7.1 and patient is crashing.D. Metabolic AlkalosisCause: loss of stomach acid (vomiting, NG suction)Often causes: secondary low potassiumLifesaving action: normal saline + potassiumChloride allows kidneys to excrete excess bicarbonatePotassium replaces lossesConsider acetazolamide in severe cases.VI. Practice Scenarios (High-Yield NCLEX Style)1. Vomiting × 3 dayspH high + bicarbonate high → metabolic alkalosisInterventions: normal saline + potassium; consider acetazolamide2. Severe DKApH extremely low + bicarbonate low → metabolic acidosisFirst action: start regular insulin infusion3. Chronic COPDpH low + CO₂ high + bicarbonate high → partially compensated respiratory acidosis Need to reach out? Send an email to Brooke at ThinkLikeaNursePodcast@gmail.com
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    13 分
  • Shock, Sepsis & SIRS: Early Clues, Fast Actions & Bedside Nursing Pearls

    Shock, Sepsis & SIRS: Early Clues, Fast Actions & Bedside Nursing Pearls
    2025/11/21
    Visit thinklikeanurse.orgComprehensive Episode Notes1. What Shock Really IsCore definition: inadequate tissue perfusion, leading to anaerobic metabolism, rising acid, cellular hypoxia, and eventual organ failure.All shock types follow the same three-stage progression:Stage 1: Compensated – tachycardia, tachypnea, cool pale skin, anxiety, decreased urine output; BP may still look normal.Stage 2: Decompensated – severe tachycardia, severe tachypnea, drop in BP, narrowed pulse pressure, mental status changes, oliguria/anuria, metabolic acidosis.Stage 3: Irreversible – refractory hypotension, multiorgan failure, disseminated intravascular coagulation, poor response to pressors or fluids.2. The Big Three Shock CategoriesA. Hypovolemic Shock — “The Empty Tank”Causes: bleeding, trauma, burns, dehydration, massive fluid shifts (DKA, vomiting, diarrhea).Key assessment:Pale, cool, clammyFlat neck veinsThready pulsesLow urine outputLab clues:Low hemoglobin/hematocrit (bleeding)High hemoglobin/hematocrit (hemoconcentration from dehydration)BUN-to-creatinine ratio over 20:1 → prerenal dehydrationPriority actions:Two large-bore IVs, rapid fluid resuscitationBlood products if bleedingKeep patient warm; control source of fluid lossB. Cardiogenic Shock — “The Broken Pump”Causes: massive heart attack, myocarditis, pulmonary embolism, cardiac tamponade.Key assessment:Cold + wetJugular vein distentionCrackles, pulmonary edema, pink frothy sputumNew S3 heart soundAdvanced hemodynamics:High wedge pressureLow cardiac indexPriority actions:Avoid aggressive fluidsReduce afterloadStart inotropes (dobutamine, milrinone)Pressors if needed (norepinephrine is first-line)Immediate cardiology intervention (cath lab, mechanical support)C. Distributive Shock — “The Leaky Pipes”Includes:SepticAnaphylacticNeurogenicAdrenal crisisEarly septic shock often looks warm:Warm, flushed skinBounding pulsesWide pulse pressureHigh cardiac output, low vascular resistanceNeurogenic shock exception:Warm, dryBradycardicCaused by spinal cord injury above T63. SIRS vs. Sepsis-3SIRS (old criteria): too sensitive, not specific; triggered by many non-infectious conditions.Sepsis-3 definition:Life-threatening organ dysfunction caused by a dysregulated response to infection.SOFA ScoreICU tool measuring organ failure across six systems.QS-SOFA Bedside ScreenSuspected infection + 2 of 3:Respiratory rate 22 or higherAltered mentationSystolic pressure 100 or less→ Activate sepsis pathway immediately.4. Defining Septic ShockSepsis PLUS:Vasopressors needed to maintain a MAP of 65Lactate level over 2 despite adequate fluid resuscitation→ Mortality increases dramatically.5. Universal Nursing Actions for ShockAirway, breathing, circulation firstHigh-flow oxygenTwo large-bore IVs immediatelyGoal-directed fluidsUrine output target: 0.5–1 per hour → early marker of organ perfusionSerial lactatesFor sepsis:Blood cultures before antibiotics if no delayBroad-spectrum antibiotics within 60 minutesPressors through central line when possibleMaintain warmth; initiate stress-ulcer and DVT prevention6. 5-Minute Bedside Differentiation TriadHypovolemic: Cold + flat veinsCardiogenic: Cold + wet lungsDistributive (early septic): Hot + flushedNeurogenic: Warm + bradycardicMaster these patterns → fast, accurate recognition. Need to reach out? Send an email to Brooke at ThinkLikeaNursePodcast@gmail.com
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    13 分
  • 18 Pharmacology Red Flags With 1 Simple & Clear Action for each

    18 Pharmacology Red Flags With 1 Simple & Clear Action for each
    2025/11/21

    Check out www.thinklikeanurse.org

    1. Opioids – Respiratory Depression

    Red Flag: Respiratory rate below 8–10
    Action: Stop the infusion immediately, administer naloxone, monitor closely for re-sedation.

    2. Heparin – HIT (Heparin-Induced Thrombocytopenia)

    Red Flag: Platelets below 100,000
    Action: Stop heparin immediately, notify provider, avoid antiplatelets.

    3. Warfarin – Excessive Anticoagulation

    Red Flag: INR above 3.5–4 or any active bleeding
    Action: Hold the dose, give vitamin K (planned) or FFP (active bleed).

    4. Digoxin – Toxicity

    Red Flag: Yellow/green halos, heart rate below 60, significant nausea
    Action: Hold digoxin, draw serum level before considering antidote.

    5. Potassium Chloride – IV Danger

    Red Flag: Severe burning, rhythm changes, undiluted infusion
    Action: Stop the infusion instantly.

    6. Vancomycin – Red Man Syndrome

    Red Flag: Intense flushing and rash during infusion
    Action: Slow the infusion, pre-treat with diphenhydramine for future doses.

    7. Phenytoin – Purple Glove Syndrome

    Red Flag: Purple, swollen, painful IV site
    Action: Stop the infusion, use slow rate and inline filter for prevention.

    8. ACE Inhibitors – Angioedema

    Red Flag: Rapid swelling of lips, tongue, or face
    Action: Stop the drug immediately, never restart ACE inhibitors.

    9. Aminoglycosides – Ototoxicity

    Red Flag: New tinnitus or hearing loss
    Action: Stop the medication, check peak and trough levels.

    10. Lithium – Toxicity From Dehydration

    Red Flag: Coarse tremor, confusion, severe nausea
    Action: Hold the dose, check level, increase fluids.

    11. Serotonin Syndrome – SSRI/SNRI Emergency

    Red Flag: High fever, agitation, rigidity, hyperreflexia
    Action: Stop the medication immediately, initiate cooling and supportive care.

    12. NSAIDs/Aspirin in Children – Reye Syndrome

    Red Flag: Child with viral illness taking NSAIDs/aspirin
    Action: Stop immediately, switch to acetaminophen.

    13. Metformin – Contrast Dye Risk / Lactic Acidosis

    Red Flag: Upcoming contrast study or muscle pain/drowsiness
    Action: Hold 48 hours before and after contrast.

    14. Magnesium Sulfate – OB Toxicity

    Red Flags: Respiratory rate below 12, absent DTRs, low urine output
    Action: Stop magnesium, give calcium.

    15. Beta Blockers – Bradycardia

    Red Flag: Heart rate below 50–60 with symptoms
    Action: Hold dose, notify provider; glucagon for severe overdose.

    16. Antiplatelets (Clopidogrel/Ticagrelor) – Surgical Bleeding

    Red Flag: Scheduled surgery within 3–5 days
    Action: Hold medication pre-op (5 days for clopidogrel, 3–5 for ticagrelor).

    17. Amiodarone – Pulmonary Toxicity

    Red Flag: Persistent dry cough, new shortness of breath, abnormal chest image
    Action: Stop amiodarone, start steroids.

    18. Chemotherapy Vesicants – Extravasation

    Red Flag: Burning, swelling, pain at IV site
    Action:

    Stop the infusion

    Do NOT remove the IV

    Aspirate the drug

    Remove needle

    Apply cold (or heat for vinca alkaloids)

    Give antidote

    Need to reach out? Send an email to Brooke at ThinkLikeaNursePodcast@gmail.com
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    15 分
  • Dirty Sixty Breakdown: NCLEX Pharmacology Red-Flags & Priority Actions

    Dirty Sixty Breakdown: NCLEX Pharmacology Red-Flags & Priority Actions
    2025/11/21
    Visit thinklikeanurse.orgEPISODE NOTES1. Why Pharmacology Is the GatekeeperLargest and most feared NCLEX subsection.Students may face 20–50+ pharm questions in a row.Scoring under 58% on pharm practice drops first-time pass chance to ~30%.NCLEX repeatedly tests the same 15–20 high-danger scenarios, not broad memorization.2. The Strategy Shift: From Memorizing Everything → Knowing the Life-Threatening Red FlagsStop memorizing hundreds of drugs.Master the 60–70 prototypes (“Dirty 60”) and the red-flag dangers they carry.NCLEX focuses on:Immediate safety threatsPriority nursing actionsReversal agentsToxicity signsSafe administration rules3. The High-Yield Antidotes (Guaranteed Questions)You will see 1–3 antidote questions on the NCLEX.High-Alert DrugAntidoteHeparinProtamine sulfateWarfarinVitamin K; FFP if actively bleedingOpioidsNaloxoneBenzodiazepinesFlumazenilAcetaminophenAcetylcysteineDigoxinDigiBindMagnesium sulfate toxicityCalcium gluconateBeta-blocker overdoseGlucagon4. The “Dirty 60” Prototype DrugsPain / AnticoagulantsOpioids: morphine, hydromorphone, fentanylAnticoagulants: heparin, enoxaparin, warfarin, one DOAC (apixaban)Endocrine / DiabetesInsulins: regular, NPH, lispro, glargineMetforminCardiac / Rhythm / BP ControlDigoxinAmiodaroneAdenosineDopamineNitroglycerinMetoprololACE inhibitors (lisinopril, enalapril)ARBs (losartan)HydralazineNeurologicalPhenytoinValproic acidLevetiracetamMagnesium sulfate (OB + seizure)AntibioticsVancomycinGentamicinTobramycinCeftriaxonePsychLithiumMajor antipsychoticsMiscellaneousAcetaminophenPotassium chlorideAlbuterolLevothyroxine5. The Most Common NCLEX Red-Flag Scenarios & Priority ActionsOpioids → Respiratory Rate Below 8–10Action:Stop infusion immediatelyGive naloxoneStay with patientHeparin → HIT (Heparin-Induced Thrombocytopenia)Red flag: platelets <100,000Action:Stop heparinLabel as allergicNotify providerNever give aspirinACE Inhibitors → AngioedemaAirway emergencyAction:Stop ACE inhibitor for lifeNever restart any drug in the classVancomycin → Red Man SyndromeFlushing during infusionAction:Slow rate to 90–120 minutesPre-treat with antihistamineNot a true allergyAminoglycosides → OtotoxicityRinging, hearing lossAction:Stop drugNotify providerCheck peak/trough levelsDigoxin ToxicityRed flags:Yellow/green halosHR <60Severe N/VAction: Holds dose, check dig level, notify providerMetformin Danger SituationsRed flags:Any imaging with IV contrastMuscle pain + drowsiness → lactic acidosisAction:Hold 48 hours before & after contrastMonitor kidneysMagnesium Toxicity (OB)Red flags:Respiratory depressionLoss of reflexesAction:Give calcium gluconate6. Calculations & IV Rules (Deadly NCLEX Traps)Two formulas you must know:Dose calculations:Desired ÷ Have × VehicleIV drip rate:Total Volume ÷ Time in minutes × Drop factor50 calculation problems daily builds automaticity.7. IV Push Safety Rules the NCLEX LovesNever IV push undiluted potassium chloride (instant cardiac arrest)Fentanyl/morphine: push over 4–5 minutesAdenosine: must be pushed in 6 seconds, followed by rapid flushBlood transfusion:Two nurses verifyStay with patient for first 15 minutes8. The 8-Week Pharmacology Mastery PlanWeeks 1–2: Content OnlyMemorize Dirty 60Memorize antidote listUse Anki/QuizletNo practice questions yetWeeks 3–4: Math Weeks50 dosage calcs per dayBuild accuracy + speedWeeks 5–6: Question Immersion100 pharm questions per dayRead every rationaleWeek 7: ConsolidationWatch Simple Nursing, Mark KlimekOnly focus on high-yield drug classesWeek 8: Final PrepMixed blocksTrack pharm separatelyGoal: 65%+ (UWorld 70–80%)Three cheat sheets to print:Dirty 60Antidote chartIV push rates + insulin peaks9. Final Thought: Lithium ToxicityWhy push fluids?Because lithium is excreted entirely through the kidneys.Hydration increases clearance and prevents worsening toxicity. Need to reach out? Send an email to Brooke at ThinkLikeaNursePodcast@gmail.com
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    13 分
  • Shock, Sodium, Potassium & pH: The High-Stakes NCLEX Breakdown

    Shock, Sodium, Potassium & pH: The High-Stakes NCLEX Breakdown
    2025/11/21
    Check out thinklikeanurse.orgComprehensive Episode NotesI. The “Critical Triangle” for NCLEXFluids, electrolytes, and acid–base interpretation form the foundation of the NCLEX physiological adaptation category.Accounts for ~11–17% of exam questions.Mastery requires recognizing patterns, sequences, and priorities.II. Fluid Volume: Absolute Loss vs DehydrationA. Absolute Volume LossFluid physically leaves the vascular space.Causes: trauma bleeding, burn plasma loss, third spacing.Third spacing = fluid shifts out of vessels into unusable spaces (e.g., pancreatitis abdomen).Treatment: volume replacement.B. Pure DehydrationLoss of free water > sodium.Hallmark: high sodium (hypernatremia).Seen in elderly, confused, poor intake.Treatment: free water replacement, not saline.III. Burn Management & The Parkland FormulaEquation: 4 mL × weight × % TBSA burns (2nd & 3rd degree).Half must be given in the first 8 hours (critical due to peak capillary leak).Preferred fluid: LR (unless potassium is high).LR contraindicated in crush injuries or pre-existing hyperkalemia → switch to normal saline.Large volumes of normal saline risk hyperchloremic metabolic acidosis.IV. Fluid Overload: Early vs Late SignsEarlyBounding pulses.Widened pulse pressure.LateCrackles.JVD.Dyspnea.Early detection prevents progression to pulmonary edema or cardiogenic complications.V. Hemodynamics & Shock DifferentiationA. Hypovolemic vs Cardiogenic ShockBoth show:Low cardiac output.High SVR.Difference:Filling pressures low in hypovolemia (tank is empty).Filling pressures high in cardiogenic (pump fails; backup into lungs).B. Early Warm Septic ShockBreaks the usual rules:Low SVR from vasodilation.High cardiac output as compensation.High mixed venous oxygen (SVO2) because tissues cannot extract oxygen.Profile: High CO + Low SVR + High SVO2 = Early sepsis.VI. Potassium: The Most Lethal ElectrolyteEmergency sequence (memorize the order):Protect the heart: IV calcium gluconate.Shift potassium into cells: Regular insulin + D50, or high-dose albuterol.Remove potassium: Binders or dialysis.Critical pearlIf potassium won’t correct → check magnesium first.Low magnesium prevents potassium retention.VII. Sodium: Emergencies & Rate of CorrectionA. Low SodiumAcute symptomatic (seizing): give 3% hypertonic saline quickly.Chronic low sodium: NEVER increase more than 8–12 per 24 hours.Risk: osmotic demyelination syndrome (ODS).B. High SodiumReplace free water slowly.Do not correct faster than ½ per hour.Risk: cerebral edema.VIII. Calcium & MagnesiumLow calcium causes neuromuscular irritability:Chvostek’s sign.Trousseau’s sign.QT prolongation.Give IV calcium gluconate slowly (10–20 minutes) to prevent bradycardia.IX. Acid–Base Interpretation (NCLEX Method)Step-by-step sequencepH (acidosis, alkalosis, or compensated).CO₂ = respiratory component (moves opposite pH).Bicarbonate = metabolic component (moves with pH).Apply ROME mnemonic:Respiratory = Opposite.Metabolic = Equal.X. Metabolic AcidosisA. Normal Gap AcidosisCauses = HARD P S (focus on):D – Diarrhea (loss of bicarbonate).S – Saline overload → hyperchloremic acidosis.B. High Gap Acidosis (MUDPILES)Focus on:D – DKA (ketone acids).L – Lactic acidosis (shock, sepsis).XI. Metabolic AlkalosisMnemonic CLU → focus on U = Upper GI losses.Vomiting, NG suction = loss of hydrochloric acid.Treatment requires:Normal saline (volume).Chloride (to exchange for bicarbonate).XII. Compensation: Winter’s FormulaExpected CO₂ ≈ 1.5 × bicarbonate + 8 (±2).Use to detect mixed disorders.Example:If expected CO₂ is 21–25 but actual is 15 → metabolic acidosis with respiratory alkalosis.XIII. Priority Actions (ABCs First)Stabilize airway/breathing before calling the provider.Emergency actions:Anaphylaxis → epinephrine IM.Tension pneumothorax → immediate needle decompression.Post-op day 2–3 SOB → assume pulmonary embolism.Red man syndrome → stop infusion, antihistamine, restart slowly.HIT → stop heparin, switch to direct thrombin inhibitor.XIV. DKA & PotassiumHigh or normal potassium on arrival is misleading.Total body potassium is low.As soon as insulin is given → potassium drops fast.Anticipate and replace aggressively.XV. Mixed Disorder Example: Aspirin ToxicityStimulates respiratory center → respiratory alkalosis.Produces organic acids → high gap metabolic acidosis.Check out thinklikeanurse.org Need to reach out? Send an email to Brooke at ThinkLikeaNursePodcast@gmail.com
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    16 分