5.2 Dysrhythmias, ECG Interpretation, and Shock States

5.2 Dysrhythmias, ECG Interpretation, and Shock States

Cardiac dysrhythmias and acute circulatory shock represent the ultimate frontiers of acute care nursing practice. Whether managing an unexpected fatal ventricular arrhythmia on telemetry or titrating vasoactive catecholamines in distributive shock, the registered nurse must combine rapid electrophysiological pattern recognition with decisive hemodynamic intervention. Systematic assessment, flawless algorithm execution, and deep pharmacological comprehension directly determine patient survival.

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Principles of Cardiac Electrophysiology & ECG Interpretation

Cardiac contraction is governed by an intrinsic conduction system that coordinates atrial and ventricular depolarization. Standard electrocardiographic paper is calibrated along a time and voltage grid that provides precise measurements:

  1 Small Box  = 0.04 seconds  (1 mm horizontal)
  1 Large Box  = 0.20 seconds  (5 small boxes, 5 mm horizontal)
  5 Large Boxes = 1.00 second
  Voltage: 10 small boxes (2 large boxes) = 1.0 mV (vertical)

              R
             / \
            /   \
           /     \
   P      /       \          T
  ---    /         \        ---
 /   \  /           \      /   \
/     \/             \    /     \
------- Q             \--/-------
                       S
|<-- PR -->|           |<-- QT -->|
|<----- QRS ----->|

Systematic 5-Step Rhythm Strip Analysis

1. Heart Rate: Calculate ventricular and atrial rates. For regular rhythms, count the number of large boxes between two consecutive R waves and divide 300 by that number ($300 / \text{large boxes}$), or count small boxes and divide 1500 by that number. For irregular rhythms, count the number of complete R-R intervals within a 6-second strip (30 large boxes) and multiply by 10.
2. Rhythm Regularity: Measure the distance between consecutive P-P intervals (atrial rhythm) and R-R intervals (ventricular rhythm) using calipers or paper strip markers. Are intervals regular, regularly irregular, or irregularly irregular?
3. P Wave Analysis: Are P waves present? Do they exhibit uniform, smooth, upright contours in Lead II? Does a single P wave precede every QRS complex? Are P waves absent, notched, inverted, or saw-toothed?
4. PR Interval Measurement: Measure from the beginning of the P wave to the beginning of the QRS complex. Normal PR Interval: 0.12 to 0.20 seconds (3 to 5 small boxes). Represents the time required for atrial depolarization, impulse conduction through the internodal tracts, and the physiological delay at the Atrioventricular (AV) node.
   • PR > 0.20 seconds: Indicates first-degree AV block.
   • PR < 0.12 seconds: Indicates impulse originating near the AV junction or an accessory bypass tract (e.g., Wolff-Parkinson-White syndrome).
5. QRS Complex Duration: Measure from the beginning of the Q (or R) wave to the end of the S wave (J-point). Normal QRS Duration: < 0.12 seconds (less than 3 small boxes; typically 0.06 to 0.10 s). Represents rapid intraventricular depolarization via the Bundle of His, bundle branches, and Purkinje network.
   • QRS >= 0.12 seconds: Indicates intraventricular conduction delay (Bundle Branch Block), ventricular pacemaker rhythm, or ectopic ventricular focus.

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Normal Sinus Rhythm & Common Dysrhythmias

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Supraventricular Dysrhythmias: Clinical Protocols

1. Symptomatic Sinus Bradycardia

• Clinical Definition: Heart rate < 60 bpm accompanied by signs of end-organ hypoperfusion: hypotension, altered mental status, diaphoresis, acute chest pain, syncope, or pulmonary congestion.
• First-Line Pharmacological Agent: Atropine Sulfate IV 1 mg bolus. Repeats every 3 to 5 minutes up to a maximum cumulative dose of 3 mg (doses < 0.5 mg are avoided as they can induce paradoxical bradycardia via central vagal stimulation).
• Refractory Interventions: If atropine fails or is contraindicated (e.g., Mobitz II second-degree or third-degree AV block with wide QRS):
  • Immediately initiate Transcutaneous Pacing (TCP): Set demand rate at 60 to 80 bpm; titrate current (milliamperes, mA) until electrical and mechanical capture (palpable pulse matching paced spike) is confirmed. Provide analgesia/sedation.
  • Initiate continuous chronotropic infusions: Dopamine infusion (5 to 20 mcg/kg/min) or Epinephrine infusion (2 to 10 mcg/min).

2. Atrial Fibrillation (AFib)

• Pathophysiology: Micro-reentrant circuits throughout the atria generate chaotic electrical discharges (atrial rate 350 to 600 bpm), bombarding the AV node. Mechanical atrial systole ceases, reducing left ventricular end-diastolic filling and slashing cardiac output by 20% to 30%.
• Stroke Risk & Anticoagulation: Stasis of uncontracted blood in the left atrial appendage (LAA) promotes rapid thrombus formation. Embolization causes ischemic cerebral infarction.
  • Risk Assessment: Stratified using the CHA2DS2-VASc score (Congestive HF, Hypertension, Age >= 75 [2 pts], Diabetes, Stroke/TIA history [2 pts], Vascular disease, Age 65–74, Sex category female).
  • Anticoagulation Rule: If AFib has been present for longer than 48 hours (or of unknown duration), DO NOT attempt elective cardioversion without prior anticoagulation! Restoring sinus rhythm can dislodge established atrial thrombi. Patients must receive therapeutic anticoagulation (warfarin, apixaban, rivaroxaban) for at least 3 consecutive weeks prior to cardioversion and for 4 weeks post-cardioversion, UNLESS a Transesophageal Echocardiogram (TEE) conclusively confirms the complete absence of left atrial thrombi.
• Acute Ventricular Rate Control: Intravenous beta-blockers (Metoprolol 2.5 to 5 mg IV push over 2 minutes) or non-dihydropyridine calcium channel blockers (Diltiazem 0.25 mg/kg IV bolus over 2 minutes, followed by continuous IV infusion at 5 to 15 mg/hr). Target resting heart rate is < 110 bpm.

3. Paroxysmal Supraventricular Tachycardia (PSVT / SVT)

• Clinical Sequence for Hemodynamically Stable SVT:
  1. Vagal Maneuvers: First-line intervention. Instruct the patient to perform the Valsalva maneuver (bearing down against a closed glottis as if having a bowel movement for 15 seconds) or perform the Modified Valsalva (valsalva strain followed immediately by passive leg elevation to 45 degrees, which significantly increases conversion rates). Carotid sinus massage may be performed exclusively by an experienced physician after auscultating for carotid bruits.
  2. Adenosine IV Administration Protocol: If vagal maneuvers fail, administer Adenosine 6 mg rapid IV push.
     • Technique: Must be administered via a large-bore peripheral line (18G or 20G) placed in the antecubital fossa or central line. Adenosine has an ultra-short serum half-life of less than 10 seconds due to enzymatic degradation in erythrocytes and endothelial cells.
     • Administer the drug as an instantaneous rapid bolus over 1 to 2 seconds, followed IMMEDIATELY by a rapid 20 mL 0.9% normal saline flush, and elevate the patient's arm above heart level.
     • If the rhythm fails to convert within 1 to 2 minutes, administer a second dose of Adenosine 12 mg rapid IV push with the same rapid flush technique.
     • Patient Education: Warn the patient that they will experience a sudden, intense sensation of chest pressure, facial flushing, shortness of breath, and a brief feeling of 'dying.' Continuous ECG recording is mandatory during injection; anticipate a transient brief period of asystole or severe bradycardia before sinus rhythm restores.

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Life-Threatening Ventricular Dysrhythmias & Resuscitation

                                [ Adult Cardiac Arrest ]
                                           │
                              [ Call Code / Start CPR ]
                              [ Attach Monitor / Defib ]
                                           │
                               [ Analyze Rhythm ]
                                           │
              ┌────────────────────────────┴────────────────────────────┐
              ▼                                                         ▼
      [ SHOCKABLE RHYTHM ]                                    [ NON-SHOCKABLE RHYTHM ]
    VF / Pulseless VTach                                           Asystole / PEA
              │                                                         │
     1. DEFIBRILLATE ASAP                                      1. CONTINUOUS CPR (2 min)
        Biphasic: 120-200 J                                       IV/IO Access
        Monophasic: 360 J                                         Epinephrine 1 mg q3-5m
              │                                                         │
     2. CPR IMMEDIATELY (2 min)                                2. CHECK RHYTHM / PULSE
        IV/IO Access                                                    │
              │                                                3. SEARCH & TREAT 5 Hs & 5 Ts
     3. DEFIBRILLATE (Shock #2)                                   (Hypovolemia, Hypoxia,
        CPR 2 min + Epinephrine 1 mg q3-5m                         Acidosis, K+, Hypothermia,
              │                                                    Tension Pneumo, Tamponade,
     4. DEFIBRILLATE (Shock #3)                                    Toxins, Thrombosis)
        CPR 2 min + AMIODARONE 300 mg
        (Second Amiodarone dose: 150 mg)

Shockable vs. Non-Shockable Algorithms (Current Resuscitation Guidelines)

1. Shockable Pathway: Pulseless VT & Ventricular Fibrillation (VF)

• Step 1: Immediate Defibrillation. As soon as the defibrillator arrives, apply pads, clear the patient, and deliver an immediate unsynchronized shock: 120 to 200 Joules biphasic (or 360 Joules monophasic). Do not delay shock for vascular access or intubation!
• Step 2: Immediate CPR. Resume chest compressions immediately following the shock without pausing to check the rhythm or palpate a pulse. Perform 2 continuous minutes (5 cycles of 30:2 or continuous compressions at 100–120/min with an advanced airway) of high-quality CPR.
• Step 3: Rhythm Check & Second Shock. After 2 minutes, pause briefly (< 10 seconds) to evaluate the rhythm. If VF/pVT persists, deliver a second shock (equal or higher energy). Resume CPR immediately.
• Step 4: Vasopressor Administration. Administer Epinephrine 1 mg IV/IO (1:10,000 concentration) during CPR after the second shock, repeating every 3 to 5 minutes throughout resuscitation.
• Step 5: Antiarrhythmic Administration. After the third shock, administer the first dose of Amiodarone 300 mg IV/IO bolus (diluted in 20 to 30 mL D5W). If refractory, administer a second dose of Amiodarone 150 mg IV/IO after an additional 2 minutes of CPR. (Alternative antiarrhythmic: Lidocaine 1.0 to 1.5 mg/kg initial dose, then 0.5 to 0.75 mg/kg).
• Step 6: Torsades de Pointes: For polymorphic ventricular tachycardia associated with a prolonged QT interval, administer Magnesium Sulfate 1 to 2 g IV/IO diluted in 10 mL D5W over 5 to 20 minutes.

2. Non-Shockable Pathway: Asystole and Pulseless Electrical Activity (PEA)

• CRITICAL RESUSCITATION RULE: NEVER DEFIBRILLATE ASYSTOLE OR PEA! Delivering electrical shocks to a depolarized, motionless myocardium causes severe thermal and electrophysiological injury and eliminates any residual endogenous pacemaker viability.
• Resuscitation Priorities:
  1. High-quality uninterrupted CPR.
  2. Establish IV/IO access; administer Epinephrine 1 mg IV/IO immediately, repeating every 3 to 5 minutes.
  3. Secure advanced airway with continuous capnography (ETCO2 < 10 mmHg indicates ineffective compressions; sudden rise to 35–40 mmHg signifies Return of Spontaneous Circulation [ROSC]).
  4. Aggressively diagnose and treat the Reversible Causes (The 5 Hs and 5 Ts):

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Defibrillation vs. Synchronized Cardioversion

Confusing defibrillation with synchronized cardioversion is a catastrophic error on clinical licensing exams and in clinical practice.

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The Four Primary Shock States: Pathophysiology & Management

Shock is defined as an acute, progressive state of systemic circulatory collapse where cellular oxygen delivery fails to meet metabolic tissue demands, culminating in generalized cellular hypoxia, transition to anaerobic glycolysis, accumulation of systemic lactic acidosis, and multi-organ dysfunction syndrome (MODS).

$\text{Mean Arterial Pressure (MAP)} = \frac{\text{Systolic BP} + 2(\text{Diastolic BP})}{3}$

Clinical goal across all shock resuscitation protocols: Maintain MAP >= 65 mmHg to preserve vital organ (cerebral, coronary, renal) capillary perfusion.

                                  [ The Four Shock States ]
                                              │
         ┌────────────────────────────┬───────┴────────────────────┬────────────────────────────┐
         ▼                            ▼                            ▼                            ▼
   [ HYPOVOLEMIC ]              [ CARDIOGENIC ]               [ SEPTIC ]               [ ANAPHYLACTIC ]
- Fluid/Blood Loss           - Pump Failure               - Severe Infection           - Severe Allergy (IgE)
- Low Preload (CVP ↓)        - High Preload (CVP/PCWP ↑)  - Massive Vasodilation       - Histamine Release
- High SVR (Constriction)    - High SVR (Constriction)    - Low SVR (Warm/Flushed)     - Bronchospasm + Laryngeal Edema
- Cold, Clammy Skin          - Pulmonary Crackles / S3    - Warm initially -> Cold     - Urticaria / Angioedema
- Tx: 30 mL/kg Saline, PRBCs - Tx: Dobutamine, Lasix     - Tx: 1-hr Bundle, Levo      - Tx: IM Epinephrine 1:1,000

1. Hypovolemic Shock

• Pathophysiology: Decreased circulating intravascular volume due to external fluid loss (hemorrhage, severe vomiting, diarrhea, burns) or internal third-spacing (pancreatitis, bowel obstruction). Reduced venous return -> decreased end-diastolic volume (preload) -> decreased stroke volume and cardiac output. Compensatory intense peripheral vasoconstriction attempts to divert blood to vital organs.
• Hemodynamic Profile: Decreased Central Venous Pressure (CVP < 2 mmHg), decreased Pulmonary Capillary Wedge Pressure (PCWP < 6 mmHg), decreased Cardiac Output/Index, markedly elevated Systemic Vascular Resistance (SVR > 1200 dynes/sec/cm⁻⁵).
• Clinical Signs: Tachycardia, weak thready pulses, hypotension, tachypnea, cool, pale, clammy skin, flat jugular veins, collapsed peripheral veins, delayed capillary refill (> 3 seconds), oliguria (< 0.5 mL/kg/hr).
• Resuscitation Bundle:
  • Establish two large-bore peripheral IV lines (14G or 16G) or a central venous catheter.
  • Rapid fluid resuscitation: Administer isotonic crystalloids (0.9% Normal Saline or Lactated Ringer's) with an initial bolus of 30 mL/kg administered rapidly over 30 to 60 minutes via pressure infusers or rapid infuser systems.
  • Hemorrhagic Shock: Initiate Massive Transfusion Protocol (MTP) using a balanced 1:1:1 ratio of Packed Red Blood Cells (PRBCs), Fresh Frozen Plasma (FFP), and Platelets to prevent dilutional coagulopathy. Use uncrossmatched O-negative blood in extreme emergencies.
  • Patient Positioning: Place patient in the Modified Trendelenburg position (lower extremities elevated 20 degrees with trunk horizontal and head slightly elevated). Strictly avoid classic full Trendelenburg positioning, as tilting the entire torso downward compresses the diaphragm with abdominal viscera, compromises ventilation, and raises intracranial pressure without sustained hemodynamic benefit.

2. Cardiogenic Shock

• Pathophysiology: Primary myocardial pump failure resulting in inadequate cardiac output despite adequate or elevated intravascular volume. Most frequently caused by massive acute anterior STEMI destroying >= 40% of left ventricular myocardium.
• Hemodynamic Profile: Decreased Cardiac Index (< 2.2 L/min/m²), profound hypotension (SBP < 90 mmHg or MAP < 65 mmHg), markedly elevated preload (CVP > 10–12 mmHg, PCWP > 18 mmHg), and severely elevated afterload (SVR > 1400–1600 dynes/sec/cm⁻⁵).
• Clinical Signs: Hypotension, rapid thready pulse, tachypnea, severe dyspnea, bilateral diffuse pulmonary crackles, S3 gallop, elevated JVD, cool pale extremities, diaphoresis, oliguria, altered mental status.
• Resuscitation Interventions:
  • Cautious Fluid Management: Fluid boluses are strictly avoided or restricted to tiny diagnostic challenges (100–250 mL) only if PCWP is documented to be low. Indiscriminate fluids precipitate fatal pulmonary alveolar flooding.
  • Positive Inotropic Therapy: Dobutamine IV infusion (2.5 to 20 mcg/kg/min) is the inotrope of choice. Stimulates myocardial beta-1 adrenergic receptors, significantly increasing contractile force (stroke volume) with mild beta-2 vasodilation that decreases afterload. (Milrinone is an alternative phosphodiesterase-3 inhibitor).
  • Vasopressor Support: If profound hypotension (MAP < 65 mmHg) threatens coronary perfusion, initiate Norepinephrine IV to restore vascular tone without inducing excessive tachycardia.
  • Mechanical Circulatory Support: Prepare for Intra-Aortic Balloon Pump (IABP), percutaneous ventricular assist devices (Impella), or venoarterial ECMO, followed by emergent coronary angiography/PCI.

3. Septic Shock

• Pathophysiology: A life-threatening subset of sepsis characterized by profound cellular, metabolic, and circulatory abnormalities. Pathogen toxins trigger systemic inflammatory cytokine cascades (TNF-alpha, IL-1, IL-6), generating widespread endothelial injury, loss of vascular barrier integrity, capillary leak, microvascular thrombosis, and massive systemic vasodilation.
• Diagnostic Criteria: Sepsis with persistent hypotension requiring vasopressors to maintain MAP >= 65 mmHg AND a serum lactate > 2.0 mmol/L (18 mg/dL) despite adequate volume resuscitation.
• Hemodynamic Profile: Profoundly decreased SVR (< 800 dynes/sec/cm⁻⁵); initially elevated or normal Cardiac Output/Index (hyperdynamic "warm shock" phase with bounding pulses and warm, flushed extremities), transitioning to hypodynamic "cold shock" as myocardial depression ensues.
• Surviving Sepsis Campaign: The 1-Hour Resuscitation Bundle:
  1. Measure Serum Lactate Level: Remeasure within 2 to 4 hours if the initial level is elevated (> 2 mmol/L) to guide resuscitation.
  2. Obtain Blood Cultures Prior to Antibiotic Administration: Draw at least two sets of blood cultures (one percutaneous venipuncture set and one set from each vascular catheter access lumen in place > 48 hours). Do not delay antibiotics by > 45 minutes if cultures prove difficult to draw.
  3. Administer Broad-Spectrum IV Antimicrobials: Infuse empiric broad-spectrum antibiotic therapy within 1 hour of recognition.
  4. Rapid Fluid Resuscitation: Administer a minimum of 30 mL/kg of IV balanced crystalloid (Lactated Ringer's or 0.9% Normal Saline) within 3 hours for hypotension or serum lactate >= 4.0 mmol/L.
  5. Apply Vasopressors: If blood pressure is unresponsive to initial fluid resuscitation, initiate continuous vasopressors during or immediately after fluid loading to achieve target MAP >= 65 mmHg:
     • First-Line Vasopressor: Norepinephrine IV (potent alpha-1 vasoconstriction restoring systemic vascular resistance, combined with modest beta-1 inotropic support).
     • Second-Line Adjunct: Vasopressin (0.03 units/min) continuous fixed-dose infusion added to norepinephrine to raise MAP or decrease norepinephrine dosage.

4. Anaphylactic Shock

• Pathophysiology: Severe, systemic, life-threatening Type I hypersensitivity allergic reaction mediated by IgE antibodies. Upon re-exposure to an allergen (e.g., penicillin, cephalosporins, IV contrast media, blood products, latex, bee venom), the allergen cross-links IgE on the surface of sensitized tissue mast cells and circulating basophils. This triggers immediate, massive degranulation and release of pre-formed vasoactive chemical mediators (histamine, leukotrienes, bradykinin, platelet-activating factor).
• Systemic Consequences:
  • Massive arterial and venular smooth muscle dilation (precipitous drop in SVR and profound distributive hypotension).
  • Widespread capillary endothelial hyperpermeability (rapid transudation of up to 35% to 50% of intravascular fluid into interstitial spaces within 10 minutes).
  • Severe non-vascular smooth muscle contraction: profound bronchoconstriction and life-threatening upper airway laryngeal edema.
• Clinical Presentation: Explosive onset (seconds to minutes after exposure):
  • Cutaneous: Diffuse erythema, pruritus, severe urticaria (hives), angioedema (swelling of lips, tongue, uvula, periorbital tissue).
  • Respiratory: Sensation of throat tightness, hoarseness, inspiratory stridor, barking cough, diffuse expiratory wheezes, severe dyspnea, tachypnea, respiratory arrest.
  • Cardiovascular: Severe hypotension, tachycardia, weak thready pulse, circulatory collapse.
  • Gastrointestinal: Severe crampy abdominal pain, nausea, vomiting, explosive diarrhea.
• Emergency Nursing Resuscitation Protocol:

                               [ Anaphylactic Shock Emergency Protocol ]
                                                  │
                    ┌─────────────────────────────┴─────────────────────────────┐
                    ▼                                                           ▼
     [ IMMEDIATE FIRST-LINE THERAPY ]                            [ SUPPORTIVE AIRWAY & FLUIDS ]
     EPINEPHRINE INTRAMUSCULAR (IM)                             - 100% High-Flow O2 via Non-Rebreather
     - Formulation: 1:1,000 (1 mg/mL)                           - Keep Supine with Legs Elevated
     - Adult Dose: 0.3 to 0.5 mg (0.3-0.5 mL)                   - Rapid IV Crystalloids: 1 to 2 L Bolus
     - Site: Anterolateral Thigh (Vastus Lateralis)             - Prepare for Emergent Intubation
     - Repeat every 5 to 15 minutes as needed                     if Stridor / Laryngeal Edema Occurs
                    │
                    └─────────────────────────────┬─────────────────────────────┘
                                                  │
                                                  ▼
                                    [ SECOND-LINE ADJUNCTIVE DRUGS ]
                               (Given AFTER Epinephrine — Never Delay Epinephrine!)
                               - IV H1 Antihistamine: Diphenhydramine 25-50 mg
                               - IV H2 Antihistamine: Famotidine 20 mg
                               - IV Corticosteroids: Methylprednisolone 125 mg
                               - Inhaled Beta-2 Agonist: Albuterol nebulizer

1. IMMEDIATE FIRST-LINE LIFESAVING INTERVENTION: Epinephrine Intramuscular (IM) 1:1,000 (1 mg/mL).
   • Adult Dose: 0.3 to 0.5 mg (0.3 to 0.5 mL) IM administered immediately into the anterolateral aspect of the middle third of the thigh (vastus lateralis). Pediatric dose: 0.01 mg/kg (maximum 0.3 mg).
   • Why IM into the Thigh? The vastus lateralis has extensive vascularity; IM injection into the thigh achieves peak therapeutic plasma concentrations four times faster than subcutaneous injection or deltoid IM injection.
   • Repeat Dosing: Repeat the IM dose every 5 to 15 minutes if symptoms fail to improve or continue to deteriorate. Up to 35% of patients require a second dose.
   • Physiological Actions of Epinephrine:
     • Alpha-1 Adrenergic Stimulation: Powerful peripheral vasoconstriction that increases systemic vascular resistance, raises blood pressure, and reduces mucosal edema in the larynx and upper airway.
     • Beta-1 Adrenergic Stimulation: Increases myocardial contractility and heart rate to support cardiac output.
     • Beta-2 Adrenergic Stimulation: Induces potent bronchodilation, relaxes bronchial smooth muscle, and fundamentally halts further mast cell and basophil degranulation by elevating intracellular cyclic AMP.
2. Remove Antigen & Discontinue Trigger: If a parenteral infusion (e.g., antibiotic or blood transfusion) is infusing, halt the infusion immediately and replace IV tubing.
3. Airway & High-Flow Oxygen: Apply 100% oxygen via a non-rebreather reservoir mask at 15 L/min. Continuous assessment for inspiratory stridor, voice changes, or progressive laryngeal edema. Have an emergency intubation tray, video laryngoscope, and cricothyroidotomy kit at the immediate bedside. Early intubation is mandatory before complete glottic closure occurs.
4. Aggressive Fluid Resuscitation: Rapidly infuse 1 to 2 Liters of isotonic crystalloid (0.9% Normal Saline) via large-bore IV access to combat profound vasodilation and massive third-spacing.
5. Secondary Adjunctive Medications (Administered AFTER Epinephrine):
   • H1 Receptor Antagonist: Diphenhydramine 25 to 50 mg IV push (relieves urticaria and itching).
   • H2 Receptor Antagonist: Famotidine 20 mg IV (synergistic blockade with H1 antagonists against peripheral vasodilation).
   • Systemic Corticosteroids: Methylprednisolone 125 mg IV or Hydrocortisone 200 mg IV. Corticosteroids have a delayed onset of 4 to 6 hours; they do not treat acute shock but prevent late biphasic allergic reactions that recur 8 to 24 hours after initial stabilization.
   • Inhaled Bronchodilators: Albuterol (Salbutamol) 2.5 to 5 mg via nebulizer for persistent bronchospasm.