Standard Treatment Guidelines- Critical Care Medicine

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Salient points:

This article focusses on:

  1.     General assessment & resuscitation of a critically ill patient

      General guidelines


      Oxygen therapy

      Endotracheal intubation

      Difficult airway algorithm



      Warning signs of severe illness

  1.     High flow nasal oxygen therapy
  2.     Non- invasive ventilation




      Monitoring during NIV

      Weaning from NIV

  1.     Invasive ventilation


      Care of patient on ventilator

      Liberation from mechanical ventilation

  1.     Shock



      Hypovolaemic shock

      Cardiogenic shock

      Obstructive shock

      Distributive shock


  1.     Cardiac arrest in adults 

Detailed summary:



  All critically ill patients should be monitored adequately and steps should be initiated to prevent further deterioration.

–  Job responsibilities of each member during resuscitation  should be clear and appropriate.

  Team should have adequate number of staffs.

  Early assistance should be taken whenever needed from other members of the team.

  Initial aim should be to determine immediate life-threatening problems.

  Before arriving at an accurate diagnosis, physiological abnormalities should be corrected first.

  Once physiological stability is achieved, diagnosis will help in deciding treatment.

  For hemodynamically unstable patients, resuscitation should be systematic and aimed toward assessment and management of A (airway), B (breathing), and C (circulation).

  All three components should be managed simultaneously; sequential approach is not necessary. 


Obstruction may be:

  •  Partial: inspiratory stridor and retraction of neck and intercostal muscles
  • Complete: total lack of air exchange.
  • If respiration is inadequate : head-tilt–chin-lift or jaw-thrust manoeuvre should be performed.

 In patients with suspected cervical spine injuries : the jaw-thrust manoeuvre  (without the head tilt) 

Clear upper airway obstruction if present: 

  •   Upper airway obstruction indications – Snoring, gurgling sound, paradoxical movement of the chest wall, abdomen and inadequate/absent chest rise during ventilation  
  • Oral or nasal (with soft malleable catheter) suctioning for no more than 10 s at a time should be performed and oxygenation should be resumed soon after. 
  • If obstruction not cleared by suctioning – use an oropharyngeal or nasopharyngeal airway.
  •   Length of airway : equivalent to distance from the tip of the nose/angle of the mouth to the tragus.
  •   Nasopharyngeal airway diameter should be less than the patient’s nostril.
  • Complete airway obstruction is silent—intubate.
  •  Assess the need for oxygen and ventilation. SpO2 , ABG.
  • Signs of distress: Breathlessness/Tachypnea/ Inability to talk/ Open-mouth breathing/ Ala nasi flaring/accessory muscle use/Paradoxical  breathing/Restlessness/ Delirium/ Drowsiness/Cool extremities/Cyanosis/Tachycardia/ Arrhythmia/ Hypotension/ Flapping tremor
  • Features of tension pneumothorax and evidence of massive pleural effusion or hemothorax should be looked upon and drained immediately.
  • Any evidence of massive lung collapse with desaturation requires  intubation, suctioning, and positive-pressure ventilation.
  • Noninvasive ventilation can be tried in relatively stable patients if they are suffering from a condition where noninvasive ventilation has been shown to  be effective.


  • Acute exacerbation of COPD : Target: 88-92%
  • Myocardial Infarction : Oxygen administration if SpO <90%
  • Post resuscitation :  Lowest oxygen administration to achieve SpO2>94%
  • Ventilated intensive care patients : Lowest O2 to achieve SpO2 of 90-94%/PaO2 of 60-80mmHg



  1. Inability to maintain airway patency. Trauma/Foreign bodies/ Infection/ HematomaTumour/ Congenital anomalies/ Laryngeal oedema/ Laryngeal spasm
  2. Inability to protect the airway against aspiration: Head injury/Drug overdose/Cerebrovascular accident, GCS<8
  3. Anticipation of a deteriorating course that will eventually lead to respiratory failure. Eg airway burns
  4. Respiratory Failure: hypoxemia, hypercapnia.


1.Severe airway trauma where Cricothyroidotomy /tracheostomy is indicated.

Difficult airway:

Look for signs of difficult airway: Long upper incisor, inter incisor distance of less than 3 cm, Overbite,TMJ translation, mandibular space compliance, thyromental distance, short and thick neck and limited neck mobility.

Intubation cart:


  1. Working Laryngoscope blades with Mcintosh blades 
  2. Face Masks, ETT, Magill’s Forceps, Stylet, Bougie
  3. Oropharyngeal/Nasopharyngeal airways
  4. Manual self-inflating bag 
  5. Cannula/catheter
  6. Supraglottic airway devices (preferably intubating SAD)
  7. Nasogastric tube
  8. Airway exchange catheter
  9. Cricothyrotomy device-wide bore cannula, scalpel, bougie, size6mmID ETT or any commercially available cricothyroidotomy kit

Desirable :

    1. McCoy Blade
    2. Video laryngoscope
    3. Flexible fiber optic bronchoscope
  • Equipment for high flow nasal oxygenation e.g. THRIVE

Drugs Used to Facilitate Intubation

  1. Thiopental : 2.5-4.5 mg/kg for 20-50 sec
  2. Propofol : 1-2.5 mg/kg for < 60 sec
  3. Midazolam : 0.2-0.02 mg/kg for 30-60sec
  4. Ketamine: 0.5-2 mg/kg for 30-60sec
  5. Etomidate : 0.2-0.3 mg/kg for 20-50sec
  6. Fetanyl : 0.001-0.005 mg/kg for 60-90sec
  7. Succinyl choline: 1-2 mg/kg for 45-60sec
  8. Rocuronium: 0.6-1.0 mg/kg for 60-90sec

Confirm tube placement :

  • EtCO2
  • 5-point auscultation
  • Direct visualization
  • CXR if clinically indicated


  • Keep the head of bed elevated at 30–45°.
  • All ETT and tracheostomy tubes (TT) should be checked for position at incisor teeth/alae nasi, adequate fixation, patency, tracheal cuff pressure (<25 mmHg), and pharyngeal leak during each shift and should be documented.


  • Adequacy of circulation should be assessed. 
  • Check for Peripheral and central pulse for rate, regularity, volume, and symmetry
  • Skin temperature
  • Heart rate and rhythm
  • Blood pressure (supine and sitting for orthostatic hypotension)
  • Capillary refill
  • Mottling score
  • Jugular venous pressure
  • Urine output
  • Ultrasonography- Point of care
  • Echocardiography-Point of care
  • Consider invasive monitoring
  • Central venous catheter insertion
  • Arterial catheter insertion
  • Advanced hemodynamic monitoring
  • Fluid responsiveness
  • Pericardial tamponade causing hemodynamic instability requiring immediate pericardiocentesis.
  • In patients with features of severe sepsis and septic shock, early broadspectrum antibiotics AFTER Appropriate cultures and guided fluid resuscitation should be done.


  • Frequent neurological examination needs to be performed in drowsy patients
  • Hypoglycemia should be checked and corrected urgently.
  • Ongoing seizures should be controlled. 
  • Urgent antibiotics  should be given for patients with bacterial meningitis.
  • Allows for delivering up to 60 liters min-1 of gas at 37 C and with absolute humidity of 44 mg H2O litres. 
  • For oxygen therapy, HFNO enables the administering of FIO2 up to 100%.

Strengths :

  • Easy to implement & manage 
  • Minimal risk of skin breakdown
  • Lower nurse workload in  comparison with NIV
  • Stability of nasal cannula in comparison with conventional high flow nasal mask
  • No claustrophobia
  • Eating drinking communicating permitted


  • Nasal mucosal irritation
  • Discomfort
  • Runny nose
  • Pneumothorax in new born
  • Alteration of smell
  • Risk of delayed intubation

Criteria for NIV

  1. In COPD exacerbation: Conditional recommendation against
  2. In ARF due to Cardiogenic pulmonary oedema: Strong recommendation
  3. In acute Asthma: No recommendation
  4. De novo respiratory failure: No recommendation
  5. Post-operative respiratory failure: Conditional recommendation
  6. Palliation: Conditional recommendation
  7. NIV for chest trauma patients with ARF: Recommended
  8. Pandemic viral illness: No recommendation
  9. ARF following extubation from invasive mechanical ventilation: Conditional recommendation
  10. NIV to facilitate weaning from mechanical ventilation: Conditional recommendation.

Contraindication : 

  • Inability to protect the airways—comatose patients, patients with CVA or bulbar involvement, confused and agitated patients, upper airway obstruction
  • Hemodynamic instability—uncontrolled arrhythmia, patients on very high doses of inotropes, recent myocardial infarction
  • Inability to fix the interface—facial abnormalities, facial burns, facial trauma, facial anomaly
  • Severe gastrointestinal symptoms—vomiting, obstructed bowel; recent gastrointestinal surgery, upper gastrointestinal bleeding
  • Life-threatening hypoxemia
  • Copious secretions
  • Non-availability of trained medical personnel


  • NIV-PS-PEEP (in ICU ventilator) In BiPAP machine: IPAP-EPAP (Difference is the driving pressure)
  • NIV-PCV (In BiPAP machine: PAC mode)
  • BIPAP machine: Spontaneous, Spontaneous/Triggered, PAC, iVAPS are available.

Monitoring during NIV:

  • Mask comfort
  • Tolerance of ventilator settings
  •  Respiratory distress
  •  Respiratory rate
  • Sensorium
  •  Accessory muscle use
  •  Abdominal paradox
  • Ventilator parameters
  • Air leak
  • Adequacy of pressure support
  •  Adequacy of PEEP
  • Tidal volume (5–7 mL/kg)
  • Patient–ventilator synchrony
  • Continuous oximetry (until stable)
  •  ABG, baseline and 1–2 h, then as indicated

Weaning from NIV:

  • Initially, give NIPPV continuously as long as possible.
  • Once the patient is tolerating periods off NIPPV, discontinue during daytime and give during night time.
  • Time for weaning : 2-3 days


Indications :

  • Apnoea/Respiratory arrest
  • Failed NIV/NIV contraindicated
  • Hypoxemic respiratory failure: moderate to severe ARDS
  • GCS 8 or less
  • Hemodynamic instability

Care of patient on ventilatory support :

  • Analgo-sedation with Dexmeditomidine, Opioids, Benzodiazepines
  • Comfortable, Co-operative and Calm
  • Muscle relaxants are used sparingly (Severe ARDS, Intubation, prone ventilation etc)
  • Monitoring and adjustments during mechanical ventilation
  • Patients should be closely monitored. 
  • Plateau pressure should be measured at least every 4 h.
  • Institute inspiratory hold in Volume controlled ventilation to measure Plateau pressure (gives idea regarding alveolar pressure).
  • In Pressure controlled ventilation Peak pressure is taken as alveolar pressure.
  • In ARDS: Lung protective ventilation with low tidal volume (Plateau pressure <30cmH O, Transpulmonary pressure <30 cm H2O, driving pressure <14cm H2O), Respiratory rate to a maximum of 35, Set according to pH and PaCO2.
  • In COPD : prolonged expiratory phase with increased expiratory time
  • Set external PEEP to at least 80% of Auto PEEP while the patient is triggering the ventilator.
  • In case of frequent high-pressure alarm look for bronchospasm, pneumothorax, atelectasis, blockade of endotracheal tube with secretions, right main bronchus intubation, leaks.

Liberation from mechanical ventilation

  • Hospitalized adults who have been mechanically ventilated for more than 24 hours (conditional recommendation, low certainty in the evidence).
  • There is insufficient evidence to recommend any rehabilitation protocol over another.
  • Recommend ventilator liberation protocol for adults who have been mechanically ventilated for more than 24 hours.
  • Perform a cuff leak test in mechanically ventilated patients who meet extubation criteria and are deemed high risk for post extubation stridor.
  • For adults who have failed a cuff leak test – administering systemic steroids at least 4 hours before extubation,


  • The underlying reason for MV has been stabilized and the patient is improving.
  • Patient is hemodynamically stable on minimal-to-no pressors.
  • Oxygenation is adequate (e.g., PaO2 /FiO2 > 200, PEEP < 5–8 cmH2O, FiO2 < 0.5). 
  • Patient is able to initiate spontaneous inspiratory efforts.
  • Patient should be afebrile (temperature <38°C), have stable metabolic status (pH>7.25), adequate hemoglobin and adequate mentation (e.g., arousable, Glasgow coma scale >13).

Predictors of successful weaning

  • Rapid shallow breathing index (RSBI) is assessed by putting patient on PS PEEP
  •  RSBI=RR/TV in litre
  •  Less than 100 is predictor of successful weaning.
  • The threshold of 100 is not binding and can be relaxed by 10–20 in patients with endotracheal tube size less than 7 and in women.
  • Minute ventilation less than 10 L/min.
  • Respiratory rate (RR) less than 35 breaths/min.
  •  Maximum inspiratory pressure more negative than −30 cm H2O.

Wearing Process

  1. SAT:
  • Stop continuous infusion of sedation daily
  • Communicate with patient, explain the procedure, and calm them.
  • Baseline parameters should be recorded and flow sheet at the patient’s bedside should be kept.
  • Keep calm peaceful environment and have the nurse or physician remain at the bedside to offer encouragement and support.
  1. Identification of failed SAT:
  • Anxiety, agitation, or pain
  • Respiratory rate >35/min
  • SpO2 <88%
  • Respiratory distress
  • Acute cardiac arrhythmia
  1. Do spontaneous breathing trial (SBT)
  • Whenever possible, position the patient upright in bed.
  • Endotracheal tube should be thoroughly suctioned and patency should be ensured.
  • Following modes can be chosen for SBT: T- piece, Pressure support ventilation.
  1. Monitor closely
  2. Extubate patient.

Checklist for Identifying candidates for a trial of spontaneous breathing

  • Respiratory: PaO2 /FiO2 >150-200 with FiO2 <50% and PEEP <8mmHg, PaCO2 Normal  or at baseline levels, Patient is able to initiate an inspiratory effort
  • Cardiovascular: No evidence of myocardial ischemia. Heart rate <140 bpm, Bp adequate with minimal or No vasopressors
  • Appropriate Mental status: Patient is arousable or GCS>13
  • Absence of Correctable Comorbid conditions: No fever, No significant electrolyte abnormalities

SBT Failure

Objective measurement

  • PaO2<50-60mmHg on FiO2 >0.5 or SaO2<90%
  • PaCO2 >50mmHg or an increase inPaCO2 >8mmHg
  • pH<7.32 or a decrease in pH>0.07
  • Rapid Shallow breathing index >105RR>35 or an increase of >50%
  • RR>35 or an increase of >50%
  • Heart rate >140 or increase of >20%
  • Systolic blood pressure>180 or an increase of > 20%
  • Systolic pressure<90
  • Cardiac arrhythmias

Subjective clinical assessment

  • Agitation and anxiety
  • Depressed mental status
  • Diaphoresis
  • Cyanosis
  • Evidence of increasing effort: Increasing accessory muscle use, facial signs of distress, Dyspnea.
  1. After extubation, the patient should be observed closely for signs of extubation failure as:
  • RR more than 25/min for 2 h
  • Heart rate more than 140 beats/min or sustained increase or decrease of more than 20%
  • Clinical signs of respiratory muscle fatigue or increased work of breathing
  • SaO2 less than 90%; PaO2 less than 80 mmHg, on FiO2 more than 0.50
  • Hypercapnia (PaCO2 >45 mmHg or >20% from pre extubation), pH < 7.33
  1. Try noninvasive ventilation (NIV)
  2. Identify difficult weaning

          Patients who fail initial weaning and require up to three SBT or as long as 7 days from the first SBT to achieve successful weaning.

  1. Causes of weaning difficulty

           Detailed examination of the patient should be done and causes of difficult weaning should be identified.

  1. Treat all the reversible causes
  2. Weaning process in difficult weaning

               1.Select the mode of ventilation: 

              – Provide adequate respiratory support and prevent diaphragmatic atrophy.

               – Pressure support ventilation 

               – Continuous positive airway pressure (CPAP)

               – Automatic tube compensation

             2.Plan tracheostomy.

  1. Do aggressive physiotherapy and mobilization
  1. Decide about home ventilation
  1. SHOCK

Definition: “a life-threatening, generalized form of acute circulatory failure associated with Inadequate oxygen utilization by the cells”.


  • Hypovolemic shock:

Hemodynamic changes : decreased preload, CO, increased SVR

Etiology: hemorrhage, capillary leak, GI losses, bums

  • Cardiogenic shock:

Hemodynamic changes : Increased Preload, after load, SVR, Decreased CO

Etiology : MI, dysrhythmias, heart failure, valvular disease

  • Obstructive shock:

Hemodynamic changes: Decreased preload, Increased SVR, decreased CO

Etilogy : PE, Pericardial tamponade, pneumothorax, LV outlet


  • Distributive shock : 

Hemodynamic changes: Decreased preload, Increased SVR, Mixed CO

Etilogy : Septic shock, anaphylactic shock, neurogenic shock


  1. Hemmorhagic shock:
  •  Assessment of  the severity of the patient and identification of the source of bleeding is crucial
  • Serial measurements of hematocrit, lactate, base deficit, and monitoring of coagulation with conventional tests and viscoelastic methods should be done 
  • Initial Management: arrest ongoing bleeding, to restore the effective circulating blood volume, and to restore tissue perfusion.
  • Damage control resuscitation (DCR)
  • Target Blood pressure: systolic blood pressure of 80–90 mmHg is recommended.
  • Type of fluid:
  • Blood
  • Synthetic Colloids to be avoided.
  • Crystalloids:
  • 0/9% Saline: Can use in TBI. Complication: Normal
  • Anion gap metabolic acidosis and AKI.
  • Avoid hypotonic crystalloids in TBI
  • Balanced salt solution: can be used
  • Vasopressors:Required in the life-threatening hypotension
  • Temperature control: Hypothermia in hemorrhagic shock should be prevented and warm the patients with hypothermia using measures such as removing wet clothing, covering the patient, infusion of warm fluid, forced warm air, and rewarming devices
  • Tranexamic Acid: reduced organ failure and mortality in traumatic shock patients. Dose: loading dose of 1 g over 10 min, followed by infusion of 1 g over 8 h within 3 hrs
  • Control of bleeding:
  • Tourniquets and Pelvic binders
  • Angiographic embolization
  • Endoscopic Hemostasis and Interventional Approach
  • Resuscitative Endovascular Balloon Occlusion of the Aorta (REBOA) (Weak evidence)
  • Ca++ correction
  • Correction of pH, Fibrinogen


  • Systolic BP <90 mmHg despite adequate filling status with signs of hypoperfusion.
  • Occurs due to primary failure of the ventricles of the heart to function effectively.

Causes :

Acute Myocardial infarction

  • Pump failure
  • Mechanical complications
  • RV infarction

Other conditions

  • End stage cardiomyopathy
  • Myocarditis
  • LV outlet obstruction
  • Acute MR

Cardinal manifestations

  • Oliguria and worsening renal function.
  • Metabolic acidosis due to increased production and decreased clearance of lactate.
  • Mental status changes ranging from confusion to coma.
  • Cool, clammy skin due to intense vasoconstriction. In patients with distributive shock and low systemic vascular resistance (SVR), extremities may be warm and flushed.

Investigations: Chest X-ray, ECG, and echocardiograph, Troponins, NT Pro BNP


  • Hemodynamic monitoring should complement (and not replace) other markers of end-organ perfusion in CS.
  • Assess the adequacy of end-organ and tissue perfusion in response to individualized targets by integrating serial markers of systemic perfusion, including (but not limited to) arterial lactate, mixed or central venous oxygen saturations, urine output, creatinine, liver function tests, mental status, temperature, and other invasive hemodynamic variables.
  • Recommend an early invasive strategy with appropriate revascularization for all suitable patients with suspected ACS-associated CS, including patients with uncertain neurological status or those who have received prior fibrinolysis, regardless of the time delay from MI onset.
  • Prepare for revascularization in the cardiac catheterization laboratory or surgical intervention for mechanical failure.
  • Hemodynamic support: Fluid is given in RV infarct with hypotension.


  1. Wet CS : dopamine inotrope/ NE
  2. Euvolemic cold and dry CS : NE/Dopamine Inotropic agent and Small fluid boluses
  3. Vasodilatory warm & wet or mixed cardiogenic and vasodilatory CS : NE
  4. RV shock: Fluid boluses, NE, Dopamine or vasopressin, inotropes, inhaled pulmonary vasodilators


  • Form of shock associated with mechanical obstruction of blood flow to the heart, specifically left ventricle.
  • Tension pneumothorax, Cardiac tamponade, Pulmonary embolism
  • Detailed history is taken.


  •  Airway
  • Oxygen supplementation / Ventilatory support
  • Tension Pneumothorax:

         Clinical features: 

  • tracheal deviation toward the contralateral side of tension pneumothorax,
  • hyper-resonance
  • diminished lung sounds on the affected side
  • subcutaneous emphysema
  • neck vein engorgement.
  • Persistent shock may result in the bradycardia and pulseless electrical activity arrest.

Investigations: USG lung, Chest X-ray, CT

Treatment: Immediate Needle decompressionICD

  • Pulmonary Embolism:

Probability score;

          Wells Probability score for Pulmonary Embolism

  • Clinical signs & symptoms of DVT   –  3
  • Pulmonary embolism is most likely diagnosis – 3 
  • Tachycardia>100 bpm –  1.5 
  • Immobilization or surgery in previous 4 weeks – 1.5
  • Hemoptysis –  1
  • Active malignancy –  1


  •  Low risk:<2
  • Intermediate risk 2-6
  • high>6
  • Pulmonary embolism unlikely0-4, likely >4 points.

Preferred imaging method for the diagnosis of acute PE in patients with either a high clinical (pre-test) probability or low/intermediate probability and elevated D dimer levels: CT pulmonary angiography

Adverse Prognosis in Acute Pulmonary Embolism

  •  ECG: Sinus tachycardia, New onset atrial arrhythmias, New RBBB, QR pattern in V1, S1Q3T3, T inversion In V1 through V4
  • Biomarker: Elevated Troponin, Elevated BNP and N terminal pro- BNP
  • CT: RV diameter/LV diameter >0.9, Ventricular septal bowing from Right to left, presence of RV enlargement
  • Echocardiography: RV dilatation and hypokinesis, RV/LV diameter>0.9, interventricular septal flattening and paradoxical leftward septal motion,Presence of TR., presence of PH (peak tricuspid jet velocity greater than 2.6m/s and loss of respiratory phasic IVC collapse, RV free wall hypokinesis with apical sparing (McConnell’s sign)


  • Systemic thrombolysis
  • IVC filter
  • Cardiac Tamponade

Acute circulatory failure due to the compression of the cardiac chambers by the pericardial effusion.

Signs & Symptoms: 

  • Dyspnoea at rest and with exertion
  • Tachycardia
  • Narrow pulse pressure
  • Neck vein engorgement
  • Pulsus paradoxus.


  • Chest radiography: Enlarged heart silhouette and epicardial fat-pad sign
  • ECG: Low-voltage QRS complexes, electrical alternans.

Treatment : Pericardiocentesis




  •  Intravascular volume depletion
  • Cardiac dysfunction
  • Peripheral vasodilation


  • Crystalloids
  • Synthetic colloids: Increased mortality & AKI, Do Not USE
  • Assess responsiveness: dynamic parameters better
  • Appropriate broad-spectrum antibiotics
  • Non responsive to Fluid resuscitation
  • Noradrenaline is preferred
  • Dopamine: ONLY if relative bradycardia present
  • MAP target: 65mmHg
  • Steroid supplementation when on increasing dose of vasopressin. HC 200mg over 24hrs or 50mg 6 Hourly
  • Stop steroids once resolution of shock

Definition : 

Anaphylaxis is an acute, potentially lethal, multisystem syndrome resulting from the sudden release of mast cell, basophil, and macrophage-derived mediators into the circulation.

Basic initial management :

  • Remove exposure to the trigger
  • Assess circulation airway, breathing, mental status, skin and body weight
  • Call for help
  • Inject Epinephrine IM in mid-anterolateral aspect of thigh 0.01 mg/kg of 1:1000 solution,to a maximum of 0.5 mg; repeat in 5- 15min
  • In case of respiratory distress or vomiting, place the patient on his back and elevate lower extremities.
  • Supplementary oxygen (6-8LPM) by face mask
  • Intravenous access should be established with wide bore cannula. When indicated give 1-2L of 0.9% saline rapidly
  • When indicated initiate cardiopulmonary resuscitation with continuous chest compressions
  • Tryptase and compliment can help in diagnosis

Airway management :

  • Rapid assessment.
  • Intubate patients with airway compromise
  • Early intubation to be considered if significant edema of tongue, uvula, or voice alteration has developed.


  • Standard of care for anaphylaxis.
  • Dose: 0.01 mg/kg of a 1:1000(1 mg/mL) solution, to a maximum of 0.5 mg in adults. Dose can be repeated every 5–15 min, as needed.
  • Route of administration : intramuscular route in the mid-anterolateral thigh
  • Can be given by slow intravenous infusion with diluted solution 1:10,000 (0.1 mg/mL), with the dose titrated according to non-invasive continuous monitoring of cardiac rate and function
  • Patients with orthostasis, hypotension, or incomplete response to epinephrine should receive fluid resuscitation with isotonic saline.

Glucocorticoids :

  •  Not lifesaving in initial hours of an anaphylactic episode
  • Delayed onset of 4 to 6 hours.
  • Prevents rebound anaphylaxis


  • Should not be substituted for epinephrine because they have minimal alpha-1 adrenergic agonist vasoconstrictor effects and do not prevent or relieve laryngeal edema and upper airway obstruction, hypotension, or shock.


  • First line:
  • Epinephrine 1:1000 IM max 0.5mg
  • Fluids
  • Oxygen
  • Second line:
  • H1 antihistamine iv Chlorpheniramine 10 mg
  • Beta 2 adrenergic agonist-Salbutamol 2.5mg/3ml via nebuliser
  • Glucocorticoid iv Hydrocortisone 200 mg or methyl prednisolone 50-100 mg
  • H2 antihistamine iv Ranitidine 50mg
  • Refractory anaphylaxis:
  • Adrenaline
  • Norepinephrine
  • Vasopressin
  • ECMO
  • Recurrent anaphylaxis :
  • Epinephrine auto injector.


AHA ACC 2015 Guidelines

  • Early CPCR
  • No interruptions
  • C-A-B
  • Early defibrillation for shockable rhythms
  • After return of “spontaneous circulation”, try to identify cause of arrest and treat
  • Surveillance for and prevention of in hospital cardiac arrest.

When to start CPCR:

  • Unresponsiveness
  • No breathing / gasping
  • No definite pulse ( pulse check not > 10 sec )

Steps of CPCR: C-A-B

C : COMPRESSIONS-Rate:100 to 120/min. Depth of at least 2 inches (5 cm)

for an average adult, while avoiding excessive chest compression depths

(greater than 2.4 inches [6 cm]).

Note : When an AED is immediately available, it is reasonable to use the defibrillator as soon as possible.


  • Perform chest compressions at 100-120/min
  • Compress to a depth of 5-6cms
  • Allow full recoil after each compression
  • Minimize pauses in compressions
  • Ventilate adequately (2 breaths after 30 compressions, each delivered over 1 second, each causing chest rise)


  • Compress at a rate slower than 100/min or faster than 120/min
  • Compress to a depth of less than 2 inches (5cms) or greater than 2.4 inches (6cms)
  • Lean on the chest between compressions
  • Interrupt compressions for greater than 10 seconds
  • Provide excessive ventilation (i.e too many breaths or breaths with excessive force)


  • Open up airway
  • Head tilt chin lift mouth open
  • Jaw thrust
  • Oropharyngeal / nasopharyngeal airway
  • LMA/COPA/cricothyroidotomy/tracheostomy


  • Rate: compression relaxation ratio: 30:2
  • Rate: 10 breaths/ min
  • Adrenaline: along with 2nd cycle or earlier dose: 1mg every 3-5 mins


When defibrilator arrives : check rhythm

Shockable rhythms:

  • Ventricular Fibrillation, Pulseless Ventricular Tachycardia
  • Energy for first shock: 120-200
  • Soon after shock start CPR
  • After 5 cycles of 30:2 look for rhythm
  • Energy for second shock may be higher than first
  • Along with the third shock consider: Inj. Amiodarone for VF/pulseless VT NOT responding to 3 shocks

Non-shockable rhythms:  Pulseless electrical activity and asystole

  • Start CPCR, Inj. Adrenaline.
  • Check for 5Hs & 5Ts, continue CPCR
  • Hs: Hypovolemia, Hypoxia, H+ ion excess, Hyper/Hypokalemia,Hypothermia
  • Ts: Tension Pneumothorax, Thrombosis-Coronary, Thrombosis- Pulmonary, Toxin, Tamponade-cardiac
  • Check for return of spontaneous circulation (ROSC) during rhythm analysis

Post cardiac arrest care:

  1. 12 lead ECG
  2. Angiogram: CAG should be performed emergently for OHCA patients with suspected cardiac etiology of arrest and ST elevation on ECG
  3. Hemodynamic goals: Avoid immediate correction of hypotension (Systolic BP<90,MAP<65mmHg)
  4. Targeted temperature management :
  • Constant temperature between 32- 36 C
  • Prevent fever in comatose patients after TTM
  • Rewarming rate: 0.5 / hour
  1. Seizures :EEG to be performed to diagnose seizures
  2. Ventilation: Maintain PaCO2 within physiological range
  3. Oxygenation : SpO2 94% OR greater

CPCR in pregnancy :

Position: manual left uterine displacement

Evacuation of gravid uterus: perimortem cesarean delivery in later half of pregnancy if not achieving ROSC with usual resuscitation and LUD.

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