Critical care

Causes of syncope

Syncope due to AV block

Stokes-Adams attack

Investigations to be done for syncope

• ECG, echo, Holter ECG and electrophysiological studies to diagnose cause

• Upright tilt test: confirms diagnosis of vasovagal syncope

• EEG, CT, MRI: diagnose neurological cause

Differentiate seizures from syncope

Treatment of syncope

Immediate action

• Place patient in supin postion with head tilted to side to maximise cerebral blood flow

• Peripheral stimulation like sprinkling cold water over face

• Clothing should be loosened

• Patient should not be allowed to rise again till weakness no longer persists

Instructions:

• Avoid situations causing syncope

• Try to assume recumbent position as soon as they feel premonitory symptoms

What is cardiac arrest

Abrupt cessation of cardiac pump function

Causes of cardiac arrest

Management of cardiac arrest

• Initial response and basic life support

• Defibrillation

• Advanced life support

• Postresuscitation care

• Long-term management

Sequence to be followed during resuscitation of an adult

1. Assessment of unreponsiveness

2. Activation of emergency medical services

3. BLS until defibrillation is available

4. Defibrillation if indicated

5. Intubation

6. Administration of appropriate medicine

What is ACLS

• Consists of ECG monitoring, endotracheal intubation and setting up IV line in large peripheral vein or central vein

• Immediate therapy: defibrillation, O2 and cardioactive drugs

• Immediate defibrillation to be performed if ECG reveals abnormality in rhythm. If unsuccesful, patient is intubated and IV line is set up while circulation is supported by external chest compressions

• IV epinephrine results in vasoconstriction and increase CO to brain

Clinical features of Hypovolemic shock

Mild hypovolemia (loss of < 20% of blood)

• Anxiety and tachycardia

Moderate (20-40% blood lost)

• Tachycardoa, tachpnea and postural hypotension

Severe (> 40% loss of blood)

• Hypotension

• Tachycardia

• Tachypnea

• Oliguria

• Signs of reduced cerebral perfusion: agitation, confusion, drowsiness, coma

• Cold and clammy extremeties

• Reduced central venous pressure

• Multiple organ failure

Diagnosis of hypovolemic shock

• History of blood loss or fluid loss

• Occult blood loss should be considered

• Measurement of hemoglobin and hematocrit may be normal and hence misleading

Management of hypovolemic shock

• Assess ABCs

• BP, pulse rate, RR, urinary output, arterial O2 saturation and mental status should be monitored

• Volume resuscitation: isotonic saline or Ringer’s lactate given through rapid IV infusion. Blood transfusion or packed cell transfusion required when there is continuing blood loss and hemoglobin < 10 g/dL. Infusion of inotropic agents such as dopamine, dobutamine or vasopressin may be required to maintain CO

• Supplemental O2 and endotracheal intubation (if needed)

What is neurogenic shock

• Caused by traumatic high spinal cord injury, spinal anesthesia or head injury

• Warm extremeties (venodilation)

• Vagal stimulation: increase in parasympathetic tone leading to hypotension, bradycardia and syncope

Management

• Norepinephrine

• Correction of hypovolemia

Causes and treatment of obstructive shock

Clinical features of septic shock

• Fever, chills, hypotension, altered mental status and features of end organ failure

• Hypoperfusion of brain: encephalopathy causing restlessness, confusion, delirium and coma

• ARDS: due to pulmonary oedema

• Acute renal failure and acute tubular necrosis

• Increased levels of serum bilirubin and hepatic enzymes

• DIC

Causes of septic shock

Investigations to be done for septic shock

• Blood culture

• TLC: leukocytosis (polymorphonuclear leukocytosis)

• Increase serum urea and creatinine (renal dysfunction)

• Increased bilirubin and hepatic enzymes

• Low platelet count, increased PT and aPTT (DIC)

• Arterial blood gas analysis: hypoxia and metabolic acidosis

• CXR: signs of ARDS

Management of septic shock

• Empirical therapy with broad spectrum antibiotics (one from group 1 or group 2 + 3)

• Fluid administration is usually required to correct hypotension: monitorred by measuring CVP

• Inotropic or vasopressor agents may also be given for hypotension

• Associated with relative adrenal insufficiency: hydrocortisone (50 mg 6 hourly for 5-6 days)

• Drotrecogin alfa (activated human protein C) as continous infusion of 24 mcg/kg/hr for 96 hrs

Causes of cardiogenic shock

Clinical features of cardiogenic shock

• Arterial hypotension

• Weak and rapid pulse

• Cold extremeties and cyanosis

• Oliguria

• Altered mentation

• If associated with MI: severe chest pain, dypnea, anxiety, sweating, S3 gallop and systolic murmurs

• If associated with LVF: raised JVP and pulmonary rales

Investigations to be done for cardiogenic shock

• CXR, ECG and echo

Management of cardiogenic shock

• O2 inhalation to maintain PaO2 of > 60 mmHg. Endotracheal intubation and mechanical ventilation may be required

• Hematocrite maintained at > 30%

• Fluid replacement to maitain preload and ventricular function

• Pressors post adequate fluid resuscitatin

• Dopamine: variable effects according dose (low: increases GFR, moderate: increases myocardial contractility and HR, high: vasoconstriction)

• Dobutamine (2-20 mcg/kg/min). May be combined with amrinone or milrinoma

• Norephinephrine: 2-10 mcg/min

• Aortic counterpulsation

• Treatment of underlying cause

Clinical manifestations of anaphylaxis

• Skin lesions: urticaria, angioedema

• Respiratory distress due to laryngeal edema, laryngospasm or bronchospasm (feeling of tightness of chest, stridor and wheezing)

• Hypotension and shock: cold extremeties, decreased urinary output, peripheral cyanosis and altered sensorium

• GI manifestations: abdominal cramps, nausea, vomitting, diarrhea

Diagnosis of anaphylaxis

• Clinical

• Based on history

• Elevated serum tryptase during episode confirms diagnosis

Treatment of anaphylaxis

• Adrenaline 0.3-0.5 mg IM or SC. Repeated injections can be given at 20 min intervals if needed

• Higher dose + glucagon may be needed in patients on beta blockers

• Airways management: 100% O2 to be administered

• If laryngeal edema doesnt respond to epinephrine: tracheostomy

• Bronchospams: inhalation of beta 2 adrenergic agonists (terbutaline, salbutamol) and IV aminophylline

• IV fluids to maintain instravascular vol

• Hypotensive patients: vasopressors (dopamine, norepinephrine)

• H2 receptor antagonists (diphenhydramine, promethazine) useful in relieving skin symptoms and abdominal cramps

• Glucocorticoids may reduce prolonged reactions or relapses (hydrocortisone 200 mg or methylprednisolon 125 mg IV)

Causes of ARDS

Clinical features of ARDS

• Rapid onset dyspnea following causative agent within 12-48 hrs

• Tachypnea, labored breathing and intercostal retraction

• Crepts on auscultation

• Multiorgan failure

Diagnosis of ARDS

Investigations to be done for ARDS

• CXR PA view

• Arterial blood gases

• Hemogram

• Blood sugar, urea and serum creatinine

• LFT

• Serum amylase/lipase

Treatment of ARDS

• Recognition and treatment of cause

• Minimising invasive procedures

• Venous thromboembolism prohylaxis

• Management of nosocomial infection

• Mechanical ventilation: Positive pressure mechanical ventilation with lowest level of PEEP and supplemental oxygen required to maintain the PaO2 above 60 mmHg or SaO2 above 90% is used. Volume cycle ventilation with small tidal volumes have been shown to reduce mortality over standard forms of mechanical ventilation.