INITIAL APPROACH AND MANAGEMENT IN SHOCK
Transcript of INITIAL APPROACH AND MANAGEMENT IN SHOCK
SHOCK IS A STATE OF CIRCULATORY INSUFFICIENCY THAT CREATES AN IMBALANCE BETWEEN TISSUE OXYGEN SUPPLY (DELIVERY) AND DEMAND (CONSUMPTION), RESULTING IN END-ORGAN DYSFUNCTION.
Tintinalli’s emergency medicine 9th edition
DEFINITION OF SHOCK
SHOCK
COMPENSATORY MECHANISMS
▸ Arteriolar vasoconstriction > redistribution of blood flow from skin, skeletal muscle, kidney, splanchnic viscera
▸ Increase HR, contractility > increase CO
▸ Constriction of venous capacitance vessels > augment venous return
▸ Release vasoactive hormones (epinephrine, norepinephrine, dopamine, cortisol) > increase arteriolar and venous tone
▸ Release antidiuretic , activated renin-angiotensin axis > maintain intravascular volume
CLINICAL PRESENTATION
Organ system Signs and symptoms
CNS Mental status change
CVS Tachycardia, arrythmia, hypotension, new murmur, low quality of pulse, increase or decrease JVP
Respiratory Tachypnea, cyanosis
Renal Reduce GFR , oliguria
Skin Pallor, pale, dusky, clammy, cyanosis, sweating, cool, and capillary refill time >2–3 s.
Metabolic Lactic acidosis, hyperglycemia, hypoglycemia, and hyperkalemia
INITIAL APPROACH AND MANAGEMENT IN SHOCK
CLASSIFICATION OF SHOCK
▸ MAP = CO x SVR
▸ MAP = ( SV x HR ) x SVR
▸ MAP = ( EDV - ESV ) x HR x SVR
▸ MAP = EDV/EDV x ( EDV - ESV ) x HR x SVR
▸ MAP = EDV x (EDV-ESV)/EDV x HR x SVR
▸ MAP = EDV x EF x HR x SVR
▸ MAP = Preload x Contractility x Rhythm x Afterload
INITIAL APPROACH AND MANAGEMENT IN SHOCK
CLARIFICATION OF SHOCK
▸ Hypovolemic shock
▸ Distributive shock
▸ Cardiogenic shock
▸ Obstructive shock
CLASSIFICATION OF SHOCK
HYPOVOLEMIC SHOCK
▸ Decreased intravascular fluid or decreased blood volume causes decreased preload, stroke volume, and cardiac output (CO).
▸ This action may lead to an autonomic increase in the systemic vascular resistance (SVR).
▸ MAP = Preload x Contractility x Rhythm x Afterload
CLASSIFICATION OF SHOCK
DISTRIBUTIVE SHOCK
▸ There is relative intravascular volume depletion due to marked systemic vasodilatation.
▸ This is most commonly seen in septic shock . Anaphylaxis, adrenal insufficiency, and neurogenic shock are additional causes of distributive shock
▸ MAP = Preload x Contractility x Rhythm x Afterload
CLASSIFICATION OF SHOCK
CARIOGENIC SHOCK
▸ The left ventricle fails to deliver oxygenated blood to peripheral tissues due to variances in contractility, as well as preload, afterload, right ventricular function.
▸ Myocardial infarcion is the most common cause of cardiogenic shock.
▸ MAP = Preload x Contractility x Rhythm x Afterload
CLASSIFICATION OF SHOCK
CARIOGENIC SHOCK
▸ Dysrhythmias are another common cause because they can lead to a decreased CO.
▸ Bradyarrhythmias result in low CO,
▸ Tachyarrhythmias can result in decreased preload and stroke volume.
▸ MAP = Preload x Contractility x Rhythm x Afterload
CLASSIFICATION OF SHOCK
OBSTRUCTIVE SHOCK
▸ Decrease in venous return or cardiac compliance due to an increased left ventricular outflow obstruction or marked preload decrease.
▸ Cardiac tamponade, pulmonary embolism, and tension pneumothorax are causes of obstructive shock
▸ MAP = Preload x Contractility x Rhythm x Afterload
RESUSCITATION
CIRCULATION
▸ To find cause and correct them
▸ Optimization of hemodynamics
▸ Hemorrhage control
▸ iv fluid
▸ Inotropes
▸ Vasopressors
RESUSCITATION
VASOPRESSOR VS INOTROPES
▸ Vasopressors increase vasoconstriction (increased SVR).
▸ Inotropes increase cardiac contractility improves cardiac output
▸ The major vasopressors include phenylephrine, norepinephrine, epinephrine, and vasopressin.
▸ Dopamine is a vasopressor with inotrope properties that is dose-dependent.
▸ Dobutamine and milrinone are inotropes.
SHOCK
HYPOVOLEMIC SHOCK
▸ Decrease of preload
▸ Increase SVR and HR to maintain CO
▸ Loss : GI loss, 3rd space loss, burns, bleeding
ANAPHYLACTIC SHOCK
TREATMENT OF ANAPHYLACTIC SHOCK▸ Epinephrine IM (dose of 0.01 mg/kg of a 1:1000 , maximum of 0.5 mg in adults
and 0.3 mg in children) into the anterolateral thigh, the dose can be repeated every 5 - 15 min
▸ For patient with inadequate response for IM route > epinephrine (1:1,000) 1 ml + NSS 1000 ml start 2 mcg/min ( 2ml/min or 120ml/hr) maximum 10 mcg/min (600ml/hr)
▸ If patient still shock after epinephrine IM > NSS bolus 10-20 ml/kg in 15 min
DISTRIBUTIVE SHOCK
SEPTIC SHOCK
▸ Sepsis : life-threatening organ dysfunction caused by a dysregulated host response to infection
▸ Septic shock : sepsis with persisting hypotension requiring vasopressors to maintain MAP 65 mmHg and having a serum lactate level >2mmol/L (18mg/dL) despite adequate volume resuscitation
SEPTIC SHOCK
TOOLS FOR IDENTIFYING HIGH RISK
▸ qSOFA : screening tools for sepsis
▸ RR at least 22 / min
▸ SBP 100 mmHg or lower
▸ Altered mental status ( GCS < 15 )
▸ SOFA is an objective scoring system to determine major organ dysfunction
SEPTIC SHOCK
INFECTION CONTROL
▸ Early broad-spectrum antibiotics should be initiated within 1st hour of recognising sepsis.
▸ Early source control should be achieved within 6 to 12 hours of diagnosis.
SEPTIC SHOCK
RESTING BLOOD PRESSURE
▸ KEEP MAP 65 mmHg ( 80 to 85mmHg may help patients with chronic hypertension)
▸ Norepinephrine is the first-line vasopressor
▸ Adding a second vasopressor or inotrope is routinely added when norepinephrine doses exceed 40 or 50 μg/min.
SEPTIC SHOCK
FLUID RESUSCITATION
▸ Assess volume with dynamic measures > passive leg raiseing test
▸ Lactate level as a resuscitation guide: >4 = high mortality rate
▸ Balanced crystalloids are preferred over isotonic solutions
▸ No proven benefit from colloids
SEPTIC SHOCK
CORTICOSTEROIDS
▸ In septic shock , they have a vasopressor-sparing role and reduce the duration of shock , ventilator , ICU stay.
▸ Hydrocortisone 200 mg in 24 hr or 50 mg iv q 6 hr.
DISTRIBUTIVE SHOCK
NEUROGENIC SHOCK
▸ Loss of peripheral sympathetic tone > vasodilatation
▸ T1-T4 cord levels This results in bradycardia or an absence of reflex tachycardia.
▸ In general, patients with neurogenic shock are warm, peripherally vasodilated, and hypotensive with a relative bradycardia.
▸ Hypotension in the trauma patient can never be presumed to be caused by neurogenic shock until other possible sources of hypotension are excluded.
SHOCK
CARIOGENIC SHOCK
▸ Stage of decrease cardiac output resulting in inadequate tissue perfusion despite adequate circulating volume.
▸ Acute myocardial infarction is most common cause
CARDIOGENIC SHOCK
TREATMENT
▸ If no sign of pulmonary congestion , give crystalloid fluid boluses 250 to 500 ml and repeat after assessing benefit or harm
▸ If there is no improvement with the fluid bolus or if pulmonary congestion develops, use vasopressors (for hypotension) or inotropes (for congestion without profound hypotension)
TEXT
TREATMENT
▸ If absence of hypotension , DOBUTAMINE is drug of choice
▸ Dobutamine increase CO
▸ Avoid when SBP < 90 mmHg because of its vasodilatory potential, Combined with NOREPINEPHRINE has more profound effect on vasoconstriction.
▸ If SBP < 70 mmHg , NOREPINEPHRINE is drug of choice.
▸ EPINEPHRINE is associated with more systemic acidosis, tachycardia, and dysrhythmias.
OBSTRUCTIVE SHOCK
TENSION PNEUMOTHORAX
▸ Clinical diagnosis
▸ Distended neck vein
▸ Decrease breath sound, hyper-resonant on percussion
▸ Tracheal shift
▸ Hypotension
TENSION PNEUMOTHORAX
NEEDLE THORACOSTOMY
▸ A study using computed tomography (CT) scan to review chest wall thickness of trauma patients noted an average chest wall thickness in the midclavicular line to be 46 mm (right) and 45 mm(left).
▸ In the same patients, the average chest wall thickness was 33 mm (right) and 32 mm (left) in the anterior axillary line.
▸ Longest needle in SRK hospital are ????
OBSTRUCTIVE SHOCK
CARDIAC TAMPONADE
▸ Fluid accumulation in pericardial sac
▸ Pressure to RV and RA
▸ Decrease venous return
▸ Decrease cardiac output
CARDIAC TAMPONADE
CLINICAL PRESENTATION
▸ Tachycardia
▸ Hypotension
▸ Neck vein dilate
▸ Distant heart sound
▸ Pulsus paradoxus > 10 mmHg
CARDIAC TAMPONADE
TREATMENT
▸ After ABC
▸ Bolus IV fluid ( 500ml-1000ml ) ,If no sign of pulmonary congestion
▸ Pericardiocentesis
OBSTRUCTIVE SHOCK
PULMONARY EMBOLISM
▸ Clinical presentation
▸ Dyspnea
▸ Chest pain
▸ Syncope
▸ Hemoptysis
PULMONARY EMBOLISM
TREATMENT
▸ Keep sat > 90%
▸ If need ventilator > low tidal volume , keep pressure < 30 cmH2O
▸ Anticoagulant
▸ Thrombolytic treatment
▸ In cardiac arrest : rTPA 50 mg iv bolus in 15 min can be replete in 15 min
SHOCK IN TRAUMA PATIENT
INITIAL ASSESSMENT
▸ Recognition of shock
▸ Heart rate, pulse pressure, respiratory rate, skin perfusion, mental status
▸ Do not wait until patient shock !!!
▸ Cause of shock
▸ Hemorrhagic : most common
▸ Non hemorrhagic : cardiogenic, cardiac tamponade, tension pneumothorax, neurogenic, septic
SHOCK IN TRAUMA PATIENT
HEMORRHAGIC SHOCK
▸ Adult blood volume is ~ 7% of BW
▸ Children blood volume is 8-9% of BW
▸ Classification of shock : class 3-4 blood transfusion is considered
HEMORRHAGIC SHOCK
INITIAL MANAGEMENT OF HEMORRHAGIC SHOCK
▸ Airway ,breathing
▸ C : hemorrhagic control, find internal bleeding, resuscitate
▸ Vascular access : 2 large-caliber(16-18) peripheral line at fore arm or antecubital vein, Central line as need, intraosseous in < 6 yr
▸ Initial fluid : warm isotonic solution (RLS,NSS) usual 1L in adult , 20ml/kg in children
▸ Penetrating trauma delay aggressive fluid until definitive control
▸ Permissive hypotension : keep MAP 50 mmHg or SBP 80-90 mmHg
▸ Once, can’t rule out TBI > KEEP SBP 65 mmHg