9.2 Shock / Hypotension Flashcards
Hypotension/shock is a frequently encountered, life-threatening emergency. Regardless of the underlying cause, certain general measures are usually indicated that can be life-saving.
Definition
Inadequate organ and tissue perfusion with oxigenated blood
Types of Shock
▸Hypovolemic ▸Cardiogenic ▸Distributive (vasodilation) ▹Septic ▹Neurogenic ▹Endocrine ▸Obstructive
Shock early signs
▸Tachypnea
▸Tachycardia
▸↓Capillary refil
▸Cool extremities
Shock late signs
▸↓BP
▸altered mental status
▸↓urine output (<0.5mL/kg/h)
Causes of Shock
-SHOCKED- S Septic, Spinal (neurogenic) H Hemorrhagic O Obstructive (Tamponade, Tension Pneumothorax, Pulmonary Embolism) C Cardiogenic K anafilaKtic E Endocrine D Drugs
Shock: Clinical Correlation
▸Cool extremities: Hypovolemic (periphereal vasoconstriction)
▸Signs of left-side heart failure: Cardiogenic
▸Warm extremities: Distributive (Peripheral vasodilation)
Organ response
A. Microcirculation
Normally, when ↓cardiac output ⇓ Systemic vascular resistance ↑BP ⇓ Adequate perfusion of Heart + Brain BUT if MAP ≦60 ⇒ Hypoperfusion of Heart + Brain
(Transport to cels depends on microcirculatory flow) ∴ ↓transport = ↓cellular metabolism = organ failure
Organ response
B. Cellular responses
Shock ⇓ ↓Nutrient transport ⇓ ↓Mithocondrial ATP ⇓ ↑H⁺ ions, ↑lactate, ↑products of anaerobic metabolismo ⇓ these metabolites override vasomotor tone ⇓ ↓BP (hypoperfusion) ⇓ ↓cellular transmembrane potential ⇓ ↑intracellular H₂O + Na⁺ (cellular swelling) ⇓ Hypocalcemia (Ca⁺ channels lost)
Organ response
C. Neuroendocrine response (Kidney)
↓BP ⇓ Baroreceptors ⇓ Kidney (↓juxtaglomerular perfusion) ⇓ ↑renin ⇓ AT1 ⇓ AT2 ⇓ ▸vasoconstriction ▸↑aldosterone (by adrenal cortex) ▸↑vasopresin (by posterior pituitary)
Organ response
C. Neuroendocrine response (Vasomotor center)
↓BP ⇓ Baroreceptors ⇓ Disinhibits the vasomotor center ⇓ A & B
A. Adrenergic output:
▸↑norepinephrine: peripheral vasoconstriction
▸↑epinephrine: glycogenolysis, gluconeogenesis and ↓insuline release
B. ↓Vagal activity:
▸↑HR
▸↑Cardiac output
Organ response
D. Cardiovascular response
▸Stroke volume:
▹Ventricular filling (preload)
▹Resistance to ventricular ejection (afterload)
▹Myocardial contractility
▸Cardiac output (mayor determinant of tissue perfusion) = stroke volume x HR
▸Hypovolemia = ↓preload
▸2/3 of circulating blood volume is in venous system (dynamic reservoir)
▹∝-adrenergic activity important compensatory mechanism.
▹BUT, neurogenic shock⇒venous dilation⇒↓preload
Organ response
E. Pulmonary response
▸Pulmonary vascular resistance increases in septic shock⇒Right heart failure
▸Hypoxia⇒Tachypnea⇒Respiratory alkalosis
Organ response
F. Metabolic derangements
Disruption of normal cycles of Carbohydrates, lipids, and protein metabolism. ⇓ ↓O₂ ⇓ Citric acid cycle ⇓ Glucose⇒Pyruvate⇒Lactate
Organ response
G. Inflammatory response
Innate immune system ⇓ Proinflammatory mediators ⇓ Progression of Shock ⇓ Development of Multiple Organ: (-injury), (-dysfunction MOD) and (-failure MOF) ⇓ If Px survives ⇓ Contrarregulatory response to balance the excessive proinflammatory response ⇓ Balance restored?⇒yes=Px does well ⇓ no⇒Px highly susceptible to secondary nosocomial infections⇒MOF
▸Macrophage release:
▹TNF-∝
▹IL-1β (endogenous pyrogen)
▹IL-6 (BEST PREDICTOR OF RECOVERY AND DEVELOPMENT OF MOF)
General basis of Shock treatment
▸ICU
▸Foley catheter (urine flow count)
▸Mental status frequently
▸Oximeter
▸Temperature:
▹>35ºC
▹endovascular countercurrent warmer (femoral vein)
▸Symathomimetic amines:
▹Dobutamine (pure β agonist): inotropic + ↓afterload⇒↓cardiac O₂ consumption
▹Dopamine: inotropic and chronotropic
▹Norepinephrine: ↑BP (vasoconstrction) + inotropic
Types of shock
Hypovolemic Shock
▸Most common shock
Hypovolemic Shock
Types of Hypovolemic Shock
▸Share same signs and symptoms ▸Hemorrhagic: ▹↓RBC mass ▹↓plasma ▸Nonhemorrhagic: ▹↓plasma ▹extravascular fluid sequestration ▹GI, Urinary, and insensible losses
Hypovolemic Shock
Hypovolemia Classification
▸Mild ▹≦20% blood volume ▹mild tachycardia ▸Moderate ▹20-40% ▹Anxious ▹Tachycardia ▹Postural ↓BP ▸ Severe ▹≧40% ▹Shock signs (↓BP, Oliguria, ↑HR) ▹Confusion (severe)
Hypovolemic Shock
Treatment
▸↑Preload (rapidly reexpansion) ▸Isotonic saline or Ringer's Lactate ▹2-3L over 20-30 mins ▸If hemodynamic instability ▹Blood transfusion (Hb≦10g/dL) ▹Fresh-frozen plasma (FFP) ▹1:1 ration ▹STOP once hemorrhage is controlled and HB>7g/dL
Hypovolemic Shock
Fluid resuscitation
▸Give until: ▹↓HR ▹↑urine output ▹Px stabilizes ▸Maintenance: 4:2:1 rule ▹First 10 kg: 4mL/kg/h ▹Second 20 kg: 2mL/kg/h ▹Remaining weight: 1mL/kg/h ▸Replace ongoing losses and deficits ▹10% of body weight
Obstructive Shock
Causes
▸Tension Pneumothorax
▸Herniation of abdominal viscera (diaphragmatic hernia)
▸Excessive positive-pressure ventilation
▸Tamponade
Obstructive Shock
Tamponade Triad, Dx & Tx
▸Beck's triad: ▹↓BP ▹↓heart sounds ▹neck vein distention ▸Echocardiography ▸Immediate pericardiocentesis or open subxiphoid pericardial window
Obstructive Shock
Tension Pneumothorax Dx, Rx & Tx
▸Dx:
▹↓ipsilateral breath sound
▹tracheal deviation (away from affected thorax)
▹Jugular venous distention
▸Rx:
▹↑intrathoracic volume
▹shifting of mediastinum to colateral side
▸Tx:
▹Immediately chest decompression (clinical findings are enough)
Neurogenic Shock
Causes, Dx and Tx
▸Dilatation of Arteries and Veins (pooling in the venous system) due to:
▹Interruption of vasomotor output (cord injury)
▹Cephalic migration of spina anesthesia
▹Devastating head injury
▸Dx:
▹Extremities often warm (difference with cardiogenic and hypovolemic)
▸Tx (ONCE HEMORRHAGE HAS BEEN RULED OUT)
▹Norepinephrine OR ∝-adrenergic agent (phenylephrine)⇒↑vascular resistance + adequate MAP
Hypoadrenal Shock
Definition
⇒Normally⇐
Illness, Qx or Trauma
⇓
↑cortisol (in excess by adrenal glands)
⇒Adrenal insufficiency⇐
complicates the host response to Illness, Qx or Trauma
Hypoadrenal Shock
Causes
▸Most common: ▹Chronic administration of high doses of exogenous glucocorticoids ▸Less common: ▹Idiopathic atrophy ▹Etomidate for intubation ▹Tb ▹Metastatic disease ▹Amyloidosis
Hypoadrenal Shock
Dx
▸ACTH stimulation test
▹Cortisol ≦9µg/dL change poststimulation
Hypoadrenal Shock
Tx
▸Dexamethasone 4mg IV
▹empiric tx meanwhile Dx test (because doesn’t interfere with ACTH test, like Hydrocortisone)
▸Hydrocortisone 100mg q6-8h
▹ONCE DIAGNOSED
Cardiogenic Shock
Definition
▸Systemic hypoperfusion due to a myocardial dysfunction
Cardiogenic Shock
Causes
▸Acute myocardial infarction (most common) ▹CS is leading cause of death in MI ▹ST elevation MI (STEMI): Shock typically associated. ▹non-STEMI: less common ▸Cardiomyopathy ▸Myocarditis ▸Cardiac tamponade ▸Critical valvular heart disease
Cardiogenic Shock
Vicious cycle
Ischemia ⇓ ↓myocardial contractility ⇓ ↓cardiac output ↓BP ⇓ A & B
A. Hypoperfusion of myocardium
⇓
Ischemia
B. Diastolic dysfunction ⇓ ↓Left Ventricle end-diastolic pressure (LVEDP) ⇓ Pulmonary congestion ⇓ Ischemia
Cardiogenic Shock
Finding studies
▸ECG (invaluable) ▹Q waves ± >2mm ST elevation ▸CXR ▹Pulmonary vascular congestion ▹Pulmonar edema ▸Echocardiogram ▹Define the etiology
Cardiogenic Shock
Lab findings
↑WBC (with left shift)
↑BUN & ↑Cr
↑Hepatic transaminases (hepatic hypoperfusion)
↑Lactic acid
↑Cardiac markers (CPK-MB, Troponine I & T)
Cardiogenic Shock
Clinical findigs
▸Chest pain
▸HR 90-110x’ and weak
▸sBP <90mmHg
Cardiogenic Shock
Tx
▸Goal is maintain adequate systemic and coronary perfusion
▹MAP >60 or sBP ≧90
▸Reperfusion-Revascularization
▸Vasopressors
Cardiogenic Shock
Vasopressor Tx
▸Norepinephrine
▹Initial vasopressor therapy
▹2-4µg/min
▹If sBP 10µg/kg/min (∝ dose): ↑BP
Septic Shock
Definition
▸Systemic inflammatory response syndrome (SIRS): 2 or more of
▹38.5ºC
▹HR >90
▹Respiratory rate >20
▹WBC 12 or 10% bands
▸Sepsis: SIRS + infection
▸Severe sepsis: sepsis + signs of end-organ dysfunction
▸Septic shock: sepsis + ↓BP (despite fluid resuscitation or need cathecolamines)
Organ dysfunction variables
▸Arterial hypoxemia ▸Oliguria (0.5 mg/dL ▸Coagulation abnormalities (INR >1.5 or aPTT >60 sec) ▸Ileus (absent bowel sounds) ▸Thrombocytopenia (12,000)
Septic Shock
Clinical findings
▸Fever ▸Tachypnea ▸↑HR ▸↓BP ▸local signs of infection ▸cool extremities
Septic Shock
Tests to ask
▸Blood cultures x3 (from different sites) ▸Urinalysis ▸Urine C&S (Culture & Sensitivity) ▸Culture of any wounds ▸CXR (pneumonia) ▸Lactate ▸CBC + differential ▸Electrolytes ▸BUN & Cr ▸Liver enzymes ▸ABG ▸INR ▸PTT
Septic Shock
Tx
▸After samples of blood have been taken
▸Maximal doses (adjust in renal Px)
▸IN THE FIRST HOUR
▸Pseudomonas unlikely:
▹(Ceftriaxone or Piperacillin-Tazobactam or Meropenem) ± Vancomycin
▸Pseudomonas possible:
▹(Ceftazidime or Meropenem or Pip-Taxo) AND (Ciprofloxacin or Gentamicin)
▸Activated protein C
▹Modulate coagulation and inflammation in severe sepsis
▸Hydrocortisone (50mg c/6hrs IV)
▹For unresponsive px to fluid resuscitation (NS) and vasopressors
▸Removal of source of infection
▹Foley and catheters should be replaced
▸Heparinization prevent thrombosis (if not contraindication)
Septic Shock
Early Goal Directed Therapy (EGDT)
(In 6 hours) 1. Antibiotics Community infection or Nosocomial (MRSA & Pseudomonas) Within the first hour of Dx 2. CVP Boost to 8-12 (normal 2-5) Normal Saline (NS) 3. Vasopressors (∝ & β) Goal MAP >65 Norepinephrine Dopamine 4. No better perfusion (SvO₂10⇒Dobutamine
Anaphylactic Shock
Definition
▸ Exaggerated immune response (classically IgE)
▸Hallmark: Onset within seconds - minutes after exposure
▸Anaphylactoid reaction: non-IgE mediated, first exposure
Anaphylactic Shock
Most common triggers
▸Foods (nuts, shellfish, etc.) ▸Stings ▸Drugs ▸Radiographic contrast media ▸Blood products ▸Latex
Anaphylactic Shock
Tx
▸Remove causative agent; secure ABCs
▸Epinephrine
▹∝ & β effects (↑BP & bronchial smooth-muscle relaxation)
▹On scene - epi-pen if available
▹Moderate (minimal airway edema, mild bronchospasm)
-Adult: 0.3-0.5 mL IM q5-20min (1:1000)
-Child: 0.01 mL/kg/dose - 0.4 mL/dose (1:1000)
▹Severe (laryngeal edema, severe bronchospasm and severe ↓BP)
-adults: 1mL IV or ETT
-child: 0.01 mL/kg IV or ETT
▸Diphenhydramine 50 mg IM or IV q4-6h
▹For urticaria-angioedema
▸Methylprednisolone 50-100 mg IV
▸Salbutamol via nebulizer if bronchospasm
▸Glucagon 5-15 µg q1min IV (Px with β-blockers or cardiac disease)
▸Monitor for 4-6 h in ER
▸Follow up with family doctor en 24-48 h
▹Can have second phase (biphasic reaction)
▸3-day course of:
▹H₁ antagonist: Cetirizine 10 mg PO day
▹H₂ antagonist: Ranitidine 150 mg PO day
▹Corticosteroid: Prednisone 50 mg PO day
