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.

1
Q

Definition

A

Inadequate organ and tissue perfusion with oxigenated blood

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2
Q

Types of Shock

A
▸Hypovolemic
▸Cardiogenic
▸Distributive (vasodilation)
 ▹Septic
 ▹Neurogenic
 ▹Endocrine
▸Obstructive
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3
Q

Shock early signs

A

▸Tachypnea
▸Tachycardia
▸↓Capillary refil
▸Cool extremities

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4
Q

Shock late signs

A

▸↓BP
▸altered mental status
▸↓urine output (<0.5mL/kg/h)

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5
Q

Causes of Shock

A
-SHOCKED-
S Septic, Spinal (neurogenic)
H Hemorrhagic
O Obstructive (Tamponade, Tension Pneumothorax, Pulmonary Embolism)
C Cardiogenic
K anafilaKtic
E Endocrine
D Drugs
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6
Q

Shock: Clinical Correlation

A

▸Cool extremities: Hypovolemic (periphereal vasoconstriction)
▸Signs of left-side heart failure: Cardiogenic
▸Warm extremities: Distributive (Peripheral vasodilation)

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7
Q

Organ response

A. Microcirculation

A
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

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8
Q

Organ response

B. Cellular responses

A
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)
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9
Q

Organ response

C. Neuroendocrine response (Kidney)

A
↓BP
⇓
Baroreceptors
⇓
Kidney (↓juxtaglomerular perfusion)
⇓
↑renin
⇓
AT1
⇓
AT2
⇓
▸vasoconstriction
▸↑aldosterone (by adrenal cortex)
▸↑vasopresin (by posterior pituitary)
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10
Q

Organ response

C. Neuroendocrine response (Vasomotor center)

A
↓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

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11
Q

Organ response

D. Cardiovascular response

A

▸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

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12
Q

Organ response

E. Pulmonary response

A

▸Pulmonary vascular resistance increases in septic shock⇒Right heart failure
▸Hypoxia⇒Tachypnea⇒Respiratory alkalosis

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13
Q

Organ response

F. Metabolic derangements

A
Disruption of normal cycles of Carbohydrates, lipids, and protein metabolism.
⇓
↓O₂
⇓
Citric acid cycle
⇓
Glucose⇒Pyruvate⇒Lactate
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14
Q

Organ response

G. Inflammatory response

A
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)

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15
Q

General basis of Shock treatment

A

▸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

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16
Q

Types of shock

Hypovolemic Shock

A

▸Most common shock

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17
Q

Hypovolemic Shock

Types of Hypovolemic Shock

A
▸Share same signs and symptoms
▸Hemorrhagic:
 ▹↓RBC mass
 ▹↓plasma
▸Nonhemorrhagic:
 ▹↓plasma
 ▹extravascular fluid sequestration
 ▹GI, Urinary, and insensible losses
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18
Q

Hypovolemic Shock

Hypovolemia Classification

A
▸Mild
 ▹≦20% blood volume
 ▹mild tachycardia
▸Moderate
 ▹20-40%
 ▹Anxious
 ▹Tachycardia
 ▹Postural ↓BP
▸ Severe
 ▹≧40%
 ▹Shock signs (↓BP, Oliguria, ↑HR)
 ▹Confusion (severe)
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19
Q

Hypovolemic Shock

Treatment

A
▸↑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
20
Q

Hypovolemic Shock

Fluid resuscitation

A
▸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
21
Q

Obstructive Shock

Causes

A

▸Tension Pneumothorax
▸Herniation of abdominal viscera (diaphragmatic hernia)
▸Excessive positive-pressure ventilation
▸Tamponade

22
Q

Obstructive Shock

Tamponade Triad, Dx & Tx

A
▸Beck's triad:
 ▹↓BP
 ▹↓heart sounds
 ▹neck vein distention
▸Echocardiography
▸Immediate pericardiocentesis or open subxiphoid pericardial window
23
Q

Obstructive Shock

Tension Pneumothorax Dx, Rx & Tx

A

▸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)

24
Q

Neurogenic Shock

Causes, Dx and Tx

A

▸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

25
Q

Hypoadrenal Shock

Definition

A

⇒Normally⇐
Illness, Qx or Trauma

↑cortisol (in excess by adrenal glands)

⇒Adrenal insufficiency⇐
complicates the host response to Illness, Qx or Trauma

26
Q

Hypoadrenal Shock

Causes

A
▸Most common:
 ▹Chronic administration of high doses of exogenous glucocorticoids
▸Less common:
 ▹Idiopathic atrophy
 ▹Etomidate for intubation
 ▹Tb
 ▹Metastatic disease
 ▹Amyloidosis
27
Q

Hypoadrenal Shock

Dx

A

▸ACTH stimulation test

▹Cortisol ≦9µg/dL change poststimulation

28
Q

Hypoadrenal Shock

Tx

A

▸Dexamethasone 4mg IV
▹empiric tx meanwhile Dx test (because doesn’t interfere with ACTH test, like Hydrocortisone)
▸Hydrocortisone 100mg q6-8h
▹ONCE DIAGNOSED

29
Q

Cardiogenic Shock

Definition

A

▸Systemic hypoperfusion due to a myocardial dysfunction

30
Q

Cardiogenic Shock

Causes

A
▸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
31
Q

Cardiogenic Shock

Vicious cycle

A
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
32
Q

Cardiogenic Shock

Finding studies

A
▸ECG (invaluable)
 ▹Q waves ± >2mm ST elevation
▸CXR
 ▹Pulmonary vascular congestion
 ▹Pulmonar edema
▸Echocardiogram
 ▹Define the etiology
33
Q

Cardiogenic Shock

Lab findings

A

↑WBC (with left shift)
↑BUN & ↑Cr
↑Hepatic transaminases (hepatic hypoperfusion)
↑Lactic acid
↑Cardiac markers (CPK-MB, Troponine I & T)

34
Q

Cardiogenic Shock

Clinical findigs

A

▸Chest pain
▸HR 90-110x’ and weak
▸sBP <90mmHg

35
Q

Cardiogenic Shock

Tx

A

▸Goal is maintain adequate systemic and coronary perfusion
▹MAP >60 or sBP ≧90
▸Reperfusion-Revascularization
▸Vasopressors

36
Q

Cardiogenic Shock

Vasopressor Tx

A

▸Norepinephrine
▹Initial vasopressor therapy
▹2-4µg/min
▹If sBP 10µg/kg/min (∝ dose): ↑BP

37
Q

Septic Shock

Definition

A

▸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)

38
Q

Organ dysfunction variables

A
▸Arterial hypoxemia
▸Oliguria (0.5 mg/dL
▸Coagulation abnormalities (INR >1.5 or aPTT >60 sec)
▸Ileus (absent bowel sounds)
▸Thrombocytopenia (12,000)
39
Q

Septic Shock

Clinical findings

A
▸Fever
▸Tachypnea
▸↑HR
▸↓BP
▸local signs of infection
▸cool extremities
40
Q

Septic Shock

Tests to ask

A
▸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
41
Q

Septic Shock

Tx

A

▸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)

42
Q

Septic Shock

Early Goal Directed Therapy (EGDT)

A
(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
43
Q

Anaphylactic Shock

Definition

A

▸ Exaggerated immune response (classically IgE)
▸Hallmark: Onset within seconds - minutes after exposure
▸Anaphylactoid reaction: non-IgE mediated, first exposure

44
Q

Anaphylactic Shock

Most common triggers

A
▸Foods (nuts, shellfish, etc.)
▸Stings
▸Drugs
▸Radiographic contrast media
▸Blood products
▸Latex
45
Q

Anaphylactic Shock

Tx

A

▸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