shock - pathophysiology, clinical features & management

SHOCKPATHOPHYSIOLOGYCLINICAL FEATURESMANAGEMENT

DR ANKIT SHARMADR ARUN KUMAR M

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SAMUEL V GROSS, 1872 “Shock is the manifestation of the rude unhinging of the machinery of life”

HISTORICAL PERSPECTIVE• Ambroise Paré (1510) – Fluids to injured patients• ‘Shock’ – 1743 – act of impact/ collision• Guthrie (1815) – described physiological instability• Crile (1899) – Importance of measuring BP• Claude Bernard – Milieu intérieur• Walter B. Cannon – Homeostasis• WW I – Disturbance of nervous system• Alfred Blalock (1934) – 4 categories of shock• Carl John Wiggers (1950) – Wiggers prep

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Definition A systemic state of tissue hypo-perfusion, which is inadequate for normal cellular respiration

Systemic – global phenomenonHypoperfusion (relative/ absolute)Inadequate cellular respiration Anaerobic, dysfunctionBody responses thereof

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Types• Hypovolemic• Cardiogenic• Septic (vasogenic)• Neurogenic• Traumatic• Obstructive

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Hypovolemic shock• Hemorrhagic• Trauma• Bleeding disorders• GI/ GU bleed

• Non- hemorrhagic • Dehydration• “Inter compartmental fluid mal-adjustments”• Third spacing

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Cardiogenic Shock• Pump failure

• Adequate but ineffective intravascular volume. • Cardiac causes • Pulmonary embolism

• High mortality rates

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Cardiogenic shock• Hemodynamic criteria: 1. Sustained Hypotension (i.e. SBP <90 mm Hg for at least 30 minutes)

2. Reduced Cardiac Index (<2.2 L/min per square meter) &

3. Elevated Pulmonary Artery Wedge Pressure (>15 mm Hg)

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SEPTIC SHOCK• Four sepsis-related clinical syndromes = Four steps of increasingly exaggerated systemic inflammatory responses

SIRSSepsis Severe Sepsis (Sepsis Syndrome) Septic Shock

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DEFINITIONS DESCRIBING THE CONDITION OF SEPTIC PATIENTS

Bacteremia: Bacteria in blood Positive blood cultures

Septicemia: Microbes or their toxins in blood

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DEFINITIONS DESCRIBING THE CONDITION OF SEPTIC PATIENTS

SIRS: Two or more of the following (1) Temperature >38°C or <36°C (2) Heart Rate > 90/ min (3) Respi rate > 24/ min (4) TLC >12,000/mm3 or <4,000/mm3)

or >10% bands on PBS◦ SIRS may have a noninfectious etiology

Sepsis: SIRS that has a proven/ suspected microbial etiology13

DEFINITIONS DESCRIBING THE CONDITION OF SEPTIC PATIENTS

Severe Sepsis (Similar to sepsis syndr): Sepsis with one or more signs of organ dysfunction:

1. Cardiovascular

2. Renal

3. Respiratory

4. Hematologic

5. Unexplained metabolic acidosis

6. Adequate fluid resuscitation14

DEFINITIONS DESCRIBING THE CONDITION OF SEPTIC PATIENTS Septic Shock: Sepsis + Hypotension

or Need for vasopressors to

maintain systolic BP 90 mmHg or MAP70 mmHg

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DEFINITIONS DESCRIBING THE CONDITION OF SEPTIC PATIENTS

Refractory septic shock: Septic shock

◦ lasting for >1 h ◦ Not responding to fluid or pressor administration

MODS: Dysfunction of more than one organ system, requiring intervention (individual organ support) to maintain homeostasis

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NEUROGENIC SHOCK• Acute loss of sympathetic vascular tone• Loss of vascular resistance

◦ Pooling in capacitance vessels◦ Reduced preload◦ Poor cardiac output◦ Inadequate pressure in arterial system to maintain

capillary perfusion

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NEUROGENIC SHOCK Etiology:

◦ High cervical spinal cord injury (vertebral body #)◦ inadvertent cephalad migration of spinal anaesthesia◦ epidural hematoma or devastating head injury

Failure of fluid resuscitation to improve hemodynamics, where no source of blood loss or sepsis can be identified

Vasopressors are necessary to treat this condition

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TRAUMATIC SHOCK• Hemorrhage overtly controlled, but patients continues to lose plasma volume into the interstitium • Secondary microcirculatory injury• Excessive pro-inflammatory response• Third spacing

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OBSTRUCTIVE SHOCK• Reduction in preload due to mechanical obstruction of cardiac filling

•Common causes: cardiac tamponade, tension pneumothorax, massive pulmonary embolus or air embolus

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PATHOPHYSIOLOGY OF SHOCK• Initial response driven by • Tissue hypoperfusion • Developing cellular energy deficit.

• Demand-supply mismatch • Neuro-endocrine & inflammatory response (proportional

to degree & duration of shock)

• The specific responses depends on etiology of shock

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22SHOCK INDUCED VICIOUS CYCLE

CELLULAR PATHOPHYSIOLOGY• Compensation/ Dysfunction/ Death

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↓ O2 concn in cells

↓

↓ oxidative phosphorylation

↓

↓ ATP synthesis

↓

shift from aerobic to anaerobic glycolysis

↓

Pyruvate converted to lactate

↓

accumulation of lactate & inorganic phosphate, thus ↓ pH

↓

intracellular metabolic acidosis lactate & other wastes exit cells ↓

systemic metabolic acidosis

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MICROVASCULAR PATHOPHYSIOLOGY• α1 receptors – vasoconstriction • ẞ2 receptors - vasodilation.• Shock norepinephrine & epinephrine from adrenal medulla → α1 receptors• Other constrictors: A-II, vasopressin, endothelin 1, and TxA2• Vasodilators: PG I2, NO and adenosine

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Hypoxia & acidosis

↓

Complement & neutrophil activation

↓

Free radical & cytokine release

↓

Injury to capillary endothelial cells

↓

Further activation of immune & coagulation systems

↓

Damage to endothelium with loss of integrity

↓

Leaky capillary endothelium

↓

Tissue edema & cellular hypoxia

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CARDIOVASCULARPATHOPHYSIOLOGY

Shock

↓

↓ Preload & ↓ Afterload

↓

↑ sympathetic output

↓

catecholamine release from adrenal medulla

↓

↑ heart rate & contractilityvenous and arterial vasoconstriction (Except in sepsis)

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• Arterial vasoconstriction with regional variations • Shunting of blood away from less essential organ beds such as the intestine, kidney, and skin • Brain & heart – autoregulatory mechanisms

CARDIOVASCULARPATHOPHYSIOLOGY

PULMONARY PATHOPHYSIOLOGY• Tachypnea• ↑ minute ventilation & ↑ CO2 excretion• Compensatory respiratory alkalosis• Resuscitation induced O2 free radical injury• ALI & ARDS• Non cardiogenic pulmonary edema

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RENAL PATHOPHYSIOLOGY• Decreased renal blood flow• RAS activation• ↓ GFR + ↑ aldosterone & vasopressin → Oliguria

• Further vasoconstriction → ↑ sodium & water retention → edema

• Toxic tubular injury & Tubular obstruction

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ENDOCRINE PATHOPHYSIOLOGY• Na+ & water retention K+ & H+ lost• Hypovolaemia ADH• Adrenergic drive Norepinephrine release•Vasoconstriction•↑ glycogenolysis & ↑ gluconeogenesis•↓ Insulin release

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CRH (Hypothalamus)

↓

ACTH (pituitary)

↓

Cortisol (Adrenal Cortex)

↓

Cortisol + Epinephrine + Glucagon Catabolic state↓

Gluconeogenesis & Insulin resistance

↓

Hyperglycemia, Muscle protein break down, lipolysis

ENDOCRINE PATHOPHYSIOLOGY

METABOLIC DERANGEMENTS• Disruption of C-P-L metabolism• Anaerobic metabolism Lactate• ↑ Hepatic gluconeogenesis• Hepatic lipogenesis ↑ TG• Protein catabolism → muscle wasting

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INFLAMMATORY & IMMUNE RESPONSE

Pro-inflammatory Anti-inflammatoryIL-1α/ẞ IL-4

IL-2 IL-10IL-6 IL-13IL-8 IL-1Ra

IFN-ϒ PGE2

TNF-α TGF-βPAF

TNFR- I/II

INFLAMMATORY & IMMUNE RESPONSE• MODS• Counter-regulatory immune response• Delayed MOF

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SEPTIC SHOCK• Culture proven etiology +/-• Any class of micro-organism • Gram (-) ve bacteria > Gram (+) ve bacteria > polymicrobial infection > fungi • Gm (-) ve bacteria = Enterobacteriaceae, pseudomonads, Haemophilus etc. •Gm (+) ve bacteria = S.aureus, coagulase (-) ve staph, enterococci, S.pneumoniae etc.

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SEPTIC SHOCKMyocardial depression

+ Hypovolemia

+ other factors

↓

Tissue hypoxia (hypodynamic pd)

↓

↑ blood lactate & ↓ central venous O2 saturation

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SEPTIC SHOCKAfter fluid administration

↓ ↓ peripheral vascular resistance

(vasodilatory phase) Hallmark of septic shock

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Clinical Features & Management

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Severity of shockCompensated shock

Decompensation• Mild shock

• Moderate shock• Severe shock

Unresuscitable Shock

MOF

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Severity of shock Compensated shock

◦ Loss of up to 15% of circulatory volume

◦ Maintain central blood volume

◦ If prolonged (>12 hrs) Ischaemia-Reperfusion effect

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Severity of shock Decompensation

◦ Loss of > 15% of circulating volume.

◦ Progressive Renal, Respiratory & Cardiovascular decompensation.

◦ Hypotension >30-40% volume loss.

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Severity of shock

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Hemorrhagic shock

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Hemorrhagic shockMost common cause of shock in the surgical or trauma patients

Young patients vs elderly patients

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Hemorrhagic shock Classification of hemorrhage

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Hemorrhagic shockApproach to Hemorrhagic shock

Identify haemorrhage

Immediate resuscitative maneuvers

Identify the site of haemorrhage

Haemorrhage control

Damage control resuscitation

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Hemorrhagic shockTreatment concurrently with diagnostic evaluation

Time dependent survival

Resuscitative maneuvers

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Hemorrhagic shockHistoryRoot cause of hemorrhage & its site

Any underlying Pathology

Any co-morbidities/medications

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Hemorrhagic shockSymptoms & Signs:Agitation, Cold clammy extremitiesTachycardia, HypotensionPallorWeak or absent peripheral pulsesProlonged capillary refill timeSystemic examinationSymptoms specific to site of Hemorrhage

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Hemorrhagic shockSite specific Symptoms & Signs:

Penetrating wounds / Blunt trauma

Sites that can harbor sufficient extra-vascular volume: Intrathoracic (2-3L/ pleural cavity)IntraabdominalRetroperitoneal# long bones

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Hemorrhagic shockInvestigations

Hematological & Biochemical Investigations

Lactate levels

Blood grouping & cross matching

Radiological investigations as indicated

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Hemorrhagic shockDamage control resuscitation

Permissive hypotension

Use of limited crystalloids and blood products

Anticipate and treat coagulopathy

Hypothermia

DCS

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Hemorrhagic shockFluid therapy

Crystalloid

Hypotonic solutions

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Hemorrhagic shockFluid therapy : Dynamic Fluid ResponseTo determine shock status

250-500ml bolus over 5-10min

HR, BP & CVP are measured

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Hemorrhagic shockResponders

• Sustained improvement in CVS status after bolus• No active bleeding, require fluids to attain normal volume status

Transient Responders

• Initial improvement followed by reverting to previous state over 10-20 min• Moderate ongoing fluid losses

Non responders

• No improvement in CVS status following bolus• Severely volume depleted and likely to have ongoing loss( persistent uncontrolled Hemorrhage)

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Hemorrhagic shockTransfusion of blood and blood products

Coagulation factor-based products

Blood product Aim

PRBC Hb 7-9 gm/dl

Platelets > 50,000/ml

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Hemorrhagic shock Monitoring of response

◦ Clinical : Conscious level, BP, Urine output◦ ECG◦ Pulse oximetry◦ CVP, Invasive BP monitoring◦ Cardiac output◦ Base deficit & serum lactate

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Hemorrhagic shock

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Traumatic shockInitial resuscitation

Control of Hemorrhage

Early stabilization of the fractures, debridement or evacuation of hematoma

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Septic Shock

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Septic shock

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SEPSIS SIX The Sepsis Six is the name given to a bundle of medical therapies designed to reduce the mortality of patients with sepsis.

The Sepsis Six consists of three diagnostic and three therapeutic steps – all to be delivered within one hour of the initial diagnosis of sepsis.

◦ Deliver high-flow oxygen.◦ Take blood cultures.◦ Administer empiric intravenous antibiotics.◦ Measure serum lactate and send full blood count.◦ Start intravenous fluid resuscitation.◦ Commence accurate urine output measurement.

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Management of severe sepsisInitial Resuscitation and Infection Issues

Hemodynamic Support and Adjunctive Therapy

Supportive Therapy of Severe Sepsis

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Initial Resuscitation and Infection Issues

A. Initial Resuscitation B. Screening for Sepsis and Performance Improvement C. Diagnosis D. Antimicrobial Therapy E. Source Control F. Infection Prevention

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A. Initial Resuscitation Resuscitation of patients with sepsis- induced tissue hypoperfusion ◦ defined as hypotension persisting after initial fluid challenge or blood

lactate concentration ≥ 4 mmol/L

EGDT (first 6 hrs of resuscitation) ◦ a) CVP 8–12 mm Hg ◦ b) MAP ≥ 65 mm Hg ◦ c) Urine output ≥ 0.5 mL/kg/hr ◦ d) Scvo2 or Svo2 70% or 65%, respectively

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B. Screening for Sepsis and Performance ImprovementRoutine screening of seriously ill patients for severe sepsis toincrease the early identification of sepsis allow implementation of early sepsis therapy

Performance improvement efforts to improve patient outcomes and decrease sepsis-related mortality.

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C. DiagnosisCultures Imaging studies1,3 β-d-glucan assay ,mannan and anti-mannan antibody assays

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D. Antimicrobial TherapyInitial empiric anti-infective therapy Broad spectrum Anti fungals

Reassessed daily for potential de-escalationCombination empiric therapyDuration & De-escalation

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E. Source ControlIntervention for source control within the first 12 hr of diagnosis.

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Haemodynamic support & Adjunctive therapyFluid therapyVasopressorsInotropic supportCorticosteroids

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Haemodynamic support & Adjunctive therapyFluid therapy

CrystalloidsAlbumin

VasopressorsNoradrenalineAdrenalineVasopressinDopamine

Ionotropic agents : Dobutamine

Corticosteroid

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Supportive therapyBlood products administration

Mechanical ventilation of sepsis

induced ARDS

Sedation, analgesia & neuromuscular

blockade

Glucose control

Renal replacement therapy

DVT prophylaxis

Stress ulcer prophylaxis

Nutrition

Setting goals of care

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Cardiogenic Shock

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Cardiogenic shock Causes:

◦ Acute MI (most common)◦ Arrythmia◦ End stage cardiomyopathy◦ Myocarditis◦ Severe myocardial contusion◦ LV outflow obstruction◦ Obstruction to LV filling◦ MR◦ Acute aortic insufficiency◦ Metabolic◦ Drug reactions

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Cardiogenic shockDiagnosis

ECG & ECHO

CXR

ABG

Cardiac enzymes

Invasive monitoring

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Cardiogenic shockTreatmentAims of treatment

Adequate oxygenation

Judicious fluid administration

Adequate Analgesia

Correcting electrolyte imbalances

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Cardiogenic shockTreatment

Ionotropic support (Dopamine/Dobutamine)

Treatment of cause

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Obstructive Shock

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Obstructive shock Causes:

◦ Tension Pneumothorax◦ Pericardial Tamponade◦ Pulmonary embolus◦ IVC obstruction [Gravid uterus, DVT, Neoplasm]◦ Increased Intra-thoracic pressure [ Excess end-expiratory pressure, Neoplasm]

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Obstructive shockDiagnosis

Diagnosis is clinical

Chest X-Ray

Echocardiography

Pericardiocentesis

Treatment of the cause

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Neurogenic Shock

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Neurogenic shockCauses

Spinal cord Trauma

Spinal cord Neoplasm

Spinal / Epidural anesthesia

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Neurogenic shock Diagnosis:

Hypotension with bradycardia

Warm extremities

Motor and sensory deficits

Radiographic evidence of vertebral fracture

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Neurogenic shockTreatment

Fluid resuscitation

Ionotropic support

Operative attempt to stabilise the vertebral fracture.

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