Shock

 Shock is a physiologic state characterized by a significant reduction of systemic tissue perfusion, resulting in decreased oxygen delivery to the tissues.

Shock : Definition

cell membrane ion pump dysfunction intracellular edema leakage of intracellular contents into the

extracellular space inadequate regulation of intracellular pH

Cellular effects

alterations in the serum pH endothelial dysfunction redox state further stimulation of inflammatory and

antiinflammatory cascades

Systemic effects of shock

sequential cell death end-organ damage multi-system organ failure death.

Initially reversible rapidly become irreversible

Dffects of oxygen deprivation

Cryptic = hidden or silent

Inadequate oxygen delivery leading to shock can occur despite the patient being hypertensive or normotensive and clinicians should not wait for the presence of hypotension before aggressively attempting to reverse shock and restore adequate tissue perfusion.

Early evaluation of serum lactate can assist in identifying “cryptic shock” (normal blood pressure accompanied by tissue level hypoperfusion).

hypertensive (cryptic) shock

 Systemic tissue perfusion is determined by the cardiac output (CO) and systemic vascular resistance (SVR):

●CO is the product of heart rate and stroke volume.

The stroke volume is related to preload, myocardial contractility, and afterload

●SVR is governed by the vessel length, blood viscosity, and vessel diameter

PHYSIOLOGY

Decreased systemic tissue perfusion is a consequence of diminished CO, SVR, or both. The CO or SVR may be elevated in shock if the other is disproportionately low.

As an example, SVR is decreased out of proportion to the elevation of the CO in hyperdynamic shock .

Complex interactions between humoral and microcirculatory processes cause patchy regional blood flow and reduced effective tissue perfusion

This results in derangement of cellular metabolic processes.

PHYSIOLOGY

HypovolemicCardiogenicDistributive.

“3” TYPES OF SHOCK

↓preload due to intravascular volume loss. leading to ↓ CO & compensatory ↑SVR

↓ PCWP is decreased.

Hypovolemic shock

Distributive (vasodilatory) shock Due to severely decreased SVR. Compensatory ↑CO The PCWP may be low or normal

Septic Adrenal crises Neurogenic (spinal shock) Anaphylactic

PCWP : DD hypovolemic from cardiogenic shock .

An example, in septic shock : hypovolemic component (due to

decreased oral intake, insensible losses, vomiting, diarrhea)

cardiogenic component (due to sepsis-related myocardial dysfunction)

distributive component (due to the effects of inflammatory and antiinflammatory cascades on vascular permeability and vasodilation).

Combined shock

Preshock Shock End-organ dysfunction.

STAGES OF SHOCK 

warm shock or compensated shock.

rapid compensatory homeostatic mechanisms for diminished tissue perfusion

Signs : tachycardia, peripheral vasoconstriction, and either a modest ↑ ↓ systemic blood pressure

Preshock 

Overwhelmed compensatory mechanisms

S/S signs of organ dysfunction appear. tachycardia, dyspnea, restlessness, diaphoresis, metabolic

acidosis, oliguria, and cool clammy skin.

↓25% in effective arterial blood volume in hypovolemic shock ↓ cardiac index to ≤2.5 L/min/m2 in cardiogenic shock, activation of innumerable mediators of the systemic

inflammatory response syndrome (SIRS) in distributive shock.

Shock Stage

⇊ urine output : ARF Acidemia decreases the cardiac output and

alters cellular metabolic processes restlessness evolves into agitation,

obtundation, and coma.

End-organ dysfunction

Hypotension Oliguria abnormal mental status metabolic acidosis

in some patients, cool and clammy skin.

Cardinal findings of shock

Hypotension occurs in the majority of shock patients.

absolute hypotension (eg, systolic BP<90 mmHg) relative hypotension (eg, a drop in systolic BP>40 mmHg).

Relative hypotension explains, in part, why a patient may be in shock despite having a high or normal BP.

Hypotension

Pathogenesis: shunting of renal blood flow to other vital

organs intravascular volume depletion both.

Oliguria

orthostatic hypotension poor skin turgor absent axillary sweat dry mucous membranes.

Signs of intravascular volume depletion

Due to vasoconstriction

Cool, clammy skin

early distributive shock prior to the onset of compensatory vasoconstriction

terminal shock due to failure of compensatory vasoconstriction.

Shock with flushed, hyperemic skin

⇩ lactate clearance by liver, kidneys & skeletal muscle Lactate production may increase due to anaerobic

metabolism if shock progresses to circulatory failure and tissue hypoxia, which can worsen the acidemia.

Metabolic acidosis

– Depending upon the cause :

hematemesis, hematochezia, melena, vomiting, diarrhea, or abdominal pain.

There may be evidence of blunt or penetrating trauma,

The patient may be postoperative.

History in Hypovolemic shock

⇩ skin turgor (in younger patients), dry skin dry axillae dry tongue & oral mucosa. postural hypotension ⇩ JVP

Occasionally : Anemia ⇈ amylase and lipase

Signs of Hypovolemic shock

Depending upon the cause. dyspnea, chest pain, or palpitations. H/O of CV disease. Lung : diffuse crackles cardiac :new murmur, gallops, or soft heart sounds. ⇧ JVP and CVP ⇩ distal arterial pulses CXR : pulmonary congestion or pulmonary edema ECG : recent or current ischemia ⇧ Cardiac enzymes. Echo may demonstrate the etiology.

Cardiogenic shock

Depending upon the cause dyspnea, productive cough dysuria, hematuria chills, myalgias, rashes, fatigue, malaise headache, photophobia, pain recent ingestion.

O/E: fever, tachypnea, tachycardia, leukocytosis, an abnormal mental status, or flushing.

Distributive shock

Causes:Hemorrhage-induced – penetrating trauma, GI bleeding, ruptured

hematoma, hemorrhagic pancreatitis, fractures, or a ruptured aneurysm.

Fluid loss-induced diarrhea, vomiting, heat stroke, inadequate

repletion of insensible losses, burns, and "third spacing".

Third-space losses are common postop & if intestinal obstruction, pancreatitis, or cirrhosis.

Hypovolemic shock

myopathic Arrhythmic Mechanical extracardiac (obstructive).

Causes of cardiogenic shock

Massive PE Tension pneumothorax Severe constrictive pericarditis Pericardial tamponade Severe pulmonary hypertension: Eisenmenger's

They may present clinically as hypovolemic shock when their primary physiologic disturbance is decreased preload, rather than pump failure.

Extracardiac (obstructive) causes

Resuscitative efforts should NOT be delayed for history, physical examination, laboratory testing, or imaging.

DIAGNOSTIC APPROACH

 The patient's baseline medical status recent complaints food and medicine allergies recent changes in medications, potential

acute or chronic drug intoxication preexisting diseases immunosuppressed states hypercoagulable conditions.

Medical history

neither sensitive nor specific for identifying the cause of shock.

Physical examination 

CBC : leukocytosis and/orbandemia >10% (sepsis)  Basic chemistry (sodium, potassium, chloride, serum

bicarbonate) RFT :urea & creatinine liver function tests amylase, lipase INR, PTT fibrinogen, fibrin split products or dimer, cardiac enzymes

(troponin or CK mb) ABG Toxicology screen lactate level. Type and crossmatch should be performed for patients who are

at risk for significant bleeding

Laboratory evaluation

Causes: increased production ( anaerobic metabolism) mitochondrial derangements affecting oxygen

utilization decreased clearance due to hepatic

dysfunction.

Increased serum lactate

CXR abdominal X-ray for intestinal obstruction abdominal CT ECG Echocardiogram urinalysis Gram stain of material from sites of possible infection

(sputum, urine, wounds) may give early clues to the etiology of infection while cultures are incubating.

Blood should be taken from two distinct venipuncture sites

Imaging

 Hemodynamic measurements titration of vasopressors guide fluid resuscitation

cardiac output pulmonary artery occlusion pressure: PAWP SVR

never been shown to improve outcomes

Pulmonary artery catheterization

35 to 60 % higher in cardiogenic shock; 60 to 90 %

MORTALITY