SHOCK: Pathophysiology and Classification.

• Shock or Cardiovascular collapse, is the final common pathway for a number of potentially lethal clinical events.

• Regardless of the underlying pathophysiology, Shock constitutes systemic hypoperfusion owing to reduction either in cardiac output or in the effective circulating blood volume.

Empiric Criteria for Shock

4 out of 6 criteria have to be met

• Ill appearance or altered mental status• Heart rate >100• Respiratory rate > 22 (or PaCO2 < 32 mmHg)• Urine output < 0.5 ml/kg/hr• Arterial hypotension > 20 minutes duration• Lactate > 4

Stages of Shock

• Insult

• Pre shock Early intervention(compensation) can arrest or reduce the damage.Shock(compensation overwhelmed)

End organ damage

Death

• Initial: state of hypoperfusion causes hypoxia.• due to lack of oxygen cells perform

lactic acid fermentation.• Lactate accumulates causing lactic acidosis.

Compensatory:

Blood loss/ trauma etc

Activation of sympathetic adrenal system

Vasoconstrictive substances ( catecholamines, angiotensin II, vasopressin, endothelin)

Activation of activation of a receptors B receptors

Constriction of micro angia opening of A V shunts

Additional Compensatory Mechanisms

• Renin-Angiotensin-Aldosterone Mechanism– AII components lead to vasoconstriction– Aldosterone leads to water conservation

• ADH leads to water retention and thirst

• Inflammatory cascade

Compensatory significances

• ① Venous constriction → stored blood return to circulation (self blood transfusion) (60~70%)

• ② Capillary pressure → fluid transfer from interstitial arterial space to circulation (self fluid infusion) (1500ml)

• Catecholamines , AII → cardiac contractility peripheral vascular resistance

• ③ Redistribution of blood → Decrease blood flow to the skin, skeletal muscle, kidneys and abdominal organs

• maintain blood supplying to heart and brain

Progressive:

• Should the cause of the crisis not be successfully treated, shock will proceed to the progressive stage and compensatory mechanisms begin to fail.

Effects of inadequate perfusion on cell function

• Microcirculation stasis

• returned blood volume

• BP CO

• Brain ischemia renal blood flow stasis in kidney stasis in skin

• Dull/coma oliguria cyanosis

Refractory:

• At this stage, the vital organs have failed and the shock can no longer be reversed.

Impairment of cell metabolism

• (1) Oxygen deficiency and glycolysis enhancement ATP↓, Lactic acid↑

• (2) Energy deficient, sodium pump dysfunction and Na+, H2O inflow Cellular edema, Hyperkalemia

• (3) Lactic acid and CO2↑ Local acidosis

Definitions of Sepsis

• Systemic Inflammatory Response Syndrome (SIRS) – 2 or > of:

-Temp > 38 or < 36 -RR > 20

-HR > 90/min -WBC >12,000 or <6,000 or more than

10% immature bands

• Sepsis – SIRS with proven or suspected microbial source

• Severe Sepsis – sepsis with one or more signs of organ dysfunction or hypoperfusion.

• Septic shock = Sepsis + Refractory hypotension-Unresponsive to initial fluids 20-40cc/kg – Vasopressor dependant

• MODS – multiple organ dysfunction syndrome-2 or more organs

Stages of Sepsis

• SIRS 7%

• Sepsis 16%

• Severe sepsis 20%

• Septic shock 70%

• MODS/ Death

Pathophysiology• Inflammatory Cascade:

– Humoral, cellular and Neuroendocrine (TNF, IL etc)

• Endothelial reaction– Endothelial permeability = leaking vessels

• Coagulation and complement systems– Microvascular flow impairment

• End result = Global Cellular Hypoxia

Three Major types of ShockType of Shock Clinical Examples Principle Mechanisms

Cardiogenic MIVentricular ruptureArrhythmiaCardiac tamponadePulmonary Embolism

Failure of myocardial pump owing to intrinsic myocardial damage, extrinsic pressure or obstruction to outflow.

Hypovolemic HemorrhageFluid loss eg. Vomiting, diarrhea, burns or trauma.

Inadequate blood or plasma volume.

Septic Overwhelming microbial infectionsEndotoxic shockGram positive septecemiaFungal sepsisSuperantigens

Peripheral vasodilation and pooling of blood; leukocyte induced damage; DIC; activation of cytokine cascades.

Type of Shock

Insult Physiologic Effect

Compensation

CompensationHeart Rate

CompensationContractility

Cardiogenic

Heart fails to pump blood out

↓CO BaroRc↑SVR

↑ ↑

Obstructive Heart pumps well, but the outflow is obstructed

↓CO BaroRc↑SVR

↑ ↑

Hemorrhagic

Heart pumps well, but not enough blood volume to pump

↓CO BaroRc↑SVR

↑ ↑

Distributive Heart pumps well, but there is peripheral vasodilation

↓SVR ↑CO ↑

No Change - in neurogenic shock

↑

No Change - in neurogenic shock

Cardiogenic Shock: Causes

↓MAP = ↓ CO (HR x Stroke Volume) x ↑SVR

• Decreased Contractility (Myocardial Infarction, myocarditis, cardiomypothy, Post resuscitation syndrome following cardiac arrest)

• Mechanical Dysfunction – (Papillary muscle rupture post-MI, Severe Aortic Stenosis, rupture of ventricular aneurysms etc)

• Arrhythmia – (Heart block, ventricular tachycardia, SVT, atrial fibrillation etc.)

• Cardiotoxicity (B blocker and Calcium Channel Blocker Overdose)

Obstructive Shock: Causes

↓MAP = ↓ CO (HR x Stroke Volume) x ↑SVR

• Heart is working but there is a block to the outflow– Massive pulmonary embolism– Aortic dissection– Cardiac tamponade– Tension pneumothorax

• Obstruction of venous return to heart– Vena cava syndrome - eg. neoplasms, granulomatous disease– Sickle cell splenic sequestration

Hypovolemic Shock: Causes

↓MAP = ↓ CO (HR x Stroke Volume) x ↑SVR

• Decreased Intravascular volume (Preload) leads to Decreased Stroke Volume– Hemorrhagic - trauma, GI bleed, AAA rupture, ectopic pregnancy– Hypovolemic - burns, GI losses, dehydration, third spacing (e.g. pancreatitis,

bowel obstruction), Adesonian crisis, Diabetic Ketoacidosis

Distributive Shock: Causes

↓MAP = ↑CO (HR x SV) x ↓ SVR

• Loss of Vessel tone – Inflammatory cascade

• Sepsis and Toxic Shock Syndrome• Anaphylaxis• Post resuscitation syndrome following cardiac arrest

– Decreased sympathetic nervous system function• Neurogenic - C spine or upper thoracic cord injuries

– Toxins• Due to cellular poisons -Carbon monoxide, methemoglobinemia, cyanide• Drug overdose (a1 antagonists)