Week 14 - Shock

What is shock

• inadequate tissue perfusion that causes insufficient delievery of nutrients and oxygen to cells

• cells switch from aerobic to anaerobic metaboism, increasing metabolic waste

• w/o proper perfusion causes cell dysfxn and death

Classifications of shock - hypovolemic shock

shock caused by inadequate circulatory blood volume

classifications of shock - cardiogenic shock

shock caused by sudden fall in CO due to acute dz in the heart

calssifications of shock - septic shock

shock caused by severe bacterial infxn (SEPSIS that gets worse)

classifications of shock - anaphylatic shock

shock caused by severe allergic rxn

classifications of shock - obstructive shock

shock caused by a physcial block impairing blood flow to critical parts of the circulation system causing inadequate tissue perfusion.

classifications of shock - neurogenic shock

shock caused by spinal cord injuries, anesthetic accidents which lead to peripheral vasodilation and blood pooling

classifications of shock - traumatic shock

shock caused by traumatic injuries to the body

Shock patho

• start w/ dec. circulating blood vol which dec. the venous return to heart.

• this causes: heart fail or dec. CO which leads to dec. BF and dec. supply O2 at cellular lvl.

• the dec. supply of O2 causes Anoxia which activates inflammatory mediators and causes shock

Cardiac output - general idea

cardiac output - vol. of blood ejected from the heart - norm: 4-8L

Heart rate - heart beats in a minute

Stroke volume - vol. of blood ejected during systole - affected by preload, afterload and contractility

cardiac output and stroke vol. - preload

vol. of blood in the ventricles after diastole

• inc. vol = inc. stretch = inc. force of contraction

• inc. w/ IV fluids

• dec. w/ diuretics

cardiac output and stroke vol - afterload

the resistance the left ventricle must overcome to pump blood

• inc. reistance = inc. forc of contraction left ventricle must overcome to pump blood

• inc. w/ vasopressors by inc. vascular resistance

what are the clinical features of shock

• very low bp - d/t fluid loss, vasodialtion, and dec. heart fxn

• shallow sighs/ resp. - d/t dec. O2 to tissues, dec. pulmonary circulation, inc. pulmonary capillary pressure and inc. airway edema

• subnormal temps. - d/t sepsis affecting hypothalamus, vasodilation

• feeble and irregular pulses

the stages of shock

1. initial stage

2. compensatory stage

3. nonprogressive stage

4. progressive stage

5. irreversible stage

the stages of shock - the initial stage

starts w/ drop in blood flow, causing hypoxia, tachycardia and anxiety which leads to anaeorbic metabolism as a response to the hypoxia

the stages of shock - compensatory stage

the body employs hormonal and neuronal meaures to improve BP and O2 delievery

• this compensates for the dec. prefusion casuing inc. BP and HR

the stages of shock - nonprogressive stage

the reflex compensatory mechanisms are activated which maintains perfusion to the vital organs

the stages of shock the progressive stage

things get worse

tissue hypoperfusion occurs causing worsening circulatory blood volume leading to inc. capillary perfusion and fluid shifts leading to metabolic imbalances (Acidosis)

stages of shock - irreversible stage

severe cell and tissue injury has already set in, even if hemodynamic stability reachieved survival CANT happen.

hypovolemic shock - causes

• blood loss: from cuts, injuries of internal bleeding

  • dehydration: burns, vomitting, diarrhea, excessive persperation, excessive diuretics

hypovolomic shock - s/sx

s/sx: inc. HR, dec. BP, dec. UO, ALOC

hypovolemic shock - compensatory mechanisms for hypovolemia:

fluid conservation

• ADH = inc. BP cuasing inc. Fluid retention and dec. UO

• aldosterone - inc. Na resorption and inc. K excretion causes inc. blood volume and water retention

• The RAAS stimulates vasocontriction and inc. production of aldosterone

hypovolemic shock - compensatory mechanisms for hypotension

inc. BP

• activating SNS response which inc. BP and vasoconstriction

• peripheral resistance to inc. BP and keep vital organs perfused

hypovolemic shock - compensatory mechanisms to redistribute blood supply

coronary and cerebral vessels are spared d/t sympathetic vasoconstriction

cardiogenic shock - causes and goals

the heart has problems contracting d/t dyastolic and systolic dysfxn

• this dec. CO and dec. perfusion

Goal: provide inotropic support to improve CO

• positive inotropic force to inc. myocardial contract and inc. CO

cardiogenic shock - S/SX

s/sx - chest pain, SOB, severe fatigue, dec. UO, dizzy, clammy skin, anxiety

cardiogenic shock - compensatory mechanisms

Frank sterling mechanism - inc. preload enhances CO and stroke volume

Hypertrophy - attempting to push more out to the system

activate neurohormonal sys - norepinephrine released inc. Heart rate and augments myocardial contractility or RAAS activation

Cardiogenic shock - patho

starts w/ cardiac event (MI, arrythmia, CHF causing myocardial pump failure. this causes: dec. CO, dec. tissue perfusion, dec. fluid movements from pulmonary vascular bed to pulmonary interstial space causing blood to back up into lungs

this ends with pulmnoary interstital edema and then alveolar edema

septic shock patho

start with an infection occuring causing the releases of lipoppolysaccharides. thi striggers TNF-a to release IL1,6, and 8. all of this leads to the release of NO and platelete activating factor at inc. amounts to the point where it affects the heart and lungs causing shock

septic shock - s/sx

can cause:

heart: low cardiac output and peripheral resistance

vessels - BV injury, thrombosis and DIC (overreactive clotting proteins)

lungs - ARDS

if pts. has super high nitric oxide and platelete activating factors is probably going into this shock

anaphylactic shock - cause

result of Ag-Ab rxn occuring after antigen person is sensitve to enters the body

anaphylactic shock patho

start with IgE antibody latching onto mast cells, causing histamine to release into the bloodstream causing vasodilation causing dec. vascular resistance. this leads to dilation of the arterioles causing dec. BP and inc. cellular permeability causing major fluid/protein loss into the tissue space causing this shocks symptoms to occur (edema, wheezing, hypovolemia)

Nuerogenic shock - causes

caused by spinal cord injuries usually above T6 or loss of vascular tone

neurogenic shock patho

starts w/ spinal cord injury causing imbalance between PSNS adn SNS with PSNS being more dominant, this causes massive vasodilation, dec. vascular tone and either dec. or the same SVR which leads to inadequate CO and dec. tissue perfusion. causing impaired cellular metabolism causing lactic acidosis and possible organ failure.

obstructive shock causes -

caused by: cardiac tamponade, tension pneumothorax and pulmonary embolisms all of which block bloods normal flow

obstructive shock - s/sx

s/sx - severe SOB, chest pains, dec. UO, rapid heart rate

obstructive shock - treatment

treatment - immediate/quick rmeoval of the block, managing pt. symptoms and stablizing their condition with meds or surgical interventions.

what is chronotropic

the hearts rate of contraction (from the SA node)

• positive effects - inc. HR

• negative effects - dec. HR

what is dromotropic

• the rate of conduction in the heart (from the AV node)

inotrpopic

the strength of contraction

• poisitve = inc. contraction

  • negative = dec. contraction

chronotropic effects - positive effects

increase the heart rate

• meds that give this:

• atropine,

• dobutamine

• epinephrine

• isoproternoll

  • caffeine

chronotropic effects - negative effects

decrease the HR

• meds that give this

• Beta blockers

• CCBs

• digoxin

• aniodarone

inotropic effcets of the heart - positive

increase heart contractility

• meds tha give this:

• digoxin

• norepi

• dobutamin

• dopamine

• adrenaline

inotropic effects of the heart - negative effects

decrease heart contractility

• meds that give this

• beta blockers

• CCBs

• sedatives

• anesthetics

• alcohol

dromotropic effects - positive

increase HR conduction

• meds that give this:

• digoxin

• epinephrine

• norepinephrine

• dobutamine

inotropic effects - negative inprtropes

dec. HR conduction

• beta blockers

• CCB

• Digoxin

• antirhythmic drugs

difference between epinephrine and norepinephrine - epinephrine

• stimulates alpha and beta adrenergic receptors

• more inc. of HR and CO

• used for anaphylactic shock

  • causes more tachycardia, anxiety, restlessness

difference between epinephrine and norepinephrine - norepinephrine

• only stimulates alpha adrenergic receptors

• signifigc inc. of vasoconstriction causing inc. SVR

• used for septic shock

• my cause peripheral ischemia d/t vasoconstriction

Life threatening complications of shock - ARDS

acute rep. distress syndrome - severe inflammation and fluid leak into aveoli

• associated w. prolonged shock and tissue hypoxia

• usually caused by ammonia and sepsis

life threatenign conditions of shock - DIC

disseminated intravascular coagulation - overactive blood clotting

• develop w/ sepsis or injury affecting normal blood clotting

life threatening conditions of shock - ARF

Acute renal failure (pre, intra and post)

• hypovolemia causes dec. BF to kidneys d/t low BP

life threatening conditions of shock - multiple organ fail

multiple organs fail due to dec. CO and dec. in perfusion due to shock