Sepsis-Shock-MODS

shock pathway

inadequate tissue perfusion --> cellular O2 deficit --> anaerobic metabolism --> increase lactate and metabolic acidosis --> cell/organ death

universal goal during sepsis

restore O2 delivery and perfusion (MAP ≥ 65 mmHg)

4 stages of shock

1. initial: cellular hypoxia --> anaerobic metabolism --> increase lactate

2. compensatory: SNS/RAAS/ADH activation --> increase HR, RR, cool clammy skin, decreased UO, narrowing pulse pressure, restlessness; BP near normal --> REVERSIBLE

3. progressive: compensation fails --> hypotension, decreased LOC, weak thready pulse, organ ischemia, worsening acidosis, decreased UO (anuria)

4. refractory/irreversible: profound hypotension unresponsive to therapy --> MODS --> death

what are the first signs of compensation for decreasing perfusion?

tachycardia, narrow pulse pressure, restlessness, rising lactate

clinical manifestations by system during shock (neuro, CV, respiratory, renal, skin, GI)

neuro --> restlessness, anxiety --> confusion --> decreased LOC

CV --> increased HR, weak thready pulse, narrow pulse pressure, decreased BP (late)

respiratory --> increased RR and depth (early), shallow (late) --> ARDS

renal --> urine output < 0.5 mL/kg/hr, increased BUN and creatinine

skin --> warm/flushed --> cool, pale, clammy, mottled

GI --> decreased bowel sounds, ilea, stress ulcers, increased lactate

how to fix preload, contractility, afterload, and content (hgb x SpO2)?

preload --> volume

contractility --> inotrope

afterload --> vasopressors

content --> oxygen/blood

increase/ decrease preload for hypovolemic, cardiogenic, obstructive, distributive

hypovolemic --> decrease

cardiogenic --> increase

obstructive --> either

distributive --> decrease

cardiac output during shock (except?)

decreased

distributive increased then decreased

SVR during shock (except?)

increased

distributive is low SVR with initially high CO

hypovolemic shock is loss of _____? examples? tx?

loss of intravascular volume

ex: hemorrhage, burns, vomiting, diarrhea, third spacing

tx: fluids

cardiogenic shock is a failure of _______? examples? treatment?

failure of the heart as a pump

ex. acute MI, HF, dysrhythmias, valve failure

tx: NO FLUIDS, inotropes (digoxin, dobutamine)

obstructive shock is a ______ to blood flow? examples? treatment?

physical block to blood flow

ex: cardiac tamponade, pension pneumothorax, massive PE

tx: remove obstruction

distributive shock is ______/loss of ______? examples? treatment?

maldistribution/loss of vascular tone

ex: septic, anaphylactic, neurogenic

tx: septic (abx, IVF), anaphylactic (IM epi), neurogenic (immobilize, atropin for brady, vasopressors)

hypovolemic shock pathway

decreased volume (hemorrhage, GI loss, burns, dehydration, third spacing) --> decrease venous return (preload) --> decrease SV --> decreased CO + increase SVR --> decreased tissue perfusion + O2 delivery --> cellular hypoxia --> organ injury

absolute loss vs relative loss

absolute loss = volume leaves the body

- hemorrhage, vomiting, diarrhea, burns, DKA

relative loss = third spacing

- fluid shifts into interstitial space

- ascites, bowel obstruction, pancreatitis, sepsis cap leak

4 classes of hypovolemic shock

class I: up to 15% blood loss,

treatment for hypovolemic shock

stop loss; isotonic fluids bolus/blood via 2 large bore IVs

MAP goal >65

cardiogenic shock pathway

pump failure (#1 MI)

decreased myocardial contractility --> decreased SV + CO --> blood backs up --> pulmonary congestion --> increased afterload --> increased cardiac workload + O2 demand --> worsening ischemia --> further pump failure

**BODY COMPENSATES THROUGH VASOCONSTRICTION RESULTING IN PULMONARY EDEMA

symptoms of cardiogenic shock

- crackles, dyspnea, pulmonary edema

- S3, JBD

- cool, clammy, mottled skin

- oliguria/anuria

treatment for cardiogenic shock

oxygen, inotrope (dobutamine), vasopressors (norepinephrine), diuretics, vasodilators (nitroglycerin), treat cause

types of distributive shock; what is common about all of them

1. septic

2. anaphylactic

3. neurogenic

massive vasodilation --> decreased SVR --> relative hypovolemia ("warm shock")

pathway for septic shock (3 stages) + early and late sx

sepsis 1: infection + 2 SIRS criteria

sepsis 2: infection + SIRS + expanded criteria

sepsis 3: infection + SIRs + >2 SOFA (organ dysfunction)

septic shock: unresponsive to fluids + vasopressors required + lactate >2

infection --> inflammation --> vasodilation, increased capillary permeability

- early: warm/flushed

- late: cold, clammy

SIR criteria (4)

temp >38C or

early/warm shock vs late/cold shock

early/warm shock:

- hyper dynamic: decreased SVR, increased CO

- warm, flushed, dry skin

- bounding pulses, brisk cap refill

- fever, tachycardia, tachypnea

- altered mentation

- wide pulse pressure

late/cold shock

- decompensated: decreased CO, hypoperfusion dominates

- cool, mottled, clammy skin

- weak, thready pulses, delayed refill

- hypotension unresponsive to fluids

- oliguria --> anuria

- worsening lactate, falling mentation

- MODS

surviving sepsis campaign

1. measure >2 lactate

2. blood cultures BEFORE abx

3. board spectrum antibiotics

4. crystalloid 30 mL/kg

5. vasopressors (norepinphrine FIRST LINE)

progression of vasopressors

levophed (norepinephrine)

vasopressin (vasopressin)

neo (phenylephrine)

treatment for septic shock

cultures FIRST --> antibiotics + fluids, norepinephrine

pathway for anaphylactic shock

allergen --> massive histamine release --> vasodilation + capillary leak + bronchospasm --> angioedema

treatment for anaphylactic shock

IM epinephrine FIRST, airway/O2, antihistamine, steroid, IVF, bronchodilators

pathway for neurogenic shock

SNS loss (SCI above T6) --> PSNS vasodilation --> hypotension + bradycardia (relative hypovolemia) --> warm/dry skin

**the only distributive shock exhibiting hypotension WITH bradycardia

treatment for neurogenic shock

IVFs, vasopressors (phenylephrine, norepinephrine), atropine (for bradycardia), spinal immboilization

pathway for obstructive shock + causes (3)

physical block to flow (cardiac tamponade, tension, pneumothorax, massive PE)

what is cardiac tamponade? what triad is indicative of this disease? treatment?

fluid in the pericardiac sac compresses the heart thus preventing filling

- Beck's triad: hypotension, JVD, muffled heart sounds

- pulsus paradoxus

- tx: pericardiocentesis

what is tension pneumothorax? characteristics? treatment?

trapped air collapses the lung and shifts the mediastinum, kinking great vessels

- absent breath sounds, tracheal deviation

- JVD, severe dyspnea, hypotension

- tx: needle decompression/chest tube

what is a pulmonary embolism? characteristics? treatment?

a large clot obstructs pulmonary outflow, straining the right ventricle

- SUDDEN dyspnea, chest pain, hypoxia

- RV strain, tachycardia

- tx: thrombolytics/embolectomy

treatment for obstructive shock

relieve the obstruction

what is MODS? #1 cause?

progressive dysfunction of 2 or more organ systems

- sepsis is #1 cases

primary vs secondary MODS

primary MODS:

- direct organ injury from a defined insult

- ex. trauma, major burns, aspiration, pneumonitis

secondary MODS:

- develops later, remote from original insult

- sepsis is classic trigger

pathway of MODS

uncontrolled SIRS --> endothelial damage --> increased cap permeability

--> microvascular coagulation + maldistribution of flow --> hyper metabolism + tissue hypoxia --> sequential organ failure

typical order of organ failure

lungs --> liver --> GI tract --> kidneys --> heart --> hematologic