Patho Shock

31問 • 2年前

問題一覧

Shock in which the body is still able to compensate for absolute or relative fluid loss (patient is able to maintain an adequate BP and cerebral perfusion)

Compensated

The late phase of shock in which the body’s compensatory mechanisms are unable to maintain adequate perfusion to the brain and organs

Decompensated

A rapid deterioration of the CV system and the compensatory mechanisms have failed and the patient will die

Irreversible

Inability of heart to pump adequate blood to tissues/organs causing hypotension and hypoperfusion despite adequate LV filling pressure and intravascular volume

Cardiogenic Shock

1. Decreased contractility: MI, cardiomyopathy, sepsis, myocarditis, pericarditis, aneurysms, dysrhythmias, contusion, metabolic abnormalities, papillary muscle rupture 2. Impaired diastolic filling: dysrhythmias 3. Obstruction: PE, cardiac tamponade, valve disorder, tumors, wall defects

Etiologies of Cardiogenic Shock

High SVR (pallor cool extremities), thirst, oliguria, low preload (RA pressure or CVP) and tachycardia

Manifestations of hypovolemic shock

Widespread and massive vasodilation related to imbalance in parasympathetic and sympathetic NS

Neurogenic shock

Anything that stimulates par parasympathetic activity and inhibits sympathetic activity (brain spinal cord trauma, conditions that deprive medulla of oxygen or glucose, depressive drugs, anesthesia, emotional stress, pain)

Etiologies of neurogenic shock

Hypotension with bounding peripheral pulses and flash cap refill, Bradycardia

Defining characteristics of neurogenic shock

Inflammatory and vasodilatory reaction to an allergic antigen.

Anaphylactic shock

Vasodilation->hypotension, peripheral pooling, tissue edema, and bronchoconstriction

Defining characteristics of anaphylactic shock

Exposure to allergic antigen (anaphylactoid type - cold, exercise, and medication contaminants)

Etiologies of anaphylactic shock

CV: hypotension, diaphoresis, pallor. Respiratory: SOB, cough, rhinorrhea, throat tightening, wheezing. GI: N/V/D, abdominal pain. Cutaneous: erythema, pruritis, urticaria, angioedema. Ominous sign - anxiety, confusion, impaired mentation.

Manifestations of anaphylactic shock

Epinephrine to stop mast cell degranulation, fluid resuscitation, antihistamines, steroids

Treatment of anaphylactic shock

Progressive dysfunction in response to an infection caused by Gram negative and positive bacteria, viruses, and fungus. PNA, bloodstream, intravascular catheter, intrabdominal, urosepsis, surgical wound.

Septic shock

SIRS—>Sepsis—>Septic Shock—>MODS

The Sepsis Spectrum

Reaction to anything that stimulates the inflammatory response (both infections and non-infectious). If homeostasis restored can be reversed, but it not and infection continues —>Sepsis.

SIRS

Temp >38C or <36C HR > 90 RR > 20 or PaCO2 <32 WBC > 12,000 or < 4,000 or > 10% bands

Defining characteristics of SIRS

Life threatening organ dysfunction caused by a dysregulated host response to infection. Commonly affects: respiratory, hematologic, cardiac, renal, hepatic, and CNS systems

Sepsis

Systolic hypotension (<90) and organ dysfunction (measured with LODS, SOFA, qSOFA)

Defining characteristics of Sepsis

SOFA measures

P/F ratio, PLT count, GCS, Bilirubin, MAP, Creatinine

SOFA is (+) if

If score increases 2 points or more indicating organ dysfunction and hypoperfusion

Quick SOFA measures if

RR >22 GCS < 15 (or lower than baseline) SBP < 100

Quick SOFA is (+) if

If 2/3 criteria are true

Hypo/hyperthermia, tachycardia, tachypnea, AMS, significant edema, positive fluid balance, hyperglycemia. Leukocytosis or leukopenia (>12,000 or <4,000, or bandemia >10%), elevated CRP and/or Procalcitonin. Hypotension, SvO2, CI>3.5. PF ratio <300, Oliguria ((<0.5ml/kg/hr x 2 hrs), Cr increase, coagulopathy, ileus, thrombocytopenia, hyperbilirubinemia. Lactic acidosis, decreased cap refill.

Sepsis manifestations

Subset of Sepsis with profound circulatory , cellular, and metabolic abnormalities (increased risk of mortality)

Septic shock

A vasopressor requirement to maintain MAP >65. Low SVR and vasodilation. Lactate >2. Without hypovolemia.

Defining characteristics of Septic Shock

Progressive dysfunction of 2+ organ systems from uncontrolled inflammatory response to severe illness or injury (Sepsis or Sepsis related disorders: burns, trauma, heat stroke). Risk factors: older age, significant tissue injury, pre-existing conditions.

MODS

Organ dysfunction related to specific ischemic or hypoperfusion. Decreased perfusion to—>local tissues/organs, or generalized hypoperfusion (subclinical)—>sets cells up for exaggerated response it it’s secondary form.

Primary MODS

Excessive inflammation reaction after a latent period following initial injury (organ is often distant from site of original injury). End result is organ failure and death 54% with 2 organ failures, 100% with 5 organ failures.

Secondary MODS

24 hrs post injury: fever, tachycardia, tachypnea, dyspnea, AMS, hypermetabolic state 24-72 hours later: respiratory failure (ARDS) 7-10 days later: hypermetabolic and hyperdynamic state. Bacteremia (enteric), hepatic, renal, GI failure. 14-21 days later: worsening organ failures can evolve to death. 21+ days later: linger - improve or die; rapidly - improve or die.

MODS Manifestations

Patho Renal

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