Shock

Cardiogenic Shock
(CO & MAP decrease)

Hypovolemic Shock
(MAP decrease)

Distributive Shock
(MAP decrease)

Cause: Total body fluid decreased ( in all fluid departments)
Risk Factors:
- Hemmorhage (trauma, GI ulcer, surgery, inadequate clotting {hemophilia, liver disease, malnutrition, bone marrow suppresion, cancer, anticoagulation therapy}
- Dehydration (vomitting, diarrhea, heavy diaphoresis, diuretic therapy, nasogastric suction, diabetes insipidus, hyperglycemia)

Pathophysiology: Loss of blood -> loss of circulating red blood cells -> decreased blood flow -> decreased MAP > 5-10 mm Hg -> baroreceptors in aortic arch and carotid sinus are triggered -> transmit info to brain -> compensatory mechanisms are stimulated -> blood is shunted to vital organs -> lactic acid levels, protein-destroying enzymes, and oxygen free radicals increase -> electrolyte and acid-base imbalances

Cause: direct pump failure (fluid volume not affected)
Risk Factors:

  • Myocardial infarction
  • Cardiac Arrest
  • Cardiac tamponade
  • Ventricular dysrhythmias (fibrillation, tachycardia)
  • Cardiac amyloidosis
  • Cardiomyopathies (viral, toxic)
  • Myocardial degeneration

Cause: fluid shifted from central vascular space (total body fluid volume normal or increased
Risk factors:

  • Neural induced (pain, anesthesia, stress, spinal cord injury, head trauma
  • Chemical induced (anaphylaxis, sepsis, capillary leak {burns, extensive trauma, liver impairment, hypoproteinemia)

Stages of Shock

Progressive Stage

  • Decrease in MAP of >20 mm Hg from the patient's baseline
  • Anoxia of nonvital organs
  • Hypoxia of vital organs
  • Overall metabolism is anaerobic
    -Moderate acidosis
    -Moderate hyperkalemia
    -Tissue ischemia
  • S/S: worsening of subjective and objective changes; may express impending doom; rapid, weak pulse, low BP, pallor to cyanosis of oral mucosa & nail beds, cool and moist skin, anuria, 5%-20% dec in O2 sats, low pH, rising lactic acid and K .
    VITAL ORGANS CAN TOLERATE THIS SITUATION FOR ONLY A SHORT PERIOD (< 1 hour)

Refractory Stage

  • Severe tissue hypoxia with ischemia and necrosis
  • Release of myocardial depressant factor from the pancreas
  • Buildup of toxic metabolites
  • Multiple organ dysfunction syndrome (MODS)
  • Death

Nonprogressive Stage

  • Decrease in MAP of 10-15 mm Hg from the pt's baseline
  • Continued sympathetic stimulation
    -Moderate vasoconstriction
    -Increased heart rate
    -Decreased pulse pressure
  • Chemical compensation
    -Renin aldosterone, and antidiuretic hormone secretion
    -Increased vasoconstriction
    -Decreased urine output
    -Stimulation of the thirst reflex
  • Some anaerobic metabolism in nonvital organs
    -mild acidosis
    -mild hyperkalemia
  • Tissue hypoxia in nonvital organs (skin, GI tract) and kidneys
  • S/S: thirst, anxiety, restlessness, tachycardia, inc. RR, dec. urine output, falling systolic BP, rising diastolic BP, narrowing PP, cool extremities, 2%-5% dec in O2 sats.
    REVERSIBLE W/ INTERVENTIONS

Initial Stage

  • Decrease in baseline mean arterial pressure (MAP) of 5-10 mm Hg
  • Increased sympathetic stimulation
    -Mild vasoconstriction
    -Increased Heart rate
  • Production of lactic acid

Multiple Organ Dysfunction Syndrome
the sequence of cells damage caused by the massive release of toxic metabolites and enzymes

Etiology:
As more dead cells break open and release harmful metabolites creating a cycle. The buildup of metabolites trigger small clots (microthrombi) to form, which block tissue oxygenation and damage more cells, thus continuing the devastating cycle. Liver, heart, brain, and kidney fx are lost first. The most profound change is damage to the heart muscle. One cause is the release of myocardial depressant factor from the ischemic pancreas.

Teaching and Interventions

  • Teach all people to prevent dehydration by having adequate fluid intake during exercise and when in hot, dry environments
  • Urge people to prevent trauma and hemorrhage by using proper safety equipment and seat belts and being aware of hazards in the home or workplace
  • Identify pts at risk for dehydration and assess for early manifestations
  • Assess all patients who have invasive procedures or trauma for obvious occult bleeding
  • Compare pulse quality and rate with baseline
  • Compare urine output with fluid intake
  • Check vital signs for patients who have persistent thirst
  • Assess for shock in any patient who develops a change in mental status, an increase in pain, or an increase in anxiety.
  • When pts have procedures and then go home, teach s/s of shock

Assessment

  • Ask about recent illness, trauma, procedures, or chronic health problems
  • Ask about the use of aspirin, other NSAIDs, and diuretics
  • Ask about fluid intake and output during the previous 24 hours
  • Assess for obvious signs or factors that could lead to shock
  • Assess gums, wounds, sites of dressings, drains, and vascular access (checkunder the pt for blood)
  • Observe for any swelling or skin discoloration that may indicate an internal hemorrhage

Clinical Manifestations
Cardiovascular: occur with dec MAP leading to compensatory responses. Assess the central and peripheral pulses for rate and quality. In the initial stage, HR inc (first manifestation). Stroke vol is dec, peripheral pulses are difficult to palpate (as shock progresses may become absent). When assessing BP, compare to baseline. Systolic pressure dec. as shock progresses and CO dec. leading to dec. pulse pressure. At this stage, BP is difficult to hear. O2 sats are 90-95% during the nonprogressive stage of shock and between 75-80% with the progressive stage.


Respiratory: Assess rate, depth, and ease of respirations. RR inc. during hypovolemic shock. When shock progresses to the stage at which lactic acidosis is present, the rr depth also inc.


Kidney/Urinary: Assess urine for volume, color, specific gravity, and the presence of blood or protein. Measure urine output every hour. (dec urine output is a sensitive indicator of early shock). Kidney can tolerate anoxia for up to 1 hr.


Skin: Assess for temp, color, and moisture (cool, cold, moist). Observe oral mucosa. As shock progresses, skin becomes mottled. Evaluate capillary refill. With shock, may be slow or absent.


CNS: Assess LOC and orientation. Pt may be restless, agitated or anxious. As hypoxia progresses, leads to lethargy and loss of consciousness.


Skeletal: Muscle weakness and pain in response to tissue hypoxia. Deep tendon reflexes are decreased or absent. Assess muscle strength. Assess deep tendon reflexes.

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Obstructive Shock

Patho: Mediator excess: cytokines, oxygen free radicals etc. -> widespread endothileal injury and dysfunction -> vasodilation and increased capillary permeability -> tissue edema -> neutrophil entrapment in microcirculation

Early manifestations: tachycardia, hypotension, narrowed pulse pressure, increased myocardial O2 consumption
Physical assessment: tachypnea, pulmonary congestion, dec capillary refill time, anxiety, confusion, agitation


  • increased PAWP, decreased renal perfusion and urine output