What is Shock?
Syndrome characterized by decreased tissue perfusion and impaired cellular metabolism.
What happens when a cell experiences Hypoperfusion?
The demand for oxygen and nutrients exceeds the supply at the microcirculatory level.
What are the four classifications of shock?
Cardiogenic, Hypovolemic, Distributive, and Obstructive.
What happens during SIRS?
Systemic inflammatory response to a variety of insults, including infection, ischemia, infarction and injury. Generalized inflammation in organs remote from the initial insult characterize SIRS.
What happens during MODS?
The failing of two or more organ systems in an acutely ill patient such that homeostasis cannot be maintained without intervention.
What is Cardiogenic Shock??
Occurs when either systolic or diastolic dysfunction of pumping action of the heart results in reduced Cardiac Output (CO).
What are causes of Cardiogenic Shock?
Systolic Dysfunction, Diastolic Dysfunction, Dysrhtyhmias (bradydysrhythmias, tachycdysrhythmias), Structural Factors (valvular stenosis or regurg, ventricular septal rupture, tension pneumothorax).
What is Systolic Dysfunction?
Inability of the heart to pump blood forward. i.e., MI, Cardiomyopathy, blunt cardiac injury, severe systemic/pulmonary hypertension, myocardial depression.
Why does Systolic Dysfunction affect the left ventricle?
Because systolic pressure and tension are greater on the left side of the heart.
What is Diastolic Dysfunction?
Inability of the heart to fill during diastole. i.e., pericardial tamponade, ventricular hypertrophy, cardiomyopathy.
What are the effects of cardiogenic shock on hemo dynamic parameters?
Increased HR, SVR, PVR, CVP, PAP, PAWP, Decreased PP, BP, CO, SVO2.
What is the pathophysiology of Cardiogenic Shock with systolic dysfunction?
Systolic dysfunction -> decreased stroke volume, decreased cardiac output -> decreased cellular oxygen supply -> decreased tissue perfusion -> impaired cellular metabolism.
What is the pathophysiology of Cardiogenic Shock with Diastolic Dysfunction?
Diastolic dysfunction -> increased pulmonary pressures -> pulmonary edema -> decreased oxygenation -> decreased cellular oxygen supply -> decreased tissue perfusion -> impaired cellular metabolism.
What are the early clinical manifestations of Cardiogenic Shock?
Tachycardia, hypotension, and narrowed pulse pressure.
On examination of a patient in Cardiogenic Shock, what will you probably observe?
Tachypneic, and crackles on auscultation of breath sounds due to pulmonary congestion, peripheral hypoperfusion, decreased urine output, anxiety, confusion, and aggitation.
What are signs of Peripheral hypoperfusion?
Cyanosis, pallor, diaphoresis, weak peripheral pulses, cool and clammy skin, delayed capillary refill.
What are studies useful in diagnosing Cardiogenic Shock?
Cardiac Enzymes, Troponin levels, BNP, ECG, Chest X-Ray, and Echo.
What causes Hypovolemic Shock?
When there is a loss of intravascular fluid volume. The volume is inadequate to fill the vascular space.
What is Absolute Hypovolemia?
External loss of whole blood (hemmorhage, surgery, GI bleeding), or loss of other body fluids (vomiting, diarrhea, diuresis, DI/DM).
What is Relative Hypovolemia?
Pooling of blood or fluids (bowel obstruction), fluid shifts (burn injuries, ascites), internal bleeding, massive vasodilation (sepsis).
What are the effects of Hypovolemic Shock on Hemodynamics?
Increased HR, SVR, PVR, Decreased PP, BP, CVP, PAP, PAW, CO, and SVO2.
What does the patients response to acute volume loss depend on?
Extent of injury or insult, age, and general state of heath.
What are the S/S of Hypovolemic Shock?
Decreased preload, SV, and cap refill. Tachypnea -> bradypnea, decreased urine output, pallor, cool, clammy, decreased cerebral perfusion -> anxiety, confusion agitation, absent bowel sounds, decreased hct, hgb, lactate. increased urine specific gravity.
How much blood loss may a patient be able to compensate for?
A loss of up to 15% (approximately 750 mL).
What happens to a patient with further loss of volume (15-30%)?
Results in a sympathetic nervous systemic (SNS) mediated response.
What happens with a fluid loss above 40%?
Loss of autoregulation in the microcirculation and irreversible tissue destruction occurs.
What is the pathophysiology of Hypovolemic Shock?
Relative/Absolute -> Decreased circulating volume -> decreased venous return -> decrease stroke volume -> decreased cardiac output -> decreased cellular oxygen supply -> decreased tissue perfusion -> impaired cellular metabolism.
What causes Neurogenic Shock?
Can occur within 30 minutes of a spinal cord injury at the fifth thoracic (T5) vertebra or above and last up to 6 weeks.
What happens to cause Neurogenic Shock?
An injury results in a massive vasodilation without compensation due to the loss of SNS vasoconstrictor tone. Leads too pooling of the blood in the blood vessels, tissue hypoperfusion, and ultimately impaired cellular metabolism.
Besides injury, what else can result in Neurogenic Shock?
Spinal anesthesia blocking transmission of impulses from the SNS, and depression of the vasomotor center of the medulla from drugs (opiods, benzos, diazepines).
What are the most important clinical manifestations in neurogenic shock?
Hypotension (from massive vasodilation), and bradycardia (from unopposed parasympathetic stimulation).
What is the clinical presentation of Neurogenic Shock?
Decreased BP, Disautoregulation of Temperature, Bradycardia, Bladder Dysfunction, Decreased skin perfusion, cool or warm, dry, flaccid paralysis below the level of the lesion, loss of reflex activity, bowel dysfunction.
What is the pathophysiology of Neurogenic Shock?
Loss of sympathetic tone (and parasympathetic response -> decreased hr) -> venous and arterial vasodilation -> decreased BP -> decreased venous return -> decreased stroke volume -> decreased cardiac output -> decreased cellular oxygen supply -> decreased tissue perfusion -> impaired cellular metabolism.
What is the effect of Neurogenic Shock on Hemodynamics?
Decreased HR, PP, BP, SVR, CVP, PAP, PAWP, CO and SVO2.
What is Anaphylactic Shock?
An acute and life threatening hypersensitivity (allergic) reaction to the sensitizing substance (e.g., drugs, chemical, vaccine, food, insect.)
What happens during Anaphylactic Shock?
Immediate rx causes massive vasodilation, release of vasoactive mediators, and an increase in capillary permability. Fluid leaks from the vascular space into the interstitial space.
What is the clinical presentation of Anaphylactic Shock?
Chest pain, third spacing, SOB, edema of larynx/epiglottis, wheezing, stridor, rhinitis, incontinence, flushing, pruitis, uticaria, angioedema, anxiety, impending doom, confusion, decreased LOC, metallic taste, swelling of lips/face, cramping, abd pain, nausea, vomiting, diarrhea.
What is the effect of Anaphylactic Shock on Hemodynamics?
Increased HR, PVR, Decreased PP, BP, SVR, CVP, PAP, PAWP, CO, and SVO2.
What is Septic Shock?
Presence of sepsis with hypotension despite fluid resuscitation along with the presence of inadequate tissue perfusion.
What is the response of the body during severe sepsis and septic shock?
Increase in inflammation and coagulation, a decrease in fibrinolysis. Endotoxins stimulate the release of cytokines. Release of platelet activating factor resulting in microthrombi and obstruction of microvasculature = damage to endothelium, vasodilation, increased capillary permeability, and neutrophil and platelet aggregation and adhesion to the endothelium.
What is the effect of Septic Shock on Hemodynamics?
Increased HR, PVR, Decreased PP, BP, SVR, CVP, PAWP, Up, down, or no change PAP, CO, or SVO2. Up or no change PVR.
What are the general variables in diagnostic criteria for sepsis?
Fever, hypothermia, heart rate >90 bpm, tachypnea, altered mental status, edema or +fluid balance, hyperglycemia w/o DM.
What are the inflammatory variables in diagnostic criteria for sepsis?
Leukocytosis, leukopenia, normal WBC count with >10% immature forms, ^ CRP, elevated procalcitonin.
What are the organ dysnfunction variables in diagnostic criteria for sepsis?
Arterial hypoxemia, acute oliguria, serum creatinine increase, coagulation abnormalities, ileus, thrombocytopenia, hyperbilirubinemia.
What are tissue perfusion variables in diagnostic criteria for sepsis?
Hyperlactatemia, decreased cap refill or mottling.
What are the clinical presentations of Septic Shock?
Up/Down Temperature, Myocardial Dysfunction, biventricular dilation, decreased EF, hyperventlation, respiratory alkalosis -> respiratory acidosis, hypoxemia, respiratory failure, ARDS, pulmonary hypertension, crackles, decreased urine output, warm and flushed - cool and mottled (late), alteration in mental status, agitation, coma (late), GI bleed, paralytic ileus, up/down WBC, decreased platelets, increased lactate, bg, urine specific gravity, decreased urine Na+.
What are the three main pathophysiologic effects of septic shock?
Vasodilation, maldistribution of blood flow, and myocardial depression.
What causes Obstructive Shock?
Develops when a physical obstruction to blood flow occurs with a decreased CO. i.e., cardiac tamponade, tension pneumothorax, superior vena cava syndrome, abdominal compartment syndrome.
What are the clinical presentations of Obstructive Shock?
Decrease Bp/Preload, tachypnea, bradypnea (late), SOB, decrease urine output, pallor, cool, clammy, decreased cerebral perfusion (anxiety, confusion, agitation), decrease to absent bowel sounds.
What is the pathophysiology of Obstructive Shock?
Structural compression -> decreased venous return and decreased outflow -> decreased stroke volume -> decreased cardiac output -> decreased cellular oxygen supply -> decreased tissue perfusion -> impaired cellular metabolism.
What happens during the compensatory stage of shock?
The body activates neural, hormonal, and biochemical compensatory mechanisms in an attempt to overcome the increasing consequences of anaerobic metabolism and to maintain homeostasis.
Why does a drop of blood pressure occur with shock?
Decrease in CO, and a narrowing of the pulse pressure. The baroreceptors in the carotid and aortic bodies immediately respond by activating the SNS.
What happens when the SNS is activated?
Stimulates vasoconstriction and the release of vasoconstrictors epinephrine and norepinephrine.
What is the clinical manifestations with the compensatory stage of shock in the neurologic system?
Oriented to person, place and time, restless, apprehensive, confused, change in LOC.
What is the clinical manifestation with the compensatory stage of shock in the cardiovascular system?
SNS response releases epinephrine/norepinephrine promoting vasoconstriction, increased in MVO2, increased contractility, increased hr, coronary artery dilation, narrowed pulse pressure, decreased bp.
What is the clinical manifestations with the compensatory stage of shock in the respiratory system?
Decreased blood flow to the lungs, increased physiologic dead space, increased ventilation perfusion mismatch, hyperventilation, increased minute ventilation.
What is the clinical manifestations with the compensatory stage of shock in the gastrointestinal system?
Decreased blood supply, decreased GI motility, hypoactive bowel sounds, increased risk for paralytic ileus.
What is the clinical manifestations with the compensatory stage of shock in the renal system?
Decreased renal blood flow, increased renin resulting in release of angiotensin, increased aldosterone resulting in Na+ and H20 absorption, increased ADH resulting in H20 reabsorption.
What is the clinical manifestations with the Progressive Stage of shock in the Neurologic System?
Decreased cerebral perfusion pressure, decreased cerebral blood flow, listless or agitated, decreased response to stimuli.
What is the clinical manifestations with the Progressive Stage of shock in the Cardiovascular System?
Increased capillary permeability -> systemic interstitial edema, decreased cardiac output -> decreased bp increased hr, decreased coronary perfusion -> dysrhythmias, myocardial ischemia, MI, decreased peripheral perfusion -> ischemia of extremities, diminished pulses, decreased cap refill.
What is the clinical manifestations with the Progressive Stage of shock in the Respiratory System?
ARDS - increased cap permeability, pulmonary vasoconstriction, pulmonary interstitial edema, alveolar edema, diffuse infiltrates, increased rr, decreased compliance, moist crackles.
What are the clinical manifestations with the Progressive Stage of shock in the Gastrointestinal System?
Vasoconstriction and decreased perfusion -> ischemic gut = erosive ulcers, GI bleeds, translocation of GI bacteria, impaired absorption of nutrients.
What are the clinical manifestations with the Progressive Stage of shock in the Renal System?
Renal tubules become ischemic -> acute tubular necrosis = decreased urine output, increased BUN/creatinine ratio, increased urine sodium, decreased urine osmolality and specific gravity, decreased urine potassium, metabolic acidosis.
What are the clinical manifestations with the Progressive Stage of shock in the Hepatic System?
Failure to metabolize drugs and waste products, cell death (^ liver enzymes), jaundice (decreased clearance of bilirubin), increased NH3 and lactate.
What are the clinical manifestations with the Irreversible Stage of shock in the Neurologic System?
Unresponsiveness, areflexia, pupils nonreactive and dilated.
What are the clinical manifestations with the Irreversible Stage of Shock in the Cardiovascular System?
Profound hypotension, decreased CO, bradycardia, irregular rhythm.
What are the clinical manifestations with the irreversible stage of shock in the respiratory system?
Severe refractory hypoxemia, respiratory failure.
What are the clinical manifestations with the irreversible stage of shock in the gastrointestinal system?
What are the clinical manifestations with the irreversible stage of shock in the renal system?
What are the clinical manifestations with the irreversible stage of shock in the hepatic system?
Metabolic changes from accumulation of waste products.
What are the clinical manifestations with the compensatory stage with skin?
Pale and cool, or warm and flushed (early onset of septic shock).
What are the clinical manifestations with the compensatory stage with lab findings?
Increased BG and pH, Decreased PaO2/PaCO2.
What are the clinical manifestations with the progressive stage and the hematologic system?
DIC -> thrombin clots in microcirculation and consumption of platelates and clotting factors.
What are the clinical manifestations with the progressive stage and thermoregulation?
Hypothermia, sepsis - hypothermia or hyper.
What are the clinical manifestations with the progressive stage and key lab findings?
Increased liver enzymes, bleeding time, and thrombocytopenia.
What are the clinical manifestations with the irreversible stage and key lab findings?
Decreased BG, Increased NH, lactate and K+, metabolic acidosis.
Which drugs are used for Cardiogenic Shock?
dobutamine (Dobutrex), dopamine (inotropin), epinephrine (Adrenalin), Norepinephrine (Levophed), nitroglycerin (Tridil), sodium nitroprusside (Nipride).
What drugs are used for Septic Shock?
dobutamine (Dobutrex), drotrecogin alfa (Xigris), hydrocortisone (solu-Cortef), norepinephrine (Levophed)
What are nursing implications for crystalloids?
Monitor for circulatory overload. DO not use LR with liver failure.
What are nursing implications for hypertonic solutions?
Monitor for hypernatremia, central line preferred.
What is Hetastarch (Hespan)?
Made from starch, volume expander used in shock except for cardiogenic and neurogenic.
What are nursing implications for Hetastarch (Hespan)?
1/2 the cost of albumin, use cautious with HF, RF, or bleeding disorders.
What is human serum albumin used for?
Increased plasma colloid osmotic pressure and rapid volume expansion for all types of shock except cardiogenic and neurogenic.
What are nursing implications for human serum albumin?
Monitor for circulatory overload. May cause chills, fever and uticaria. More expensive.
What are nursing implications for dextran (dextra 40, dextran 70)?
Increases risk of bleeding, monitor for allergic reactions and acute renal failure.
What is dextran (dextra 40, dextra 70) used for?
Hyperosmotic glucose polymer for volume expansion, limited use in shock.
What should you do with crystalloid and colloid solutions before massive fluid resuscitation?
Warm the fluids.
How long do you monitor a patients end-organ perfusion to ensure that tissue perfusion is adequate?
Every 2 hours for the first 6 hours.
What labs are used with a shock patient to assess nutritional status?
Serum protein, total albumin, BUN, serum glucose, and serum electrolytes.
What is the goal of a patient in Cardiogenic Shock?
Restore blood flow to the myocardium by restoring the balance between oxygen supply and demand.
What can drugs be used for in Cardiogenic Shock?
Decreasing workload of the heart by dilating coronary arterieis (nitrates), reducing preload (diuretics), reducing afterload (Vasodilators), and reducing heart rate and contractility (beta blockers).
What is the goal of using an circulatory assist device such as a Intraaortic Balloon Pump or Ventricular Assist Device?
To decreased SVR and the left ventricular workload so the heart can recoer.
What is the fluid resuscitation rule for Hypovolemic Shock?
3:1 - 3 mL of isotonic crystalloid for eery 1 mL of estimated blood loss.
How much fluid replacement does a patient with Septic Shock need?
As much as 6 - 10 L of isotonic crystalloids and 2 - 4 L of colloids in the first 6 hours to achieve a target CVP of 8 - 12 mm Hg.
When can vasopressors be added for a patient with Septic Shock?
When the CVP is greater than or equal too 8 mm Hg.
What are drug considerations for Vasopressin (Pitressin)?
Infuse at low doses (e.g., 0.01 to 0.03 units/min), do not titrate, use cautiously in patients with CAD.
What do you need to do before starting Antibiotics with Septic Shock?
Obtain cultures (e.g., blood, wound exudate, urine, stool sputum).
What mechanisms can trigger SIRS?
Mechanical tissue trauma, abscess formation, ischemic or necrotic tissue, endotoxin release, global perfusion deficits, regional perfusion deficits.