Exam 3 Flashcards
SIRS (Systemic inflammatory response syndrome) triggers
Trauma
Abscess
Ischemic/necrotic tissue
Microbial invasion (bacterial, viral, fungal)
Endotoxin release
Global perfusion deficits
Regional perfusion deficits
MODS
Multiple organ dysfunction syndrome
Failure of 2+ organ systems
Result of SIRS
Patho of SIRS and MODS
Result of inflammatory response
Organ and metabolic dysfunction
Respiratory Manifestations of SIRS and MODS
Alveolar edema
Decreased surfactant
Increased shunting
V/Q mismatch
End result: ARDS
Cardiovascular Manifestations of SIRS and MODS
Myocardial depression and massive vasodilation
Results in decreased SVR and BP
Baroreceptors respond to enhance CO
Albumin and fluid move out of blood vessels
Neurological Manifestations of SIRS and MODS
Mental status changes due to hypoxemia, inflammatory mediators, or impaired perfusion
Often early sign of MODS
Renal Manifestations of SIRS and MODS
Acute kidney injury (AKI)
Hypoperfusion
Release of mediators
Activation of renin-angiotensin-aldosterone system
Nephrotoxic drugs, especially antibiotics
GI Manifestations of SIRS and MODS
Motility decreased: abdominal distention and paralytic ileus
Decreased perfusion: risk for ulceration and GI bleeding
Potential for bacterial translocation
Hypermetabolic Manifestations of SIRS and MODS
Hyperglycemia-hypoglycemia
Insulin resistance
Catabolic state
Liver dysfunction
Lactic acidosis
Nursing interventions of SIRS and MODS
Infection prevention
Maintain oxygenation
Nutritional and metabolic needs
Support failing organs
Initial stage of shock
Not clinically apparent
Lactic acid accumulates and must be removed by blood and broken down by liver
Compensatory stage of shock
Clinically apparent
Baroreceptors activate SNS
- vasoconstriction, RASS, impaired GI motility, cool, clammy skin
Cardiovascular manifestations in Progressive stage of shock
When compensatory mechanisms fail
Decreased cellular profusion and altered capillary permeability
- Protein leaks into interstitial space, increased edema
Anasarca (diffuse profound edema)
Pulmonary manifestations in Progressive stage of shock
Fluid moves from pulmonary vasculature to interstitium
Pulmonary edema
Bronchoconstriction
Alveolar edema
Decreased surfactant
Worsening V/Q mismatch
Tachypnea
Crackles
Cardiac manifestations in Progressive stage of shock
CO falls
Weak pulses
Ischemia of distal extremitites
GI manifestations in Progressive stage of shock
Mucosal barrier becomes ischemic
- Ulcers, bleeding, decreased nutrient absorption
Renal manifestations in Progressive stage of shock
Renal tubular ischemia
May result in AKI
Hepatic manifestations in Progressive stage of shock
Failure to metabolize drugs and waste
Jaundice
Elevated enzymes
Loss of immune function
Risk for DIC and bleeding
Irreversible stage of shock
Exacerbation of anaerobic metabolism
Accumulation of lactic acid
↑ Capillary permeability
Profound hypotension and hypoxemia
Tachycardia worsens
Failure of one organ system affects others
Recovery unlikely
Hypovolemic Shock cause
Hypovolemic shock results from a decrease in circulating volume—particularly following loss of more than 15 to 30% of normal blood volume.
Hemorrhage
GI loss (e.g., vomiting, diarrhea)
Fistula drainage
Diabetes insipidus
Hyperglycemia
Diuresis
Cardiogenic Shock
Results from the heart’s inability to adequately circulate blood to the tissues
Systolic or diastolic dysfunction
Compromised cardiac output (CO)
Cardiogenic shock precipitating causes
Myocardial infarction
Cardiomyopathy
Blunt cardiac injury
Severe systemic or pulmonary hypertension
Cardiac tamponade
Myocardial depression from metabolic problems
Early manifestations of cardiogenic shock
Tachycardia
Hypotension
Narrowed pulse pressure
↑ Myocardial O2 consumption
Cardiogenic shock expected assessment findings
Tachypnea, pulmonary congestion
Pallor and cool, clammy skin
Decreased capillary refill time
Anxiety, confusion, agitation
↑ In pulmonary artery wedge pressure
Decreased renal perfusion and UOP
Hypotension
Tachycardia
Delayed capillary refill
Cool, mottled extremities
Jugular venous distention
Dyspnea and crackles if pulmonary edema is present
Oliguria, altered mental status
Distributive Shock
Vasodilation and redistribution of blood volume
Obstructive Shock
Occurs as a result of impairment in cardiac ventricular filling or ventricular emptying
Hypovolemic shock tx
Isotonic solution (NS)
Colloid (blood products)
Cardiogenic shock tx
Dopamine
Norepinephrine
Diuretics and nitroglycerin for pulmonary edema
Cause of neurogenic shock
Can occur within 30 minutes of a spinal cord injury at the fifth thoracic (T5) vertebra or above
Can occur in response to spinal anesthesia
Neurogenic shock
Hemodynamic phenomenon
Can last up to 6 weeks
Results in massive vasodilation, leading to pooling of blood in vessels
Manifestations of neurogenic shock
Hypotension without compensatory tachycardia
Bradycardia
Temperature dysregulation (resulting in heat loss)
Dry skin
Poikilothermia (taking on the temperature of the environment)
Bowel and bladder dysfunction
Priapism
Decreased filling pressures (MAP, CVP/RAP, PAWP)
Loss of sympathetic innervation below level of injury results in (neurogenic shock)
Vasodilation-hypotension
Warm, dry skin
Loss of urinary bladder tone
Paralytic ileus
Loss of perspiration
Loss of cutaneous and DTR’s
Parasympathetic innervation continuing unopposed results in (neurogenic shock)
Neurogenic shock tx
Crystalloids first
Dopamine, norephinephrine, or phenylephrine
Atropine for bradycardia
Anaphylactic shock tx
Epinephrine
Diphenhydramine
Ranitidine or famotidine
Septic shock tx
Norepinephrine
Dopamine
Phenylephrine
Vasopressin
Manifestations of hypovolemic shock
Anxiety
Tachypnea
Increase in CO, heart rate
Decrease in stroke volume, PAWP, urinary output
Hypotension; orthostatic hypotension
Tachycardia
Reduced capillary refill
Dry mucus membranes
Poor skin turgor
Thirst; weight loss; Oliguria
Altered mental status
Tx for pulmonary edema in cardiogenic shock
Diuretics
Preload reducers (nitroglycerin)
High flow oxygen
CPAP, BiPAP
Mechanical ventillation
Tx for decreased cardiac output during cardiogenic shock
Positive inotropes
Intraaortic balloon pump
Perecutaneous coronary interevntion
Surgical correction of structural defect
Major effects of septic shock
Vasodilation
Maldistribution of blood flow
Myocardial depression
- Decreased ejection fraction
- Ventricular dilation
Clinical manifestations of septic shock
Tachypnea/hyperventilation
Temperature dysregulation
↓ Urine output
Altered neurologic status
GI dysfunction
Respiratory failure is common
Septic shock
Presence of sepsis with hypotension despite fluid resuscitation
Presence of inadequate tissue perfusion resulting in hypoxia
Clinical manifestations of septic shock
↑ Coagulation and inflammation
↓ Fibrinolysis
- Formation of microthrombi
- Obstruction of microvasculature
Hyperdynamic state: increased CO and decreased SVR
Obstructive Shock cause
Develops when physical obstruction (clot) to blood flow occurs with decreased CO
- From restriction to diastolic filling of the right ventricle due to compression
- Can cause Abdominal compartment syndrome
Obstructive Shock clinical manifestations
Decreased CO
Increased afterload
Variable left ventricular filling pressure
Obstructive Shock
Hypotension, pulsus paradoxus; tachycardia
Muffled heart tones (indicates cardiac tamponade)
Reduced capillary refill
Tachypnea, JVD, crackles
Unilateral absence of breath sounds (tension pneumothorax)
Tracheal deviation (tension pneumothorax)
Oliguria
Altered mental status
