Exam 3 Flashcards by Morgan Sowder

SIRS (Systemic inflammatory response syndrome) triggers

Trauma
Abscess
Ischemic/necrotic tissue
Microbial invasion (bacterial, viral, fungal)
Endotoxin release
Global perfusion deficits
Regional perfusion deficits

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MODS

Multiple organ dysfunction syndrome
Failure of 2+ organ systems
Result of SIRS

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Patho of SIRS and MODS

Result of inflammatory response
Organ and metabolic dysfunction

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Respiratory Manifestations of SIRS and MODS

Alveolar edema
Decreased surfactant
Increased shunting
V/Q mismatch
End result: ARDS

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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

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Neurological Manifestations of SIRS and MODS

Mental status changes due to hypoxemia, inflammatory mediators, or impaired perfusion
Often early sign of MODS

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Renal Manifestations of SIRS and MODS

Acute kidney injury (AKI)
Hypoperfusion
Release of mediators
Activation of renin-angiotensin-aldosterone system
Nephrotoxic drugs, especially antibiotics

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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

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Hypermetabolic Manifestations of SIRS and MODS

Hyperglycemia-hypoglycemia
Insulin resistance
Catabolic state
Liver dysfunction
Lactic acidosis

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Nursing interventions of SIRS and MODS

Infection prevention
Maintain oxygenation
Nutritional and metabolic needs
Support failing organs

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Initial stage of shock

Not clinically apparent
Lactic acid accumulates and must be removed by blood and broken down by liver

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Compensatory stage of shock

Clinically apparent
Baroreceptors activate SNS
- vasoconstriction, RASS, impaired GI motility, cool, clammy skin

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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)

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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

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Cardiac manifestations in Progressive stage of shock

CO falls
Weak pulses
Ischemia of distal extremitites

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GI manifestations in Progressive stage of shock

Mucosal barrier becomes ischemic
- Ulcers, bleeding, decreased nutrient absorption

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Renal manifestations in Progressive stage of shock

Renal tubular ischemia
May result in AKI

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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

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Irreversible stage of shock

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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

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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

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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

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Myocardial infarction
Cardiomyopathy
Blunt cardiac injury
Severe systemic or pulmonary hypertension
Cardiac tamponade
Myocardial depression from metabolic problems

Early manifestations of cardiogenic shock

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Tachycardia
Hypotension
Narrowed pulse pressure
↑ Myocardial O2 consumption

Cardiogenic shock expected assessment findings

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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

Exam 3 Flashcards

(46 cards)