Week 1; Concepts of Complexity Flashcards
DKA Review
Occurs with type I diabetes, on-diagnosed diabetes – undetected, 3 P’s (polyuria, polydipsia, polyphagia).
Can occur with Type II
DKA causes
Stressful situation, skipping meals – “starvation mode” – starts burning fats, corticosteroids, infection, trauma, omission of insulin, medications that antagonize insulin
DKA assessment findings
Kussmaul respirations – rapid deep breaths, lower CO2 (sign of metabolic acidosis), fruity breath, nausea, abdominal pain (frequent in pediatric patients), dehydration or electrolyte loss, polyuria, polydipsia, weight loss, dry skin, sunken eyes, lethargy, coma
DKA vs HHS
DKA symptoms occur suddenly as opposed to HHS – occur gradually
DKA lab findings
Serum glucose > 300 mg/dL or >200 mg/dL for pediatrics, positive urine ketones, serum pH <7.35, serum HCO3 <15 mEq/L, Ketones-positive, serum Na varies low, normal, or high, BUN >30 mg/dL, creatinine >1.5 mg/dL, serum potassium increased(mild); decreased (severe)
DKA interventions
- Correct Dehydration
- glucose level
- correct metabolic acidosis
- electrolyte balance
HHS (hyperosmolar hyperglycemic nonketotic state)
Results from a sustained osmotic diuresis. Serious, life-threatening, slow onset. Results in severe dehydration. Patient secretes just enough insulin to prevent
ketosis. EXTREME hyperglycemia – blood is
concentrated (hyperosmolarity). Mostly in Type II in pt with infection or older adult
HHS causes
Kidney disease, MI, sepsis, pancreatitis, stroke, some medications-glucocorticoids, diuretics, phenytoin, beta blockers, and calcium channel blockers.
HHS assessment findings
Polyuria, polydipsia, hypovolemia, dehydration, hypotension, tachycardia, hypoperfusion, weight loss, weakness, nausea/vomiting, abdominal pain, stupor, coma, seizures
HHS interventions
Admit to ICU if blood glucose > 700 mg/dL
Establish, maintain ventilation
Correct shock with adequate IV fluids Normal saline is
preferred.
* 1liter per hour until central venous pressure begins to rise.
* Half-normal saline for others.
If client is comatose, NG suction
Maintain fluid volume
Administer insulin to reduce blood glucose
Assess mental status and consult physician if changes
occur.
Fluid replacement therapy
IV fluids or blood: most effective treatment for
hypovolemic shock. Fluids also used to treat septic, neurogenic and anaphylactic shock. Fluids administered alone or in combination; crystalloid solutions, colloid solutions, blood and blood products are administered in massive amounts through two large-bore peripheral lines or a central line
Hypovolemic shock review
Hypovolemic shock affects all body systems
* Effects vary according to age, general state of health, extent of injury or severity of illness, time before treatment is provided, rate of volume loss
* Manifestations result directly from decrease in blood volume, initiation of compensatory mechanisms
* Shock stage progresses with sustained loss of ≥100 mL
Cardiogenic shock review
Cardiogenic shock occurs when heart’s pumping ability cannot maintain CO, perfusion. Caused by MI (most common cause), cardiac tamponade, restrictive pericarditis, cardiac arrest, dysrhythmias, pathologic changes in valves, cardiomyopathies, complications of cardiac surgery, electrolyte imbalances, drugs affecting cardiac muscle contractility, head injuries causing damage to cardioregulatory center
Obstructive shock review
Caused by obstruction in heart, great vessels. Impedes venous return or prevents effective cardiac pumping. Caused by impaired diastolic filling, increased right ventricular afterload, increased left ventricular afterload. Manifestations result from decreased CO and BP → reduced tissue perfusion, cellular metabolism.
Distributive shock (vasogenic shock)
Several types of shock resulting from widespread
vasodilation, decreased PVR. Blood volume does not change → relative hypovolemia
Septic shock (septicemia)
Leading cause of death for patient in ICUs. Part of progressive syndrome: systemic inflammatory response
syndrome. Most often result of gram-negative bacterial infection. May also follow gram-positive Staphylococcus, Streptococcus infections
Neurogenic shock
Parasympathetic overstimulation → sustained vasodilation
* Dramatic reduction in systemic PVR
* Causes: head injury or trauma to spinal cord, insulin reactions, CNS drugs, anesthesia, severe pain, exposure to heat
S/S of shock
Signs of early shock may be nonspecific; as body compensates for hypotension, hypovolemia, signs of shock include: tachycardia, increased respiratory effort, decreased urine output, diaphoresis, drop in systolic BP, narrowing of pulse pressure, reduced cerebral blood flow → decreased LOC, progression to cardiopulmonary failure, death
Shock treatment
ALL should receive oxygen
Also fluids (colloids) and drugs