NMS Flashcards
Total body water
65% Intracellular
35% Extracellular- 25% Interstitial, 10% Intravascular
2/3 rule
Total body water comprises approximately 2/3 of body weight; of this, 2/3 is intracellular, and one third extracellular. Of the extracellular, 2/3 is interstitial, and 1/3 is intravascular.
Blood volume
Approx. 7% of body weight
Body water excreted
- urine- minimum = 0.5 mL/kg/hr
2. insensible loss (sweat, respiration, stool) = 600-900 mL/24 hr
Fluid requirement
First 10 kg = 4 cc/kg/hr
Second 10 kg = 2 cc/kg/hr
1 cc/kg/hr for every kg above
1/2 normal Saline (0.5% NaCl)
77 mEq/L Na+
77 mEq/L Cl-
Osmolarity = 154 mOsm/L
Normal Saline (0.9% NaCl)
154 mEq/L Na+
154 mEq/L Cl-
Osmolarity = 308 mOsm/L
Hypertonic Saline (3.0% NaCl)
513 mEq/L Na+
513 mEq/L Cl-
Osmolarity = 1027 mOsm/L
Lactated Ringer’s
130 mEq/L Na+ 4 mEq/L K+ 2.7 mEq/L Ca++ 98 mEq/L Cl- 28 mEq/L Lactate
Osmolarity = 525 mOsm/L
Plasmalyte
140 mEq/L Na+ 5 mEq/L K+ 3 mEq/L Mg++ 98 mEq/L Cl- 27 mEq/L Acetate 23 mEq/L Gluconate
Osmolarity = 294 mOsm/L
Signs of acute volume loss
tachycardia
hypotension
decreased urine output
Signs of gradual volume loss
loss of skin turgor
thirst
alterations in body temperature
changes in mental status
Signs of acute hypervolemia
acute shortness of breath
tachycardia
complications- acute CHF
Signs of chronic hypervolemia
peripheral edema
pulmonary edema
hyponatremia
serum Na+ < 130 mEq/L
Hyperosmolar hyponatremia
Dilutional
Causes: hyperglycemia, mannitol infusion, other osmotic particles present
Tx: correct hyperglycemia or other source
Normo-osmolar hyponatremia
Pseudohyponatremia
Causes: hyperglycemia, hyperlipidemia, hyperproteinemia
Tx: none required
Hypo-osmolar hyponatremia
True hyponatremia
Hypovolemic
Hypervolemic
Euvolemic
Hypovolemic hypo-osmolar hyponatremia
most common
total body sodium low
hypovolemia = ADH secretion, decreased free water excretion
Increased intake of free water from thirst or infusion of hypotonic solution
Dx: Urine osmolarity HIGH, Na LOW
Tx: isotonic fluid infusion, Na+ replacement if deficit is severe
Hypervolemic hypo-osmolar hyponatremia
total body sodium high
low cardiac output (less blood to kidneys, free water not excreted)
hypoalbuminemic (ex: cirrhosis) or other edematous state salt (Renin-angiotensin) and free water (ADH) cannot be excreted
Dx: Urine osmolarity HIGH, Na LOW
Tx: treat underlying medical condition, NaCl and free water restriction
Euvolemic hypo-osmolar hyponatremia
syndrome of inappropriate antidiuretic hormone (SIADH)
can be stimulated by stress response to trauma and surgery.
free water retained
Dx: Urine osmolarity HIGH, urine Na HIGH
Tx: free water restriction
Acute hyponatremia symptoms
acute cerebral edema
seizures
coma
Chronic hyponatremia symptoms
usually well tolerated
confusion/decreased mental status
irritability
decreased deep tendon reflexes
Hypernatremia
serum Na+ > 150 mEq/L
Sxs: volume depletion (tachy, hypotension)
dehydration (dry mucous membranes, decreased skin turgor)
lethargy
confusion
coma (water shift into intracellular in CNS)
Hypovolemia hypernatremia
volume deficit, more free water lost than Na+
Tx: calculate free water deficit
replace half within 8 hrs
second half over 16 hrs
Hypervolemia hypernatremia
iatrogenic infusion of too much sodium
rare
Tx: decrease Na+ infusion
free water infusion
diuretics
Free water deficit
= 0.6 x BW in kg x (pNA/140 - 1)
Hypokalemia
serum K+ < 3.5 mEq/L
Severe < 3.0 mEq/L or less
Sxs: ileus, weakness, respiratory failure, cardiac dysrhythmias
ECG changes in hypokalemia
seen when K+ < 3.0 mEq/L
T-wave flattening T-wave inversion depressed ST segments U wave development prolonged QT interval ventricular tachycardia
Causes of hypokalemia
renal- diuretics, vomiting, renal tubular acidosis
extrarenal- diarrhea, burns
intracellular shift- insulin, alkalotic state
medical disease- hyperaldosteronism, cushing syndrome
Treatment of hypokalemia
every 10 mEq of K+ should increase serum concentration by 0.1 mEq/L
Hyperkalemia
serum K+ > 6 mEq/L
Sxs: diarrhea, cramping, nervousness, weakness, flaccid paralysis, cardiac dysrhythmias
ECG changes in hyperkalemia
peaked T waves
widened QRS
ventricular fibrillation
Causes of hyperkalemia
Renal failure with inappropriate consumption/admin of K+
Extracellular shift- rhabdomyolysis, massive tissue necrosis, metabolic acidosis, hyperglycemia
Medical disease-Addison’s disease
Treatment of hyperkalemia
Acutely- IV Ca++, stablizes cardiac myocyte membrane to prevent dysrhythmias; glucose/insulin to shift K+ intracellularly; Bicarbonate to shift K+ intracellulary
Removal- ion-exchange resin (K-exylate) binds K+ in colon; Lasix only if kidneys can excrete; Dialysis
Respiratory acidosis
decreased ventilation relative to CO2 production, increased CO2 concentration
Causes: most common- decreased alveolar ventilation (respiratory depression, CNS disorder, physical), increased CO2 production (excess enteral carbs)
Tx: increase alveolar ventilation
Metabolic acidosis
loss of HCO3-, accumulation of strong anions, accumulation of weak acids
Causes: weak acid (anion gap; renal failure, lactic acidosis, DKA, toxins), strong anion (no gap; hyperchloremic acidosis), loss of bicarb (no gap; excess renal excretion, diarrhea)
Tx: underlying metabolic condition
bicarb only if pH < 7.2
Respiratory alkalosis
increase in alveolar ventilation with decrease in CO2 levels
Causes: anxiety, pain, shock, sepsis, toxins, CNS dysfunction, over ventilation
Tx: decrease ventilation, most self-limited
Metabolic alkalosis
pH over 7.45 and HCO3- > 26 mEq/L
causes: vomiting, diarrhea (loss of gastric contents), drugs that limit renal excretion of HCO3- (steroids, diuretics)
Primary hemostasis
Platelet adherence- glycoprotein Ib and vWF
Platelet activation- produce thromboxane A2 (vasoconstrict); Glycoprotein IIb/IIIa expressed for platelet-platelet adhesion (fibrinogen needed)
Extrinsic pathway
Tissue Factor (TF) binds Factor VII -> VIIa acivates Factor X -> Xa converts prothrombin -> thrombin (Va cofactor) -> fibrinogen -> fibrin
XIIIa mediates cross linking of fibrin
Intrinsic pathway
Factor XIIa activates XI -> XIa activates IX -> IXa activates X -> Xa converts prothrombin -> thrombin (Va cofactor) ->fibrinogen -> fibrin
XIIIa mediates cross linking of fibrin
Protein C and S
degrade factors V and VIII
Antithrombin III
inhibits thrombin-Xa complexes
Fibrinolysis
t-PA and urokinase-type plasminogen activator (uPA) convert plasminogen -> plasmin which cleaves fibrin
Prothrombin time (PT)
measures extrinsic cascade
measurement of vitamin K-dependent coag factors (II, VII, X)
used to monitor warfarin therapy
Activated partial thromboplastin time (aPTT)
measures intrinsic cascade
used to monitor pts on IV unfractionated heparin
Hemophilia A
Factor VIII deficiency
Hemophilia B
Factor IX deficiency
von Willibrand disease
most common congenital coagulopathy (1-2%)
vWF deficiency, treated with intranasal/IV DDVAVP
Clean wound
incision made under sterile conditions, nontraumatic procedure, does not enter bowel, tracheobronchial tree, genitourinary system, or oropharynx
should be closed primarily, infection rate less than 2%
Clean-contaminated wound
bowel, tracheobronchial tree, genitourinary system, or oropharynx was entered under sterile conditions. No evidence of active infection
should be closed primarily, infx rate 3-4%
Contaminated wound
major contamination of wound during procedure (ex: stool from colon), fresh traumatic wounds
should be left open, infx rate 7-10%
Dirty and infected wounds
established infection present before procedure (ex: appendiceal abscess)
should be left open, infx rate 30-40%
Normal wound healing phases
- Coagulation phase
- Inflammatory phase ~ 1 wk
a. cellular- PMN (24-48 hr) and macrophages remove necrotic tissue and debris; epithelial bridging
b. vascular- angiogenesis
c. mediators - Proliferative phase- fibroblasts form collagen, wound strength increases, wound contraction, 3 wks
- Wound remodeling- scar formation
Primary closure
skin edges approximated shortly after wound incurred
Secondary intention
wounds with risk or current infection left open, heal by epitheliazation and wound contraction
Delayed primary closure
heavily contaminated wounds, left open 3-5 days, then primarily closed
Skin grafts
graft contains epidermis and portion of dermis, provide epithelial coverage for healing
Flaps
Rotation flap- retains normal blood supply, rotated to fill in a defect
Free flap- removed from normal blood supply, moved to another area, vasuclature reanastomosed (ex: toe to hand to form thumb)
Fick equation
to determine caloric requirements
cardiac output x arterial-venous oxygen content difference = oxygen consumption
Systemic vascular resistance (SVR)
SVR = [(MAP - CVP)/CO] x 80
normal: 800-1200 dynes.sec/cm5
Pulmonary vascular resistance (PVR)
PVR = [(MPAP - PCWP)/CO} x 80
normal: 20-120 dynes.sec/cm5
Dopamine
low dose (1-3 ug/kg/min)- receptors in kidney and intestine, increases blood flow
med dose (3-10 ug/kg/min)- beta receptor agonist, increase in cardiac contractility, incr CO
high dose (>10 ug/kg/min)- alpha agonist and vasoconstrictor
Dobutamine
affects both beta-1 and -2 receptors, increase in cardiac output, vasodilation
Norepinephrine
alpha agonist, vasoconstriction, mild beta activity, some increase in cardiac contractility
Epinephrine
alpha agonist, some beta agonist effect. vasoconstriction and increased cardiac output
Phenylephrine
alpha agonist, pure arterial constriction