Fluid & Hemodynamics Flashcards
Edema
Excess fluid in interstitial space. Extracellular space, outside of vessel.
Pitting vs. non-pitting
Pitting = transudate (e.g. CHF). Non-pitting = EXUDATE, lymphatics eventually
3 fluids in Edema
Transudates, exuedates, and lymphedema
Transudates
Oncotic pressure keeps fluid in vessels (80% is from albumin). Hypoalbuminemia –> transudate leaking. Hydrostatic pressure pushes fluid out.
What produces transudates?
Decreased oncotic pressure and increased hydrostatic pressure. Albumin made in liver. Chronic liver disease -> low albumin. Malabsorption, nephrotic syndrome, third degree burn, kwashiorkor.
Bee sting
Exudate - Anaphylactic reaction is histamine (Type-1) -> increased vessel permeability. Airway, Epi (1:1000 SQ)
Cirrhosis of liver
Pitting edema and ascites. Ascites: transudate; dec. oncotic pressure and inc. hydrostatic in portal HTN. Legs: transudate from dec. oncotic pressure.
Non-pitting type of edema 2/2 s/p radical mastectomy
Lymphedema. Lymphogranulonum venereum - scarring lymphatics; Peu D’ Orange. Risk of lymphangiosarcoma.
ECF
Vascular (1/3) and interstitial (2/3)
ICF
2/3 larger than ECF.
For every 3 L NS you put into a person
1 L in vascular; 2 L in interstitial fluid.????
Osmolality
Measure of solutes in a fluid. Sodium, glucose, BUN are major compartments. 2 x Na (140) + glucose/18 + BUN/3
Osmosis
Na and Glucose are limited to ECF. Na is the main determiner of osmosis since osmolality is determined primarily by [Na]ecf. Urea is PERMEABLE so doesn’t control osmosis
Hyperglycemia
ICF -> ECF. DILUTIONAL Hyponatremia
Tonicity
Referred against plasma tonicity. Isotonic, hypotonic, hypertonic. Tonicity is related to: Total body Na / Total body water
Isotonic loss of fluid
Lost equal amounts of Na+ and water. Mostly loss of ECF. Serum Na+ conc. is normal. Examples - hemorrhage, diarrhea.
Most common cause of low osmolality in plasma =
Hyponatremia. ICF will gain water. (e.g. SIADH 2/2 SCLC -> restrict WATER NOT Salt). Serum Na+ < 120 think SIADH
Hypertonic loss of fluid
Lost more salt than water. Hyponatremia. E.g. - diuretics.
SIADH
T2DM - chloropropamide (sulfonylureas) —> SIADH
Hypertonic gain of fluid
Still get hyponatremia. Pitting edema states (RHF, cirrhosis)
Total body Na+
When increased = PITTING EDEMA; Most of your Na+ is in interstitial (3/4 of ECF).
Hypernatremia
ICF shrunk. Primary aldosteronism, Diabetes insipidus (too much ADH), Osmotic diuresis (losing more water than salt in urine, e.g. glucose, mannitol), baby diarrhea (b/c it’s hypotonic not isotonic); Give back a hypotonic salt solution.
What has to be in pedialyte in order to reabsorb Na+ in GI?
Glucose or galactose. (NOT fructose) B/c co-transporter in small intestine.
Sweat
Hypotonic salt solution. Too much sweat —> hypernatremia
Arterial blood volume
Effective arterial blood volume = SV
What does our body do with hypovolemia?
Baroreceptors - both low (venous) and high (arterial) pressure owns. High pressure - IX, X. Low CO –> underfill arch vessels and carotids, we get a sympathetic nervous tissue response. Catecholamines -> venoconstriction -> inc. blood to right heart. Beta-adrenergic –> inc. inotropy and chronotropy. Systemic arterioles (usually vasoconstrictor in diastole in order to perfuse heart via coronary arteries). RAAS–> vasoconstriction, aldo will reabsorb Na and water. SV low -> low RBF -> RAAS. ADH release -> pure water retention (not good).
Peritubular capillary pressures
Reabsorb most Na+ in proximal tubule. Rest of it in DCT by aldosterone (aquoporin). Reabsorb into peritubular capillaries. Starling forces must be favorable. If RBF decreased when CO down, hydrostatic pressure decreased and peritubular oncotic pressure increased –> reabsorption of fluid back into blood stream
Decreased CO
e.g. hemorrhage. PCT reabsorbs isotonic fluid. Aldo also reabsorbs isotonic. ADH contributes pure water fluid —> NET hypotonic fluid is reabsorbed normally back into ECF
Increased CO
E.g. volume overload. Baroreceptors stretched innervated by IX and X. We will get a parasympathetic nervous response. RAAS not activated w/ inc. RBF. ADH not activated. Glomerulotubular balance –> not reabsorbed. LOSE hypotonic fluid. ANP (released with volume overload state, RA or LA dilation) will get rid of Na+ via filtration (diuretic)
Total body Na+
Determined by CLINICAL EXAM. “Dehydration” - poor skin tugor, dry mucus membranes
tx for pitting edema
Restrict salt AND water b/c both were increased w/ low CO –> hypotonic fluid reabsorption by kidney. diuretics will get rid of salt > water.
Hypovolemic shock
Causes - diarrhea, hemorrhage, DI?? (NO b/c losing pure water –> shifting fluid BUT NOT hypovolemic). FIRST STEP = NORMAL Saline. Then look for what caused the hypovolemia.
DI
Normal clinical exam
Orthostatic - “tilt test” = hypovolemic
Lying flat - maintained CO w/o gravity. W/ sit-up, decrease venous return to right side of heart. When hypovolemic –> dec. Bp and inc. pulse.
Hypovolemic person
Treated w/ NS. Person seems to be dehydrated still. Now give 0.5% NS. Give the patient WHAT they lost eventually.
DKA
Osmotic diuresis. Hypotonic fluid loss. 1st step = NS to make them normotensive (liters). 2nd step = 0.5% NS + insulin
Diabetes insipidus
Out of surgery. Na = 165 mEq/L. Bp is stable and lucid. Pt lost pure water. Tx with pure water; DW5 IV. Can’t give saline b/c then they’d be salt-overloaded
Hypovolemic shock etio
Hemorrhage, diarrhea. Cold and clammy b/c of vasoconstriction b/c of catecholamine and AII. Bp is low. Pulse is increased. Dec. CO.
Septic shock
Most commonly caused by E. coli in the hospital. From indwelling urinary catheter. Gram NEG = endotoxin in cell wall = LPS. C3a-C5a = anaphylotoxin -> mast cells release histamine -> vasodilation of arterioles. Skin feels WARM. Endotoxins damage endothelial cells –> releasing NO and PGI2 = vasodilation. Turbulent water but tissue CAN’T get oxygen. Blood returns to heart too quickly –> increased CO. HIGH-OUTPUT failure.
Pousille’s law
TPR (arterioles) = viscosity of blood / radius ^4; viscosity is controlled by Hgb. Anemic is low viscosity = lower resistance. polycythemia is higher. TPR controls diastolic blood pressure.
Swan-Ganz catheter
Cardiac output. Systemic vascular resistance = TPR (a calculation). Mixed venous-arterial O2 concentration: best test for tissue hypoxia. Low CO = more time to oxygenate; Extracts more oxygen in tissue in hypovolemic shock —> LOW mixed venous-arterial O2 concentration. In septic shock, mixed venous-arterial O2 Sat is HIGH b/c tissues not extracting.
PC wedge pressure
A measure of LVEDF ~ LA pressure.
Hypovolemic/cardiogenic shock
LOW CO. SVR = high = vasoconstriction. Mixed SpO2 = LOW. PCWP is LOW in hypovolemic shock but HIGH in cardiogenic shock.
Septic Shock
HIGH CO. SVR = low = vasodilation. Mixed SpO2 = HIGH. PCWP is LOW in septic shock.
Which organ suffers greatest from dec. Bp?
Kidneys! Medulla (only gets 10% of CO). Brain is 2nd but Circle of Willis. During shock = OLIGURIA —> ATN. Inc renal blood flow (dobutamine!). Coagulation necrosis —> renal tubular casts block urine flow. Sickle cell trait –> kidney disease b/c sickling in medulla b/c of LOW oxygen tension –> microinfarctions. Microscopic hematuria.
Henderson-Hasselbach equation
pH ~ bicarb / PCO2
Compensation
Bodies attempt to maintain normal pH. Metabolic alkalosis –> increase PCO2 (respiratory acidosis is compensation for metabolic alkalosis)
Respiratory alkalosis tx?
Breathe in bag. Make them rebreathe CO2. Most common cause is anxiety.
Respiratory center?
Medulla oblongata. Controls breathing rate. All pregnant women have respiratory alkalosis b/c estrogen and progesterone increase RR. AV fistulas in the pulmonary.
Endotoxins
Overstimulate respiratory system. Respiratory alkalosis. In shock. Metabolic acidosis (lactic acidosis). pH normal.
Salicylate intoxication
Overstimulate respiratory system -> respiratory alkalosis. Salicylic acid = AG metabolic acidosis. pH normal.
Steeple vs. thumbprint sign
Croup. Lesion is at the trachea. Thumbprint sign = H flu epiglottitis.
Phrenic nerve for diaphragm
Elevated diaphragm on X-ray -> respiratory acidosis. ALS. Guillan Barre. Polio.
