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rules of thumb
pure resp. acidosis:
- chg PCO2 10 <--> chg pH 0.08
- acute: chg PCO2 10 <--> chg HCO3 1 mEq
- chronic: chg PCO2 10 <--> chg HCO3 4 mEq
pure met. acidosis
- (Winter's formula for pure metabolic acidosis with compensation. Get HCO3 from lytes.)
- PCO2 = 1.5(HCO3) + 8
pure resp alkalosis
- acute: chg PCO2 10 <--> chg HCO3 2 mEq
- chronic: chg PCO2 10 <--> chg HCO3 5 mEq
A-a gradient: (A: alv., a: artl.)
- PAO2 = (713 * FiO2) - pCO2/0.8
- P(A-a) = PAO2 - PaO2 norm < 10
- pulm. art press.: 30/14 (10-25, 5-15 mm. Hg)
- mean pulm cap wedge press.: 12 (5-13 mm) approx. = to left atrial pressure and LVEDP.
Post MI best @ 14-18 mm. If exceeds @ 30 have pulmonary edema. If mitral valve OK this
reflects LVEDP, which in turn reflects LVEDV and end diastolic fiber length (preload). For
each mm of PEEP > 25 the PCWP will be increased by 1 mm over the true LVEDP/LAP. With
lo albumin CHF with lower PCWP.
- LVEDP: 12 (5-12 mm).
- PAD: Pressure in pulm artery, measured with balloon down. In ideal cases may approx.
PCWP, pulm hyptnsn dissociates PAD/PCWP.
- CVP: 1-5 mm; reflects RVEDP/preload, approx. = RAP. If CVP > 15 no resp to incr
- cardiac index: normal 2.5-3.6 L/min/m2. Typical CO is 4-6 L/min. Hypoperfusion at
1.8-2.2, shock at < 1.8.
- PVR: 800-1200.
- mitral valve parameters: Norm 4.5-6.0 cm2.
- < 2.5: incr. atrial pressures
- < 1.5: over 25 mm LAP
- < 1.0: symptoms and pulmonary edema.
- typical cardiogenic shock: CI @ 1.8, BP @ 90, incr. PVR, oliguria, pulm vasc cong on
CXR. If PCWP is low or normal give fluids and maintain PCWP @ 15-20 mm.
- Venous Oxygen saturation and A-V O2 gradient:
- This is a measure of the balance between total body O2 supply and demand. Use with CO
- mixed venous saturation: normal 70-80%, heart failure < 60%, shock < 40%.[18
- A-V O2 gradient: normal 3.5-5.0. In cardiogenic shock the A-V gradient widens. In early
sepsis it narrows (incr. CO and microvascular shunting), in late sepsis it widens.
- normal anion gap: diarrhea, small bowel drainage, ureterosigmostomy, RTA, hyporeninemic
hypoaldost. (seen in chronic interstitial renal disease -- hyperkalemic -- as with
ureterostomies), acetazolamide, TPN, DKA with lots of saline (renal excrtn organic acids).
If NO GI LOSS must R/O treatable renal problems: drugs (NSAIDS), pyelo, OBSTRUCTION,
calculi, idiopathic RTA.
- incr. anion gap: ketoacidoses (diabetic, alcoholic, starvation: accel. ketogenesis and
lipolysis due to lo insulin), lactic acidosis, renal failure, salicylates, meth., parald.,
- low anion gap: consider multiple myeloma. If urine dip protein neg (alb) and sulfasal
test protein pos --> mult. myeloma.
- look at the urinary Cl and at BP
- Urinary Cl, BP and metabolic alkalosis
- UK < 30: diarrhea, low intake
- UK > 50
- UCl <10
- (a) n/g suction
- (b) vomiting (bulemia)
- (c) post hypercapnea
- (a) incr. BP
- (b) low BP
- non-PTH carcinoma
- Na 23, Cl 35, NaCl 58, K 39, Ca 40, Mg 24.3, Acetate 59, Glucose
Ideally we want to know what LV preload is, and where a given heart lies on the its
unique Starling curve. LV end diastolic myofibril length (hence LVEDV) is one axis of the
Starling curve, we can't measure this but we can estimate LVEDP -- the next best thing.
PROBLEMS: PEEP, positive intrathoracic pressure, catheter placement above lt atrium (zone
I or II), MS, AR, pulm htypertn stiff LV all dissociate PCWP, LVEDP, LVEDV, and preload!
Afterload is even harder to measure. If we know cardiac output we can estimate
peripheral vascular resistance (PVR). In the normal heart stroke volume (SV) (hence CO) is
determined mostly by preload and heart rate and is not affected by afterload. In the
weakened heart SV is reduced by increased afterload; hence vasodilator therapy.
Contractility increase means an increased SV without change in preload.
- sodium: for oliguria, hyponatremia
- potassium: for hypokalemia, met. alk - chloride: for metabolic alkalosis
- basically 10 mEq is the cutoff for everything -- that's about the lowest K gets, and a
Cl over 10 with hypochloremia suggests renal Cl loss.
- metabolic alkalosis is a stimulant for renal excretion of K ( switch for H). Persistent
metabolic alkalosis is usually due to Cl loss in urine or GI tract. Hence hypokalemia,
incr. urinary K, hypochloremia, low urinary Cl results from vomiting. If Cl is down met.
alk. will correct with volume and K.
Author: John G. Faughnan.
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