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151 Cards in this Set

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Normal Alveolar-Arterial gradient in non-ventilated patient = _-_ mmHg
Normal Alveolar-Arterial gradient in non-ventilated patient = 10-15 mmHg

Normal A-a gradient is <10 mmHg, but can range from 5–20 mmHg.
For every decade a person has lived, their A-a gradient is expected to increase by 1 mmHg.
An abnormally increased A-a gradient suggests a defect in diffusion, V/Q (ventilation/perfusion ratio) defect, or right-to-left shunt.
How is A-a gradient calculated?
A-a gradient = PAO2 − PaO2
PAO2 = alveolar = calculated from alveolar gas equation
PaO2 = arterial = from ABG
what ABG change should be anticipated in elderly pts?
Decreased PO, unchanged PCO.
-Arterial PO falls by approximately 5 mm Hg per decade of life. This is due to ventilation perfusion mismatching associated with aging, which leads to increased shunt and dead space ventilation.

-ALso, ventilatory responses to hypoxia and hypercapnia fall by 50% and 40%, respectively, with aging. The exact mechanism is unknown but likely involves reduced chemoreceptor function.
effect of ACE-inhibitor on potassium
ACE-I increase K
how do ACE inhibitors lower the glomerular pressure gradient?
-Can precipitate ARF in patients c/ _
ACE-I lowers the glomerular pressure gradient by efferent arteriole vasodilation
-Can prescipite renal failure in patients c/ renal artery stenosis
hypoxic pulm vasoconstriction is worsened by what acid/base status?
Hypoxic pulmonary vasoconstriction is worsened by acidosis
Activated protein C: what is is used for in pts c/ sepsis and multiorgan failure
Activated protein C = Xigris
Inactivates the inhibitor of protein C -> FIBRINOLYSIS
What is the best initial therapy for a patient with acute pancreatitis who develops a Na of 122 on the second day of hospital admission?
FLUID RESTRICTION Pseudohyponatremia can occur in pancreatitis & hyperglycemia. For each increment of glucose over 100, add 2 to the Na value. Na deficit = .6 x kg weight x (140-Na)
How does ADH work?
ADH: -stimulated by intravascular hypovolemia, osmolality of ECF
-Stimulated peri-op by pain, anxiety, some narcotics => may be 5-50x highter post-op, then normalize w/in 3-5 days
-V1: vasocontriction of vascular sm muscle
-V2 (intrarenal) H20 reabsorption @ collecting ducts
-V3 (extrarenal): release of factor 8, vWF
most sensitive test for adrenal insufficiency
corticotrophin stim test most sensitive test for adrenal insufficiency
how does aldosterone work?
Aldosterone:
-Stimulated by Angiotensin 2, K
-Causes transcription of Na/K ATPase, Na/H ATPase -> reabsorb Na, secrete H and K in distal convoluted tubule ->
Water reabsorption
For diagnosing ALI, an S/F ratio of _ corresponds with P/F ratio of _
For diagnosing ALI, an S/F ratio of 235 corresponds with P/F ratio of 200
normal inspiration is associated with greater ventilation of zone _ alveoli
normal inspiration is associated with greater ventilation of zone 3 alveoli (dependent portion of lung)
zone _ alveoli may contribute to physiological dead space of the respiratory system
Physiologic dead space:
-Emphysematous lung
-lung involved in PE
-proximal 2/3 of subsegmental (+ eerything proximal)
-zone 1 alveoli
__ type AA's: leucine, isoleucine, valine
-metabolized in __
-all essential
Branched-chain AA's: leucine, isoleucine, valine
-metabolized in muscle
-all essential
Angiotensin 2 is formed mostly in the _
Its role is to …….
Angiotensin:
ACE converts Angiotensin 1 to Angiotensin 2 (highest concentration is in lung) ->
ALDOSTERONE RELEASE, vasocontstriction, increased HR and contractility
How is anion gap calculated?
What are the anion gap acidoses
Anion gap acidosis = MUDPILES:
Methanol
UREMIA
DKA
paraldehyde
LACTATE
ethylene glycol
salicylates
-Anion gap = Na - HCO - Cl. Normal gap <12
For diagnosing ARDS, an S/F ratio of _ corresponds with P/F ratio of _
For diagnosing ARDS, an S/F ratio of 315 corresponds with P/F ratio of 300
What is the basic ventilation strategy for ARDS:
Ventilation for ARDS:
-Pressure-control ventilation
-Permissive hypercapnea
-Correct pH c/ bicarb
What conditionally essential amino acid is shunted into nitric oxide synthase during times of stress?
Arginine is considered a conditionally essential amino acid. Humans do not produce adequate amounts to meet metabolic needs following acute surgical illness. This relative deficiency is felt to result from the upregulation of arginase 1 which shunts arginine away from nitric oxide synthase and production of nitric oxide. Nitric oxide is the body's most potent endogenous vasodilator.
The magnitude of a left-to-right shunt in the presence of an ASD is determined by...
Difference in compliance b/w left and right atria
The blood will tend to fill the more compliant ventricle which will usually be the right, until chronic pulmonary hypertension yields right ventricular hypertrophy.
what type of cells cause fever 2/2 atelectasis?
what cytokine?
alveolar macrophages are activated by atelectasis, cause fever via IL-1
___ macrophages =
source of fever in atelectasis
alveolar macrophages =
source of fever in atelectasis
Atrial natiuretic peptide:
-Released from atria when stretched
effect in the kidney is ... -> end effect ...
Atrial natiuretic peptide:
-Released from atria when stretched
-Inhibits Na and water absorbtion -> natiuresis, diuresis
what are the brain death criteria?
Deep tendon reflexes and even local pain stimulation reflexes may be present when brain is dead.

Brain death criteria include:
Lack of brain stem reflexes (doll's eyes, cold caloric, corneal, gag, cough)
Lack of motor response to noxious stimuli
Lack of pupillary light reflexes
APNEA - no respiratory drive with pCO2 of 60 mm Hg
Fluid leaves the capillary at the arterial end because _ type pressure exceeds _ type pressure.
Fluid leaves the capillary at the arterial end because hydrostatic pressure exceeds oncotic pressure.
symptoms of carcinoid syndrome are ameliorated by drug _
symptoms of carcinoid syndrome are ameliorated by SOMATOSTATIN
what is normal cardiac index?
normal cardiac index = 2.5-4 L/min
A postsurgical patient you are managing has a history of congestive heart failure. Despite fluid resuscitation, the patient remains hypotensive with an elevated SVR. Management considerations could include
Post-op hypotension in patient with CHF - can try: B1 agonist, nitroprusside, phosphodiesterase inhibitor, IV fluids + afterload reduction
_ deficiency =>
hyperglycemia (relative diabetes)
neuropathy
Chromium deficiency =>
hyperglycemia (relative diabetes)
neuropathy
Carbon monoxide poisoning:
-Carboxyhemoglobin is elevated if >10% in nonsmoker or >20% in smoker
-CO binds Hgb -> carboxyHgb -> falsely increases O2 sat on monitor
-Tx: 100% O2 displaces CO, hyperbaric O2 if severe
Carbon monoxide poisoning:
-Carboxyhemoglobin is elevated if >10% in nonsmoker or >20% in smoker
-CO binds Hgb -> carboxyHgb -> falsely increases O2 sat on monitor
-Tx: 100% O2 displaces CO, hyperbaric O2 if severe
_ deficiency:
anemia
neutropenia
Copper deficiency:
anemia
neutropenia
Cori cycle:
-glucose metabolized to _ -> metabolized to _ in the __
Cori cycle:
-glucose metabolized to lacatate -> metabolized to glucose in liver
Adrenal secretion of cortisol has negative feedback on what gland?
Adrenal secretion of cortisol has negative feedback on the HYPOTHALAMUS
#1 non-iatrogenic cause of Cushing's syndrome = _
-Diagnosed by ...
-Localized by...
-Treatment is ...
PITUITARY ADENOMA = 80-80% of non-iatrogenic Cushing's syndrome
-Cortisol supressed by high- or low-dose Dex supression test.
-Usually MICROadenomas
-Need petrosal sampling to figure out which side. MRI also helps
-Vertical incisions to find adenoma
-Tx: most tumors removed c/ transsphenoidal approach.
-Unresectable or residual tumors treated c/ XRT
CVP: 7 +/- 2
CVP: 7 +/- 2
enzyme which catalyzes the conversion of arachidonic acid to prostaglandins is
cyclooxygenase catalyzes the conversion of arachidonic acid to prostaglandins is
what is the role of IL-4 and IL-10?
IL-4 and IL-10 are anti-inflammatory cytokines
define dead space
-roughly _cc
Dead space:
-ventilated, not perfused
-about 150 cc
Dobutamine:
-5-15 ug/Kg/kin => beta 1 (mostly contractility)
->15 ug/Kg/min => beta 2 (vasodilation, increased HR)
Dobutamine:
-5-15 ug/Kg/kin => beta 1 (mostly contractility)
->15 ug/Kg/min => beta 2 (vasodilation, increased HR)
Dopamine:
-0-5 ug/Kg/min => dopamine R's (renal)
-6-10 ug/Kg/min => beta adrenergic (cardiac contractility)
->10 ug/Kg/min => alpha adrenergic (vasoconstiction, increased BP)
Dopamine:
-0-5 ug/Kg/min => dopamine R's (renal)
-6-10 ug/Kg/min => beta adrenergic (cardiac contractility)
->10 ug/Kg/min => alpha adrenergic (vasoconstiction, increased BP)
2 names for the molecule that acts via cGMP pathway to promote relaxation of vascular sm muscle
EDRF = endothelium derived relaxing factor = NO
-made from ARGININE in endothelial cells-> activates guanylate cyclase (cGMP path) -> vascular sm muscle relaxation
-increased in sepsis
(endothelin => vascular sm muscle constriction)
Metabolic disturbance 2/2 NG suction is _
NG suction -> hypochloremic, hypokalemic, metabolic alkalosis c/ paradoxical aciduria
-Lose HCl, HCO3 in gastric suctioning ->
Kidney compensates for H2O loss by absorbing Na in exchange for K (-> hypokalemia)
-Kidney compensates for K loss by absorbing K in exchange for H (-> aciduria)
Tx: D5 1/2 NS + 20mEq KCl
Metabolic disturbance 2/2 pyloric stenosis in child is _
Vomiting -> hypochloremic, hypokalemic, metabolic alkalosis c/ paradoxical aciduria
-Lose HCl, HCO3 in gastric suctioning ->
Kidney compensates for H2O loss by absorbing Na in exchange for K (-> hypokalemia)
-Kidney compensates for K loss by absorbing K in exchange for H (-> aciduria)
Tx: D10 + 10 mEq KCl
patient has following lung changes - what lung disease is it?
EMPHYSEMA:
-increased minute ventilation
-increased airway resistance (2/2 destruction of these terminal bronchioles, early collapse of remaining bronchioles)
-Early (increased) closing volume (2/2 coalesced alveoli)
-Adverse length-tension relationship of diaphragm.
Epinephrine
-Initial dose = 2 ug/min
-Low dose => beta 1 (cardiac contractility, rate), beta 2 (bronchial and vascular sm muscle relaxation), can decrease BP @ low doses
-High dose => alpha 1 (vascular sm muscle constriction), alpha 2 (venous sm muscle constriction), increases cardiac ectopic pacer activity, myocardial O2 demand
Epinephrine
-Initial dose = 2 ug/min
-Low dose => beta 1 (cardiac contractility, rate), beta 2 (bronchial and vascular sm muscle relaxation), can decrease BP @ low doses
-High dose => alpha 1 (vascular sm muscle constriction), alpha 2 (venous sm muscle constriction), increases cardiac ectopic pacer activity, myocardial O2 demand
_ chain and _ chain fatty acids go via portal system c/ AAs + carbs
only medium and short chain fatty triglycerides go to portal system c/ AAs + carbs
how is fat transported from bowel to central circulation?
Fat digestion:
-micelles go to enterocytes -> chylomicrons go to lymphatics -> junction of L IJ + SCV
_ chain fatty acids = preferred food for colon
short chain fatty acids = preferred food for colon
how are medium-chain fatty acids absorbed?
MCT (6–12 carbons) are more rapidly hydrolyzed and have greater solubility than LCT. This allows absorption directly into the portal vein and require little or no pancreatic or bile salts for absorption
LR is comprised of _
LR is comprised of Na 130, Cl 109, K 4, Ca 2.7, HCO3 28 mEq/L
NS is comprised of _
NS is comprised of NaCl 154 mEq/L
equation for maintenance fluid in a child
Maintenance fluid:
40 mL/hr for 1st 10 Kg
20 mL/hr for 2nd 10 Kg
1 mL/Kg/hr for rest of body weight
how is free water deficit calculated?
free water deficit = body weight × 0.6 × (1 – 140/actual serum sodium)
Glutamine:
-preferred food for _ bowel
-why are levels decreased in stress?
Glutamine:
-preferred food for small bowel
-#1 AA in bloodstream => decreased levels in stress b/c glutamine goes to kidney to form ammonium, help acidosis (but sm bowel still the #1 consumer)
-decreases bacterial translocation, increases mucosal health c/ chemo or XRT to bowel
-delivered to sm bowel enterocytes by intestinal lumen or blood stream.
In major illness, the major carrier of nitrogen from skeletal muscle breakdown is amino acid _
In major illness, the major carrier of nitrogen from skeletal muscle breakdown = GLUTAMINE
Goldman index = 9 factors for increased risk of periop cardiac complications.
Goldman index by points:
11: uncompensated CHF (elevated CVP/JVD,S3 gallop)
10: MI in past 6 mo
7: >5 PVC/min any time pre-op
7: non-sinus rhythm or PACs on pre-op EKG
othes: age >70; intra-peritoneal/intra-thoracic/aortic surgery; emergency surgery; important aortic stenosis; poor general medical condition
Hydralazine = alpha blocker
Hydralazine = alpha blocker
An 85 year old male with metastatic prostate cancer presents to the ER with mental status changes and an abnormal QT interval. What is the best initial therapy?
SALINE INFUSION
Neoplasm is the most common cause of hypercalcemia in the hospitalized patient. The malignancy most commonly associated with hypercalcemia is breast cancer due to its high rate of bone metastasis. Prostate cancer is the second most common cause. Medical treatment of hypercalcemia should start with IV saline infusion followed by loop diuretics. Dialysis should be reserved for refractory hypercalcemia or life threatening episodes. Long term medical management of hypercalcemia can include use of lasix, mithramycin, calcitonin, &/or aldaronic acid.
Tip of an IABP should be located at _
Tip of an IABP should be 2 cm below the top of the aortic arch
-Higher than that => can occlude the arch vessels
-Lower than that => can occlude the mesenteric vessels
IABP improves coronary blood flow by _
IABP:
-Improves coronary blood flow, increasing SBP -> augments flow to coronaries, then decreases afterload by deflating during systole
(inflates on T wave, deflates on P wave)
Contraindication to IABP = _
Aortic regurgitation = contraindication to IABP
IABP improves coronary blood flow by INFLATING IN DIASTOLE TO AUGMENTING FLOW TO CORONARIES, then decreases afterload by deflating during systole
(inflates on T wave, deflates on P wave)
intrinsic factor is produced by _ cells in the _ and _ of the stomach
intrinsic factor is produced by PARIETAL cells in the FUNDUS and CORPUS of the stomach
Isoproterenol
-Intial dose = 1-2 ug/min
-Beta 1 (myocardial contractiliy, rate), Beta 2 (bronchial and vascular sm muscle relaxation)
-Arrhythmogenic, increases metabolic demand of heart (rarely used), can decrease BP
Isoproterenol
-Intial dose = 1-2 ug/min
-Beta 1 (myocardial contractiliy, rate), Beta 2 (bronchial and vascular sm muscle relaxation)
-Arrhythmogenic, increases metabolic demand of heart (rarely used), can decrease BP
Kreb's cycle = ___ ATPs from 1 glucose (anaerobic glycolysis = _ ATP + _ lactate)
Kreb's cycle = 38 ATP from 1 glucose
(anaerobic glycolysis = 2 ATP + 1 lactate)
_ deficiency (essential fatty acids) =>
dermatitis
hair loss
vision change
linoleic acid deficiency (essential fatty acids) =>
dermatitis
hair loss
vision change
Long chain fatty acids enter the body via _, in the form of _ or _
Long chain fatty acids enter the body via LYMPHATICS (terminal lacteals), in the form of LONG CHAIN FATTY ACIDS or CHYLOMICRONS
how do loop diuretics work?
Loop diuretics:
-inhibit active Na reabsorption @ thick ascending limb of Henle
-increase venous capacitance => may relieve pulm edema before significant natiuresis
-increase renal blood flow by stimulating vasodilatory prostaglandins
-reach intratubular site of action by active proximal tubular secretion (not by glomerular filtration)
Medium + short-chain fatty acids enter the body via _
Medium + short-chain fatty acids enter the body via PORTAL CIRCULATION
(along with carbs, protein)
In metabolic acidosis, the renal regulation of body fluid pH depends primarily on secretion of _ ion in exchange for _ ion
In metabolic acidosis, the renal regulation of body fluid pH depends primarily on SECRETION OF H+ in exchange for NA
Methemoglobinemia:
-Nitrites (e.g. Hurricaine spray) bind Hgb ->
decreases O2 sat to 85%
-Tx: methylene blue
Methemoglobinemia:
-Nitrites (e.g. Hurricaine spray) bind Hgb ->
decreases O2 sat to 85%
-Tx: methylene blue
Metoclopramide stimulates release of _ by blocking _ receptors
Metoclopramide stimulates release of ACETYL CHOLINE by blocking DOPAMINERGIC receptors
How does low Mg cause hypo-Ca?
Low Mg inhibits PTH =>
replace Mg if difficulty correcting Ca
Milrinone
-Phosphodiesterase inhibitor => increases cAMP
-Increases Ca flux -> cardiac contractility
-Also causes vascular smooth muscle relaxation, vasodilation
Milrinone
-Phosphodiesterase inhibitor => increases cAMP
-Increases Ca flux -> cardiac contractility
-Also causes vascular smooth muscle relaxation, vasodilation
Erythromycin binds the _ receptor, located in 3 locations…
Erythromycin binds the MOTILIN receptor
Located in 3 locations: stomach, duodenum, colon
how is Na level corrected in hyperglycemia?
Hyperglycemia:
for every 100 glucose over 100, add 2 to Na
How is Na deficit calculated?
Na deficit:
- 0.6 (wt in Kg) (140-Na).
replace max of 1 mEq/hr to avoid CPM
What vitamin deficiency?
red swollen skin lesions, cheilosis, mouth angular scars and stomatitis, and dementia.
Niacin deficiency includes: red swollen skin lesions, cheilosis, mouth angular scars and stomatitis, and dementia.
Nipride: arterial and venous dilator
-CN toxicity @ doses >_ ug/Kg/min x _ hrs => check _ levels, signs of metabolic acidosis
-Tx for CN toxicity = _ -> sodium nitrate
Nipride: arterial and venous dilator
-CN toxicity @ doses >3 ug/Kg/min x 72 hrs => check thiocyanate levels, signs of metabolic acidosis
-Tx for CN toxicity = amyl nitrite -> sodium nitrate
Nitroglycerine:
-Predominantly venodilation
-Modest effect on coronaries
-Decreases _-> decreases myocardial wall tension
Nitroglycerine:
-Predominantly venodilation
-Modest effect on coronaries
-Decreases preload -> decreases myocardial wall tension
the 2 main harms of nitroprusside are ...
Nitroprusside can cause:
-Thiocyanate toxicity -> hypoxia
-Coronary steal (arteries in CAD already mazimally dilated, so additional arteriolar dilation steals perfusion away)
Nitric oxide:
-Precursor is _
-Acts on enzyme _ -> increases _ -> end effect _
Nitric oxide:
-Precursor is arginine
-Acts on guanylate cyclase -> increases cGMP -> vasodilation
Norepinephrine:
-Initial dose = _ ug/min
-Low dose => _ R's (contractility)
-High dose => _ R's (vascular sm muscle constriction), _ R's (venous sm muscle constriction)
-Potent splanchnic vasoconstrictor
Norepinephrine:
-Initial dose = 4 ug/min
-Low dose => beta 1 (contractility)
-High dose => alpha 1 (vascular sm muscle constriction), alpha 2 (venous sm muscle constriction)
-Potent splanchnic vasoconstrictor
Basal caloric expenditure is ~___
Roughly how many g protein/Kg/day?
Basal caloric expenditure:
-25 Kcal/Kg/day (~1g protein/Kg/day needed)
Typical O2 in coronary sinus is _%
Typical O2 in coronary sinus is 30%
(heart consumes a lot of O2)
O2 dissociation curve:
Normal p50 @ which 50% of O2 R's are saturated = _
L-shifted by 3 things…
O2 dissociation curve: normal p50 = 27 mmHg
L shift = oxygen more bound to Hgb:
-Low CO2
-Low temp
-High pH
O2 dissociation curve:
Normal p50 @ which 50% of O2 R's are saturated = _
R-shifted by 4 things…
O2 dissociation curve: normal p50 = 27 mmHg
R shift = oxygen less bound to Hgb:
-High CO2
-Low pH
-2-3 DPG
-ATP
oliguria = <__ mL urine in 24 hrs
oliguria: <600 mL UOP/24 hrs (<25 mL/hr)

Oliguric acute renal failure => get a FENA.
-FeNa > 3% => ATN.
-Urine osmolality >400, Urine spec grav >1.02, Urine Na <20 => prerenal azotemia.
what is the formula for O2 consumption?
O2 consumption = CO x (arterial O2 content - venous O2 content)
-normal 5:1 ration of O2 delivery: consumption. Consumption is supply-independent until low level of delivery is reached
what is the formula for O2 delivery?
O2 delivery = CO x O2 content = CO x (Hgb x 1.34 x O2 sat + pO2 x 0.003)
_ = limiting factor for oxygen transport in the alveolus
Oxygen transport is perfusion limited in that once hemoglobin is fully saturated, continued exposure to the alveolus as a result of increase in transit time results in no further net uptake by hemoglobin

Although carbon dioxide is substantially more diffusible through the alveolar-capillary barrier than oxygen, a higher initial diffusion gradient exists for oxygen, which by combining with hemoglobin is able to maintain this gradient advantage such that approximately equivalent amounts of oxygen and carbon dioxide are eventually exchanged. Chemical binding with hemoglobin takes oxygen out of solution such that its partial pressure is reduced and the gradient for diffusion is increased.
what is the typical concentration of Na, K, HCO3 in pancreatic secretions?
Pancreatic secretions:
Na 140
K 5
HCO3 100
PCWP: 11 +/- 4
PCWP: 11 +/- 4
what number is used to monitor dynamic compliance of lungs?
PEAK pressure = measure of dynamic compliance
Phenylephrine:
-Alpha 1 => vasoconstriction
Phenylephrine:
-Alpha 1 => vasoconstriction
_ deficiency:
weakness (resp)
encephalopathy (needed for ATP)
Phosphate deficiency:
weakness (resp)
encephalopathy (needed for ATP)
Potassium concentration in body fluids:
-Saliva
-Gastric
-Pancreas/duodenum
Potassium concentration in body fluids:
-Saliva 20 mEq
-Gastric 10 mEq
-Pancreas/duodenum 5 mEq
Alkalosis causes hypokalemia by _
Alkalosis causes hypokalemia by driving K into cells and into urine (exchanged for H+)
which part of the bowel has highest concentration of potassium in its secretions?
COLON has highest K concentration in its secretions
Pre-renal azotemia:
FeNa <_%
Urine Na < _
BUN/Cr >_
Urine osmolality >_ mOsm
Pre-renal azotemia:
FeNa <1%
Urine Na <20
BUN/Cr >20
Urine osmolality >500 mOsm
lab findings with prerenal azotemia (vs. ATN)
oliguric acute renal failure => get a FENA.
-FeNa > 3% => ATN.
-Urine osmolality >400, Urine spec grav >1.02, Urine Na <20 => prerenal azotemia.
normal pulm capillary wedge pressure = _ +/- _
normal PCWP = 11 +/- 4
what is the effect of high PEEP on wedge pressure?
excessive PEEP artificially raises wedge pressure
optimal site of placement of PA catheter = zone _
optimal site of placement of PA catheter = zone 3
-avoids the effects of pulmonary pressures on wedge pressures
When placing a Swan-Ganz catheter, what is the relative distance from the internal jugular vein to the pulmonary artery?
The distance from the right internal jugular vein to the pulmonary artery is 40cm. This can easily be remembered by the rule of 5s: 40cm from the Right IJ to the PA 45cm from the Right SC to the PA 50cm from the Left IJ to the PA 55cm from the left SC to the PA
Swan distance to wedge in L subclavian = _ cm
Swan distance to wedge:
R SCV 45 cm
R IJ 50 cm
L SCV 55 cm
L IJ 60 cm
Pulmonary vascular resistance is measured by _
Pulmonary vascular resistance is measured only by SWAN-GANZ CATHETER
normal PA pressure
PA pressure: 20-30/6-15
normal cardiac output = _ to _ L/min
Cardiac output: 4-8 L/min
normal cardiac index is...
Cardiac index: 2.5-4 L/min
How is PVR calaculated?
PVR = [(PA pressure - wedge)/CO] x 80
Pre-renal failure:
FeNa__
Urine Na __
BUN/Cr__
Urine osmolality __
Pre-renal failure:
FeNa< 1%
Urine Na< 20
BUN/Cr >20
Urine osmolality >500 mOsm
Aldosterone:
-Stimulated by Angiotensin 2
-Causes transcription of Na/K ATPase, Na/H ATPase -> reabsorb Na, secrete H and K in distal convoluted tubule ->
Water reabsorbtion
Aldosterone:
-Stimulated by Angiotensin 2
-Causes transcription of Na/K ATPase, Na/H ATPase -> reabsorb Na, secrete H and K in distal convoluted tubule ->
Water reabsorbtion
why are elderly people have impaired ability to concentrate urine?
Renal response to ADH is diminished in elderly pts causing a reduced ability to concentrate urine.
Kidney receives _% of cardiac output
Kidney receives 25% of cardiac output
-But does not require a lot of O2 expenditure to clear solutes, so oxygen tension in renal vein is relatively high, ~80%
what are the 2 triggers for renin release?
what does renin do?
Renin:
-Decreased pressure at JGA and/or increased Na concentration at macula densa ->
Renin released ->
converts angiotensinogen to angiotensin I
Renin:
-Relased in response to 2 things…
Converts _ to _
Renin:
-Decreased pressure at JGA and/or increased Na concentration at macula densa ->
Renin released ->
converts angiotensinogen to angiotensin
how is respiratory quotient calculated?
respiratory quotient = CO2 produced/O2 consumed
-0.7 => fat used
-1.0 => carb used
->1 => overfeeding
What is respiratory quotient?
-0.7 => _ used
-1.0 => _ used
Respiratory quotient = CO2 produced/O2 consumed
-0.7 => fat used
-1.0 => carb used
what vitamin deficiency causes magenta tongue?
Riboflavin deficiency causes magenta tongue?
how is serum osmolality calculated?
normal serum osmolarity = 275-299 mOsm/Kg H20
osmolality = 2 × Na (mEq/L) + glucose (mg%)/18 + BUN (mg%)/2.8
what is normal serum osmolarity?
normal serum osmolarity = 275-299 mOsm/Kg H20
osmolality = 2 × Na (mEq/L) + glucose (mg%)/18 + BUN (mg%)/2.8
Cytokine induced hypotension is primarily stimulated by induction of enzyme _ mediated through the proinflammatory cytokines _ and _.
Cytokine induced hypotension is primarily stimulated by induction of nitric oxide synthetase mediated through the proinflammatory cytokines TNF-α and IL-1.
-IL-1 also induces fever
-TNF-alpha also promoted WBC adhesion to endothelium
A 23-year-old woman with malabsorption due to short gut syndrome has been receiving total parenteral nutrition in her home for one year. She now has hair loss, dry skin, and a reddish skin rash. These symptoms are evidence of a deficiency of
essential fatty acids
how are short-chain fatty acids provided to the colonocytes?
Oligosaccharides which cannot be broken down and absorbed are fermented by bacteria in the colon providing end products of short-chain fatty acids (primarily butyrate and propionate) which are the primary oxidative fuel of the colonocyte.
A 52-year-old male patient with lung cancer is admitted with the following laboratories: Serum sodium: 127 mEq/L. Serum potassium: 4 mEq/L. Serum uric acid: 3 mg/dL. Serum osmolality: 256 mOsm/kg. Urine osmolality: 340 mOsm/kg. Urine sodium: 55 mEq/L. On examination, he is normovolemic.
How should his fluid be managed?
SIADH: 2/2 high ADH
-low UOP, low Na, low serum osmolarity (normal 275-299 mOsm/Kg)
-Tx: fluid restriction, then vasopressin R antagonist (diuresis) for goal Na >120 and improved neuro sx.
-Don't give NS if pt has normal volume status (may worsen condition) Can give 3% if treatment fails
The major oncotic force of the interstitium is _
The major oncotic force of the interstitium is hyaluronate, a proteoglycan, not albumin
Starvation:
Brain begins using _ from fatty acids
(normally brain and RBCs are dependent on _)
-Late starvation: liver depleted of alanine => gluconeogenesis shifts to kidney
Starvation:
Brain begins using ketones from fatty acids
(normally brain and RBCs are dependent on glutamine)
-Late starvation: _ depleted of alanine => gluconeogenesis shifts to the _
Steroid hormones bind a receptor located at the cell, then affect transcription by _
Steroid hormones bind a receptor in the CYTOPLASM -> enter nucleus as STEROID-RECEPTOR COMPLEX
SvO2:
Nornal range = _-_
Decreased by 2 mechanisms …
SvO2 = Mixed venous O2 saturation. Normal = 65-75% Decreased by:
-Decreased O2 delivery: MI, cardiac tamponade, low Hgb, low O2 sat
-Increased O2 consumption: malignant hyperthermia
SvO2:
Nornal range = _-_
Increased by 2 mechanisms …
SvO2 = Mixed venous O2 saturation Normal = 65-75% Increased by:
- Shunting of blood: sepsis, cirrhosis, L->R cardiac shunt
-Decreased O2 extraction: CN toxicity, hyperbaric O2, hypothermia, paralysis, coma, sedation
normal SvO2 is ..
SvO2: 70 +/- 5
normal SVR is...
SVR: 800-1400
normal SVR index is ...
SVR index: 1500-2400
what are the two main processes by which intubated pts get pneumotx?
Tension pneumotx 2/2:
- trauma to pharynx or piriform sinus during intubation
-Peak pressures >50 cm H20 x 12 hrs (43% of pts c/ PIP >70 cm H2O)
Total body water:
-% for infants, men, and women
-if TBW is 60%, then _% cellular, _% intestinal, _% plasma
Total body water:
-Infant 80%
-Men 60%
-Women 50%
-Substract 10% if obese

If TBW is 60%, then 40% cellular, 15% intestinal, 5% plasma
How do you compute a 24-hour UUN?

-6.25 g of protein contains 1g nitrogen
-N balance = (Protein/6.25) - (24 hr urine N + 4g)
Vasopressin:
-V1 R's: vascular sm muscle constriction
-V2 R's intrarenal: water reabsorbtion @ collecting ducts
-V2 R's extrarenal: release of factor VIII, vWF
Vasopressin:
-V1 R's: vascular sm muscle constriction
-V2 R's intrarenal: water reabsorbtion @ collecting ducts
-V2 R's extrarenal: release of factor VIII, vWF
Increasing PEEP can decrease a pt's UOP by mechanism …
PEEP can prevent blood from traversing pulm capillaries ->
decreased preload ->
decreased cardiac output
Lung dead space:
-~150cc in normal adults
-Everything proximal to resp bronchioloes, i.e. airway that is ventilated but not perfused
-Incrased by excessive PEEP (which collapses alveolar capillaries), PE, ARDS, pulm HTN
Lung dead space:
-~150cc in normal adults
-Everything proximal to resp bronchioloes, i.e. airway that is ventilated but not perfused
-Incrased by excessive PEEP (which collapses alveolar capillaries), PE, ARDS, pulm HTN
Vital capacity = max amount of air exhaled after max inhalation
Vital capacity = max amount of air exhaled after max inhalation
Residual volume is ~_% of total lung volume
Residual volume = air left in lung after maximal exhalation
~20% of total lung volume
Functional residual capacity = volume of air left in lungs after normal exhalation = residual volume + expiratory reserve volume
Functional residual capacity = volume of air left in lungs after normal exhalation = residual volume + expiratory reserve volume
How does atelectasis cause fever?
Atelectasis:
Alveolar macrophages activated -> release IL-2 -> acts on hypothalamus to cause fever
Pre-renal failure:
FeNa< 1%
Urine Na< 20
BUN/Cr >20
Urine osmolality >500 mOsm
Pre-renal failure:
FeNa< 1%
Urine Na< 20
BUN/Cr >20
Urine osmolality >500 mOsm
Rapid shallow breathing index = most sensitive parameter for predicting successful extubation
= RR/Tidal Volume
Rapid shallow breathing index = most sensitive parameter for predicting successful extubation
= RR/Tidal Volume
Vit _ deficiency =>
can decrease vit C stores
Vit A deficinecy =>
can decrease vit C stores
what are the steps of Vit D metabolism?
Vitamin D:
-made in skin -> 25-OH in liver -> 1-OH in kidney-> active
-Increases Ca binding protein to increase intestinal absorbtion of Ca
what vitamin deficiency should be suspected in a patient with bile drain AND broad-spec abx?
Vitamin K being a fat-soluble vitamin is likely to be malabsorbed with bile diversion. Bile is required for adequate fat and fat-soluble vitamins. Approximately 50% of the vitamin K in the human comes from bacterial production in the colon. The broad spectrum antibiotic rapidly destroys a significant portion of the anaerobic bacteria in the colon. They are the primary vitamin K producers.
what vitamin deficiency causes taste atrophy
Zinc deficiency causes taste atrophy
_ deficiency =>
perioral rash
hair loss
poor healing
change in taste
Zinc deficiency =>
perioral rash
hair loss
poor healing
change in taste