McNeil's notes: lytes, physiology, toxicology, hypothermia, burns, embolism, radiology, potpourrie(-stats/epi/ethics) Flashcards
Labs in diabetes insipidus show:
a. Hyponatremia.
b. Hypoglycemia.
c. High urine specific gravity.
d. Low urine osmolarity
e. Urine specific gravity
e. Urine specific gravity
1) patient post transsphenoidal resection pituitary tumour. Now has mild DI . Just complain of thirst and Na 145. Best treatment option is:
a. fluids ad lib
b. R/L at 150 cc / hour
c. D5 at 150 cc/ hr
d. DDAVP
a. fluids ad lib
DDAVP for Na > 150
The body system MOST sensitive to changes in sodium homeostasis is: A. CVS B. CNS C. Respiratory D. Musculoskeletal
Answer: CNS
The clinical features of acute hyponatremia are related to osmotic water shift leading to increased ICF volume, specifically brain cell swelling. Therefore, the symptoms are primarily neurologic, and their severity is dependent on the rapidity of onset and absolute decrease in plasma [Na+ ].
The major symptoms of hypernatremia are neurologic and include altered mental status, weakness, neuromuscular irritability, focal neurologic deficits, and occasionally coma or seizures.
- Washington Manual of Medical Therapeutics, 30th ed., Copyright © 2001
In a patient diagnosed with multiple myloma, had the following lab result, Creatinine 178, Urea 5, Na 128, K 3.5 & Albumin 22. the cause of hyponatremia is:
a. SIADH
b. Pseudohyponatremia
c. Renal failure
d. Volume overload
e. Dehydration
Answers given:
pseudohyponatremia
pseudohyponatremia seem with MM and high TG, and hyperglycemia
Pseudohyponatremia is a laboratory artifact that is present when the plasma contains very high concentrations of protein (multiple myeloma, intravenous immunoglobulin infusion) or lipid (hypertriglyceridemia, hypercholesterolemia). It does not occur when a direct ion-selective electrode determines the sodium concentration, a technique that is increasingly used in clinical laboratories. In true hyponatremia, the measured osmolality is low, whereas it is normal in pseudohyponatremia.
- Kliegman: Nelson Textbook of Pediatrics, 18th ed.
Depends on the osmolality
There are two situations in which sodium can be fictitiously low as a result of the presence of substances that alter the volume of plasma water in which sodium is measured.
Pseudohyponatremia is common in the setting of hyperglycemia or the use of some other restricted solute that causes high plasma osmolality.
Pseudohyponatremia also can occur as a result of an increase in relatively high-molecular-weight substances, such as occurs with Bence-Jones proteins in multiple myeloma or in hyperlipidemia.
- Abeloff: Abeloff’s Clinical Oncology, 4th ed.
Adrenal insufficiency - orthostatic hypotension and hyponatremia are common; hyperpigmentation and hyperkalemia and volume depletion occur in primary adrenal failure (disease of adrenal glands versus secondary which is caused by disorders the pituitary or hypothalamus); may become pre-renal; multiple myeloma-monoclonal malignancy of plasma cells that produce paraprotein and is characterized by replacement of bone marrow and bone destruction; often presents with bone pain, anemia and infection; labs: rouleaux/rare plasma cells/pancytopenia, monoclonal protein, heavy and light chains on SIE, decreased normal immunoglobulins, BJ proteins, hyperCa, increased Cr, increased ESR, and narrow anion gap; renal failure secondary to: myeloma kidney (light chain deposition), hypercalcemic nephropathy, pyelo, amyloid, obstruction, plasma cell infiltration, hyperuricemia, and hyperviscosity of renal blood flow; diuretics-side effects depend on class; thiazides cause hypokalemia, hypoMg, hyperlipidemia, hyperCa, hyperglycemia, hyperuremia, hyponatremia, and rarely azotemia; loop diuretics cause hypoMg, hypoCa, and hypoK; K-sparing diuretics of course cause hyperK!
65 year old male patient presents with symptomatic hyponatremia his NA is 117.What is the best way to treat his hyponatremia:
a. Slow infusion hypertonic saline
b. Rapid infusion of hypertonic saline
c. D5W
d. D5 ½ NS
e. D5 ¼ NS
a. Slow infusion hypertonic saline
Risk central pontine demyelination
Hyponatremia can be either hypovolemic, hypervolemic, and euvolemic. The treatment will usually vary depending on which of these is present. In a patient with severe hyponatremia however, (Na
Calculate the approximate sodium deficit in a 70kg man with a serum sodium of 120mmol/L.
a. 280
b. 410
this only seems to have been asked 1 year so probably low yield.
Sodium Deficit = Total Body Water * Normal Wt in kg * (Desired Na - Pt’s Na) (TBW = 0.6 if male and 0.5 if female)
70*0.6 = 42kg water = 42L water (140-120)mmol/L*42L = 840mmol needed
Post-op laryngectomy, headache, decreased LOC. AVSS, normal urine output. Sodium 118. What is the most likely diagnosis
a) SIADH
b) Dilutional hyponatremia
c) Depletional hypokalemia
b) Dilutional hyponatremia (seems like a long surgery)
??? or could be DKA with pseudohyponatremia? depends on the question
1) Hyponatremia: when do you treatment it with Na replacement (When pt is symptomatic or if Na less than 120)
a.
a.
In patient with cirrhosis and ascites, hyponatremia is associated with:
a. Expanded extravascular fluid volume
b. Expanded intravascular fluid volume
c. Renal loss of Na
d. Depleted intravascular volume
Answer: Expanded intravascular fluid volume
The net effect is avid renal sodium and water retention because the patient is effectively volume depleted even though extracellular sodium stores, the plasma volume, and the cardiac output are increased. The sodium retention leads to the development of ascites unless the patient is adequately treated with dietary sodium restriction and diuretics.
- Up To Date 2007 Hyponatremia in Cirrhosis
proteins go extravascular–>intravascular hypovolemia
ADH increases as cirrhosis gets worse–>retain salt and water
lose ability to excrete water as cirrhosis worsens
end up hyponatremic with increased total body sodium. worsened by those that continue to drink alcohol. Better to be on low sodium diet.
initially would be vascular low volume but as things get worse can’t pee water so would be hypervolemic hyponatremic.
Hypercalcemia causes all of the following except:
a) Polyuria
b) carpopedal spasm
c) proximal mm weakness
d) coma
b) carpopedal spasm
IV lasix is associated with all except: All are complications of Lasix therapy EXCEPT: a. Hyperuricemea. b. Hyponatremia. c. Hypercalcemia. d. Metabolic alkalosis
c. Hypercalcemia.
actually can be used for tx of hyperCa
Loop diuretics inhibit the Na+/K+/2Cl- cotransporter in the ascending limb of the loop of Henle (see Fig. 136-1 ). They are highly protein bound and not filtered by the glomerulus. Loop diuretics are actively secreted into the proximal tubule by the organic anion pathway and reach their site of action intraluminally. They also indirectly inhibit reabsorption of calcium and magnesium by their effect on transepithelial potential difference.
- Walsh: Palliative Medicine , 1st ed.
Which of the following is the site of calcium and iron absorption in the gastrointestinal tract?
- duodenum
- distal ileum
- proximal ileum
- jejunem
- duodenum
Which of the following will NOT cause hypercalcemia? A. Thiazide diuretics B. Sarcoidosis C. Paget’s disease D. Multiple fractures
Answer: Multiple fractures
Common question. This is always the answer
[Paget’s] may also cause hypercalcemia, especially if the patient becomes bed-bound.
- Bradley: Neurology in Clinical Practice, 5th ed.
In addition to the well-known association of hypercalcemia in sarcoidosis ….
- Abeloff: Abeloff’s Clinical Oncology, 4th ed.
Young, normally active patients with high bone turnover rates are subject to the development of hypercalcemia when suddenly forced into immobility, as may occur during forced bed rest after injury or major illness.
- Townsend: Sabiston Textbook of Surgery, 18th ed.
In Paget’s disease, the following abnormality is MOST likely to occur:
a. elevated serum calcium
b. elevated alkaline phosphatase
c. elevated serum phosphate
Answer: elevated alkaline phosphatase
High alk phos.normal or high calcium ,normal phos
Paget’s disease can cause bone pain and deformity. An elevated bone-specific alkaline phosphatase and characteristic radiographic changes can help make the diagnosis. Joint pain caused by secondary osteoarthritis in areas of involvement of bone from Paget’s disease most commonly occurs in the hip, knee, or vertebrae. Spinal stenosis from Paget’s disease of the spine has been reported.
- Goldman: Cecil Medicine, 23rd ed.
Extracellular calcium homeostasis is almost invariably normal despite the massive increase in bone turnover. Hypercalciuria and more rarely hypercalcemia may occur with prolonged immobilization or fracture.
A 40 yo presents with hypocalcemia and hyperparathyroidism. What is the MOST likely diagnosis? A. Renal Failure B. Osteomalacia C. Parathyroid Adenoma D. Vitamin D Deficiency
D. Renal failure
Secondary hyperparathyroidism is caused by any condition that gives rise to chronic hypocalcemia, which in turn leads to compensatory overactivity of the parathyroid glands. Renal failure is by far the most common cause of secondary hyperparathyroidism, although several other diseases, including inadequate dietary intake of calcium, steatorrhea, and vitamin D deficiency, may also cause this disorder.
- Kumar: Robbins and Cotran Pathologic Basis of Disease, Professional Edition , 8th ed.
Uptodate 2016: Vitamin D deficiency osteomalacia is the only osteomalacia in their table that has both hypocalcemia and hyperparathyroidism
Parathyroid adenoma = hypercalcemia
All of the following are used in the treatment of hypercalcaemia except:
a. Steroid
b. Rehydration
c. Lasix
d. Calcitonin
e. None of the above
a. none of the above (although steroid is only used in granulomatous disease : lymphoma, sarcoidosis)
Other EXCEPT answers:
- Thiazide (avoid as may increase reabsorption of calcium in DCT)
- Insulin
MANAGEMENT (9)
- Forced diuresis with isotonic saline and lasix (mainstay in those with normal kidneys, dialysis possible in those with RF)
- Bisphosphonates
- Mithramycin
- Calcitonin
- Corticosteroids (in sarcoidosis)
- IV phosphates (disodium or monopotassium phosphate, use as absolute last resort)
- Gallium nitrate
- Chloroquine phosphate (in sarcoidosis)
- Surgical excision of excess functioning tissue
- Morell Notes
A patient with Trousseau’s sign, prolonged QT interval and hyperactive DTR. He has :
Answer given: Hypocalcemia
But more likely hypomagnesemia.
- Trousseau’s sign is seen in hypocalcemia and hypomagnesemia.
- Hyperactive DTRs are somewhat more specific for hypomagnesemia
- QT shortening is seen with hypocalcemia
Hypocalcemia
Hypercalcemia can produce a number of nonspecific findings, as follows:
* Hypertension and bradycardia may be noted in patients with hypercalcemia, but this is nonspecific.
* Abdominal examination may suggest pancreatitis or the possibility of an ulcer.
* Patients with long-standing elevation of serum calcium may have proximal muscle weakness that is more prominent in the lower extremities; they also may have bony tenderness to palpation.
* Hyperreflexia and tongue fasciculations may be present.
* Anorexia or nausea may occur.
* Polyuria and dehydration are common.
* Lethargy, stupor, or even coma may be observed.
Hypercalcemia may produce ECG abnormalities related to altered trans-membrane potentials that affect conduction time. QT interval shortening is common, and, in some cases, the PR interval is prolonged. At very high levels, the QRS interval may lengthen, T waves may flatten or invert, and a variable degree of heart block may develop. Digoxin effects are amplified.
- http://emedicine.medscape.com/article/766373-diagnosis
Hypomagnesemia Physical # Neuromuscular irritability * Hyperactive deep tendon reflexes * Muscle cramps * Muscle fibrillation * Trousseau and Chvostek signs * Dysarthria and dysphagia from esophageal dysmotility # CNS hyperexcitability * Irritability and combativeness * Disorientation * Psychosis * Ataxia, vertigo, nystagmus, and seizures (at levels
Hypomagnesemia MOST likely causes: A. Decreased deep tendon reflexes B. Tremor C. Constipation D. Muscle paralysis
B. Tremor
Tip: Hypoeverything makes you slow
EXCEPTION: hypoMg and hypoCa make you twitch
Clinical and laboratory manifestations:
a. Neuromuscular: weakness, hyperreflexia, fasciculations, tremors, convulsions, delirium, coma
b. Cardiovascular: cardiac arrhythmias
c. Hypokalemia refractory to potassium replacement
d. Hypocalcemia refractory to calcium replacement
- Ferri: Practical Guide to the Care of the Medical Patient, 7th ed.
At serum magnesium levels less than 1 mEq/L, patients have tremor, hyperactive deep-tendon reflexes, hyperreactivity to sensory stimuli, muscular fibrillations, positive Chvostek and Trousseau signs, and carpopedal spasms progressing to tetany. Mental status changes may become evident and may include irritability, disorientation, depression, and psychosis. Cardiac arrhythmias and reversible respiratory muscle failure can also occur in severe hypomagnesemia.
- http://emedicine.medscape.com/article/922142-overview
Clinical Manifestations of hypomagnesemia
Cardiac manifestations (7):
1. tachyarrhythmias (unstable VT)
2. digitalis toxicity enhanced as both inhibit the membrane pump
3. prolonged QT
4. T-wave flattening
5. prolonged PR interval
6. A. fib
7. Torsades de pointes
Neurologic manifestations: Changes in mental status, seizures, Tremors, Hyperreflexia
All uncommon, non-specific and have little clinical value
Tremor is the most characteristic finding with hypomagnesemia but tetany is first sign.
- Morell Notes
35 year old male patient with ulcerative colitis and chronic diarrhoea presents with hypocalcaemia, and you prescribed calcium gluconate two weeks later present with tetany. What is the most likely diagnosis:
a. Hypomagnesaemia
b. Hyponatremia
c. Hypokaemia
d. Exacerbation of ulcerative colitis
e. None compliance to medication
a. Hypomagnesaemia
Tetany associated with hypocalcemia.
Hypocalcemia in this case caused by hypomagnesemia, causing decreased PTH secretion and inhibition of PTH effect on bone.
Hypomagnesaemia is caused by all of the following except:
a. Cisplastin
b. Loop diuretics
c. Cyclosporine
d. Aminoglycosides
e. Malabsorbtion
Sources mention all answers!
I refuse to learn this list, but here it is for you keeners:
Primary nutritional disturbances
Inadequate intake, total parenteral nutrition, refeeding syndrome
Gastrointestinal disorders
Specific absorptive defects, malabsorption syndromes, prolonged diarrhea, prolonged nasogastric suction, pancreatitis
Endocrine disorders
Hyperparathyroidism, hypoparathyroidism, hyperthyroidism, primary hyperaldosteronism, Bartter’s syndrome, diabetic or alcoholic ketoacidosis, administration of epinephrine, SIADH, hungry bone syndrome after parathyroidectomy
Chronic alcoholism, alcoholic withdrawal, increased renal excretion
Ethanol ingestion; idiopathic; after renal transplantation; drugs (cisplatin, aminoglycoside, amphotericin B, diuretics, pentamidine, theophylline); recovery phase of acute tubular necrosis; colony-stimulating factor therapy
-Miller: Miller’s Anesthesia, 7th ed.
HYPOMAGNESEMIA (Etiology)
a Gastrointestinal and nutritional
i. Defective gastrointestinal absorption (malabsorption)
ii. Inadequate dietary intake (e.g., alcoholics)
iii. Parenteral therapy without magnesium
iv. Chronic diarrhea, villous adenoma, prolonged nasogastric suction, fistulas (small bowel, biliary)
b Excessive renal losses
i. Diuretics
ii. RTA
iii. Diuretic phase of ATN
iv. Endocrine disturbances (diabetic ketoacidosis, hyperaldosteronism, hyperthyroidism, hyperparathyroidism), SIADH, Bartter’s syndrome, hypercalciuria, hypokalemia
v. Cisplatin, alcohol, cyclosporine, digoxin, pentamidine, mannitol, amphotericin B, foscarnet, methotrexate
vi. Antibiotics (gentamicin, ticarcillin, carbenicillin)
c Redistribution: hypoalbuminemia, cirrhosis, administration of insulin and glucose, theophylline, epinephrine, acute pancreatitis, cardiopulmonary bypass
d. Miscellaneous: sweating, burns, prolonged exercise, lactation, “hungry-bones” syndrome
- Ferri: Practical Guide to the Care of the Medical Patient, 7th ed.
Loop diuretics inhibit the apical membrane Na+/K+/2Cl− cotransporter of the TAL and abolish the transepithelial potential difference, thereby inhibiting paracellular Mg2+ reabsorption. Hypomagnesemia is therefore a frequent finding in patients receiving chronic loop diuretic therapy
- Brenner: Brenner and Rector’s The Kidney, 8th ed
The earliest clinical sign of hypermagnesemia is:
a. stupor
b. convulsion/seizure
c. decreased DTRs
d. something else
Answer: these something elses: hypotension, nausea, vomiting, facial flushing, urinary retention, and ileus. BUT These are so common so I would say they shouldn’t clinically make you think of hyperMg unless you’re an internal medicine resident and listing your top 100 DDx
If those aren’t there, probably decreased DTR
Causes of hypermagnesemia:
renal insufficiency, antacid overuse, adrenal insufficiency, hypothyroidism, excessive intake (e.g. tx of eclampsia).
Signs and symptoms
Clinical: nausea, vomiting, weakness, mental status changes, hyperreflexia, hyperventilation
EKG findings include AV block and prolonged QT interval
Treatment
1- discontinue or remove external sources; large amounts found in antacids and cathartics
2- IV calcium gluconate for emergent symptoms
3- dialysis in renal failure patients
- Mont Reid Surgical Handbook, pg 26
Magnesium toxicity is a serious and potentially fatal condition. Mild hypermagnesemia (serum magnesium level >4 to 6 mg/dL) causes hypotension, nausea, vomiting, facial flushing, urinary retention, and ileus. Above serum magnesium levels of 8 to 12 mg/dL, flaccid skeletal muscular paralysis and hyporeflexia may ensue, together with bradyarrhythmias, respiratory depression, coma, and cardiac arrest. A low, or even negative serum anion gap may sometimes be seen.
- Goldman: Cecil Medicine, 23rd ed.
Cardiac toxicity in hyperkalemia would be BEST treated with: A. Insulin B. Metoprolol C. Calcium D. Bicarbonate
Intravenous calcium is used to stabilize the myocardium by lowering the threshold potential. It has no effect on the serum potassium level. Improvement in the ECG is usually evident within 2 to 5 minutes.
- Ferri: Practical Guide to the Care of the Medical Patient, 7th ed.
The following are clinical signs of hyperkalemia except:
a. peaked T waves
b. wide QRS
c. diarrhea
d. tetany
Answer: diarrhea
In hyperkalemia, there is a depolarizing effect on the resting membrane potential and potassium channel conductance is increased, leading to the classic electrocardiographic changes of hyperacute peaked T waves associated with rapid repolarization ( Fig. 118-2). Because of the increased potassium conductance, hyperkalemia antagonizes the normal slow depolarization of pacemaker tissue that is usually associated with a decrease in potassium conductance. Hyperkalemia, like acetylcholine, commonly results in sinus bradycardia. Heart block, loss of P waves on the electrocardiogram, and prolonged QRS intervals are all seen in cases of severe hyperkalemia, usually in excess of 6 mmol/L.
- Goldman: Cecil Medicine, 23rd ed
Neuromuscular signs and symptoms of hyperkalemia include muscle cramps, weakness, paralysis, paresthesias, tetany, and focal neurologic deficits, but these are rarely specific enough to suggest the diagnosis in themselves
- Marx: Rosen’s Emergency Medicine, 7th ed.
EKG Summary:
- loss of P wave
- prolonged QRS
- hyperacute T wave
2) What are the signs of hypokalemia?
a) Depressed ST, inverted T, wide QRS
b) Depressed ST, inverted T, narrow QRS
c) Elevated ST, inverted T, wide QRS
d) Elevated ST, inverted T, narrow QRS
A) Depressed ST, inverted T, wide QRS
Low serum potassium not only hyperpolarizes most cells, leading to an increase in the resting potential, but also has effects on certain potassium channels required for repolarization. Thus, hypokalemia decreases or slows potassium conductance, the prolonged repolarization phase accounting for the characteristic electrocardiographic findings of broad, flattened T waves. U waves are also indicative of this delay in repolarization.
- Goldman: Cecil Medicine, 23rd ed.
Electrocardiographic changes in hypokalemia include broad flat T waves, ST depression, and QT prolongation; these are most marked when serum K+ is
3) Which of the following is a sign of hypokalemia:
a. U wave
b. Peaked T waves
c. ST segment elevation
d. Increased deep tendon reflexes
e. None of the above
U wave
All of the following may cause hypokalemia EXCEPT: A. Vitamin B12 B. Ventolin C. Insulin D. Digoxin E. Corticosteroids
Answer: digoxin can lead to malignant hyperkalemia (Digibind, used for digoxin toxicity, is a cause)
Etiology and classification:
a. Cellular shift (redistribution) and undetermined mechanisms
i. Alkalosis (each 0.1 increase in pH decreases serum potassium by 0.4 to 0.6 mEq/L)
ii. Insulin administration
iii. Vitamin B12 therapy for megaloblastic anemias, acute leukemias
iv. Hypokalemic periodic paralysis: rare familial disorder manifested by recurrent attacks of flaccid paralysis and hypokalemia
v. β-Adrenergic agonists (e.g., terbutaline), decongestants, bronchodilators, theophylline, caffeine
vi. Barium poisoning, toluene intoxication, verapamil intoxication, chloroquine intoxication
vii. Correction of digoxin intoxication with digoxin antibody fragments (Digibind)
b. Increased renal excretion
i. Drugs
(a) Diuretics, including carbonic anhydrase inhibitors (e.g., acetazolamide)
(b) Amphotericin B
(c) High-dose sodium penicillin, nafcillin, ampicillin, or carbenicillin
(d) Cisplatin
(e) Aminoglycosides
(f) Corticosteroids, mineralocorticoids
(g) Foscarnet sodium
ii. Renal tubular acidosis (RTA)
iii. Diabetic ketoacidosis, ureteroenterostomy
iv. Magnesium deficiency
v. Postobstruction diuresis, diuretic phase of acute tubular necrosis (ATN)
vi. Osmotic diuresis (e.g., mannitol)
vii. Bartter’s syndrome: hyperplasia of juxtaglomerular cells leading to increased renin and aldosterone, metabolic alkalosis, hypokalemia, muscle weakness, and tetany (seen in young adults)
viii. Increased mineralocorticoid activity (primary or secondary aldosteronism), Cushing’s syndrome, or physiologic increases in mineralocorticoid activity (dehydration)
ix. Chronic metabolic alkalosis from loss of gastric fluid (increased renal potassium secretion)
c. Gastrointestinal loss
i. Vomiting, nasogastric suction
ii. Diarrhea
iii. Laxative abuse
iv. Villous adenoma
v. Fistulas
d. Inadequate dietary intake (e.g., anorexia nervosa)
e. Cutaneous loss (excessive sweating)
f. High dietary sodium intake, excessive use of licorice
g. Hypomagnesemia
- Ferri: Practical Guide to the Care of the Medical Patient, 7th ed
What is the commonest cause of hypokalemia associated with INCREASED urine potassium?
a. prolonged thiazide diuretic use
b. spironolactone use
c. primary hyperaldosteronism
Answer: A vs C (thiazide more common than 1 hyperaldosteronism)
“The most common causes of hypokalemia due to urinary potassium losses include diuretic use, a primary increase in mineralocorticoid activity, increased distal delivery of nonreabsorbable anions, and loss of gastric secretions.” uptodate 2016
The four most common causes of hypokalemia are reduced intake, gastrointestinal losses, excessive renal losses of potassium (e.g., with excess of mineralocorticoids or diuretics), and potassium shifts from the ECF to the intracellular fluid (e.g., owing to insulin administration).
- Miller: Miller’s Anesthesia, 7th ed.
Renal loss of K+ is by far the most common cause of hypokalemia. With rare exceptions, hypokalemia due to increased renal wasting of potassium can be attributed to an increased activity of aldosterone or other mineralocorticoids. Increased aldosterone could be a primary disorder as in primary hyperaldosteronism or due to increased renin secretion as in secondary hyperaldosteronism.
Examples of secondary hyperaldosteronism that result in hypokalemia include renal artery stenosis, diuretic therapy, and malignant hypertension, and congenital defects in renal salt transport such as Bartter’s syndrome and Gitelman’s syndrome.
- McPherson & Pincus: Henry’s Clinical Diagnosis and Management by Laboratory Methods, 21st ed.
Normal hemodynamic changes during pregnancy include all of the following except:
a) Hemodilution
b) increased red cell mass
c) leukocytosis
d) eosinophilia
d) eosinophilia
Turns out babies are not parasites
Increase in TBW (by 40%) – 2/3 increase in extravascular. Increase in plasma volume. Disproportionate increase in plasma volume over RBC volume – hemodilution. Despite erythrocyte production there is a physiologic fall in the HB and hematocrit readings. (likely Eosinophilia)
As a consequence of the increased minute ventilation, maternal Pao2 levels during late pregnancy range from 104 to 108 mm Hg, and maternal Paco2 ranges from 27 to 32 mm Hg.
- Townsend: Sabiston Textbook of Surgery, 18th ed.
Physiologic leukocytosis during pregnancy makes it more difficult to evaluate infectious abdominal processes, particularly late in the 3rd trimester, when the WBC is even higher.
- Gabbe: Obstetrics: Normal and Problem Pregnancies, 5th ed.
Which is not associated with pregnancy?
a. low CO2
b. metabolic acidosis
c. decreased Hct
d. leukocytosis
e. high ESR
b. metabolic acidosis
Minute ventilation begins to rise by the end of the first trimester and continues to increase until term. Progesterone mediates this response by direct stimulation of respiratory drive and by increasing sensitivity of the respiratory center to CO2.[16] This results in a mild respiratory alkalosis—Pco2 falls to approximately 27 to 32 mm Hg—and a compensatory increase in renal excretion of bicarbonate. This large increase in minute ventilation allows maintenance of high-normal Po2 despite the 20% to 33% increase in oxygen consumption in pregnancy.
- Brenner: Brenner and Rector’s The Kidney, 8th ed.
Physiology maternal hyperventilation causes a compensatory metabolic acidosis with a decrease in maternal Hco3. The mother therefore has less buffering capacity for metabolic acidosis
ESR elevated in: inflammatory states (acute-phase reactant), collagen-vascular diseases, infections, myocardial infarction, neoplasms, hyperthyroidism, hypothyroidism, rouleaux formation, elderly, pregnancy
- Rakel: Textbook of Family Medicine, 7th ed.
Hematocrit is 30–50% normal
- Gabbe: Obstetrics: Normal and Problem Pregnancies, 5th ed
Resistant is proportional to:
a. Length and 1/radius to power of 4
b. Radius and 1/ length to power of 4
c. Length to power of 4 and 1/radius
d. Radius to power of 4 and 1/length
a. Length and 1/radius to power of 4
Which of the following changes in vital signs is not seen when a patient goes from standing to supine?
a) decreased heart rate
b) decreased SV
c) Decreased SVR
Standing – blood to pool in feet, less venous return, and reduced CO, compensatory increase HR/BP
What is the primary determinant of myocardial oxygen supply in a healthy person:
a) blood pH
b) sympathetic activity
c) oxygen content of the blood
d) myocardial oxygen demand
Previous answer D, but it’s actually C I think
“The delivery of oxygen (DO2) to the myocardium (oxygen supply) is determined by two factors: coronary blood flow (CBF) and the oxygen content (concentration) of the arterial blood (CaO2).” - Some random website
Blood flow to coronaries based on preload (diastolic flow)
“Heart rate is the single most determinant of myocardial oxygen demand”
Which of the following are effects of thromboxane A2?
a. platelet aggregation
b. vasodilatation
c. vasoconstriction
d. bronchodilatation
e. increased vascular permeability
a. platelet aggregation
Thromboxanes are synthesised predominantly by platelets and act to promote:
• vasoconstriction
• platelet aggregation
• bronchoconstriction in lung.
They act as autocoid local hormones due to their short half lives, and they are excreted in the kidney.
TxA2 is the predominant cyclooxygenase product formed by platelets and human monocytes. It stimulates platelet aggregation and secretion and is mitogenic for and constricts vascular and bronchial smooth muscle. These biologic properties are shared by the prostaglandin endoperoxides. A single gene encodes a human thromboxane receptor, which is a member of the G protein-coupled receptor superfamily.
- Goldman: Cecil Textbook of Medicine, 21st ed., Ch 233
Thromboxane A2 (TXA2) is a thromboxane. It is produced by activated platelets and has prothrombotic properties: it stimulates activation of new platelets as well as increases platelet aggregation. This is achieved by mediating expression of the glycoprotein complex GP IIb/IIIa in the cell membrane of platelets.
Aspirin irreversibly inhibits platelet cyclooxygenase 1 (and 2) preventing the formation of prostaglandin H2, and therefore thromboxane A2.
Nonselective NSAIDS, such as ibuprofen, reversibly inhibit both cyclooxygenase1 and 2, and thus alter thromboxane A2 synthesis and platelet aggregation.
Selective NSAIDS, known as the COX-2 inhibitors (eg, Celebrex®, Vioxx®, Bextra®), inhibit cyclooxygenase 2 without affecting cyclooxygenase 1. Thus, their effects predominantly alter prostacyclin versus thromboxane A2
Which one or more of the following is primarily responsible for increasing the cardiac output in patient with acute mild to moderate normovolemic anemia?
a) Tachycardia
b) Increased contractility.
c) Increased afterload.
d) Decreased sympathetic nervous activity.
e) Decreased blood viscosity
Answer key says E. I think that’s wrong
I think the answer would be B based on below: CMAJ 1997 review article conclusions
Cardiac output increases with increasing degrees of normovolemic anemia provided that blood volume is adequate
Increased cardiac output in normovolemic anemia is a result of increased stroke volume
The contribution of increased heart rate to the increase in cardiac output following normovolemic anemia is variable
Changes in blood viscosity result in many of the hemodynamic changes in normovolemic anemia
Normovolemic anemia is accompanied by increased sympathetic activity
Normovolemic anemia causes increased myocardial contractility
Normovolemic anemia causes a decrease in systemic vascular resistance
BUT also it states:
If cardiac function is normal, the increase in venous
return or left ventricular preload will be the most important determinant of the increased CO during normovolemic anemia.
Bradykinin has which of the following properties?
a) Vasoconstriction
b) Vasodilation
c) Decreased permeability of capillaries
d) Increased platelet aggregation
b) Vasodilation
Bradykinin is a potent endothelium-dependent vasodilator, causes contraction of non-vascular smooth muscle, increases vascular permeability and also is involved in the mechanism of pain. Bradykinin also causes natriuresis, contributing to a drop in blood pressure. Can also cause dry cough in patients on ACEI.
Implicated in inflammation, anaphylaxis, septic shock
Principal effects (6):
1. Stimulate production of NO (→ VD, ↓ plt aggregation)
2. Vasodilation
3.↑ capillary permeability
4. Activation of phospholipase and thus amplification of inflammatory response, e.g., ↑ PG I2 and ↓ plt aggregation
5. Pain
6. Bronchoconstriction
The endothelium creates a substance that effects blood pressure, capillary permeability, and vascular flow, what is it?
a. Nitric Oxide.
b. Bradykinin.
c. Acetylcholine.
d. Prostacyclin.
e. Norepinephrine.
a. Nitric Oxide.
Vascular actions of NO include the following:
* Direct vasodilation (flow dependent and receptor mediated) * Indirect vasodilation by inhibiting vasoconstrictor influences (e.g., inhibits angiotensin II and sympathetic vasoconstriction) * Anti-thrombotic effect - inhibits platelet adhesion to the vascular endothelium * Anti-inflammatory effect - inhibits leukocyte adhesion to vascular endothelium; scavenges superoxide anion * Anti-proliferative effect - inhibits smooth muscle hyperplasia
There are three isoforms of NOS. Two of these (cNOS) exist constitutively and the third (iNOS) is inducible. cNOS can be found in endothelium, myocardium, endocardium, skeletal muscle, platelets, and neural tissue.
Nitric oxide has the potential to be both protective and damaging in anaphylaxis (Box 59.4). It relaxes bronchial smooth muscle while dilating vascular smooth muscle. In addition to the peripheral vasodilatation, it can enhance vascular permeability. Its effect on smooth muscle thus can improve bronchospasm while worsening hypotension.
- Adkinson: Middleton’s Allergy: Principles and Practice, 7th ed.
Effects of NO include all except:
a. Selective vasodilatation of pulmonary circulation with less effect on systemic circulation
b. Decrease reperfusion injury in transplanted lung
c. May have beneficial effect in ARDS
d. Increase Cyclic GMP
???
NO has limited improvement in oxygenation in pts with ARDS and ALI. There is no effect on mortality and s/e. It is NOT recommended.
old answer:
Nitric oxide (NO) is an endogenous substance whose primary function appears to be vascular smooth muscle relaxation. The concept of inhaled NO as a practical means by which to achieve selective and therapeutic pulmonary vasodilation is based on the presumption that NO is so rapidly inactivated in blood that diffusion into a pulmonary capillary can produce local vasodilation without systemic effects.
Available data suggest that inhalation of NO by patients with severe Acute Lung Injury reduces pulmonary artery pressures in ventilated lung areas, improves blood flow to these areas, and subsequently improves arterial oxygenation without producing systemic vasodilation.
A therapeutic potential for inhaled NO to act as a selective pulmonary vasodilator was demonstrated by Frostell and colleagues in 1991, who showed that breathing NO gas resulted in rapid and profound pulmonary vasodilation in an awake lamb model of pulmonary hypertension produced by infusion of a stable thromboxane analog ( Fig. 31-3 ).[2] Because NO binds rapidly to hemoglobin (Hb) with high affinity, the vasodilatory effect of inhaled NO is limited to the lung. This is in sharp contrast to intravenously infused vasodilators, which often cause systemic vasodilation and lead to systemic arterial hypotension. This unique ability of inhaled NO to cause highly selective pulmonary vasodilation has prompted a large number of preclinical and clinical studies.
- Miller: Miller’s Anesthesia, 7th ed.
Inhaled NO has also been used to treat pulmonary hypertension associated with COPD, cardiac surgery, heart and lung transplantation, and acute lung injury.
- Mason: Murray & Nadel’s Textbook of Respiratory Medicine, 4th ed.
Nitric oxide (NO) is a potent pulmonary vasodilator and has been used for a number of years to improve oxygenation in the face of acute respiratory distress syndrome (ARDS) and severe pulmonary hypertension. - Miller: Miller's Anesthesia, 7th ed.
Most of the effects of NO on the cardiovascular system are mediated by activation of the enzyme soluble guanylate cyclase, which catalyzes formation of the second messenger cyclic guanosine monophosphate (cGMP) from guanosine 5′-triphosphate. NO stimulates soluble guanylate cyclase to synthesize cGMP, which in turn activates cGMP-dependent protein kinase and thereby leads to vascular relaxation.
- Miller: Miller’s Anesthesia, 7th ed.
Endothelium-derived nitric oxide or relaxing factor (EDNO or EDRF) can be released in response to acetylcholine stimulation, hypoxia, endotoxin, cellular injury, or mechanical shear stress from circulating blood. Its vasodilatory activity has been demonstrated in large (conduit) arteries and in resistance vessels of most mammalian species, including human beings.
EDNO induces vasodilation and platelet deactivation.
- Goldman: Cecil Textbook of Medicine, 21st ed
Hypoxic pulmonary vasoconstriction is due to :
a. Increase follow in pulmonary vessels
b. Decrease PO2 in alveoli
c. Metabolic acidosis
d. All of the above
e. None of the above
Answer: decreased PO2 in alveolar gas
HYPOXIC PULMONARY VASOCONSTRICTION (HPV) is an adaptive vasomotor response to alveolar hypoxia, which redistributes blood to optimally ventilated lung segments by an active process of vasoconstriction, particularly involving the small, muscular “resistance” pulmonary arteries (PA).
HPV shunts blood from poorly oxygenated areas to better ventilated lung segments, thereby optimizing ventilation-perfusion matching, reducing shunt fraction, and optimizing systemic O2 delivery in conditions such as atelectasis and pneumonia
Although it is generally accepted the mechanism of HPV involves a direct effect of decreased oxygen tension on the pulmonary artery smooth muscle cell to increase cytosolic Ca2+ and cause contraction, the biochemistry of the oxygen sensing, the intracellular signaling pathways that link oxygen sensing to Ca2+ signaling, the relative roles of extra- and intracellular sources of Ca2+, and the role of the endothelial cell remain unresolved.
- Mason: Murray & Nadel’s Textbook of Respiratory Medicine, 4th ed.
The process of active redistribution of pulmonary blood flow to maintain optimal V/Q relationship is called Hypoxic Pulmonary Vasoconstriction (HPV). Pulmonary arterial vasoconstriction occurs as the alveolar PO2 of a given lung region Falls below 70 torr. The exact mechanism by which local hypoxia is detected and cconstriction is mediated is not clear.
- Essentials of Basic Science in Surgery
A patient was just put in reverse trendlenberg position and he developed hypotension the most likely cause of hypotension is:
a. Dysfunction of baroreceptors
b. External compression of IVC
c. Decrease cardiac contractility
d. Hypovolemia
e. Dysfunction of chemoreceptors
a. Dysfunction of baroreceptors
Trendelenburg poisition = IVC dilates but is compressed by abdominal contents, and thus LESS pre-load. CO/SV increase only modestly
The loss of pedal pulses following exercise is most often related to which of the following conditions?
a. Increased venous return
b. Redistribution of blood flow
c. Proximal arterial stenosis
d. Decreased cardiac output
b. Redistribution of blood flow
Systemic diastolic BP is determined by :
a. Stroke volume
b. Peripheral vascular resistant
c. Cardiac output
d. Viscosity
b. Peripheral vascular resistant
Most normal pressure to maintain CPP at
a. 30mmHg
b. 70mmHg
c. 30mmH2O
d. 70mmH2O
b. 70mmHg
Answer: 70mmHg (80-100)
Cerebral perfusion pressure (CPP)which is equal to the Mean Arterial Pressure (MAP) minus the Intra-Cranial Pressure (ICP) is an important measurement that is used to monitor therapy in head trauma patients. The lowest acceptable CPP is 60 mmHg.
Maintaining cerebral blood flow requires using an elevated minimal CPP threshold when treating the injured brain. A CPP level of at least 70 mmHg is suggested.
- Schwartz
MAP = 1/3(Systolic-Diastolic) + Diastolic MAP = 1/3 pulse pressyre + diastolic
Vascular injury is less likely to be present when ABI is :
a. 0.3
b. 0.5
c. 0.7
d. 0.9
d. 0.9
The Ankle Brachial Pressure Index (ABPI) is the ratio of the blood pressure in the lower legs to the blood pressure in the arms. Compared to the arm, lower blood pressure in the leg is a symptom of blocked arteries (peripheral vascular disease). The ABPI is calculated by dividing the systolic blood pressure in the arteries at the ankle and foot by the higher of the two systolic blood pressures in the arms.
above 1.2 – Abnormal - Vessel hardening from PVD- Refer routinely
1.0 - 1.2 - Normal range No treatment
0.9 - 1.0 Acceptable
0.8 - 0.9 Some arterial disease - Manage risk factors
0.5 - 0.8 Moderate arterial disease - Routine specialist referral
under 0.5- Severe arterial disease- Urgent specialist referral
What is the most reliable indicator of tissue perfusion?
a) Heart rate
b) Urine output
c) Skin color
d) Skin temperature
b) Urine output
As signs of a reduced tissue perfusion and end-organ oxygenation, a decreased urinary output (
If the end diastolic pressure is kept the same, how can you increase the CI (cardiac index)?
a) Increase SVR
b) Increase pulmonary vascular resistance
c) Increase HR
d) Decrease venous capacitance
e) Increase coronary artery blood flow
c) increase HR
This is the only one that makes a bit of sense
Cardiac index (CI) is a haemodynamic parameter that relates the cardiac output (CO) from left ventricle in one minute to body surface area (BSA)
So should increase with tachycardia
Preload refers to the passive stretch on the myocardium just prior to contraction, or the ventricular wall tension at the end of diastole. In the intact heart, preload corresponds to the end-diastolic volume or end-diastolic pressure. According to Starling’s law, the higher the preload, the greater the force of ventricular contraction and the greater the stroke volume. When heart failure develops, cardiac output may be maintained within normal limits by an increase in preload. Diastolic filling increases in part due to an increase in venous return resulting from vasoconstriction and intravascular volume expansion. However, in severe heart failure, the ventricular function curve may be flat at higher end-diastolic volumes; thus cardiac output may not be augmented by an increase in filling, and a marked increase in end-diastolic pressure causes pulmonary venous congestion ( Fig. 65-3 ).
Afterload refers to the ventricular wall stress during systole or the force that the ventricle must overcome to eject its contents. According to Laplace’s law, systolic wall stress is directly proportional to ventricular pressure and chamber radius and inversely proportional to ventricular wall thickness. The major determinant of left ventricular afterload is systemic vascular resistance.
Noble: Textbook of Primary Care Medicine, 3rd ed., Copyright © 2001 Mosby, Inc.
Which of the following would not be useful in improving tissue oxygenation when delivery/extraction is impaired?
a) Fluid to keep the CVP >15
b) Supplemental O2
c) Dopamine to increase cardiac output
d) Bronchodilators
e) Helium-oxygen mixture
a) fluids?
I don’t really know what they mean by delivery/extraction impaired.
B, C, and D make sense! Below is the evidence for why E would make sense.
It has been recognized for some time that breathing heliox, a gas consisting of 20% oxygen and 80% helium (hence a density approximately one-third that of air), results in prompt improvement in dyspnea, work of breathing, and arterial blood gas abnormalities in patients with upper airway obstruction.[146] This benefit stems from the density dependence of the flow-related pressure drop across the upper airway in cases of severe upper airway obstruction, disorders typically producing highly turbulent flow across the narrowed airway.
- Murray & Nadel: Textbook of Respiratory Medicine, 3rd ed., Copyright © 2000
Insuflation for laporoscopy causes
a – decreased preload
b – increased cardiac output
a – decreased preload
Cardiac Index is a – HR x SV b – number of myocytes c – avO2 difference x hemocrit x cardiac output d – Cardiac output / Body surface area
d – Cardiac output / Body surface area
Tension pneumothorax is associated with all of the following except?
a. increased SV
b. increased intrapleural pressure
Answer: increased SV
Carbon dioxide is transported in the blood primarily as:
a) dissolved CO2
b) carbonic acid
c) carboxyhemoglobin
d) bicarbonate salt (HCO3)
d) bicarbonate salt (HCO3)
Transport of carbon dioxide in the blood is considerably more complex. A small portion of carbon dioxide, about 5 percent, remains unchanged and is transported dissolved in blood. The remainder is found in reversible chemical combinations in red blood cells or plasma. Some carbon dioxide binds to blood proteins, principally hemoglobin, to form a compound known as carbamate. About 88 percent of carbon dioxide in the blood is in the form of bicarbonate ion.
Asthmatic patient wheezing in the clinic what is the best way to control his asthma pre op:
a. Steroid IV
b. Steroid inhaled
c. Bronchodilators
d. All of the above
e. None of the above
Answer: Bronchodilators
A preoperative chest radiograph is necessary only for evaluation of infections or pneumothorax. Bronchodilators, inhaled and oral steroids, and antibiotics (if taken) need to be continued on the day of surgery. β-Agonists are the most useful prophylactic intervention to lower the risk for bronchospasm on induction of anesthesia. A short course of steroids (20 to 60 mg of prednisone daily for 3 to 5 days) preoperatively may be useful in any patient who is not at baseline and surgery must proceed.
- Miller: Miller’s Anesthesia, 7th ed.
Elderly lady in the ICU post op, intubated. C.I. 1.6 (low), CVP of 10 (highish), PCWP > 20 (high), pulmonary artery pressure :30 (mean is 25). What is your Dx?
a. hypervolemia
b. hypovolemia
c. CHF
d. Sepsis
e. Pulmonary embolus
Answer: CHF
CI 1.6 (N=2.4-4.0), PCWP (N=6-12), PA Pressure (N Systolic 15–30 mm Hg Diastolic 5–12 mm Hg), SVR of 1500 (N=900-1200)
What will decrease intrapulmonary shunting
a. increase anatomic dead space
b. alveolar collapse
c. pulm edema
d. pneumonia
Answer: increase anatomic dead space
Pulmonary shunt is a physiological condition which results when the alveoli of the lungs are perfused with blood as normal, but ventilation (the supply of air) fails to supply the perfused region.
Dead space ventilation increases when the alveolar–capillary interface is destroyed (e.g., emphysema), when blood flow is reduced (e.g., heart failure, pulmonary embolism), or when alveoli are overdistended by positive-pressure ventilation.
Intrapulmonary shunt fraction increases when the small airways are occluded (e.g., asthma, chronic bronchitis), when alveoli are filled with fluid (e.g., pulmonary edema, pneumonia) or when alveoli collapse (e.g., atelectasis), and when capillary flow is excessive (e.g., nonembolized regions of lung in pulmonary embolism).
Alveolar hypoventilation is best assessed by:
a. PaO2
b. SaO2
c. PaCO2
d. pH
Answer: PaCO2
Alveolar PAO2 =150 - 1.25 x PaCO2
Carbon dioxide retention develops when Pimax
Causes of elevated PCWP :
a. LVF
b. RVF
c. PE
d. Tricuspid regurgitation
a. LVF
B&C&D would incr CVP
PCWP as measured by a pulmonary artery catheter, is the pressure measured in a pulmonary artery distal to an occlusion of that artery. Physiologically, distinctions can be drawn among pulmonary venous pressure, pulmonary artery pressure, pulmonary wedge pressure, and left atrial pressure. it is considered the gold standard for determining the cause of acute pulmonary edema; this is likely to be present at a PWP of >20mmHg. It has also been used to diagnose severity of left ventricular failure and mitral stenosis[5]
PCWP represents
a. RA pressure
b. LA pressure
c. RV pressure
b. LA pressure
Note: it is an indirect measure of it
If a Swan-Ganz catheter is in place in the pulmonary artery, cardiac output is measured and attempts are made to maintain the cardiac index at a normal level. In many patients the pulmonary capillary wedge pressure (PCWP) provides a reasonable guide to left atrial pressure or preload.
- Schartz Ch 18
Cause of decreased alveolar ventilation in obese pt is :
a. Decreased descent of the diaphragm
b. Increased upper airway resistance
c. Decreased lung compliance
a. Decreased descent of the diaphragm
The most frequent abnormality in pulmonary function in obesity is a decrease in the expiratory reserve volume attributable to cephalad displacement of the diaphragm by adipose tissue. In severely obese individuals and in those with the OHS, total lung capacity and vital capacity may be reduced. In such patients, the residual volume may actually be increased relative to total lung capacity because of small airway closure and gas trapping. This is supported by the finding of larger total lung capacity by body box plethysmography than by helium dilution.13 Similarly, spirometry is typically normal in simple obesity, whereas severely obese individuals or those with the OHS may exhibit reductions in FEV1 and FVC, even though the ratio of these two variables is preserved or even increased
Respiratory quotient question: carbon dioxide production / oxygen consumption?
RQ carbs = 1.0
RQ protein = 0.8
RQ fat = 0.7
Ratio of the volume of carbon dioxide produced when a substance is oxidized, to the volume of oxygen used. The oxidation of carbohydrate results in an RQ of 1.0; of fat, 0.7; and of protein, 0.8.
If >0.7 – ketosis and if >1 = hyperalimentation – increased carb:fat ratio
Vital capacity is calculated as:
a. TLC – RV; also VC = IRV + TV + ERV
b. TLC - (Exp Re serve Vol + TV)
c. IC + FRC
d. IC + TV
e. none of the above
Answer: TLC – RV
Patient sustains first degree burn to face and neck, second degree burn to one arm, anterior trunk and one lower extremity. Calculate percent burn
a. 35%
b. 25%
c. 45%
d. 55%
first degree burns don't count Second degree burns - arm = 4.5+4.5 = 9% - ant trunk = 18% - lower extremity (whole) = 9+9 = 18% - total= 45%
A patient suffers a 3rd degree burn to their torso, both legs, and half of one arm. ??assuming 70kg
The necessary fluid requirements include:
a. Crystalloid at 500 cc/hr for 8 hrs, then 1 L/hr for 16 hrs
b. Crystalloid at 750 cc/hr for 8 hrs, then 850 cc/hr for 16 hrs
c. Crystalloid at 1 L/hr for 24 hours
d. Crystalloid at 1180cc/hr for 8 hours, then 800 cc/hr for 16 hrs
Calculations don’t make sense for me…
TBSA =
Torso (36) + Legs (36) + ½ arm (4.5) [assuming total torso] or
Torso (18) + Legs (36) + ½ arm (4.5) [assuming ant. torso]
Total fluids in 24 = TBSA * weight in kg (assume 70) * 4 =
21420 or
16380
Hourly rate for first 8 hrs = Total * ½ / 8 =
1338. 75 or 1023. 753
Adding maintenance (110cc/hr] =
1438. 75 or 1123. 75
Given these calculations, no answers are appropriate. Generally, the rate in the first 8 hours should be twice the rate in the second, unless you include maintenance. This would give D (no maintenance) but the last 16 hours should be half the rate.
80 kg female burn patient presented 30 min after 20% 3rd degree burn , what is the fluid for the first 8hrs: a. RL 400cc/h b. RL 270cc/h c. NS 400cc/h d. NS 270cc/h
a.
Parkland Formula
4cc x BW (kg) x % BSA burned = 24 hour replacement
½ in first 8 hours, remaining ½ over next 16 hours
4 x 80 x 20 = 6400 cc over 24hrs. 6400 x .5 = 3200 cc ( volume over next 8 hrs)
3200cc/8hrs = 400 cc/hr
use RL
A burn patient has a urine output of 45, 70, 50 cc over 3 subsequent hours. What would you do next?
a) Bolus 1L RL
b) Increase by 1/3 rate
c) Decrease by 1/3 rate
d) Monitor for another hour and reassess
Answer: Decrease by 1/3 rate (target = 0.5cc/kg/hr)
What is the BEST measure of the adequacy of burn resuscitation? A. MAP B. CVP C. sBP D. Urine output
D. Urine output
Man sustained electrical burn, has tea-colored urine, best management
a) Mannitol and bicarb.
b) Lasix and bicarb.
c) Keep urine output >0.5 cc/kg.
d) Acidify urine.
c) Keep urine output >0.5 cc/kg.
Essentially there is good evidence that making a lot of urine is good, but less good evidence that the other things can help
2016:uptodate
The rate is adjusted to maintain the desired diuresis of approximately 200 to 300 mL/hour.
The optimal fluid for the prevention of heme-induced AKI is not known
Limited data suggest that alkalinization of urine may benefit patients with severe rhabdomyolysis (so long as they are making urine, otherwise severe metabolic acidosis).
Patients with gross pigmenturia are at risk for myoglobin-induced acute tubular necrosis (Color Fig. 12-10). This situation is most common in patients who have sustained high-voltage electrical injury or deep thermal burns. In these patients, pigment must be cleared from the urine promptly. This is ideally accomplished with crystalloid loading, maintaining a brisk urine output of 2 mL/kg/h or more. Also helpful is alkalinization of the urine. This is best accomplished by administration of 0.12 to 0.5 mEq/kg/h of sodium bicarbonate intravenously as a part of the resuscitative fluid, with careful observation of the serum pH. Occasionally, osmotic diuresis using mannitol is required; however, the administration of osmotic diuretics obscures the urine output as a measure of intravascular volume status. Therefore, a pulmonary artery or central venous catheter should be placed when mannitol must be used so that cardiac filling pressures can be used to judge the adequacy of fluid administration.
- Greenfield
Young lady with face and neck first degree burns and right arm and chest/abdomen second degree burns, and high carbon monoxide, how much daily fluid in first 24 hours? a-2L b-5L c-7L d-9L
Assuming 4.5% R anterior arm, 18% chest/abdomen = 22.5%
assuming 70kg
47022.5 = 7560 (6.3L)
If inhalation component, then increase the fluid requirements by 40-50%
6.3*1.5 = 9.45L
Answer: 9L (if you think is inhalational injury)
Add 2 cc/kg%TBSA for inhalational injuries
- Morell Notes
Parkland underestimates fluid req in inhalation injury
Why do you use a dry dressing over the top of a partial thickness burn?
a) Keep it dry
b) Reduce scab formation
c) Reduce the bacterial count
Answer: Reduce bacterial count
Occlusive dressings support a moist wound healing environment that is optimal for healing. A moist environment has been shown to enhance re-epithelialization and angiogenesis and to reduce pain, partly since these dressings do not need to be changed daily.
- Marx: Rosen’s Emergency Medicine, 7th ed.
If the bandage is allowed to become saturated with fluid draining from the wound or to become dirty, it may promote infection.
- Auerbach: Wilderness Medicine, 5th ed.
A patient suffered a 3rd degree bum on his forearm 4 days ago. Now he presents with fever, spreading erythema, worsening arm pain, and elevated white count. The best course of management includes:
a. elevate/splint/antibiotics/secondarily debride
b. immediate eschar debridement
c. IV Abtx
Answer: immediate eschar debridement
Circumferential burns of an extremity or of the trunk pose special problems. Swelling beneath the unyielding eschar may act as a tourniquet to blood and lymph flow, and the distal extremity may become swollen and tense. More extensive swelling may compromise the arterial supply. Escharotomy may be required. To avoid permanent damage, escharotomy must be performed before arterial ischemia develops.
Burn shock is associated with:
a. Decreased SVR
b. Increased ICF
c. Increase ICP
d. Decrease ICP
e. Increase SVR
decreased cardiac output or increased SVR
Two processes lead to postburn hypovolemia: an increase in microvascular permeability in the burn wound and an increase in the osmolarity of surface burn tissue. A large intravascular to extravascular plasma shift occurs. The phase of rapid loss of intravascular fluid persists for about 24 to 36 hours.
- Goldman: Cecil Medicine, 23rd ed.
Excessive leakage of plasma, especially in the first eight hours post-burn, causes hypovolemia, hypoproteinemia, hemoconcentration, electrolyte imbalances and acid base disturbances. Plasma volume is reduced by as much as 23-27%, with a reduction in cardiac output and an increase in peripheral vascular resistance.
- http://www.totalburncare.com/orientation_burn_shock.htm
A marked increase in peripheral vascular resistance accompanied by a decrease in cardiac output occurs in the first 18 to 24 hours postinjury.
- Bope: Conn’s Current Therapy 2010, 1st ed
Cardiovascular System (Plastic Seminar, see diagram)
➢ Dramatic effect on the cardiovascular system
➢ During the initial (emergent/ebb) phase of burn injury lasting the first 72 hours there is:
o Increased capillary permeability
o Decreased plasma volume
o Decreased cardiac output
➢ This initial burn shock may mimic hypovolemic shock because the decrease in circulating volume can result in tachycardia, hypotension, decreased cardiac output, decreased central venous pressure, decreased pulmonary artery pressures and decreased urine output
➢ The above cardiovascular responses result from Neurogenic and humoral influences (ie vasocontriction) rather than from hypovolemia
➢ The Flow Phase follows the ebb phase by approximately 24 hours
➢ During the Flow Phase burn shock is resolved and capillary integrity is re-established ==> mobilization of fluid and diuresis
➢ Several process involved in postburn vascular changes:
o Loss of intravascular volume to burn and nonburn tissue
o Increase in osmotic pressure in burn tissue can increase burn edema
o Hypoproteinemia results in cellular swelling
➢Alterations in electrolytes is common and should be monitored:
o Hyperkalemia ==> seen in initial resuscitative phase (due to release from damaged cells
o Hypokalemia can result secondarily from hemodilution
o During the acute phase alterations in Na, K, Mg, Ca, and Ph need to be monitored and corrected
A burn patient developed progressive anemia due to:
a. Ag sulfasiadine causing marrow suppression
b. Fluid redistribution
c. Hemolysis
d. Protein consumption
b. Fluid redistribution (I disagree, I think it’s silver sulfadiazine that causes aplastic anemia. I think that’s what they are getting to. Especially the “progressive anemia part”)
McNeil’s answer:
Hematologic Changes
➢ Initially laboratory values reflect hemoconcentration that reverses with fluid resuscitation
➢ Hemolysis can also occur resulting in anemia and leukocytosis
➢ Altered tissue oxygenation and sluggish blood flow can occur from a hypercoagulable state secondary to hypovolemia
DIFFERENTIAL DIAGNOSIS OF HEMOLYTIC ANEMIA
> ACQUIRED HEMOLYTIC ANEMIA
> Microangiopathic hemolytic anemia
> Physical or chemical injuries
> Burn related
- Goldman: Cecil Medicine, 23rd ed.
Severe burns can also cause fragmentation hemolysis from the thermal injury.
- Bope: Conn’s Current Therapy 2010, 1st ed.
Trauma (e.g., march hemoglobinuria), thermal injury from severe burns, and osmotic lysis secondary to freshwater drowning or mistaken intravenous infusion of high volumes of hypotonic fluids are additional causes of mechanical damage to otherwise normal erythrocytes.
- Goldman: Cecil Medicine, 23rd ed.
These sources don’t really mention progressive anemia.
