Friday, October 30, 2009
Alice in intensiveland
"Alice in intensiveland" is an wonderful article by Bartlett RH which appeared in Chest 1995; 108: 1129-39. This article has commented in an hilarious manner regarding the nonsenses one should not do in ICU. A must read.
Monday, October 19, 2009
Wolff-Parkinson-White Syndrome
WPW Syndrome: Paroxysmal tachycardias mediated by accessory pathways that cross the AV node and electrically link the atria and ventricles, when combined with a short P-R interval (< 0.12 seconds), a wide QRS, and secondary repolarization abnormalities.
Wolff-Parkinson-White pattern or ventricular preexcitation - When this ECG pattern is seen without the tachycardia.
First described in 1930 in an article by Louis Wolff, Sir John Parkinson, and Paul Dudley White in 11 patients.
• Accessory bypass tracts detectable on an ECG - reported in 0.15 to 0.25 %.
• Familial association - 0.55 %.
• 2:1 male: female predominance.
• Tachyarrhythmia - depends on the population studied and varies from 13% in a healthy outpatient population to 80% in the hospital setting.
• Incidence of sudden death in the 0-4% range.
• Approx. 5–10% of patients with documented bypass tracts have concomitant structural heart disease.
o Ebstein anomaly is the most common, accounting for 25–50%,
o Corrected transposition of the great arteries (levo-TGA), and
o Hypertrophic cardiomyopathy.
• Association of right-sided accessory pathways with structural heart disease is strong. 45% of patients with right-sided vs 05% of those with left-sided.
• Most common bypass tract is an accessory atrioventricular (AV) pathway called Kent bundle.
• Another common preexcitation syndrome, Lown-Ganong-Levine (LGL), has an accessory pathway - James fibers, which connect the atria serially to the His bundle.
• Pathways can cross the AV groove anywhere in its course to connect the left or right atrium to its respective ventricle except the region between the aortic and mitral valves. The distribution of accessory pathways,
- 46–60% are located in the left free wall,
- 25% within the posteroseptal space,
- 13–21% in the right free wall, and
- 2% in the anteroseptal space.
ECG
Each location produces a distinct ECG pattern but in the 13% of patients with two or more bypass tracts the ECG tracing can be confounding and show multiple QRS morphologies. During sinus rhythm, an atrial impulse will reach the ventricles via both the AV node and the accessory AV pathway. The latter conducts the atrial impulse to the ventricles before the AV node, resulting in ventricular pre-excitation and a short PR interval. On reaching the ventricles, the pre-excitation impulse is not conducted via the specialised conducting system. Hence, early ventricular activation will be slowed, resulting in a slurred upstroke of the QRS complex, the so-called delta (d) wave.The abnormal ventricular activation also gives rise to secondary S-T segment and T-wave abnormalities. d-wave polarity in a 12-lead ECG may help localise the anatomical position of the accessory pathway.
In type A WPW the accessory pathway is usually situated on the left with pre-excitation of the left ventricle. Positive R waves in the right precordial leads, short PR & a delta wave giving rise to wide QRS complex
Type B WPW has a dominantly negative QRS complex in V1 and the accessory pathway tends to be on the right with pre-excitation of the right ventricle.
CLINICAL - AVRT or AF can occur with WPW.
During AVRT, the re-entry impulse usually travels down the AV node and back up the accessory pathway. Ventricular activation is via the normal conducting pathways and the QRS will be narrow. This is called orthodromic conduction.
Occasionally, the re-entry impulse may pass in the opposite direction (down the accessory pathway and up the AV node), resulting in a wide QRS-complex tachycardia due to abnormal slow ventricular activation. This is antidromic conduction. Treatment is the same as for AVRT.
AF is common in WPW 11-38%, and may be life-threatening. Most impulses are conducted via the accessory pathway, leading to wide QRS complexes. The ECG of WPW with AF usually shows rapid, irregular QRS complexes with variable QRS width. Ventricular response is very rapid, leading to hypotension or cardiogenic shock. This arrhythmia may degenerate to VF.
Symptoms range from palpitations to syncope, episodes of tachycardia may be associated with dyspnea, chest pain, decreased exercise tolerance, anxiety, dizziness, or syncope.
ELECTROPHYSIOLOGIC TESTING
•To confirm the presence of an AP
•To differentiate this condition from other forms of SVT
•To find the pathway participating in the tachycardia and aid in ablative therapy
TREATMENT
Treatment usually involves synchronised DC shock.
Antiarrhythmic drugs may be used when patients are haemodynamically stable and the ventricular rate is not excessively rapid.
•Drugs that prolong the refractory period of the accessory pathway are useful (e.g. sotalol, amiodarone, flecainide and procainamide).
•Drugs that shorten the refractory period (e.g. digoxin) are contraindicated as they may accelerate ventricular rate.
•Verapamil and lidocaine may increase the ventricular rate during AF, and are also best avoided.
•b-Adrenergic blockers have no effect on the refractory period of the accessory pathway.
Catheter Ablation of APS
In conjunction with a diagnostic EP test. Once the AP is localized to a region of the heart, precise mapping and ablation is performed using a steerable electrode catheter. The largest prospective, multicenter clinical trial to evaluate the safety and efficacy of radiofrequency ablation was reported by Calkins and colleagues. This study involved analysis of 1050 patients, of whom 500 had APs. Overall success curing APs was 93 percent. Following an initially successful procedure, recurrence of AP conduction is found in approximately 5 percent of patients.
Complications
•Obtaining vascular access (hematomas, DVT, perforation of the aorta, AV fistula, PTx),
•Catheter manipulation (valvular damage, microemboli, perforation of the coronary sinus or myocardial wall, coronary dissection and/or thrombosis), or
•Delivery of RF energy (AV block, myocardial perforation, coronary artery spasm or occlusion, transient ischemic attacks, or cerebrovascular accidents).
Calkins and coworkers reported the incidence of
•major complications - 3 %
•minor complications - 8 %.
•procedure-related mortality - 0 - 0.2 %.
The two most common types of major complications reported during catheter ablation of APs are inadvertent complete AV block and cardiac tamponade.
Cryoablation has become available as an alternative energy source for creation of myocardial lesions. The main advantage of cryoenergy, compared to radiofrequency energy, is that the risk of heart block appears to be lower.
Aymptomatic Preexcitaion
Mostly have a good prognosis. Because of the small but real risks associated with invasive procedures, EPS is not routinely recommended for risk stratification and/or ablative therapy. ACC/AHA/ESC Guidelines for Management of Patients With Supraventricular Arrhythmias gives catheter ablation a 2a classification for treatment of patients with asymptomatic preexcitation.
The detection of intermittent preexcitation—which is characterized by an abrupt loss of the delta wave, normalization of the QRS complex, and an increase in the P-R interval during a continuous ECG recording—is evidence that an AP has a relatively long refractory period and is unlikely to precipitate VF. The loss of preexcitation after administration of antiarrhythmic drugs like procainamide has also been used to indicate a low-risk subgroup. These noninvasive tests are generally considered inferior to EPS testing in the assessment of risk of sudden cardiac death. Because of this, they play little role in patient management at present.
Studies have identified markers that identify patients at increased risk –
(1) a short preexcited RR interval <250 msec during spontaneous or induced AF (2) a history of symptomatic tachycardia, (3) multiple APs, and (4) Epstein anomaly.
Wolff-Parkinson-White pattern or ventricular preexcitation - When this ECG pattern is seen without the tachycardia.
First described in 1930 in an article by Louis Wolff, Sir John Parkinson, and Paul Dudley White in 11 patients.
• Accessory bypass tracts detectable on an ECG - reported in 0.15 to 0.25 %.
• Familial association - 0.55 %.
• 2:1 male: female predominance.
• Tachyarrhythmia - depends on the population studied and varies from 13% in a healthy outpatient population to 80% in the hospital setting.
• Incidence of sudden death in the 0-4% range.
• Approx. 5–10% of patients with documented bypass tracts have concomitant structural heart disease.
o Ebstein anomaly is the most common, accounting for 25–50%,
o Corrected transposition of the great arteries (levo-TGA), and
o Hypertrophic cardiomyopathy.
• Association of right-sided accessory pathways with structural heart disease is strong. 45% of patients with right-sided vs 05% of those with left-sided.
• Most common bypass tract is an accessory atrioventricular (AV) pathway called Kent bundle.
• Another common preexcitation syndrome, Lown-Ganong-Levine (LGL), has an accessory pathway - James fibers, which connect the atria serially to the His bundle.
• Pathways can cross the AV groove anywhere in its course to connect the left or right atrium to its respective ventricle except the region between the aortic and mitral valves. The distribution of accessory pathways,
- 46–60% are located in the left free wall,
- 25% within the posteroseptal space,
- 13–21% in the right free wall, and
- 2% in the anteroseptal space.
ECG
Each location produces a distinct ECG pattern but in the 13% of patients with two or more bypass tracts the ECG tracing can be confounding and show multiple QRS morphologies. During sinus rhythm, an atrial impulse will reach the ventricles via both the AV node and the accessory AV pathway. The latter conducts the atrial impulse to the ventricles before the AV node, resulting in ventricular pre-excitation and a short PR interval. On reaching the ventricles, the pre-excitation impulse is not conducted via the specialised conducting system. Hence, early ventricular activation will be slowed, resulting in a slurred upstroke of the QRS complex, the so-called delta (d) wave.The abnormal ventricular activation also gives rise to secondary S-T segment and T-wave abnormalities. d-wave polarity in a 12-lead ECG may help localise the anatomical position of the accessory pathway.
In type A WPW the accessory pathway is usually situated on the left with pre-excitation of the left ventricle. Positive R waves in the right precordial leads, short PR & a delta wave giving rise to wide QRS complex
Type B WPW has a dominantly negative QRS complex in V1 and the accessory pathway tends to be on the right with pre-excitation of the right ventricle.
CLINICAL - AVRT or AF can occur with WPW.
During AVRT, the re-entry impulse usually travels down the AV node and back up the accessory pathway. Ventricular activation is via the normal conducting pathways and the QRS will be narrow. This is called orthodromic conduction.
Occasionally, the re-entry impulse may pass in the opposite direction (down the accessory pathway and up the AV node), resulting in a wide QRS-complex tachycardia due to abnormal slow ventricular activation. This is antidromic conduction. Treatment is the same as for AVRT.
AF is common in WPW 11-38%, and may be life-threatening. Most impulses are conducted via the accessory pathway, leading to wide QRS complexes. The ECG of WPW with AF usually shows rapid, irregular QRS complexes with variable QRS width. Ventricular response is very rapid, leading to hypotension or cardiogenic shock. This arrhythmia may degenerate to VF.
Symptoms range from palpitations to syncope, episodes of tachycardia may be associated with dyspnea, chest pain, decreased exercise tolerance, anxiety, dizziness, or syncope.
ELECTROPHYSIOLOGIC TESTING
•To confirm the presence of an AP
•To differentiate this condition from other forms of SVT
•To find the pathway participating in the tachycardia and aid in ablative therapy
TREATMENT
Treatment usually involves synchronised DC shock.
Antiarrhythmic drugs may be used when patients are haemodynamically stable and the ventricular rate is not excessively rapid.
•Drugs that prolong the refractory period of the accessory pathway are useful (e.g. sotalol, amiodarone, flecainide and procainamide).
•Drugs that shorten the refractory period (e.g. digoxin) are contraindicated as they may accelerate ventricular rate.
•Verapamil and lidocaine may increase the ventricular rate during AF, and are also best avoided.
•b-Adrenergic blockers have no effect on the refractory period of the accessory pathway.
Catheter Ablation of APS
In conjunction with a diagnostic EP test. Once the AP is localized to a region of the heart, precise mapping and ablation is performed using a steerable electrode catheter. The largest prospective, multicenter clinical trial to evaluate the safety and efficacy of radiofrequency ablation was reported by Calkins and colleagues. This study involved analysis of 1050 patients, of whom 500 had APs. Overall success curing APs was 93 percent. Following an initially successful procedure, recurrence of AP conduction is found in approximately 5 percent of patients.
Complications
•Obtaining vascular access (hematomas, DVT, perforation of the aorta, AV fistula, PTx),
•Catheter manipulation (valvular damage, microemboli, perforation of the coronary sinus or myocardial wall, coronary dissection and/or thrombosis), or
•Delivery of RF energy (AV block, myocardial perforation, coronary artery spasm or occlusion, transient ischemic attacks, or cerebrovascular accidents).
Calkins and coworkers reported the incidence of
•major complications - 3 %
•minor complications - 8 %.
•procedure-related mortality - 0 - 0.2 %.
The two most common types of major complications reported during catheter ablation of APs are inadvertent complete AV block and cardiac tamponade.
Cryoablation has become available as an alternative energy source for creation of myocardial lesions. The main advantage of cryoenergy, compared to radiofrequency energy, is that the risk of heart block appears to be lower.
Aymptomatic Preexcitaion
Mostly have a good prognosis. Because of the small but real risks associated with invasive procedures, EPS is not routinely recommended for risk stratification and/or ablative therapy. ACC/AHA/ESC Guidelines for Management of Patients With Supraventricular Arrhythmias gives catheter ablation a 2a classification for treatment of patients with asymptomatic preexcitation.
The detection of intermittent preexcitation—which is characterized by an abrupt loss of the delta wave, normalization of the QRS complex, and an increase in the P-R interval during a continuous ECG recording—is evidence that an AP has a relatively long refractory period and is unlikely to precipitate VF. The loss of preexcitation after administration of antiarrhythmic drugs like procainamide has also been used to indicate a low-risk subgroup. These noninvasive tests are generally considered inferior to EPS testing in the assessment of risk of sudden cardiac death. Because of this, they play little role in patient management at present.
Studies have identified markers that identify patients at increased risk –
(1) a short preexcited RR interval <250 msec during spontaneous or induced AF (2) a history of symptomatic tachycardia, (3) multiple APs, and (4) Epstein anomaly.
Friday, October 9, 2009
Hypophosphatemia
Background
Phosphate is the most abundant intracellular anion and is essential for
- membrane structure,
- transport in all cells.
- production of ATP, which provides energy for nearly all cell functions.
- as an essential component of DNA and RNA.
- production of 2,3-diphosphoglycerate (2,3-DPG) in RBC’s, which facilitates release of oxygen from hemoglobin
Approximately 85% of the body's phosphorus is in bone as hydroxyapatite,
while most of the remainder (15%) is present in soft tissue.
Only 0.1% of phosphorus is present in extracellular fluid, and it is this
fraction that is measured with a serum phosphorus level.
Normal Serum phosphate or phosphorus levels are 0.81-1.45 mmol/L.
Hypophosphatemia is defined as
mild: 0.65-0.81 mmol/L,
moderate: 0.32-0.65 mmol/L,
severe: < 0.32 mmol/L. Mild to moderately severe hypophosphatemia is usually asymptomatic. Major clinical sequelae usually occur only in severe hypophosphatemia.
Pathophysiology
Phosphorus homeostasis is complex and regulated by the actions of several hormones.
- Parathyroid hormone causes phosphate to be released from bone and inhibits renal reabsorption of phosphorus, resulting in phosphaturia
- Vitamin D aids in the intestinal reabsorption of phosphorus.
- Thyroid hormone & growth hormone act to increase renal reabsorption of phosphate.
- Phosphatonins -Factors responsible for inhibition of renal phosphate reabsorption.
Major causes of hypophosphatemia
Internal redistribution
Increased insulin secretion, particularly during refeeding
Acute respiratory alkalosis
Hungry bone syndrome
Decreased intestinal absorption
Inadequate intake
Antacids containing aluminum or magnesium
Steatorrhea and chronic diarrhea
Vitamin D deficiency or resistance
Increased urinary excretion
Primary and secondary hyperparathyroidism
Vitamin D deficiency or resistance
Hereditary hypophosphatemic rickets
Oncogenic osteomalacia
Fanconi syndrome
Other – osmotic diuresis, acetazolamide, acute volume expansion
Internal re-distribution
1) Respiratory alkalosis moves phosphate into cells leading to activation of
phosphofructokinase which stimulates intracellular glycolysis leading to phosphate
consumption as phosphorylated glucose precursors are produced.
Any cause of hyperventilation (eg, sepsis, anxiety, pain, heatstroke, alcohol
withdrawal, diabetic ketoacidosis [DKA], hepatic encephalopathy, salicylate
toxicity) can precipitate hypophosphatemia.
2) Administering carbohydrate lowers serum phosphate by stimulating the release of insulin which moves phosphate and glucose into cells.
The so-called refeeding syndrome occurs when starving or chronically malnourished patients are refed or given intravenous (IV) glucose, and typically produces a hypophosphatemic state by treatment day 3 or 4. In addition, during refeeding cells switch to an anabolic state, resulting in further phosphate depletion as this essential substrate is incorporated into cells and cell products.
3) Catecholamines and beta-receptor agonists also stimulate phosphate uptake into cells.
4) Certain rapidly growing malignancies (eg, acute leukemia, lymphomas) may consume phosphate preferentially, leading to hypophosphatemia.
5) Hungry bone syndrome — Parathyroidectomy (for hyperparathyroidism) or rarely thyroidectomy (for hyperthyroidism) in patients with preexisting osteopenia can rarely result in marked deposition of calcium and phosphate in bone in the immediate postoperative period.
In most cases of intracellular phosphate shift, serum phosphate normalizes once the precipitating cause is removed.
Increased urinary excretion
1) Parathyroid hormone stimulates the kidneys to excrete phosphate,hypophosphatemia is a common sequela of primary and secondary hyperparathyroidism.
2) Urinary loss of phosphate occurs with acute volume expansion due to a dilution of serum calcium, which in turn triggers an increase in the release of parathyroid hormone.
3) Osmotic diuresis, such as seen in hyperosmolar hyperglycemic syndrome (HHS)also produces increased urinary excretion of phosphorus. Diuretics, including loop diuretics, thiazides and carbonic anhydrase inhibitors (eg acetazolamide) interfere with the ability of the proximal tubule to reabsorb phosphorus, thus producing hyperphosphaturia and potentially leading to hypophosphatemia.
4) Patients with transplanted kidneys,congenital defects (X-linked hypophosphatemia [XLH] and autosomal dominant hypophosphatemic rickets [ADHR]), or Fanconi syndrome (proximal tubule dysfunction) also may excrete excess urinary phosphate.
Decreased intestinal absorption
Phosphate may be lost via the gut, as in chronic diarrhea, malabsorption syndromes, severe vomiting, or NG suctioning. Phosphate may also be bound in the gut, thereby preventing absorption (eg,chronic use of sucralfate, or phosphate-binding antacids, including aluminum hydroxide, aluminum carbonate, and calcium carbonate).
Decreased dietary intake
This is a rare cause of hypophosphatemia because of the ubiquity of phosphate in foods. Certain conditions such as anorexia nervosa or chronic alcoholism may lead to hypophosphatemia in part via this mechanism.
Manifestations of phosphate deficiency
1) Muscular weakness
2) Rhabdomyolysis via ATP depletion and the consequent inability of muscle cells to maintain membrane integrity. Patients undergoing acute alcohol withdrawal are especially vulnerable to rhabdomyolysis secondary to hypophosphatemia, which is caused by the rapid uptake of phosphate into muscle cells. Rhabdomyolysis occurs more rarely in patients being treated for DKA or being refed after starvation.
3) Respiratory insufficiency
4) Myocardial depression, reduced threshold for ventricular arrhythmias.
5) Impaired neurologic function, manifested by confusion, seizures, and coma. Peripheral neuropathy and ascending motor paralysis, similar to Guillain-Barré syndrome. Extrapontine myelinolysis has also been reported.
6) The hemolytic anemia ,attributed to the inability of erythrocytes to maintain integrity of cell membranes in the face of ATP depletion, leading to their destruction in the spleen.
7) Compromised oxygen delivery to the tissues due to decreases in erythrocyte 2,3-DPG
8) Leukocyte function is affected, which results in impaired chemotaxis and phagocytosis.
Treatment
Treatment of hypophosphatemia is twofold.
o Correct any precipitating causes of hypophosphatemia.
o Replace total body phosphates.
Depending on the clinical situation, replacement options include dietary phosphate, oral phosphate preparations, and IV phosphate.The most important consideration in choosing replacement therapy is whether the patient has signs or symptoms of phosphate depletion.
Mild to moderately severe, asymptomatic hypophosphatemia may require oral phosphate replacement; however, correcting factors that led to the hypophosphatemia usually is sufficient.
Severe/symptomatic Hypophosphatemia -Patients with symptoms of hypophosphatemia or with serum phosphate levels less than 0.32 mmol/L require IV phosphate replacement.
The intracellular nature of phosphate makes interpreting a low serum phosphate level difficult and predicting the amount required to replenish cellular stores nearly impossible.
Phosphate salt
IV preparations are available as sodium phosphate (Na2HPO4 and NAH2PO4)or potassium phosphate (K2HPO4 and KH2PO4).
Response to IV phosphorus supplementation varies widely and may be associated with hyperphosphatemia and hypocalcemia. Rate of infusion and choice of initial dosage should be based on severity of hypophosphatemia and presence of symptoms.
Thanks to Dr Harjit Mahay for contributing this wonderful article.
Phosphate is the most abundant intracellular anion and is essential for
- membrane structure,
- transport in all cells.
- production of ATP, which provides energy for nearly all cell functions.
- as an essential component of DNA and RNA.
- production of 2,3-diphosphoglycerate (2,3-DPG) in RBC’s, which facilitates release of oxygen from hemoglobin
Approximately 85% of the body's phosphorus is in bone as hydroxyapatite,
while most of the remainder (15%) is present in soft tissue.
Only 0.1% of phosphorus is present in extracellular fluid, and it is this
fraction that is measured with a serum phosphorus level.
Normal Serum phosphate or phosphorus levels are 0.81-1.45 mmol/L.
Hypophosphatemia is defined as
mild: 0.65-0.81 mmol/L,
moderate: 0.32-0.65 mmol/L,
severe: < 0.32 mmol/L. Mild to moderately severe hypophosphatemia is usually asymptomatic. Major clinical sequelae usually occur only in severe hypophosphatemia.
Pathophysiology
Phosphorus homeostasis is complex and regulated by the actions of several hormones.
- Parathyroid hormone causes phosphate to be released from bone and inhibits renal reabsorption of phosphorus, resulting in phosphaturia
- Vitamin D aids in the intestinal reabsorption of phosphorus.
- Thyroid hormone & growth hormone act to increase renal reabsorption of phosphate.
- Phosphatonins -Factors responsible for inhibition of renal phosphate reabsorption.
Major causes of hypophosphatemia
Internal redistribution
Increased insulin secretion, particularly during refeeding
Acute respiratory alkalosis
Hungry bone syndrome
Decreased intestinal absorption
Inadequate intake
Antacids containing aluminum or magnesium
Steatorrhea and chronic diarrhea
Vitamin D deficiency or resistance
Increased urinary excretion
Primary and secondary hyperparathyroidism
Vitamin D deficiency or resistance
Hereditary hypophosphatemic rickets
Oncogenic osteomalacia
Fanconi syndrome
Other – osmotic diuresis, acetazolamide, acute volume expansion
Internal re-distribution
1) Respiratory alkalosis moves phosphate into cells leading to activation of
phosphofructokinase which stimulates intracellular glycolysis leading to phosphate
consumption as phosphorylated glucose precursors are produced.
Any cause of hyperventilation (eg, sepsis, anxiety, pain, heatstroke, alcohol
withdrawal, diabetic ketoacidosis [DKA], hepatic encephalopathy, salicylate
toxicity) can precipitate hypophosphatemia.
2) Administering carbohydrate lowers serum phosphate by stimulating the release of insulin which moves phosphate and glucose into cells.
The so-called refeeding syndrome occurs when starving or chronically malnourished patients are refed or given intravenous (IV) glucose, and typically produces a hypophosphatemic state by treatment day 3 or 4. In addition, during refeeding cells switch to an anabolic state, resulting in further phosphate depletion as this essential substrate is incorporated into cells and cell products.
3) Catecholamines and beta-receptor agonists also stimulate phosphate uptake into cells.
4) Certain rapidly growing malignancies (eg, acute leukemia, lymphomas) may consume phosphate preferentially, leading to hypophosphatemia.
5) Hungry bone syndrome — Parathyroidectomy (for hyperparathyroidism) or rarely thyroidectomy (for hyperthyroidism) in patients with preexisting osteopenia can rarely result in marked deposition of calcium and phosphate in bone in the immediate postoperative period.
In most cases of intracellular phosphate shift, serum phosphate normalizes once the precipitating cause is removed.
Increased urinary excretion
1) Parathyroid hormone stimulates the kidneys to excrete phosphate,hypophosphatemia is a common sequela of primary and secondary hyperparathyroidism.
2) Urinary loss of phosphate occurs with acute volume expansion due to a dilution of serum calcium, which in turn triggers an increase in the release of parathyroid hormone.
3) Osmotic diuresis, such as seen in hyperosmolar hyperglycemic syndrome (HHS)also produces increased urinary excretion of phosphorus. Diuretics, including loop diuretics, thiazides and carbonic anhydrase inhibitors (eg acetazolamide) interfere with the ability of the proximal tubule to reabsorb phosphorus, thus producing hyperphosphaturia and potentially leading to hypophosphatemia.
4) Patients with transplanted kidneys,congenital defects (X-linked hypophosphatemia [XLH] and autosomal dominant hypophosphatemic rickets [ADHR]), or Fanconi syndrome (proximal tubule dysfunction) also may excrete excess urinary phosphate.
Decreased intestinal absorption
Phosphate may be lost via the gut, as in chronic diarrhea, malabsorption syndromes, severe vomiting, or NG suctioning. Phosphate may also be bound in the gut, thereby preventing absorption (eg,chronic use of sucralfate, or phosphate-binding antacids, including aluminum hydroxide, aluminum carbonate, and calcium carbonate).
Decreased dietary intake
This is a rare cause of hypophosphatemia because of the ubiquity of phosphate in foods. Certain conditions such as anorexia nervosa or chronic alcoholism may lead to hypophosphatemia in part via this mechanism.
Manifestations of phosphate deficiency
1) Muscular weakness
2) Rhabdomyolysis via ATP depletion and the consequent inability of muscle cells to maintain membrane integrity. Patients undergoing acute alcohol withdrawal are especially vulnerable to rhabdomyolysis secondary to hypophosphatemia, which is caused by the rapid uptake of phosphate into muscle cells. Rhabdomyolysis occurs more rarely in patients being treated for DKA or being refed after starvation.
3) Respiratory insufficiency
4) Myocardial depression, reduced threshold for ventricular arrhythmias.
5) Impaired neurologic function, manifested by confusion, seizures, and coma. Peripheral neuropathy and ascending motor paralysis, similar to Guillain-Barré syndrome. Extrapontine myelinolysis has also been reported.
6) The hemolytic anemia ,attributed to the inability of erythrocytes to maintain integrity of cell membranes in the face of ATP depletion, leading to their destruction in the spleen.
7) Compromised oxygen delivery to the tissues due to decreases in erythrocyte 2,3-DPG
8) Leukocyte function is affected, which results in impaired chemotaxis and phagocytosis.
Treatment
Treatment of hypophosphatemia is twofold.
o Correct any precipitating causes of hypophosphatemia.
o Replace total body phosphates.
Depending on the clinical situation, replacement options include dietary phosphate, oral phosphate preparations, and IV phosphate.The most important consideration in choosing replacement therapy is whether the patient has signs or symptoms of phosphate depletion.
Mild to moderately severe, asymptomatic hypophosphatemia may require oral phosphate replacement; however, correcting factors that led to the hypophosphatemia usually is sufficient.
Severe/symptomatic Hypophosphatemia -Patients with symptoms of hypophosphatemia or with serum phosphate levels less than 0.32 mmol/L require IV phosphate replacement.
The intracellular nature of phosphate makes interpreting a low serum phosphate level difficult and predicting the amount required to replenish cellular stores nearly impossible.
Phosphate salt
IV preparations are available as sodium phosphate (Na2HPO4 and NAH2PO4)or potassium phosphate (K2HPO4 and KH2PO4).
Response to IV phosphorus supplementation varies widely and may be associated with hyperphosphatemia and hypocalcemia. Rate of infusion and choice of initial dosage should be based on severity of hypophosphatemia and presence of symptoms.
Thanks to Dr Harjit Mahay for contributing this wonderful article.
Thursday, October 8, 2009
Management of the pregnant trauma patient
Trauma in 5% of pregnancy, of which greater than 50% are MVAs, and of these 82% of fetal deaths occur during the accident.
*MVA 1/2, Falls 1/5, Assaults 1/5, Burns 1/100
Life threatening trauma results in 50% fetal loss rate.
The most common cause of fetal death after blunt trauma is abruption.
Anterior abdominal penetrating trauma will (unless proven otherwise) injure the fetus >20/40 weeks gestation.
Peri-mortem caesarian has poor prognosis.
Note there are preventive (non-medical) measures which exist are effective when followed. (physical abuse, alcohol, seat-belts)
Principles (on top of basic trauma principles)
Changes in maternal physiology.
Radiation/medication risks greater in early pregnancy.
Fetus viable after 23-24 weeks.
Two-patients: good management of mother is good for fetus usually.
Fetus hates hypoxaemia and hypovolaemia.
Remember the signs of fetal distress (tachycardia, decreased variability, decelerations)
Multi-disciplinarian approach
Trauma surgeon, emergency physician, technicians, obstetricians, neonatologist, many specialist nursing staff.
Prehospital issues
History
Beware of the distended abdomen. Also avoid direct pressure on abdomen (e.g. MAST)
Lateral decubitus
Transfusion with O negative
Emergency care issues (on top of ATLS principles)
All investigations (including radiology) and interventions for the mother necessary should be performed (e.g. DPL)
Estimation of gestation from fundal height; any fetus >23 wks should prompt immediate monitoring, which includes tocography and FHS. (umbilicus 20wks) NB 25% of trauma after 2240 wks gestation is complicated by premature labour
Secondary survey includes rectal and vaginal exam (cervical effacement, dilation, blood/amniotic fluid, etc), except in 3rd trim, where there's need to exclude placenta praevia
FAST is useful (intraabdominal bleed sensitivity 83%)
Kleihauer-Betke test, if positive this is relevant to Rhesus negative mothers.
ABG respiratory alkalosis, dilutional anaemia
Intensive care issues
Think pregnancy conditions and post-partum conditions.
DVT, PE prophylaxis
Blunt Trauma
Not as problematic in <13/40 gestation, unless there is pelvic fracture with 25% chance of fetal loss. Placenta is never elastic, even if myometrium is after 20wks: abruptions usually suspected with uterine activity. Think coagulopathy/DIC and fetal loss. Penetrating Trauma after 20wks uterus usually protective. Tetanus toxoid should be given. C-section C-section post trauma for >25/40wks gestation has 45% survival and 72% maternal survival rate.
Peri-mortem c-section is often futile. Consider after 4minutes of CPR to help fetal survival and aid maternal resuscitation.
Reference:
Kenneth L M, Goetzl, L. Trauma in pregnancy. Critical Care Medicine 2005 Vol. 33, No. 10 (Suppl.)
Thnks to William Ng for contributing this wonderful article.
*MVA 1/2, Falls 1/5, Assaults 1/5, Burns 1/100
Life threatening trauma results in 50% fetal loss rate.
The most common cause of fetal death after blunt trauma is abruption.
Anterior abdominal penetrating trauma will (unless proven otherwise) injure the fetus >20/40 weeks gestation.
Peri-mortem caesarian has poor prognosis.
Note there are preventive (non-medical) measures which exist are effective when followed. (physical abuse, alcohol, seat-belts)
Principles (on top of basic trauma principles)
Changes in maternal physiology.
Radiation/medication risks greater in early pregnancy.
Fetus viable after 23-24 weeks.
Two-patients: good management of mother is good for fetus usually.
Fetus hates hypoxaemia and hypovolaemia.
Remember the signs of fetal distress (tachycardia, decreased variability, decelerations)
Multi-disciplinarian approach
Trauma surgeon, emergency physician, technicians, obstetricians, neonatologist, many specialist nursing staff.
Prehospital issues
History
Beware of the distended abdomen. Also avoid direct pressure on abdomen (e.g. MAST)
Lateral decubitus
Transfusion with O negative
Emergency care issues (on top of ATLS principles)
All investigations (including radiology) and interventions for the mother necessary should be performed (e.g. DPL)
Estimation of gestation from fundal height; any fetus >23 wks should prompt immediate monitoring, which includes tocography and FHS. (umbilicus 20wks) NB 25% of trauma after 2240 wks gestation is complicated by premature labour
Secondary survey includes rectal and vaginal exam (cervical effacement, dilation, blood/amniotic fluid, etc), except in 3rd trim, where there's need to exclude placenta praevia
FAST is useful (intraabdominal bleed sensitivity 83%)
Kleihauer-Betke test, if positive this is relevant to Rhesus negative mothers.
ABG respiratory alkalosis, dilutional anaemia
Intensive care issues
Think pregnancy conditions and post-partum conditions.
DVT, PE prophylaxis
Blunt Trauma
Not as problematic in <13/40 gestation, unless there is pelvic fracture with 25% chance of fetal loss. Placenta is never elastic, even if myometrium is after 20wks: abruptions usually suspected with uterine activity. Think coagulopathy/DIC and fetal loss. Penetrating Trauma after 20wks uterus usually protective. Tetanus toxoid should be given. C-section C-section post trauma for >25/40wks gestation has 45% survival and 72% maternal survival rate.
Peri-mortem c-section is often futile. Consider after 4minutes of CPR to help fetal survival and aid maternal resuscitation.
Reference:
Kenneth L M, Goetzl, L. Trauma in pregnancy. Critical Care Medicine 2005 Vol. 33, No. 10 (Suppl.)
Thnks to William Ng for contributing this wonderful article.
Monday, September 7, 2009
Assessment and Management Of Airway Burns
The term “inhalational injury” has been used to describe the aspiration of toxic products of combustion, but also more generally any pulmonary insult associated with a burn injury. Patients with cutaneous burns are two to three times more likely to die if they also have lower airway burns. Death may be a direct result of lung injury but is usually due to the systemic consequences of such injury. It may be impossible to distinguish lung injury caused at the time of the burn directly to the lungs by a burn from injury due to the systemic consequences of the burn. Inhalation injury, age, and burn size are the three most commonly cited predictive factors for prolonged ventilator dependence, hospital stay, and death in burn patients. The injuries can generally be divided into three classes:
- thermal injury (restricted to upper airway structures except in cases of blast injury or steam inhalation),
- local chemical irritation throughout the respiratory tract, and
- systemic toxicity (eg, inhalation of toxins such as carbon monoxide or cyanide).
In the clinical setting, diagnosis of inhalation injury is usually a subjective decision based on a combination of history and physical exam, and confirmed by diagnostic studies (eg, fiberoptic bronchoscopy).
History includes -
mechanism of exposure, (eg, flame, electricity, blast injury, steam, or hot liquid)
quality of inhaled irritants (eg, house fire, industrial toxins), and
duration of exposure eg, trapped in an enclosed space or
conditions that limit avoidance behavior such as intoxication, loss of consciousness, or physical disability).
Physical exam can provide
an estimate of the intensity of exposure and includes findings such as
evidence of exposure of the respiratory tract to extreme heat (facial burns or singed facial or nasal hair),
soot deposited on the face or carbonaceous sputum,or
early manifestations of respiratory compromise such as airway obstruction by edema or parenchymal damage.
Defining diagnostic criteria for inhalation injuries is made difficult by the extreme heterogeneity of clinical presentation as evaluated therefore, diagnosis is with a high index of suspicion of airway burns in patients with one or more of the warning signs.
Warning signs of airway burns - Suspect airway burn if:
• Burns occurred in an enclosed space
• Stridor, hoarseness, or cough
• Burns to face, lips, mouth, pharynx, or nasal mucosa - Singed nasal hairs; red, tender oral membranes; or obvious intraoral or pharyngeal burns indicate likely airway burn.
• Soot in sputum, nose, or mouth
• Dyspnoea, decreased level of consciousness, or confusion
• Hypoxaemia (low SpO2 or PaO2) or increased carbon monoxide levels (>2%)
Onset of symptoms may be delayed
Mechanisms of pulmonary insult after lower airway burns
• Mucosal inflammation • Ciliary paralysis
• Mucosal burn • Reduced surfactant
• Bronchorrhoea • Obstruction by debris
• Bronchospasm • Systemic inflammatory response
The pathophysiology of airway burns is highly variable, depending on the environment of the burn and the incomplete products of combustion. The clinical manifestations are often delayed for the first few hours but are usually apparent by 24 hours. Airway debris—including secretions, mucosal slough, and smoke residue—can seriously compromise pulmonary function.
Management of Airway burns—key clinical points
• Restricting fluids increases mortality
• If in doubt, intubate
• Give 100% oxygen until carbon monoxide toxicity excluded
• Ventilatory strategies to avoid lung injury (low volume or pressure)
• Aggressive airway toilet
• Early surgical debridement of wounds
• Early enteral feeding
There is no specific treatment for airway burns other than ensuring adequate oxygenation and minimising iatrogenic lung insult. Prophylactic corticosteroids or antibiotics have no role in treatment. Studies on Beta 2 agonists, Nebulized Heparin,Tocopherol, Inhaled NO are also inconclusive or lack sufficient data.
Control of the airway, by endotracheal intubation, is essential before transporting any patient with suspected airway burn. Rapid fluid administration, with inevitable formation of oedema, may lead to life threatening airway compromise if control of the airway is delayed. Endotracheal intubation before oedema formation is far safer and simpler. Oxygen (100%) should be given until the risk of carbon monoxide toxicity has been excluded, since high concentrations of oxygen will clear carbon monoxide from the body more rapidly than atmospheric concentrations. Importantly, carbon monoxide toxicity may result in a falsely elevated pulse oximetry saturation.
Airway burns are associated with a substantially increased requirement for fluid resuscitation. Reducing the fluid volume administered, to avoid fluid accumulation in the lung, results in a worse outcome. Invasive monitoring may be required to guide fluid administration, especially with failure to respond to increasing volumes of fluid. Fluid administration should not be guided by calculated fluid requirements alone.Adequate oxygen delivery to all the tissues of the body is essential to prevent multi-organ failure.
Aggressive airway toilet is essential. Early surgical debridement, enteral feeding, mobilisation of the patient, and early extubation are desirable. Antibiotics should be reserved for established infections and guided by regular microbiological surveillance.
Several ventilatory strategies have been proposed to improve outcome following airway burns. Adequate systemic oxygenation and minimising further alveolar injury is the primary clinical objective. Prolonging survival will permit spontaneous lung recovery.
- thermal injury (restricted to upper airway structures except in cases of blast injury or steam inhalation),
- local chemical irritation throughout the respiratory tract, and
- systemic toxicity (eg, inhalation of toxins such as carbon monoxide or cyanide).
In the clinical setting, diagnosis of inhalation injury is usually a subjective decision based on a combination of history and physical exam, and confirmed by diagnostic studies (eg, fiberoptic bronchoscopy).
History includes -
mechanism of exposure, (eg, flame, electricity, blast injury, steam, or hot liquid)
quality of inhaled irritants (eg, house fire, industrial toxins), and
duration of exposure eg, trapped in an enclosed space or
conditions that limit avoidance behavior such as intoxication, loss of consciousness, or physical disability).
Physical exam can provide
an estimate of the intensity of exposure and includes findings such as
evidence of exposure of the respiratory tract to extreme heat (facial burns or singed facial or nasal hair),
soot deposited on the face or carbonaceous sputum,or
early manifestations of respiratory compromise such as airway obstruction by edema or parenchymal damage.
Defining diagnostic criteria for inhalation injuries is made difficult by the extreme heterogeneity of clinical presentation as evaluated therefore, diagnosis is with a high index of suspicion of airway burns in patients with one or more of the warning signs.
Warning signs of airway burns - Suspect airway burn if:
• Burns occurred in an enclosed space
• Stridor, hoarseness, or cough
• Burns to face, lips, mouth, pharynx, or nasal mucosa - Singed nasal hairs; red, tender oral membranes; or obvious intraoral or pharyngeal burns indicate likely airway burn.
• Soot in sputum, nose, or mouth
• Dyspnoea, decreased level of consciousness, or confusion
• Hypoxaemia (low SpO2 or PaO2) or increased carbon monoxide levels (>2%)
Onset of symptoms may be delayed
Mechanisms of pulmonary insult after lower airway burns
• Mucosal inflammation • Ciliary paralysis
• Mucosal burn • Reduced surfactant
• Bronchorrhoea • Obstruction by debris
• Bronchospasm • Systemic inflammatory response
The pathophysiology of airway burns is highly variable, depending on the environment of the burn and the incomplete products of combustion. The clinical manifestations are often delayed for the first few hours but are usually apparent by 24 hours. Airway debris—including secretions, mucosal slough, and smoke residue—can seriously compromise pulmonary function.
Management of Airway burns—key clinical points
• Restricting fluids increases mortality
• If in doubt, intubate
• Give 100% oxygen until carbon monoxide toxicity excluded
• Ventilatory strategies to avoid lung injury (low volume or pressure)
• Aggressive airway toilet
• Early surgical debridement of wounds
• Early enteral feeding
There is no specific treatment for airway burns other than ensuring adequate oxygenation and minimising iatrogenic lung insult. Prophylactic corticosteroids or antibiotics have no role in treatment. Studies on Beta 2 agonists, Nebulized Heparin,Tocopherol, Inhaled NO are also inconclusive or lack sufficient data.
Control of the airway, by endotracheal intubation, is essential before transporting any patient with suspected airway burn. Rapid fluid administration, with inevitable formation of oedema, may lead to life threatening airway compromise if control of the airway is delayed. Endotracheal intubation before oedema formation is far safer and simpler. Oxygen (100%) should be given until the risk of carbon monoxide toxicity has been excluded, since high concentrations of oxygen will clear carbon monoxide from the body more rapidly than atmospheric concentrations. Importantly, carbon monoxide toxicity may result in a falsely elevated pulse oximetry saturation.
Airway burns are associated with a substantially increased requirement for fluid resuscitation. Reducing the fluid volume administered, to avoid fluid accumulation in the lung, results in a worse outcome. Invasive monitoring may be required to guide fluid administration, especially with failure to respond to increasing volumes of fluid. Fluid administration should not be guided by calculated fluid requirements alone.Adequate oxygen delivery to all the tissues of the body is essential to prevent multi-organ failure.
Aggressive airway toilet is essential. Early surgical debridement, enteral feeding, mobilisation of the patient, and early extubation are desirable. Antibiotics should be reserved for established infections and guided by regular microbiological surveillance.
Several ventilatory strategies have been proposed to improve outcome following airway burns. Adequate systemic oxygenation and minimising further alveolar injury is the primary clinical objective. Prolonging survival will permit spontaneous lung recovery.
Saturday, September 5, 2009
Critical Care/Medical Sites of Interest
Hi everyone, I am trying to collect and make list of all useful websites in CRITICAL CARE. Here is the beginning and if you know some, please share for benefit of all.
Critical Care Medicine
http://www.ccmtutorials.com
http://www.aic.cuhk.edu.hk/web8/index.htm
http://www.lhsc.on.ca/Health_Professionals/CCTC/edubriefs/index.htm
http://www.uihealthcare.com/vh/
http://cim.ucdavis.edu/
http://www.thoracic.org/sections/clinical-information/critical-care/index.html
http://www.anzics.com.au/
http://www.lhsc.on.ca/programs/critcare/pge/
http://www.dicm.co.uk/papers.htm - Great UK based website, primarily for those doing the UK DICM but a treasure trove of evidence for any intensivist
Evidence Based Medicine
http://www.ebmny.org/">http://www.ebmny.org/">http://www.ebmny.org/
http://www.cche.net/usersguides/ebm.asp
http://www.cebm.utoronto.ca/
http://www.cebm.net/
Anesthesia
http://www.virtual-anaesthesia-textbook.com/vat/main.shtml
Acid Base
Acid Base Tutorial - http://www.acid-base.com/
Acid Base Physiology - http://www.anaesthesiamcq.com/AcidBaseBook/ABindex.php
Mechanical Ventilation
http://www.ccmtutorials.com/rs/mv/index.htm">http://www.ccmtutorials.com/rs/mv/index.htm">http://www.ccmtutorials.com/rs/mv/index.htm
http://www.aic.cuhk.edu.hk/web8/mech%20vent%20intro.htm
Sepsis
http://www.sepsisforum.org/">http://www.sepsisforum.org/">http://www.sepsisforum.org/
http://www.elililly.com/
http://www.ardsfoundation.com/
http://ssc.sccm.org/
http://www.ardsnet.org/
Radiology
http://www.learningradiology.com/
http://www.anatomyatlases.org/
Chest XRay
http://www.meddean.luc.edu/lumen/MedEd/medicine/pulmonar/cxr/cxr.htm
http://www.meddean.luc.edu/lumen/MedEd/medicine/pulmonar/cxr/atlas/cxratlas_f.htm
http://www.learningradiology.com/lectures/facultylectures/BASIC%20CXR-mod-Adam_files/v3_document.htm
http://www.usfca.edu/fac-staff/ritter/chestxra.htm
Trauma
http://www.trauma.org/
Pupil assessment
http://cim.ucdavis.edu/EyeRelease/Interface/TopFrame.htm
Delirium
http://www.icudelirium.org/delirium/CAM-ICUTraining.html
Anatomy
http://www.pbs.org/wnet/brain/3d/
http://www.meddean.luc.edu/lumen/MedEd/GrossAnatomy/anatomy.htm
http://msjensen.cehd.umn.edu/webanatomy/
http://www.imaios.com/en/e-Anatomy
IABP
http://www.aic.cuhk.edu.hk/web8/IABP%20pressure%20waveforms.htm
ECHO
http://www.criticalecho.com (By Kishore CMC Vellore)
Brain Herniation
http://rad.usuhs.mil/rad/herniation
Critical Care Medicine
http://www.ccmtutorials.com
http://www.aic.cuhk.edu.hk/web8/index.htm
http://www.lhsc.on.ca/Health_Professionals/CCTC/edubriefs/index.htm
http://www.uihealthcare.com/vh/
http://cim.ucdavis.edu/
http://www.thoracic.org/sections/clinical-information/critical-care/index.html
http://www.anzics.com.au/
http://www.lhsc.on.ca/programs/critcare/pge/
http://www.dicm.co.uk/papers.htm - Great UK based website, primarily for those doing the UK DICM but a treasure trove of evidence for any intensivist
Evidence Based Medicine
http://www.ebmny.org/">http://www.ebmny.org/">http://www.ebmny.org/
http://www.cche.net/usersguides/ebm.asp
http://www.cebm.utoronto.ca/
http://www.cebm.net/
Anesthesia
http://www.virtual-anaesthesia-textbook.com/vat/main.shtml
Acid Base
Acid Base Tutorial - http://www.acid-base.com/
Acid Base Physiology - http://www.anaesthesiamcq.com/AcidBaseBook/ABindex.php
Mechanical Ventilation
http://www.ccmtutorials.com/rs/mv/index.htm">http://www.ccmtutorials.com/rs/mv/index.htm">http://www.ccmtutorials.com/rs/mv/index.htm
http://www.aic.cuhk.edu.hk/web8/mech%20vent%20intro.htm
Sepsis
http://www.sepsisforum.org/">http://www.sepsisforum.org/">http://www.sepsisforum.org/
http://www.elililly.com/
http://www.ardsfoundation.com/
http://ssc.sccm.org/
http://www.ardsnet.org/
Radiology
http://www.learningradiology.com/
http://www.anatomyatlases.org/
Chest XRay
http://www.meddean.luc.edu/lumen/MedEd/medicine/pulmonar/cxr/cxr.htm
http://www.meddean.luc.edu/lumen/MedEd/medicine/pulmonar/cxr/atlas/cxratlas_f.htm
http://www.learningradiology.com/lectures/facultylectures/BASIC%20CXR-mod-Adam_files/v3_document.htm
http://www.usfca.edu/fac-staff/ritter/chestxra.htm
Trauma
http://www.trauma.org/
Pupil assessment
http://cim.ucdavis.edu/EyeRelease/Interface/TopFrame.htm
Delirium
http://www.icudelirium.org/delirium/CAM-ICUTraining.html
Anatomy
http://www.pbs.org/wnet/brain/3d/
http://www.meddean.luc.edu/lumen/MedEd/GrossAnatomy/anatomy.htm
http://msjensen.cehd.umn.edu/webanatomy/
http://www.imaios.com/en/e-Anatomy
IABP
http://www.aic.cuhk.edu.hk/web8/IABP%20pressure%20waveforms.htm
ECHO
http://www.criticalecho.com (By Kishore CMC Vellore)
Brain Herniation
http://rad.usuhs.mil/rad/herniation
Tuesday, September 1, 2009
Assessment for extubation
Despite advances in mechanical ventilation and respiratory support, the science of determining if the patient is ready for extubation is still very imprecise. A lot depends on the clinician’s threshold for reduction in ventilatory support, than does the modes of ventilatory wean.
Patients who can be extubated safely can be divided into three phases-
1. Freedom from the primary problem that prompted mechanical ventilation
2. Identifying whether the patient will sustain spontaneous respiration and ventilation and also when the patient is failing the assessment
3. What to look for immediately before extubation.
These assessments are multifaceted and usually include the overall patient condition, hemodynamic stability, neurological and muscular status and adequacy of gas exchange.
Commonly used clinical parameters that predict successful weaning from
mechanical ventilation.
Parameter with Desired value
Respiratory rate Less than 30-38 breaths/minute
Tidal volume 4-6 mL/kg
Minute ventilation 10-15 L/minute
Negative inspiratory force -20 to –30 cm H2O
Maximal inspiratory pressure (MIP) -15 to –30 cm H2O
Mouth occlusion pressure 100 msec after the
onset of inspiratory effort (P0.1) divided by MIP 0.3
Rapid shallow breathing index (RSBI)
(respiratory rate divided by tidal volume) 60-105
Rapid shallow breathing index rate
[(RSBI2 – RSBI1)/RSBI1] x 100 Less than 20%
CROP score (an index including compliance,
rate, oxygenation and pressure) 13
PaO2/FiO2 ratio >150-200
Despite high sensitivity, however, these parameters lack specificity.
All the patients who are deemed fit for extubation should undergo some means of assessment to see if they will tolerate extubation. It is routine to perform Spontaneous breathing trial (SBT), by means of – CPAP of 5 cm of H2O, T –Piece trial, or Pressure support of 7 cm of H2O. Once the patient is on SBT we should watch for indicators of failure, which are –
1. Inadequate gas exchange
Arterial oxygenation saturation (SaO2) <85% - 90% PaO2 <50 – 60 mmHg pH < 7.32 Increase in PaCO2 >10 mmHg
2. Unstable ventilatory/respiratory pattern
Respiratory rate >30 – 35 breaths/minute
Respiratory rate change over 50%
3. Hemodynamic instability
Heart rate >120 – 140 beats/minute
Heart rate change greater than 20%
Systolic blood pressure >180 mmHg or <90 mmHg Blood pressure change greater than 20% Vasopressors required 4. Change in mental status
Agitation
Anxiety
Somnolence
Coma
5. Signs of increased work of breathing
Nasal flaring
Paradoxical breathing movements
Use of accessory respiratory muscles
6. Onset of worsening discomfort ± diaphoresis
Another parameter that is widely used is the Rapid shallow breathing index (RSBI), from which we can calculate the RSBI rate which is the measure of change of RSBI over time, and may offer more predictive value .A RSBI rate of less than 20% is 90 % sensitive and 100% specific for predicting weaning success .It has a positive predictive value of 100% and negative predictive value of over 81 %.
Finally, once it is confirmed that patient can sustain spontaneous breathing , we can extubate the patient provided—
1 .Presence of a patent airway –assessed with “Cuff leak test”( dividing expiratory volume by inspiratory volume and multiplying with 100)
2. Patients’ ability to consistently protect the airway and clear secretions –assessed by the presence of adequate cough and gag reflex.
3. Mental status compatible with maintenance of airway and secretion clearance.
4. Absence of any other reasons for potential post-extubation failure—
- severe pain
- presence of apnea
- poorly controlled seizures
- risk of massive upper GI bleeding.
Thanks to Dr Harjit Mahay for contributing this wonderful article.
Patients who can be extubated safely can be divided into three phases-
1. Freedom from the primary problem that prompted mechanical ventilation
2. Identifying whether the patient will sustain spontaneous respiration and ventilation and also when the patient is failing the assessment
3. What to look for immediately before extubation.
These assessments are multifaceted and usually include the overall patient condition, hemodynamic stability, neurological and muscular status and adequacy of gas exchange.
Commonly used clinical parameters that predict successful weaning from
mechanical ventilation.
Parameter with Desired value
Respiratory rate Less than 30-38 breaths/minute
Tidal volume 4-6 mL/kg
Minute ventilation 10-15 L/minute
Negative inspiratory force -20 to –30 cm H2O
Maximal inspiratory pressure (MIP) -15 to –30 cm H2O
Mouth occlusion pressure 100 msec after the
onset of inspiratory effort (P0.1) divided by MIP 0.3
Rapid shallow breathing index (RSBI)
(respiratory rate divided by tidal volume) 60-105
Rapid shallow breathing index rate
[(RSBI2 – RSBI1)/RSBI1] x 100 Less than 20%
CROP score (an index including compliance,
rate, oxygenation and pressure) 13
PaO2/FiO2 ratio >150-200
Despite high sensitivity, however, these parameters lack specificity.
All the patients who are deemed fit for extubation should undergo some means of assessment to see if they will tolerate extubation. It is routine to perform Spontaneous breathing trial (SBT), by means of – CPAP of 5 cm of H2O, T –Piece trial, or Pressure support of 7 cm of H2O. Once the patient is on SBT we should watch for indicators of failure, which are –
1. Inadequate gas exchange
Arterial oxygenation saturation (SaO2) <85% - 90% PaO2 <50 – 60 mmHg pH < 7.32 Increase in PaCO2 >10 mmHg
2. Unstable ventilatory/respiratory pattern
Respiratory rate >30 – 35 breaths/minute
Respiratory rate change over 50%
3. Hemodynamic instability
Heart rate >120 – 140 beats/minute
Heart rate change greater than 20%
Systolic blood pressure >180 mmHg or <90 mmHg Blood pressure change greater than 20% Vasopressors required 4. Change in mental status
Agitation
Anxiety
Somnolence
Coma
5. Signs of increased work of breathing
Nasal flaring
Paradoxical breathing movements
Use of accessory respiratory muscles
6. Onset of worsening discomfort ± diaphoresis
Another parameter that is widely used is the Rapid shallow breathing index (RSBI), from which we can calculate the RSBI rate which is the measure of change of RSBI over time, and may offer more predictive value .A RSBI rate of less than 20% is 90 % sensitive and 100% specific for predicting weaning success .It has a positive predictive value of 100% and negative predictive value of over 81 %.
Finally, once it is confirmed that patient can sustain spontaneous breathing , we can extubate the patient provided—
1 .Presence of a patent airway –assessed with “Cuff leak test”( dividing expiratory volume by inspiratory volume and multiplying with 100)
2. Patients’ ability to consistently protect the airway and clear secretions –assessed by the presence of adequate cough and gag reflex.
3. Mental status compatible with maintenance of airway and secretion clearance.
4. Absence of any other reasons for potential post-extubation failure—
- severe pain
- presence of apnea
- poorly controlled seizures
- risk of massive upper GI bleeding.
Thanks to Dr Harjit Mahay for contributing this wonderful article.
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