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  • The next reception of the Iranian endourology of Musavibakhor in the Clinic Ibn Sino

    Thursday, November 6 professional Iranian endourology Sayed Habibullah Musavibakhor will begin accepting patients in Clinic Ibn Sino. The people suffering from kidney stones and other types of urological diseases, will be able to pre-enroll in Clinic Ibn Sino. Take the opportunity which provides Clinic Ibn Sino and extracted arrival of such highly skilled doctors of the world level which is endourology Musavibakhor.

     
  • The Iranian ophthalmologist of Ahmadali Firdavsi will visit the Clinic of Ibn Sino

    On Thursday, October 30 a Doctor Akhmadaly Firdavsi will visit the Clinic of Ibn Sino, who is the skilled expert in the field of ophthalmology and he has broad experience in conservative and physiotherapeutic treatment of the following diseases:

    - Phacoemulsification (cataract removal with the subsequent implantation of an artificial lens).

    - Squint operation of eye muscles (strabismus).

     
  • The neurosurgeon Abbos Bakhtiyori will visit our Clinic of Ibni Sino

    The next visit of the Iranian neurosurgeon Abbos Bakhtiyori on Sunday, October 12 will give the opportunity to perform such complex operations as backbone hernia, a laminectomy, a foraminotomy, a discectomy; spondylolisthesis (eliminating the curvature of the spine using a CD), spondylolis (eliminating the fragility of the spine using CD) and other types of neurosurgical surgery.

     

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Scientific articles

Acid-base disturbances

Karimov Kh. expert in resuscitation

The normal extracellular fluid (ECF) pH is 7.35-7.45. Regulation of normal pH depends on lungs and kidneys. Maintenance of pH is essential for normal cellular function. Three general mechanisms exist to keep to within a narrow window:

 Chemical buffering is mediated by HCO3- in the ECF and by protein and phosphate buffers in the intracellular fluid (ICF). The normal HCO3- is 21-26mEq/L.

 

Alveolar ventilation minimizes variations in the pH by altering the partial pressure of carbon dioxide (pCO2).  The normal pCO2- is 35-45mm Hg.

Renal H+ handling allows the kidney to adapt to changes in acid-base status via HCO3- reabsorption and excretion of titratableacid  and NH4

 

                                          Metabolic acidosis

Metabolic acidosisis characterized by  a decrease in the plasma HCO3- due to either HCO3- loss or the accumulation of acid.

Etiology

  1. A low cardiac output state , which is often associated with peripheral vasoconstriction from hypothermia or use vasoconstrictive drugs, is the primary cause of metabolic acidosis in the cardiac surgery patients.
  2. Low-dose epinephrine. This may reflect metabolic type B lactic acidosis caused by metabolic factors that increase lactic acid production, such as hyperglycemia and lipolysis.
  3. Intra-abdominal catastrophes such as mesenteric ischemia.
  4. Sepsis.
  5. High dose of nitroprusside.
  6. Renal failure.
  7. Acute hepatic disfunction.
  8. Diabetic ketoacidosis.

Effects

The presence of a progressive or significant metabolic acidosis is often an indication a serious ongoing problem that must be corrected before adverse consequences occur. These include:

Cardiovascular effects:

-          Decreased contractility and cardiac output, reduction in hepatic and renal blood flow

-          Attenuation of the positive inotropic effects of catecholamines

-          Venoconstriction and arteriolar dilatation which decrease systemic pressures.

-          Increased pulmonary vascular resistance.

-          Sensitization to reentry arrhythmias.

Respiratory effects:

-          Dyspnea and tachypnea

-          Decreased respiratory muscle strength

Metabolic changes:

-          Increased metabolic demands

-          Hyperglycemia caused by tissue insulin resistance and inhibition anaerobic glycolysis.

-          Increased hepatic production of  lactate,

-          Hyperkalemia.

-          Increased protein catabolism

Cerebral function:

-          Inhibition of brain metabolism and cell volume regulation.

-          Obtundation and coma.

Assessment

Measurement of anion gap (AG) is important to define the etiology of acidosis, with normal range being 3-13mEq/L. High AG generally reflects additional acid production and high AG metabolic acidosis is most common after cardiac surgery. A normal or low AG represents loss of bicarbonate.

Treatment.

Treatment of metabolic acidosis depends on the cause and severity.

-          Sodium bicarbonate is administered in a dose calculated from the following:

0.5xbody weight in kg x base deficit = mEq NaHCO3

This should be administered over several hours in the patients with severe metabolic acidosis with careful monitoring of the serum sodium concentration. Because the bicarbonate is metabolized to CO2, this can worsen a respiratory acidosis in a patients with compromised pulmonary function.

 

-          Carbicarb is an equimolar solution of sodium bicarbonate and sodium carbonate. One of its advantages is that it does not undergo significant breakdown into CO2 and H2O. The recommended dose is:

0.2xbody weight in kg x base deficit = mEqsodium

          -         Tromethamine 0.3 M is most beneficial in patients with hypernatremia and mixed metabolic/respiratory acidosis, because it limits   

CO2 generation and will not rise the serum sodium. In contrast to NaHCO3  it does not lower serum potassium, but it can produce hypoglycemia and respiratory depression. It is contraindicated in renal failure.

                                       body weight in kg x base deficit = ml of Tromethamine 0.3 M

In a mechanically ventilated patient it is not unreasonable to hyperventilate the patient to lower the pCO2, this will increase the intracellular and extracellular pH.

Metabolic alkalosis

Metabolic alkalosisis characterized by  an elevation in the plasma HCO3- due to either H+ loss or HCO3- gain.

Etiology

  1. Excessive diuresis which promotes hypovolemiaand depletion of hydrogen ions and chloride.
  2. Nasogastric drainage and inadequate electrolyte replacement by IV solution.
  3. Total parenteral nutrition with inappropriate solute composition.
  4. Secondary as compensation for respiratory acidosis.

Pathophysiology

Hypovolemia stimulates aldosterone secretion, which causes sodium retention, which then prevents excretion of sodium bicarbonate. Aldosterone also increases hydrogen secretion into the tubules, increasing bicarbonate reabsorption. Potassium loss directly increases bicarbonate reabsorption. Decreased available chloride delivered to the distal tubules results in less chloride-bicarbonate exchange and thus less bicarbonate excretion.

Adverse effects

-          Lowers the serum potassium level, leading to atrial and ventricular arrhythmias and neuromuscular weakness.

-          Has a adverse effects on the cardiovascular response to the catecholamines that is comparable to that of acidosis.

-          Shifts the oxygeh-hemoglobin dissociation curve to the left, impairing oxygen delivery to the tissues.

-          Produces arteriolar constriction which can compromise cerebral and coronary perfusion.

-          Neurologic abnormalities including headache, seizures, tetani, and lethargy may occur , because of associated hypocalcemia induced by alkalosis. These effects are usually seen with a pH >7.60.

-          Decreases the central respiratory drive, leading to hypoventilation, CO2 retention and hypoxemia.

Treatment

Metabolic alkalosis is sustained by volume depletion as well as by potassium and chloride depletion. Potential contributors to alkalosis should be assessed.

-          Reduce dose of loop diuretics to avoid volume depletion, Use proton pump inhibitors to minimize loss of gastric acid.

-          Avoid lactated Ringer’s solution and acetat, that are metabolized to bicarbonate.

The administration of chloride (KCL or NaCL) is the primary treatment for metabolic alkalosis. In hypovolemic patients 0.9%NaCL is the primary replacement  fluid, and KCL may be given for hypokalemia. In patients with total body water overload, typical in the postoperative state or with CHF, infusion of sodium chloride may exacerbate the edema. Alternative means of treating alkalosis in these states include the following:

-          Acetazolamide (Diamox) 250-500mg IV can be given in conjunction with a loop diuretic to increase urine output. It can lead to potassium depletion, so normokalemia should be present before it is started.

-          Hydrochloric acid 0.1 N may be administered through a central line at a rate of 10-20mEq/h.

Respiratory acidosis

Respiratory acidosis characterized by an elevation pCO2 resulting from alveolar hypoventilation.Norm pCO2 -35-45mmHg

Etiology

  1. Respiratory center depression. (sedatives, stroke)
  2. Chronic pulmonary disorders.
  3. Airway obstruction.
  4. Neuromuscular disorders
  5. Severe pulmonary edema and cardiopulmonary arrest

The second goal of mechanical ventilation is that of alveolar ventilation , which regulates the level of pCO2 This si controlled by setting the tidal volume and respiratory rate on the ventilator and should provide a minut ventilation of approximately 8-10L/min. The level of pCO2 is determined by the arterial blood gases.   Symptoms of respiratory acidosis result from changes in the cerebrospinalfluidpH.  Initial symptom and signs may include headache and restlessness, which may progress to generalized hyperreflexia/asterixis and coma.

Treatment

 Moderate hypercarbia in the fully ventilated patient is corrected by increasing either the respiratory rate or tidal volume. Significant hypercarbia usually ndicates a mechanical problem such as ventilator malfunction, endotracheal tube malposition or a pneumothorax. In the intubating patient sedation can be obtained with short-acting narcotics or other sedavies. These include:

-          Poropofol 25-75mg/kg/min

-          Morphine sulfate 2.5-5mg IV q1-2h.

-          Midazolam 2-4mg IV q1h.

-          Dexmedetomidine 1mg/kg over 10min, followed by a continuous infusion of 0.2-0.7mg/kg/h.

-          Shivering is best controlled using meperidine 25-50mg IV.

Respiratory alkalosis

Respiratory alkalosis characterized by a decrease in pCO2 resulting from hyperventilation. Norm pCO2 -35-45mmHg

Etiology

  1. Pneumonia, pulmonary edema, interstitial lung disease and asthma.
  2. Pain and fever.
  3. Hypoxemia, sepsis, delirium.
  4. Mechanical overventilation.

Severe respiratory alkalosis may acutely causes seizures, tethany, cardiac arrhythmias or loss of consciousness. Mild hypocarbia is quite acceptable in the immediate postoperative period, especially when the patient is hypothermic. Sever hypocarbia can lead to:

-           hypokalemia and  may predispose to ventricular arrhythmias

-          Shift the oxygen-hemoglobin dissociation curve to the left, decreasing oxygen release to the tissues.

-          Induce cerebral vasoconstriction reducing cerebral blood flow.

Note:hypocarbia with a normal pH is masking a metabolic acidosisthat may need to be evaluated and addressed.

Treatment

Management of hypocarbia is best accomplished by lowering the respiratory rate and/or tidal volume. If no specific issues can be identified, additional sedation or selection of a different medication (propofol, fentanyl or dexmedetomidine) may be necessary to minimize the patient’s respiratory drive.

References:

  1. Manual of perioperative Care in Adult Cardiac Surgery.  Robert M.Bojar
  2. Harrison’s manual of medicine.
  3. The Washington Manual of Medical Therapeutics

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