THE APPROACH TO COMPLICATIONS DURING HEMODIALYSIS

Hazel Daphne Nialga Philippine Society of Nephrology National Kidney and Transplant Institute July 15 , 2011
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ACUTE COMPLICATIONS DURING HEMODIALYSIS

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Acute complications during hemodialysis

Common complications
INTRODUCTION Acute complications commonly occur during routine hemodialysis treatments. They include the following: 1. Hypotension 25 to 55 percent of treatments 2. Cramps 5 to 20 percent 3. Nausea and vomiting 5 to 15 percent 4. Headache 5 percent 5. Chest pain 2 to 5 percent 6. Back pain 2 to 5 percent 7. Itching 5 percent 8. Fever and chills Less than 1 percent
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HYPOTENSION
The incidence of a symptomatic hypotension during (or immediately following) dialysis ranges from 15 to 50 percent of dialysis sessions

There are two clinical patterns of dialysis-associated hypotension: 1. Episodic hypotension, which occurs during the latter stages of dialysis and associated with vomiting, muscle cramps, and other vagal symptoms (such as yawning). 2. Chronic persistent hypotension, which may occur in longterm patients in whom predialysis systolic blood pressures of less than 100 mmHg ,are frequently observed.
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ETIOLOGY
Common causes

A. Volume related (excessive or rapid decreases in blood volume) 1. A rapid reduction in plasma osmolality, which causes extracellular water to move into the cells.

2. Large weight gain 3. Rapid fluid removal in an attempt to attain "dry weight (Short dialysis ) 4. Inaccurate determination of true "dry weight" . 5. Use of a lower sodium concentration in the dialysate.
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Water movement during standard hemodialysis

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B. Inadequate vasoconstriction:
1. 2. a. b. 3. 4. 5. 6.
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High dialysis solution temprature (> 36c) Autonomic neuropathy (50 percent of patients on HD) Defect in the baroreceptor/afferent side Downregulation of alpha-adrenergic receptors Use of acetate rather than bicarbonate as a dialysate buffer. Intake of antihypertensive medications that can impair cardiovascular stability. Sudden release of adenosine during organ ischemia. [eg. Anemia (HCT< 20 - 25%)]. Ingestion of a meal immediately before or during dialysis
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Therapeutic implications
a. Lower dialysis solution temperature b. Avoid intradialytic food ingestion in hypotension-prone patients c. Minimize tissue ischemia during dialysis d. Midodrine in refractory cases: A dose of 10 mg orally one-half to 2 hours before a dialysis session is typical Active cardiac ischemia is a contraindication
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e. Consider a trial of sertraline 50- 100mg/day 4 to 6 weeks of therapy with the selective serotonin reuptake inhibitor sertraline reduces the frequency of intradialytic hypotension. The drug improves autonomic function

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C. Cardiac factors:
1. Diastolic dysfunction (stiff concentric hypertrophy heart) the effects of hypertension
coronary artery disease uremia itself

2. Impairment of cardiac compensatory mechanisms (Heart rate and contractility) Arrhythmia (atrial fibrilation), which are volumeunresponsive causes of hypotension. Ischemia
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Therapeutic implications:
1. A dialysis solution calcium concentration of 1.75 mM (3.5 mEq/l) 2. Dialysis solution magnesium levels (a higher or a lower level should be used is controversial ).

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Uncommon causes:
I. Pericardial tamponade , that is volume-unresponsive cause of hypotension. II. Myocardial infarction III. Valvular disorders IV. Occult hemorrhage V. Hemolysis VI. Septicemia VII. Dialyzer reaction, which may cause wheezing and dyspnea as well as hypotension VIII.Air embolism
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DIAGNOSIS
Most Patients with hypotension complaint of feeling dizzy, lightheadedness, nausea, vomiting, and dyspnea. Some patients suffer muscle cramps, lack of alertness, darkening of vision. In some patients, there are no symptoms until the BP falls to very low and dangerous level. For this reason, BP must be monitored on a regular basis throughout HD session.

TREATMENT

The acute management of low blood pressure associated with hemodialysis: I. Ultrafiltration should either be stopped or the rate decreased. II. The patient should be placed in the Trendelenburg position.
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Trendelenburg position

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III. The blood flow rate should be reduced, if hypotension is severe or the patient is not responding to other treatment measures. IV. Intravascular volume may be replaced with mannitol or saline [currently used an intravenous bolus of saline (100 ml or more) as first-line therapy for hypotension]. The prompt recognition of life-threatening causes of low blood pressure is essential. Particular concerns should include occult sepsis, previously unrecognized cardiac and/or pericardial disease, and gastrointestinal bleeding.
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Patients with chronic, debilitating hemodialysis hypotension due to the inability to adequately respond to rapid changes in blood volume may be more likely to tolerate the gradual volume changes associated with peritoneal dialysis.
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PREVENTION
Accurate setting of the "dry weight: At present, the determination of dry weight is largely determined empirically by trial and error. The dry weight is set at the weight below which unacceptable symptoms, such as cramping, nausea, and vomiting, or hypotension occur.
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Other modalities to more objectively estimate dry weight : I. Plasma atrial natriuretic peptide (ANP)levels II. A noninvasive assessment of conductivity is an accurate estimate of the extracellular volume and can detect underhydration after dialysis (bioimpedance measurements). III. Ultrasound assessment of the inferior vena cava Steady, constant ultrafiltration Newer dialysis machines remove volume steadily and evenly over the course of the dialysis session
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Avoid large interdialytic weight gain (IDWG) or short treatment
To avoid for rapid UF rate 1. patients should be limit IDWG to <1 kg per day,( by limiting of salt intake). 2.An increase in treatment time is also an effective way of decreasing UF rate and frequency IDH.
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Increased dialysate sodium concentration and sodium modeling
The following three sodium dialysate concentration strategies: I. A constant sodium concentration of 140 meq/L II.Sodium modeling: a) Linear sodium ramping (155 to 140 meq/L) b) Stepwise sodium ramping (155 meq/L for three hours and 140 meq/L for one hour)
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The use of a higher dialysate sodium concentration (140 meq/L) has been among the most efficacious and best tolerated therapies for episodic hypotension limitations of dialysate sodium modeling: The lack of correlation between blood volume degree and onset of hypotension Significant individual and interdialysis variations in sodium levels Thirst and weight gain with postdialysis hypertension
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I.
II. III.
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Acute complications during hemodialysis

Combination sodium modeling and ultrafiltration

Ultrafiltration profiling is characterized by the ultrafiltration rate being intermittently stopped or decreased gradually, thereby resulting in plasma refilling. The combination of ultrafiltration and sodium profiling can further enhance plasma refilling; in turn, this can result in greater stability during hemodialysis.
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Acute complications during hemodialysis

Sequential ultrafiltration and isovolemic dialysis

A similar goal of maintenance of the plasma osmolality can be attained by initial ultrafiltration alone (without dialysis) followed by isovolemic dialysis in which little or no further fluid removal occurs due to reduced transmembrane pressures. A large volume of fluid to be removed without inducing hemodynamic instability.
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Acute complications during hemodialysis

Water movement during isolated ultrafiltration

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Bicarbonate dialysate buffer
Bicarbonate is now widely available and adaptable to all new dialysis machines. The blood pressure is generally better maintained with bicarbonate. Acetate accumulation in the blood has vasodilator activity that can promote the development of hypotension.
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Temperature control The use of low dialysate temperature can improve hemodynamic stability by improving cardiovascular contractility and increasing venous tone.

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Improvement in cardiovascular performance
The frequency of dialysis-associated hemodynamic instability is greatly increased in patients with a prior history of congestive heart failure, cardiomegaly, or ischemic heart disease. Cardiovascular performance can be enhanced in many dialysis patients in the following ways: I. Increasing the dialysate calcium concentration. II. Using cool temperature hemodialysis, which can also increase vascular resistance. III. Correction of anemia with erythropoietin.
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Midodrine Among patients with autonomic neuropathy and perhaps others with severe hemodialysis hypotension not responsive to the above measures, the selective alpha-1 adrenergic agonist midodrine may be effective and well tolerated
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Carnitine Carnitine supplementation has reduced the incidence of hypotensive episodes and muscle cramps. Avoidance of food Food ingestion during dialysis leads to a significant decline in systemic vascular resistance that can contribute to a fall in blood pressure.
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Adenosine release Adenosine is an endogenous vasodilator that has been related to hypotensive episodes in a subset of patients on hemodialysis. This response can be blunted in some patients by the administration of caffeine, which may act as an adenosine receptor antagonist in this setting.
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Vasopressin infusion It has been observed that vasopressin release is not increased in hemodialysis patients undergoing volume removal. Constant infusion of a non-pressor dose of vasopressin has been significantly associated with a decreased incidence of symptomatic hypotensive episodes and increased fluid removal.
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Comparative efficacy In general, the best tolerated and most effective strategy is sodium modeling. High sodium and cool temperature dialysis were also effective.

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Muscle cramps
Etiology:
The pathogenesis of muscle cramps during dialysis is unknown.

Changes in plasma osmolality and/or extracellular fluid volume have been implicated The four most important predisposing factors are :
I. II. III. IV.
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Hypotension Hypovolemia (patient below dry weight) High UF rate (large weight gain) Use of low-sodium dialysis solution (Hyponatremia)
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Muscle cramps most commonly occur in association with hypotension. Cramping is also more common during the first month of dialysis than in subsequent periods. Pathophysiology These factors all tend to favor vasoconstriction resulting in muscle hypoperfusion leading to secondary impairment of muscle relaxation.
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Hypomagnesemia and hypocalcemia may cause treatment-resistant muscle cramping during dialysis. Predialysis hypokalemia will be exacerbated by the usual level of dialysis solution potassium (2mM) and may precipitate cramping as well.
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Other factors that related with hemodialysisassociated cramps: Carnitine deficiency Elevated serum leptin levels Low PTH values and high serum creatine phosphokinase concentrations The origin of a cramp is neural, not muscular.
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 CLINICAL FEATURES Most commonly involve the muscles of the lower extremity Cramps occur more often in older, nondiabetic, anxious patients.

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 1. 2. 3. 4.

Acute complications during hemodialysis Management

Concomitantly Hypotension & muscle cramps Treatment with 0.9% saline Ultrafiltration be stopped or the rate decreased Trendelenburg position Blood flow rate should be reduced Hypertonic solutions ( saline, glucose 50%, mannitol 12.5 to 37.5 g/dialysis). Forced stretching of the muscle involved (eg. Ankle flexion for calf cramping). Nifedipine(10 mg) Massage moist heat
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 Prevention

Acute complications during hemodialysis

I. Prevention of hypotensive episodes II. Raisening of dialysate-sodium levels to just below the threshold for induction of postdialysis thirst. III.Avoiding low predialysis levels of mg2+, Ca2+, K+. IV.Quinine sulfate . Quinine sulfate before dialysis 250-325 mg (Not FDA approved). V. Carnitine supplementation in dialysis patients. VI.Vitamin E(400 IU) VII.Oxazepam ( 5-10 mg, given 2 hrs prior to dialysis). VIII.Prazosin. IX.Stretching exercises of affected muscle groups. X. Nifedipine, phenytoin, creatine monohydrate, carbamazepine, amitriptyline, and gabapentin.
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HEADACHE, NAUSEA, AND VOMITING
Longer treatment times combined with large degree of urea removal and/or ultrafiltration significantly enhance the incidence of headache, nausea, and vomiting during dialysis. A variant of the dialysis disequilibrium syndrome may underlie these symptoms in many patients. Dialysis disequilibrium is thought to be due to water movement into the brain as a result of a reverse osmotic shift induced by urea removal.
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HEADACHE: 1. Etiology largely unknown. A subtle manifestation of the disequilibrium syndrome Caffeine withdrawal (coffee drinkers) Metabolic disturbances (eg, hypoglycemia, hypernatremia, hyponatremia), uremia, subdural hematoma, and medication-induced headaches should be considered in patients with recurrent dialysis-associated headaches. Magnesium deficiency psychological factors
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2. Prevention:
1. In this setting, initially altering the dialysis prescription in favor of less intensive and more frequent treatments may avoid these complications. 2. Decreasing dialysis solution sodium 3. A cup of strong coffee 4. A cautious trial of magnesium supplementation
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3. Management
Acetaminophen A cup of strong coffee

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1. 2. 3. 4. 5. 6. 7. 8.
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Nausea or vomiting occurs in up to 10% of routine dialysis treatment.

The causes of nausea and vomiting:

Hypotension(most episodes) Dialysis Disequilibrium Syndrome(DDS) type A and type B varieties of dialyzer reactions Exacerbated Gastroparesis Contaminated or incorrectly formulated dialysis solution(high sodium, calcium). Upper respiratory infection Narcotic usage Hypercalcemia
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Management:
1. To treat hypotension
2. Persistent nausea and vomiting unrelated to hemodynamics may benefit from metoclopramide.

Prevention:
1. Avoidance of hypotension during dialysis. 2.single predialysis metoclopramide(5-10mg).

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CHEST PAIN
Often associated with some back pain, occurs in 1%-4% of dialysis treatments
Chest pain that occurs while a patient is being dialyzed may be associated with: I. Hypotension II. Dialysis disequilibrium syndrome III. Angina IV. Hemolysis V. Pericarditis VI. Air embolism (rarely) VII.pulmonary embolism (extremely uncommon )
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I. Angina Angina should always be considered as the underlying cause of chest discomfort in the patient undergoing dialysis. If clinically indicated, ECG and cardiac enzyme evaluation should therefore be performed. If dialysis is continued, the administration of oxygen and aspirin , reduction of the desired ultrafiltration, and/or blood pump speed and administration of nitrates or morphine should be considered on an individual basis.
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II. Hemolysis Hemolysis may present as chest pain, chest tightness, or back pain. If hemolysis is not recognized early, severe hyperkalemia may ensue and lead to death. These findings highly suggestive of substantial hemolysis include:
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These findings highly suggestive of substantial hemolysis include:
A. B. C. D. A port wine appearance of the blood in the venous line. Complaints of chest pain, shortness of breath, and/ or back pain A falling hematocrit A pink color of the plasma in centrifuged specimens.
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The etiology of hemolysis in hemodialysis patients includs: A.Problems with the dialysis solution: I. Overheating II.Hypotonicity III.Contamination with formaldehyde, bleach(Sodium hypochlorite) , chloramine, or nitrates from the water supply, and copper from copper tubing or piping.
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B. Red blood cell trauma due to: I. Improperly functioning roller clamps on dialysis machines II. Kinking of the blood lines III. Poorly constructed blood tubing

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Treatment:
I. To stop dialysis immediately II.Clamp the blood lines (do not return the blood to avoid increasing the risk of hyperkalemia) III.Prepare to treat hyperkalemia and the potentially severe anemia IV.Hospitalization for observation ( for lifethreatening hyperkalemia
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III. Air embolism

It can lead to death unless quickly detected and treated Air embolism is rare in hemodialysis patients, in part because of the presence of air detectors in hemodialysis machines. Diagnosis: Foam in the venous blood line should make one suspect that air is entering the dialysis system.
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Acute complications during hemodialysis

Disconnection of connecting caps and/or blood lines can also lead to air embolism in patients being dialyzed with central venous catheters. In the seated patient, air tends to migrate into the cerebral venous system without entering the heart, as a result, this patient may lose consciousness and seizure. The recumbent patient may initially develop dyspnea, cough, and perhaps chest tightness.
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Acute complications during hemodialysis Treatment: I. Clamping the venous line II. Stopping the blood pump III. The patient should be positioned on the left side in a supine position with the chest and head tilted downward.
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Itching
Itching appearing only during the treatment, especially if accompanied by other minor allergic symptoms, may be a manifestation of low-grade hypersensitivity to dialyzer or blood circuit component.

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Standard symptomatic treatment using antihistamines is useful.

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Fever and chills

The causes of fever and chills during HD including:

I.

Bacteremia:
Bacteremia related to the access site infection (venous access, AV fistulas and grafts). Bacteremia may result from contamination of hemodilysis machines ( inadequate disinfection of water treatment , distribution systems or reprocessed dialyzers).

II.

Pyrogen reaction:
Low-grade fever during hemodialysis may be related to pyrogens present in the dialysis solution rather to actual infection.
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a)
b)

Charecteristics of fever:
Patients are afebrile prior to dialysis but become febrile during dialysis. Fever resolves spontaneously after cessation of dialysis. There is one exception to the rule : fever and chills that occur shortly after catheter manipulation (eg, commencement or cessation of dialysis) suggests catheter associated bacteremia. Blood cultures shoulds always be obtained in any febrile HD patients.
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c)

Acute complications during hemodialysis

I. II. III. IV. V. VI. VII. VIII.
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Less common but serious complications

These include:
Disequilibrium syndrome Hypersensitivity reactions Arrhythmia Cardiac tamponade Intracranial bleeding Seizures Hemolysis Air embolism
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A.

Dialysis disequilibrium syndrome

INTRODUCTION The dialysis disequilibrium syndrome (DDS) is a central nervous system disorder described in dialysis patients. It is characterized by neurologic symptoms of varying severity that are thought to be due primarily to cerebral edema.
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New patients just being started on hemodialysis are at greatest risk, particularly if the BUN is markedly elevated (above 175 mg/dL or 60 mmol/L).

B.
1. 2.

PATHOGENESIS
The cause of the disequilibrium syndrome is controversial The symptoms of DDS are caused by water movement into the brain, leading to cerebral edema. Two theories have been proposed to explain why this occurs: A reverse osmotic shift induced by rapidly urea removal (the plasma becomes hypotonic with respect to the brain cells). Acute changes in the PH of the cerebrospinal fluid and a fall in cerebral intracellular pH.
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I.

Reverse osmotic shift

The reduction in BUN lowers the plasma osmolality, thereby creating a transient osmotic gradient that promotes water movement into the cells. In the brain, this water shift produces cerebral edema and a variable degree of acute neurologic dysfunction. Urea is generally considered an "ineffective" osmole, but there is insufficient time for urea equilibration when hemodialysis rapidly reduces the BUN; as a result, urea transiently acts as an effective osmole, promoting water movement into the brain.
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II. Intracerebral acidosis and idiogenic osmoles Some investigators have proposed that a decrease in cerebral intracellular pH, occurring via an uncertain mechanism, is of primary importance . Both displacement of bound sodium and potassium by the excess hydrogen ions and enhanced production of organic acids can increase intracellular osmolality and promote water movement into the brain
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C. CLINICAL MANIFESTATIONS The classic DDS refers to acute symptoms developing during or immediately after hemodialysis. Mild disequilibrium: Early findings include headache, nausea, disorientation, restlessness, blurred vision, and asterixis. Severe disequilibrium: More severely affected patients progress to confusion, seizures, coma, and even death.
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It is now recognized, however, that many milder signs and symptoms associated with dialysis such as muscle cramps, anorexia, and dizziness developing near the end of a dialysis treatment are also part of this syndrome
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D. DIAGNOSIS AND DIFFERENTIAL DIAGNOSIS The development of the above symptoms during dialysis is strongly suggestive of DDS. Differential diagnosis of DDS include: 1. uremia itself 2. subdural hematoma 3. cerebral infarction 4. intracerebral hemorrhage 5. Meningitis 6. metabolic disturbances (hyponatremia, hypoglycemia) 7. drug-induced encephalopathy
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E. PREVENTION

The initial dialyses should be gentle, but repeated frequently. The aim is a gradual reduction in BUN, which will be protective but may not prevent mild symptoms such as headache and malaise.
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I 1. 2. Slow urea removal methods Initial heamodialysis prescription, arranged with: Cession time of two hours. Relatively low blood flow rate (150 to 250 mL/min) A small surface area dialyzer (0.9 to 1.2 m2) Concurrent rather than countercurrent blood and dialysate flow.

3. 4.
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1. This regimen is repeated daily for three or four days. 2. If the patient shows no signs of DDS, then: a) The blood flow rate can be increased by 50 mL/min per treatment (up to 300 to 400 mL/min) b) The duration of dialysis can be increased in 30 minute increments (up to four or more hours, as necessary for adequate solute removal).
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II. Patients who also have marked fluid overload can be treated with ultrafiltration (which removes less urea per unit time) followed by a short period of hemodialysis. III. The patient can be started on peritoneal dialysis in which the low rate of peritoneal blood flow results in a urea clearance per unit time that is much lower than that with hemodialysis.
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IV. Some physicians recommend: 1. Prophylactic phenytoin (1000 mg loading dose followed by 300 mg/day until uremia is controlled) 2. The administration of 12.5 g of hypertonic mannitol intravenously every hour of dialysis in high-risk patients with marked azotemia (BUN above 150 to 200 mg/dL [54 to 71 mmol/L]) or an underlying alteration in mental status.
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F. Management
1. Mild disequilibrium The management of mild nonspecific disequilibrium symptoms, such as nausea, vomiting, restlessness, and/or headache, is symptomatic In the acutely uremic patient with such symptoms who is undergoing dialysis, the blood flow rate should be slowed and consideration should be given to stopping the dialysis session earlier than planned.
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2. Severe disequilibrium Dialysis is stopped in the patient with seizures, coma, and/or obtundation. Patency of the airway should also be ensured The differential diagnosis of severe DDS should be considered. Severe DDS with seizures can be reversed more rapidly by raising the plasma osmolality with either 5 mL of 23 percent saline or 12.5 g of hypertonic mannitol.
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Management is supportive in the patient with severe DDS and coma, that including: a) The airway should be controlled. b) The patient ventilated if necessary. c) Intravenous mannitol may be of benefit. In this setting, improvement should occur within 24 hours .
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I. II. III. IV. 76

ARRHYTHMIAS
Ventricular arrhythmias are common during dialysis and between treatments. Supraventricular arrhythmias are also common. Risk factors for arrhythmias and sudden death in dialysis patients include: coronary artery disease advanced age myocardial dysfunction left ventricular hypertrophy 22/21/

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I. II. During hemodialysis, the incidence of arrhythmias may be enhanced because of: Rapid fluctuations in hemodynamics and electrolyte concentrations The induction of hypoxemia in patients with a high incidence of myocardial disease The treatment of arrhythmias, is similar to their treatment in the nondialysis patient.
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THE END
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