**3. Cardiovascular complications of hemodialysis**

Prevalence of cardiovascular diseases in dialysis patients increased as compared to the normal population. The most important reason of this increase is the increased number of incidences of diabetes mellitus (DM) and hypertension in this patient group. Cardiovascular diseases accounts for approximately 45% of the causes of mortality in dialysis patients (Shastri&Sarnak,2010). Besides the patient-related factors, the hemodialysis therapy itself brings about a number of cardiovascular complications.

### **3.1 Hypotension**

The frequency of intradialytic hypotension (IDH) in patients receiving hemodialysis therapy has been assessed in various studies. For example, in a study made by Andrulli et al on 123 hemodialysis patients, IDH was considered to prevail if there was a decrease of 30 mmHg or more in Systolic blood pressure (SBP) or if IDH appeared symptomatically and the prevalence of IDH in the group that has a tendency to hypotension was found to be 44% (Andrulli et al., 2002). In another study made by Emily S et al, IDH was found in 608 (24%) of 2559 dialysis

Acute Complications of Hemodialysis 267

the dialisate should be optimized (Maggiore et al., 1982; Maggiore Q et al., 2002). A bicarbonate-based dialysate may be preferred (Sopngano et al.,1988; Velez et al.,1984), a dialysate with high calcium content may be used if the patient's calcium situation allows it (Maynard et al.,1986) and a sodium profiling may be carried out in the relevant patients (Emili et al.,1999; Schreiber, 2001). Nevertheless, conflicting results were obtained in the meta-analyses made for sodium profile applications. Therefore, it is recommended that it should be carried out in a way to avoid sodium overloading in selected patients (Stiller et al.,2001). Ultrafiltration profiles and relative blood volume measurements may relieve

In patients with sudden symptomatic hypotension, the patient's hemodynamic stability should be achieved first. To do this, the UF is closed, the patient is brought to a trendelenburg position and then a bolus of iv fluid is administered. These fluids may be normal saline, hypertonic saline, albumin, mannitol or hydroxyethylstarch (HES) (Schreiber, 2001). They may be given one by one or in incremental profiles (Emili et al.,1999). Additional dialysis sessions should be considered in patients gaining kilos more than 3% of their weight and those who are susceptible to hypotension. However, most of the patients do not agree with extra sessions. Therefore, a medical treatment may be considered for the patients with increased hypotension episodes in spite of all these measures. The treatment agents that were evidenced to have positive effects in pharmacologic therapy are carnitine, sertraline and midodrine (Perazella, 2001). L-carnitine is a naturally available amino acid and assumes the duty of carrying longchain fatty acids to the mitochondria. It is either synthesized endogenously in the kidneys and liver or taken in by a diet. It may be insufficient in patients with chronic kidney failure. It was demonstrated in many studies that an iv administration of 20 mg/kg during each dialysis reduced the intradialytic hypotension (Perazella, 2001; Lynch et al.,2008). There are also studies showing that the use of sertraline, which is a reuptake inhibitor of the selective serotonin, in doses of 50 to 100 mg/day also reduced IDH (Perazella, 2001; Yalcin et al.,2003). Midodrine is an α1 agonist. Hypotension was shown to be reduced with its use 30 minutes before hemodialysis (the initial dose of 2.5 mg is increased to 30 mg by titration) in patients

Hypertension (HT) is the most frequently observed complication in chronic hemodialysis patients. Over 80% of the patients have HT histories and the blood pressures of two thirds of these are not under control. The target values of blood pressure in hemodialysis patients are not clear today. While K-DOQI recommends a pre-dialysis blood pressure target of 140/90 mmHg and post-dialysis blood pressure target of 130/180 mmHg, such recommendation is not based on strong evidence (Hemodialysis Adequacy 2006 Work Group,2006). As a result of many observational studies, it was shown that low blood pressure (BP) increased mortality; the lowest mortality was in those with a pre-dialysis blood pressure between 140-160/70-90 mmHg and the highest mortality was in those patients with > 180/100 mmHg (Agarwal,2005; Lacson &Lazarus, 2007; Peixoto & Santos,2010). An intradialytic increase of >10 mmHg BP was observed in 12 to 13% of hemodialysis patients (Inrig et al.2007, Inrig et al., 2009). In another study made by the same researchers, it was shown that intradialytic hypertension caused mortality in patients with a pre-dialysis hypotension (<120/80 mmHg) (Inrig et al., 2009). Most of them are hypertensions associated with high blood volume in the etiology of hemodialysis patients. Considering the prolonged patient survey among the hemodialysis

hemodialysis-related hypotension (Donauer et al.,2000; Andrulli et al.,2002).

with IDH (Perazella, 2001; Cruz et al.,1997).

**3.2 Hypertension** 

patients (Emili et al., 1999). Although the figures change in different studies, IDH is observed between 20 and 50% of the cases and continues to be an important problem (Cruz et al.,1997; Daugirdas, 2001). IDH is a significant clinical issue as it involves impairment in the quality of life, increased treatment costs and loss of time and effort on the part of the employees and leads to incidences of high mortality and morbidity such as cardiovascular, cerebrovascular and mesentery ischemia in the patients of the risk group (Emili et al., 1999; Daugirdas, 2001). There are two mechanisms suggested in the pathogenesis of IDH. First is failure to keep the plasma volume at an optimum level and the second is cardiovascular abnormalities. The first mechanism is related to excessive weight gain that requires low serum osmolarity and large volume ultrafiltration and the second to autonomic dysfunction, a shift of blood flow to the gastrointestinal area during eating, a decrease in vasoconstructive compounds and an increase in vasodilatatory compounds, vasodilatation associated with acetate-based dialysate, and impairment of compensatory response due to hypertrophy or ischemia (Emili et al., 1999). The causes of intradialytic hypotension are shown in the table 2. IDH may be accompanied by symptoms such as cramps, dizziness, nausea, vomiting, excessive fatigue and debility or it may show no symptoms at all (Perazella,2001). It becomes more symptomatic in the aged and women, and in the presence of a cardiac disease, autonomic neuropathy and DM (Perazella,2001, Davenport,2006). IDH-based extremity interactions may be seen in a chronic hypotensive patient when there is a drop in blood pressure < 30 mmHg and in a normotensive or hypertensive patient when the drop in blood pressure is > 30 mmHg (Schreiber, 2001).

#### **Factor associated with the patient**

 Excessive interdialytic weight gain (more than 3% of body weight) Myocardial infarction Left ventricular hypertrophy Diastolic dysfunction Aritmia Pericardial tamponade Autonomic neuropathy Taking antihipertensive or other medications that lower blood pressure before dialysis İnterdialitic food consumption **Factros associated with the hemodialysis**  High ultrafiltration rate Dialysis with acetate High dialysate temperature Electrolyte abnormalities **Factors associated with the doctor**  Incorrect calculation of dry body weight

Table 2. Intradialytic hypotension causes

#### **Prevention and treatment of intradialytic hypotension**

Educating the patient should be the first consideration in preventing IDH. The patient should be educated to restrict his/her salt consumption so that the interdialytic weight gain is limited to 3% of his/her weight, to avoid taking any antihypertensive drugs before dialysis, and to avoid eating during dialysis (Schreiber, 2001). If the patient has anemia, it should be corrected. The patient's dry weight should be reassessed and the temperature of

patients (Emili et al., 1999). Although the figures change in different studies, IDH is observed between 20 and 50% of the cases and continues to be an important problem (Cruz et al.,1997; Daugirdas, 2001). IDH is a significant clinical issue as it involves impairment in the quality of life, increased treatment costs and loss of time and effort on the part of the employees and leads to incidences of high mortality and morbidity such as cardiovascular, cerebrovascular and mesentery ischemia in the patients of the risk group (Emili et al., 1999; Daugirdas, 2001). There are two mechanisms suggested in the pathogenesis of IDH. First is failure to keep the plasma volume at an optimum level and the second is cardiovascular abnormalities. The first mechanism is related to excessive weight gain that requires low serum osmolarity and large volume ultrafiltration and the second to autonomic dysfunction, a shift of blood flow to the gastrointestinal area during eating, a decrease in vasoconstructive compounds and an increase in vasodilatatory compounds, vasodilatation associated with acetate-based dialysate, and impairment of compensatory response due to hypertrophy or ischemia (Emili et al., 1999). The causes of intradialytic hypotension are shown in the table 2. IDH may be accompanied by symptoms such as cramps, dizziness, nausea, vomiting, excessive fatigue and debility or it may show no symptoms at all (Perazella,2001). It becomes more symptomatic in the aged and women, and in the presence of a cardiac disease, autonomic neuropathy and DM (Perazella,2001, Davenport,2006). IDH-based extremity interactions may be seen in a chronic hypotensive patient when there is a drop in blood pressure < 30 mmHg and in a normotensive or hypertensive patient when the drop in blood pressure is > 30 mmHg (Schreiber, 2001).

Excessive interdialytic weight gain (more than 3% of body weight)

Taking antihipertensive or other medications that lower blood pressure before dialysis

Educating the patient should be the first consideration in preventing IDH. The patient should be educated to restrict his/her salt consumption so that the interdialytic weight gain is limited to 3% of his/her weight, to avoid taking any antihypertensive drugs before dialysis, and to avoid eating during dialysis (Schreiber, 2001). If the patient has anemia, it should be corrected. The patient's dry weight should be reassessed and the temperature of

**Factor associated with the patient** 

 Myocardial infarction Left ventricular hypertrophy Diastolic dysfunction

 Pericardial tamponade Autonomic neuropathy

 High ultrafiltration rate Dialysis with acetate High dialysate temperature Electrolyte abnormalities **Factors associated with the doctor** 

İnterdialitic food consumption **Factros associated with the hemodialysis** 

Incorrect calculation of dry body weight

**Prevention and treatment of intradialytic hypotension** 

Table 2. Intradialytic hypotension causes

Aritmia

the dialisate should be optimized (Maggiore et al., 1982; Maggiore Q et al., 2002). A bicarbonate-based dialysate may be preferred (Sopngano et al.,1988; Velez et al.,1984), a dialysate with high calcium content may be used if the patient's calcium situation allows it (Maynard et al.,1986) and a sodium profiling may be carried out in the relevant patients (Emili et al.,1999; Schreiber, 2001). Nevertheless, conflicting results were obtained in the meta-analyses made for sodium profile applications. Therefore, it is recommended that it should be carried out in a way to avoid sodium overloading in selected patients (Stiller et al.,2001). Ultrafiltration profiles and relative blood volume measurements may relieve hemodialysis-related hypotension (Donauer et al.,2000; Andrulli et al.,2002).

In patients with sudden symptomatic hypotension, the patient's hemodynamic stability should be achieved first. To do this, the UF is closed, the patient is brought to a trendelenburg position and then a bolus of iv fluid is administered. These fluids may be normal saline, hypertonic saline, albumin, mannitol or hydroxyethylstarch (HES) (Schreiber, 2001). They may be given one by one or in incremental profiles (Emili et al.,1999). Additional dialysis sessions should be considered in patients gaining kilos more than 3% of their weight and those who are susceptible to hypotension. However, most of the patients do not agree with extra sessions. Therefore, a medical treatment may be considered for the patients with increased hypotension episodes in spite of all these measures. The treatment agents that were evidenced to have positive effects in pharmacologic therapy are carnitine, sertraline and midodrine (Perazella, 2001). L-carnitine is a naturally available amino acid and assumes the duty of carrying longchain fatty acids to the mitochondria. It is either synthesized endogenously in the kidneys and liver or taken in by a diet. It may be insufficient in patients with chronic kidney failure. It was demonstrated in many studies that an iv administration of 20 mg/kg during each dialysis reduced the intradialytic hypotension (Perazella, 2001; Lynch et al.,2008). There are also studies showing that the use of sertraline, which is a reuptake inhibitor of the selective serotonin, in doses of 50 to 100 mg/day also reduced IDH (Perazella, 2001; Yalcin et al.,2003). Midodrine is an α1 agonist. Hypotension was shown to be reduced with its use 30 minutes before hemodialysis (the initial dose of 2.5 mg is increased to 30 mg by titration) in patients with IDH (Perazella, 2001; Cruz et al.,1997).

#### **3.2 Hypertension**

Hypertension (HT) is the most frequently observed complication in chronic hemodialysis patients. Over 80% of the patients have HT histories and the blood pressures of two thirds of these are not under control. The target values of blood pressure in hemodialysis patients are not clear today. While K-DOQI recommends a pre-dialysis blood pressure target of 140/90 mmHg and post-dialysis blood pressure target of 130/180 mmHg, such recommendation is not based on strong evidence (Hemodialysis Adequacy 2006 Work Group,2006). As a result of many observational studies, it was shown that low blood pressure (BP) increased mortality; the lowest mortality was in those with a pre-dialysis blood pressure between 140-160/70-90 mmHg and the highest mortality was in those patients with > 180/100 mmHg (Agarwal,2005; Lacson &Lazarus, 2007; Peixoto & Santos,2010). An intradialytic increase of >10 mmHg BP was observed in 12 to 13% of hemodialysis patients (Inrig et al.2007, Inrig et al., 2009). In another study made by the same researchers, it was shown that intradialytic hypertension caused mortality in patients with a pre-dialysis hypotension (<120/80 mmHg) (Inrig et al., 2009).

Most of them are hypertensions associated with high blood volume in the etiology of hemodialysis patients. Considering the prolonged patient survey among the hemodialysis

Acute Complications of Hemodialysis 269

dialysis. Calcium channel blockers are not dialyzable and can safely be used. In conclusion, RAS blockers may be used as the first line and alternative drugs such as combined alpha and beta blockers, calcium channel blockers and direct vazodilatators may be employed as the

Arrhythmias are complications that are frequently observed in patients attending to hemodialysis. They mostly occur during and after dialysis. Prevalence of arrhythmia varies between 17 to 76% (Buemi et al.,2009). Prevalence of arrhythmia was reported to be 5 to 75% in another study (Genovesi et al., 2008). ECG abnormalities were found in 65% of the patients in a study made by Abe S and associates (Abe et al.,1996). In a study made by Severi S et al, an increase in the heart rate was seen in 30% of the patients at the end of the hemodialysis (Severi et al.,2001). The differences in the figures of the studies are associated

Arrhythmia etiology of the hemodialysis patient group is multi-factorial. The dialysis therapy itself may lead to changes that can alter excitability of myocardium. Dialysis may be pro-arrhythmic as it changes the fluid composition in the body, the PH and the concentrations of heat and electrolytes. Patients with chronic kidney diseases who are undergoing a dialysis therapy are prone to arrhythmia since they usually have ischemic heart disease, left ventricle hypertrophy or autonomic neuropathy in high prevalence. Finally, the drugs used by some of the patients receiving anti-arrhythmic therapy may also be dialyzable. Such patients may, for this reason, be susceptible to arrhythmia during or after hemodialysis (Kimura et al.,1989; Weber et al., 1984). Prevalence of atrial fibrillation as one of the arrhythmia types was reported to be 27%, which is way above 0.5-1% seen in the general population (Genovesi et al.,2008). Another two types of arrhythmia, the complex ventricular arrhythmia and premature ventricular complexes, in particular increase the mortality and morbidity. Complex ventricular arrs (those defined as having a Lown score of

3 and more) prevail at a rate of 35% in the HD patient group (Burton et al.,2008).

NKF-DOQI recommends that due to the susceptibility of hemodialysis patients to arrhythmia, every dialysis patient should undergo a 12-lead ECG regardless of his/her age and if an arrhythmia is found, he/she should be treated as in the normal population. In case of an atrial fibrillation, B blockers, calcium channel blockers and amiodarone may be used for controlling the rate (K/DOQI Workgroup, 2005). While the indications of using anticoagulants in preventing a stroke in patients with atrial fibrillation in the general population are distinct, this issue is controversial in the hemodialysis population because this patient group is prone to bleeding (Sood et al., 2009). In the trial made by Quinn RR et al, the cost of using either acetylsalicylic acid or warfarin in hemodialysis patients with atrial fibrillation was compared and no difference was found between the two costs (Quinn et al., 2007). At present, an anticoagulant therapy can be applied in a similar way as in the normal population, but the susceptibility of patients to bleeding and the reactions with other medication they use should be borne in mind and the patients should be closely monitored (Abbott et al.,2007). Doses should be adjusted depending on whether or not the drugs used in treatment are dialyzable and have potential side-effects or some drugs should be avoided

second line in patients with heart failure (Inrig,2010; Hörl MP& Hörl WH,2004).

with patient characteristics and arrhythmia types.

altogether (K/DOQI Workgroup, 2005).

**3.3 Arrhythmias** 

**Treatment** 

population in the Tassin dialysis center and the absence of any hypertension, lack of hypertension can be thought of as a synonym of normovolemia and presence of hypertension as a synonym of hypervolemia (Kooman, 2009). The volume balance in hemodialysis patients are adjusted by daily sodium intake, amount of urine, and removal of excess fluid through ultrafiltration. An imbalance of these factors leads to hypertension and a poor cardiovascular outcome (Hörl et al., 2002). A study showed that a weight gain of more than 4.8% between two dialysis sessions increased mortality (Foley et al.,1998). The patients need to be brought back to their dry weights to treat a HT associated with excess volume. The dry weight is clinically determined by measuring the BP and considering the presence of any signs of excess volume and the patient's tolerance to ultrafltration (Sherman, 2002). However, it should be noted here that there could be excessive volume in patients without any signs of hypervolemia (Mitch&Wilcox, 1982). Therefore, besides physical examination, chest radiography, vena cava echography and bioimpedance techniques can be employed in assessing the volume status and the changes in blood volume during dialysis can be monitored by observing the level of natriuretic peptide and the changes in hematocrit and proteins (Koomanet al., 2009).

Besides excessive volume, the other causes of hypertension in hemodialysis patients include arterial stiffness associated with atherosclerosis, salt-related decline in NO formation, overactivation of the sympathetic nervous system, activation of the renninangiotensin-aldosterone system, presence of other vasoconstructive agents, inadequacy of vasodilatatory compounds, erythropoietin therapy and genetic tendency (Hemodialysis Adequacy 2006 Work Group,2006).

#### **Treatment**

It is being argued in recent years that home measurements or ambulatory blood pressure measurements may be more realistic in diagnosing hypertension (Peixoto & Santos,2010). As no definite target BP values are provided to hemodialysis patients, it is suggested that the prehemodialysis BP is kept between 130-160 mmHg / 80-100 mmHg (140/90 mmHg) until more objective data is published (Hemodialysis Adequacy 2006 Work Group,2006; Peixoto & Santos,2010). In hypertensive HD patients, the first consideration should be whether the patient is in his/her dry weight. If not, intake of Na chloride should be restricted to 5 gm, weight gain between two dialyses to 1 kg during the week and to 1.5-2 kg at weekends; sodium profiling and use of dialisate with high amounts of sodium should be avoided; and the patients should not be made to lose more than 1-2 kg in a week when bringing them to their dry weight (Hemodialysis Adequacy 2006 Work Group,2006). Additional dialysis sessions and prolongation of dialysis time may also be helpful to attain the dry weight (Culleton et al.,2007). Some patients persist to remain hypertensive even though they are brought to their dry weight. In such cases, antihypertensive therapies are required. The rennin-angiotensinaldosterone system (RAAS) blockers may be preferred as a first step. KDOQI recommends that they are to be preferred especially in patients with diabetics and/or heart failure (K/DOQI Workgroup, 2005). However, angiotensin converting enzyme inhibitors (ACE), which are RAAS blockers, are dialyzable with the exception of fosinopril. Therefore, a transition should be made to non-dialyzable fosinopril or angiotensin receptor blockers (ARB) in patients with intradialytic hypertension and patients taking RAS blockers should be monitored for any sideeffects. There is not adequate number of studies made on aldosterone antagonists or Alliskrein. Beta blockers may be preferred in patients with coronary arterial disease and heart failure. Since water-soluble B blockers are dialyzable, additional doses should be given after dialysis. Calcium channel blockers are not dialyzable and can safely be used. In conclusion, RAS blockers may be used as the first line and alternative drugs such as combined alpha and beta blockers, calcium channel blockers and direct vazodilatators may be employed as the second line in patients with heart failure (Inrig,2010; Hörl MP& Hörl WH,2004).

#### **3.3 Arrhythmias**

268 Technical Problems in Patients on Hemodialysis

population in the Tassin dialysis center and the absence of any hypertension, lack of hypertension can be thought of as a synonym of normovolemia and presence of hypertension as a synonym of hypervolemia (Kooman, 2009). The volume balance in hemodialysis patients are adjusted by daily sodium intake, amount of urine, and removal of excess fluid through ultrafiltration. An imbalance of these factors leads to hypertension and a poor cardiovascular outcome (Hörl et al., 2002). A study showed that a weight gain of more than 4.8% between two dialysis sessions increased mortality (Foley et al.,1998). The patients need to be brought back to their dry weights to treat a HT associated with excess volume. The dry weight is clinically determined by measuring the BP and considering the presence of any signs of excess volume and the patient's tolerance to ultrafltration (Sherman, 2002). However, it should be noted here that there could be excessive volume in patients without any signs of hypervolemia (Mitch&Wilcox, 1982). Therefore, besides physical examination, chest radiography, vena cava echography and bioimpedance techniques can be employed in assessing the volume status and the changes in blood volume during dialysis can be monitored by observing the level of natriuretic peptide and

Besides excessive volume, the other causes of hypertension in hemodialysis patients include arterial stiffness associated with atherosclerosis, salt-related decline in NO formation, overactivation of the sympathetic nervous system, activation of the renninangiotensin-aldosterone system, presence of other vasoconstructive agents, inadequacy of vasodilatatory compounds, erythropoietin therapy and genetic tendency (Hemodialysis

It is being argued in recent years that home measurements or ambulatory blood pressure measurements may be more realistic in diagnosing hypertension (Peixoto & Santos,2010). As no definite target BP values are provided to hemodialysis patients, it is suggested that the prehemodialysis BP is kept between 130-160 mmHg / 80-100 mmHg (140/90 mmHg) until more objective data is published (Hemodialysis Adequacy 2006 Work Group,2006; Peixoto & Santos,2010). In hypertensive HD patients, the first consideration should be whether the patient is in his/her dry weight. If not, intake of Na chloride should be restricted to 5 gm, weight gain between two dialyses to 1 kg during the week and to 1.5-2 kg at weekends; sodium profiling and use of dialisate with high amounts of sodium should be avoided; and the patients should not be made to lose more than 1-2 kg in a week when bringing them to their dry weight (Hemodialysis Adequacy 2006 Work Group,2006). Additional dialysis sessions and prolongation of dialysis time may also be helpful to attain the dry weight (Culleton et al.,2007). Some patients persist to remain hypertensive even though they are brought to their dry weight. In such cases, antihypertensive therapies are required. The rennin-angiotensinaldosterone system (RAAS) blockers may be preferred as a first step. KDOQI recommends that they are to be preferred especially in patients with diabetics and/or heart failure (K/DOQI Workgroup, 2005). However, angiotensin converting enzyme inhibitors (ACE), which are RAAS blockers, are dialyzable with the exception of fosinopril. Therefore, a transition should be made to non-dialyzable fosinopril or angiotensin receptor blockers (ARB) in patients with intradialytic hypertension and patients taking RAS blockers should be monitored for any sideeffects. There is not adequate number of studies made on aldosterone antagonists or Alliskrein. Beta blockers may be preferred in patients with coronary arterial disease and heart failure. Since water-soluble B blockers are dialyzable, additional doses should be given after

the changes in hematocrit and proteins (Koomanet al., 2009).

Adequacy 2006 Work Group,2006).

**Treatment** 

Arrhythmias are complications that are frequently observed in patients attending to hemodialysis. They mostly occur during and after dialysis. Prevalence of arrhythmia varies between 17 to 76% (Buemi et al.,2009). Prevalence of arrhythmia was reported to be 5 to 75% in another study (Genovesi et al., 2008). ECG abnormalities were found in 65% of the patients in a study made by Abe S and associates (Abe et al.,1996). In a study made by Severi S et al, an increase in the heart rate was seen in 30% of the patients at the end of the hemodialysis (Severi et al.,2001). The differences in the figures of the studies are associated with patient characteristics and arrhythmia types.

Arrhythmia etiology of the hemodialysis patient group is multi-factorial. The dialysis therapy itself may lead to changes that can alter excitability of myocardium. Dialysis may be pro-arrhythmic as it changes the fluid composition in the body, the PH and the concentrations of heat and electrolytes. Patients with chronic kidney diseases who are undergoing a dialysis therapy are prone to arrhythmia since they usually have ischemic heart disease, left ventricle hypertrophy or autonomic neuropathy in high prevalence. Finally, the drugs used by some of the patients receiving anti-arrhythmic therapy may also be dialyzable. Such patients may, for this reason, be susceptible to arrhythmia during or after hemodialysis (Kimura et al.,1989; Weber et al., 1984). Prevalence of atrial fibrillation as one of the arrhythmia types was reported to be 27%, which is way above 0.5-1% seen in the general population (Genovesi et al.,2008). Another two types of arrhythmia, the complex ventricular arrhythmia and premature ventricular complexes, in particular increase the mortality and morbidity. Complex ventricular arrs (those defined as having a Lown score of 3 and more) prevail at a rate of 35% in the HD patient group (Burton et al.,2008).

#### **Treatment**

NKF-DOQI recommends that due to the susceptibility of hemodialysis patients to arrhythmia, every dialysis patient should undergo a 12-lead ECG regardless of his/her age and if an arrhythmia is found, he/she should be treated as in the normal population. In case of an atrial fibrillation, B blockers, calcium channel blockers and amiodarone may be used for controlling the rate (K/DOQI Workgroup, 2005). While the indications of using anticoagulants in preventing a stroke in patients with atrial fibrillation in the general population are distinct, this issue is controversial in the hemodialysis population because this patient group is prone to bleeding (Sood et al., 2009). In the trial made by Quinn RR et al, the cost of using either acetylsalicylic acid or warfarin in hemodialysis patients with atrial fibrillation was compared and no difference was found between the two costs (Quinn et al., 2007). At present, an anticoagulant therapy can be applied in a similar way as in the normal population, but the susceptibility of patients to bleeding and the reactions with other medication they use should be borne in mind and the patients should be closely monitored (Abbott et al.,2007). Doses should be adjusted depending on whether or not the drugs used in treatment are dialyzable and have potential side-effects or some drugs should be avoided altogether (K/DOQI Workgroup, 2005).

Acute Complications of Hemodialysis 271

Acute MI is diagnosed in the normal population at the presence of a high cardiac enzyme level, classical chest pain and ECG changes. However, there are some differences in MI presentation and laboratory findings of hemodialysis patient group. This situation causes a delay in diagnosing MI in this group and thus a less frequent use of the thrombolytic and early coronary angiography/coronary stent applications for treatment of MI as compared to

For example, MI-associated classical chest pain is seen less in patients with renal failure in correlation with the intensity of such renal failure. The cause of this is thought to be the impairment of sensory and autonomic nerve functions seen in patients with renal failure. It was demonstrated in a study made by Komukai et al that as the renal function disorders increased, the prevalence of painless MI also increased (Komukai et al., 2007). In another study conducted by Pitsavos C et al, it was shown that MI patients with renal failure admitted to the hospital late and the possible reason for such late admission was thought to be the less occurence of alerting symptoms such as chest pain in this patient group (Pitsavos et al., 2007). Late admissions certainly mean that coronary interventions are less and mortality is more. Cardiac troponin T (cTnT) and creatine kinase-MB, which are two of the enzymes used in the verification of a myocardial infarction diagnosis, were seen in high levels in the hemodialysis patient group without the presence of coronary ischemia. cTnT in particular was shown to be as high as 17 to 23.8% in this patient group (Chew, 2008). This situation leads to controversies in diagnosing MI in the hemodialysis patient group. Researches are still in progress to find an ideal marker that supports an MI diagnosis. For the time being, it is advisable to monitor the

Another point to take into consideration is that 15 to 40% of the patients are seen to have ST depression during hemodialysis (Abe et al., 1996; Conlon et al., 1998). Dialysis therapy itself may cause subclinical myocardial ischemia in this patient group which is prone to

There is not sufficient data about the reliability of conducting a dialysis within 48 hours after a myocardial infarction (MI). In such a case, the volume status of the patient should be assessed together with its biochemical parameters and the hemodialysis therapy should be adjusted in a way to avoid hypotension (Coritsidis et al., 2009). The treatment of acute MI is recommended to be the same as in the normal population (K/DOQI Workgroup, 2005).

Neurologic complications may develop in the patients of end-stage renal failure due to a multiple metabolic disorder caused by a chronic kidney disease and due to the dialysis procedure. These complications may appear in the form of variations in consciousness, headache, nausea, vomiting, myoclonus, tremor, focal and generalized seizures,

Dialysis Disequilibrium syndrome (DDS) was first defined by Kennedy AC (Kennedy ,1970, Chen et al.,2007). Although the pathogenesis of DDS is controversial, the first theory blamed in etiology is the fast urea removal theory. According to this theory, the fast removal of urea from plasma in patients who newly started a hemodialysis therapy creates an osmotic gradient between the brain cells and plasma and the fluid enters the brain cells due to this osmotic gradient (Kennedy,1970; Attur et al.,2008; Chen et al.,2007; Trinh-Trang-Tanet

cardiac enzyme levels in patients clinically suspected of having an MI.

atherosclerosis and left ventricular hypertrophy (Selby& McIntyre, 2007).

cerebrovascular events (infarct and bleeding) and disequilibrium syndrome.

the normal population.

**4. Neurologic complications** 

**4.1 Disequilibrium syndrome** 
