I Hate Dialysis Message Board
Dialysis Discussion => Dialysis: General Discussion => Topic started by: Hemodoc on April 07, 2011, 01:07:03 PM
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By Peter Laird, MD
One of the greatest challenges to improving outcomes in hemodialysis patients is reducing the incidence of sudden cardiac death. In fact, more hemodialysis patients die as the result of sudden cardiac death from arrhythmia's than they do from actual myocardial infarctions (heart attacks). Hemodialysis patients also present with different symptoms during a myocardial infarction than those without renal disease and dialysis therapy with less complaints of chest pain and higher risk of cardiac arrest while hospitalized. Yet, the underlying pathophysiology of this observed increased risk of sudden cardiac death remains largely unstudied to date.
In addition to sudden cardiac death, many dialysis patients are at high risk of intradialytic hypotension (IHD) during hemodialysis itself. Elevated ultrafiltration rates higher than 10 ml/h/kg significantly increase the risk of IHD as well as congestive heart failure in the long run. Myocardial ischemia during hemodialysis leads to long standing myocardial stunning and hybernation, all of which predispose patients to increased frequency of hemodynamically significant episodes of IHD, especially in those patients with known congestive heart failure and myocardial fibrosis with left ventricular enlargement (LVH). Any studies evaluating the hemodynamic effects of differing dialysis modalities should include baseline characteristics and intradialytic cardiovascular parameters to ensure the safety of the intervention. In addition, these types of studies should not include any patients at high risk for poor cardiovascular outcomes.
The study in question evaluated differing potassium levels on hemodialysis patients by testing blood pressure responses and peripheral vascular resistance in three separate dialysis solutions, one point below, one point above and normal potassium dialysate levels. However, the authors did not monitor for myocardial ischemia during the different sessions, nor did they exclude those elderly patients with known risks of sudden cardiac death from underlying LVH.
Haemodynamic consequences of changing potassium concentrations in haemodialysis fluids
Results. Comparing K-1 and K+1, differences were found within the tertiles regarding systolic (+5.3, +6.6, +2.3 mmHg, p<0.05, <0.05, ns) and mean blood pressure (+4.3, +6.4, -0.5 mmHg, p<0.01, <0.01, ns), as well as peripheral resistance (+212, +253, -4 dyne.sec.cm-5, p<0.05, <0.05, ns). The stroke volume showed a non-statistically-significant inverse trend (-3.1, -5.2, -0.2 ml). 18 hypotension episodes were recorded during the course of the study. 72% with K-1, 11% with K and 17% with K+1 (p<0.01 for comparison K-1 vs. K and K-1 vs. K+1).
Conclusions. A rapid decrease in the concentration of serum potassium during the initial stage of the dialysis obtained by reducing the concentration of potassium in the dialysate translated into a decrease of systolic and mean blood pressure mediated by a decrease in peripheral resistance. The risk of intra-dialysis hypotension inversely correlates to the potassium concentration in the dialysate.
Unfortunately, despite the well documented occurrence risk of low potassium, none of these high risk elderly patients with a high prevalence of known ischemic cardiomyopathy had any cardiac monitoring for ST depression during dialysis, nor did they follow these patients for hypoxia which low potassium baths are likewise documented causing. In addition, myocardial ischemia and myocardial stunning are likewise induced by low potassium dialysate levels yet the authors once again did not measure these parameters as well. In such, this elderly group of patients with known ischemic cardiomyopathy in my opinion were placed at great risk by this experimental protocol which I am sure would be approved in and United States university setting.
Lastly, because the experimental parameters measured were of the most fundamental and in essence primitive clinical sophistication, the conclusions of this experiment on causation of the results observed are essentially nonexistent since many different clinical scenarios can account for the observed results. The authors so noted in their discussion some of these short fallings on their data:
However, if we take into account the experimental data obtained from animals besides the typical metabolic circumstances of kidney failure that requires dialysis, it is surprising to observe the haemodynamic pattern that is traced and which, contrary to expectations, shows a hypertensive effect for acute decrease in serum potassium. In fact, the experimental hypokalaemia model demonstrates a vasoconstriction and an increase in myocardial contractility [11-13]. The difference between the theoretical and the observed pattern could be due to the method employed to evaluate peripheral resistance (indirect, non-invasive measurements using beat-to-beat in our case) and the metabolic circumstances of dialysis with sharp variations in other factors that together can modify haemodynamics (calcaemia, osmolarity, acid-base balance, temperature), as well as concomitant counterregulatory phenomena, particularly the sympathetic and renin- angiotensin systems. The fact that hypokalaemia sensitizes myocardium to hypoxic related dysfunction [26] together with the selection for the study of an elderly population (mean age 70.3 years) with a high incidence of ischemic cardiomyopathy (10 out of 24 subjects) could have influenced the incidence of intra-dialytic hypotensions and the results. Moreover two other reasons could potentially explain a blood pressure reduction related to acute potassium decrease in the dialysis population: hypokalaemia may exacerbate autonomic dysfunction while intra-dialytic potassium loss accounts for a decrease in total osmoles [7].
Regardless of the pathophysiological explanations of the haemodynamic consequences, the results are potentially relevant in that (i) dialysate potassium concentration could theoretically be modulable in a profile, as proposed for other electrolytes like sodium and bicarbonate and (ii) more attention could be paid to controlling the potassium balance with alternative measures (diet, chelating agents, avoidance of medications which inhibits the renin-angiotensin system if unnecessary [27] and possibly prescription of mineralocorticoids [28]).
Thus, the authors in this ill advised and poorly executed study advance proposed clinical solutions to the resultant observations even though they have not elucidated the underlying pathophysiology of the data observed. The ethical prohibition against experimentation that places patients at risk were not applied to this study with elderly patients, nearly half of which with known ischemic cardiomyopathy, no documented electrocardiographic monitory and oxygen saturation accompanied the simply blood pressure results. Nor did the authors evaluate any of these patients for regional wall motion abnormalities during the differing potassium levels. A simple measure of cardiac enzymes could have substituted for the more expensive cardiac imaging. In addition, the authors did not comment on the measured levels of potassium in the patients. It is already known that giving a 3 K bath to dialysis patients with a potassium level higher than 5.6 is dangerous with 17% of the hypotensive episodes noted in the high potassium groups:
Prevention of Sudden Cardiac Death in Dialysis Patients: A Nephrologist's Perspective
Notably, the inappropriate use of a high-potassium dialysate (Greater than or equal to 3 mEq/L) in patients with a serum potassium greater than 5.6 mEq/L was associated with an increased risk of death.24
I am thus confounded by the lack of effective safety measures utilized, the known high risk interventions in high risk patients with ischemic cardiomyopathy, the lack of defined pathophysiologic etiology of the data observed by virtue of only basic hemodynamic monitoring of the peripheral blood pressure alone all draw attention to how poorly designed study that truly is that adds little to the discussion of intradialytic hypotension in dialysis patients due to variable potassium levels.
Unfortunately, hemodialysis patients benefit little from all of the experiments performed to date even when marked benefits are discovered, the American nephrology community in general chooses to simply ignore those findings such as the FHN and more frequent hemodialysis. However, evaluating this study reveals the cavalier approach that these researchers undertook in placing elderly, high cardiovascular risk patients to known cardiovascular stresses with the not unexpected results obtained of increased intradialytic hypotension. In a word, I am appalled.
http://www.hemodoc.com/2011/04/troubling-study-on-hemodynamic-consequences-of-altering-potassium-levels-in-dialysate.html