1. The Cardiac Side of the Cardio-Renal Dilemma
Dr. Ellie Stadnick MD MSc FRCPC
Cardiologist
University of Ottawa Heart Institute
May 9, 2016

2. Patients with refractory heart failure should be offered chronic dialysis… maybe….

3. Disclosures Advanced Heart Failure Cardiologist
I actually like nephrology
I prescribe more furosemide than I care to admit

4. HF is Common and Costly
The most common reason for hospitalization in the elderly
Major driver of cost is hospitalizations
Population Group
Prevalence
Incidence
Mortality
Hospital Discharges
Cost
Total population
5,000,000
550,000
>55,000
>1,000,000
>$35 billion

5. HF Prognosis
1.0
0.8
0.6
0.4
0.2
Survival
No HF (n=1728)
NYHA Class I (n=36)
NYHA Class II (n=79)
NYHA Class III (n=62)
NYHA Class IV (n=59)
Time after inclusion (yrs)
NYHA = New York Heart Association
Smith WM. Am J Cardiol 1985;55:3A-8A.

6. The 2 x 2 Matrix of CHF WET DRY WARM WET + WARM DRY + WARM COOL
WET + COOL
DRY + COOL

7. Nohria et al. J Am Coll Cardiol. 2003;41(10):1797-1804.

8. Frank-Starling Relationship

9. The Relationship
Complex interplay between the heart and the kidneys

10. The Kidney for Cardiologists
Low cardiac output to kidney leading to reduction in GFR (Pre-renal).
Too much venous congestion leading to impaired renal perfusion (Too Much “back-pressure”)
Diuresis causing intravascular depletion (Too Much Too Fast)
Prolonged pre-renal leading to kidney injury (renal/ATN).
Intrinsic renal disease secondary to hypertension or diabetes found in many of cardiac patients.

11. Cardio-Renal Syndrome
One view used to be that CRS is caused by a weak heart unable to provide enough forward flow to essentially cause ‘pre-renal’ failure
It is more complex than that
A recent classification scheme describes 5 subtypes (Ronco et al. JACC 2008;52: )

12. CRS 1 – Acute decompensated HF

13. CRS 2 – Chronic HF

14. CRS 3 – AKI causing HF

15. CRS 4 – CKD causing HF

16. CRS 5 – Systemic dz affecting both

17. Ways to Break the Cycle 1. Improve the Loading Conditions: Decongest
More aggressive diuresis (IV, sequential nephron blockade)
Nitrates
Dialysis/Ultrafiltration if oliguric despite all efforts

18. Diuretic Resistance

19. Diuretic Resistance
JACC 2010;56:

21. Ways to Break the Cycle 2. Improve Forward Flow Decrease Afterload
ACEi/ARB (not ideal in AKI)
Nitrates/Hydralazine
Increased contractility
Digoxin (not in AKI)
Inotrope IV infusions
Revascularization options (ideally not in AKI)
Cardiac Transplantation?
Important Renal Considerations!

22. Medications in Systolic Heart Failure
ACE inhibitors/ARBS
Beta-blockers
Aldosterone Antagonists
Diuretics (possibly)
Digoxin (possibly)
Nitrates (possibly)
Hydralazine (possibly)

23. ACE inhibitors and ARBs
MORTALITY BENEFIT in systolic heart failure along with anti-remodeling benefits.
Short term may worsen GFR (due to efferent arteriole dilation) and increased risk of hyperkalemia.
Long-term preserves GFR in patients with CKD.

24. Beta Blockers MORTALITY BENEFIT in systolic heart failure.
Chronic management strategy; NO role in the acute setting
May consider stopping them if inotropic support is required.

25. Aldosterone Antagonists
MORTALITY BENEFIT in systolic heart failure
Examples: Spironolactone and Eplerenone
Be mindful of potassium levels

26. Diuretics NO MORTALITY BENEFIT, but improve symptoms of congestion.
Will need higher doses (+/- second diuretic for synergistic effect) to achieve adequate diuresis in CKD patients.
Such a strategy may result in an elevation in serum creatinine.
If there is significant congestion; however, aggressive diuresis may actually improve LV function and decrease venous congestion thereby improving renal perfusion leading to improved GFR

27. Digoxin
NO MORTALITY BENEFIT, BUT REDUCES SYMPTOMS AND HOSPITALIZATIONS
Renal clearance and so risky to use in people with CKD, especially in those with fluctuating renal function.
Risk for digoxin toxicity and lethal arrhythmias especially with electrolyte abnormalities that often accompany CRS

28. Hydralazine and Nitrates
Preferential arterial dilator used to treat hypertension.
Helpful for after-load reduction.
When coupled with nitrates in A-HeFT trial had mortality benefit in addition to beta-blockers and ACE inhibitors.
Nitrates
Primary venodilators and some arterial dilation
In A-HeFT trial given orally, but can be transdermal or IV infusion.
Reduce preload and after-load, both in an attempt to unload a failing heart. .

29. Inotrope therapy
Small trials have shown dobutamine to decrease renal sympathetic activity and increase renal plasma flow rate and GFR (Al-Hesayen et al. Journal of Cardiovascular Pharmacology May 2008, Vol 51)
Dobutamine, Milrinone: Role is controversial. Short term use often used for rescue; however inotrope use is associated with increased mortality

30. Acute Management Hold ACEi/ARB Hold Spironolactone
Usually will continue beta blocker at current dose or half-dose

31. Acute Management Step one: Step two: Step three:
Assess volume status (wet or dry?)
Do you need a PA Catheter ?
Step two:
Assess Perfusion (warm or cold?)
Step three:
Initiate therapy
COLD: INOTROPES/VASODILATE
WET: REMOVE FLUID

32. Acute Management Step four: Step five:
If still volume overloaded (and creatinine is rising) …DIALYSIS INDICATION….
Step five:
LVAD or other mechanical circulatory support
What would this patient want?
What is the long term plan?

33. Chronic Management
Is there any role for revascularization by PCI or CABG?
Consider higher risk of contrast nephropathy in patients with CKD
Consider increased surgical risk in patients with CKD

34. A Word About CRT Cardiac Resynchronization Therapy.
Ideally indicated in severe LV systolic dysfunction with a wide LBBB on ECG.
Pacing the left and right ventricles simultaneously may improve overall cardiac function and forward flow.

35. End of the Line
Circ J 2011; 75

36. End of the Line
Slaughter MS et al. N Engl J Med 2009;361:

37. End of the Line
If patients like this continue to have parameters of impaired perfusion despite volume removal and pharmacologic optimization, then device therapies or cardiac transplantation may be considered.
Unfortunately, unless renal function is recoverable, these patients are often not candidates for cardiac transplantation

38. In Summary
Optimize hemodynamic loading conditions to improve renal perfusion and function first. Optimize diuretic and medical therapy
Using ACEi/ARBs and spironolactone often proves to be challenging in such patients.
Avoid digoxin in such patients.
Consider hydralazine and nitrates as a viable alternative.
Hemodialysis/Ultrafiltration may be an option in a select population of patients to optimize loading conditions

39. Questions…?

40. What matters? Quality of Life / Prognosis Cost
Need to balance the suffocating feeling of dyspnea with the inconvenience of dialysis
Palliation / Supportive Care
Cost
Hope to save money by reducing hospitalizations
Other more costly treatments that we provide