Right Heart Failure and

Cardio – Renal Syndrome

Thida Tabucanon, MD, W. H. Wilson Tang, MD
Cardiol Clin. 2020 May ; 38(2): 185–202.
doi:10.1016/j.ccl.2020.01.004.
Inflammation and Cardio – Renal Syndrome

Production of Pro Decrease cardiac

inflammatory cytokines function
Heart Failure
• Neurohormonal activation
• Venous Congestion Vascular Dysfunction

Increase vascular
Renal fibrosis Permeability
Cardio Renal
Progressive renal Promote absorption of Syndrome
dysfunction pro inflammatory
endotoxin from bowel
Neurohormonal activation in HF

RAAS
Angiotensin II  TNF biosynthesis in
myocardium and renal tissue  activated NF
kappa B  IL6, MCP 1 and other
inflammatory cytokine in kidney

SNS
Increase HR  Increase TNF ,
IL-6 and IL 1 in myocardium cells
and cardiac blood vessel
 Venous Congestion

LPS  promotes
Gram negative bacterial
Mesenteric venous secretion of
translocation through
congestion  bowel wall inflammatory cytokines
the endothelial cells of
edema and increased (TNF-α, IL-1 family, IL-6,
intestinal villi and
vascular permeability IL-8, IL-10 family, IL-12
endotoxin release (LPS)
family, IL-15 & TGF-β

CARDIO
RENAL
SYNDROME
Intravascular Volume RV dysfunction and
Expansion  Vascular Peripheral congestion  dilatation ventricular
inflammation and release inflammatory interdependence  LV
endothelial cell marker (IL-6 and remodeling  reduce
activation (NO and endothelin 1) CO and renal arterial
prostacyclin) pressure
Diagnostic Strategies for Congestion and CRS

Serum and Urine Renal Ultrasono- Intra abdominal

Biomarkers graphy Pressure
 Serum and Urine Biomarkers

Cardiac Marker for

BNP – NT myocardial Stretch, Renal biomarker
Cystatin
pro BNP associated with from tubules 
C (CysC)
renal dysfunction measure GFR

Cardiac biomarker Diagnostic and

Troponin Prognostic,
elevated in CRS, Albumin
and associated with
associated with in Urine
glactin 3 mortality and
mortality rate
admission for HF

Urine NGAL = CysC +

proximal tubular injury Prognostic value for
NGAL Troponin
Serum NGAL = HF adverse events in
+ NT pro
with renal dysfunction AHF
BNP
Renal Ultrasonography

● Renal vein flow pattern using doppler ultrasound  depend on RAP and strongly correlated with clinical
outcomes
● Continuous renal flow pattern = normal rap, discontinuous renal flow pattern = increased RAP and monophasic
pattern = highest RAP and poor outcomes (<40% survival at 1 year).
● Renal flow pattern > renal resistive index (RI) to have incremental prognostic value that reflect renal venous
congestion
● Limitation : require expertise to perform, and needs validation for consistency of Doppler waveform sampling by
operators and in a diverse group of patients
Intra-abdominal Pressure

● Splanchnic congestion due to RHF

● Measuring IAP could be using intra-bladder pressure
using intra bladder catheter connected to transducer
● Increased IAP  elevated pressure greater than normal
range (5 – 7 mmHg)
Medical Treatment Options for RHF and CRS

Reduce Loop of
Systemic Henle, Short
Congestion Peak of action

Natriuresis,
Furosemide,
Diuretic reduce
DECONGESTION Return Balance Torsemide, LOOP DIURETIC
Resistance volume
Bumetanide
overload

Diuretic, UF Protein bound

and Dialysis anion
Loop Diuretic

● Higher dose is needed to achieve same therapeutic

effect  higher dose is associated with greater
diuresis, weight loss and transient WRF
● DOSE-AHF trial  continuous vs bolus strategy of
diuretic administration  no difference in symptom
relief and in change of renal function, neither in
mortality
● Continuous administration associated with more
hyponatremia, need for vasopressors,
rehospitalization and death at 6 months
● Transition to oral therapy depend on medication half
life (4-6 hr for furosemide and bumetanide, 8-12h
for torsemide)
 Progressive impedance of venous return
from kidney in venous congestion, effective
decongestion may improve renal perfusion
and increase diuresis and natriuresis

Excessive diuresis without

adequate right heart reserve can
reduce preload and impair CO 
Relative iv hypovolemia and
decrease diuresis and natriuresis
Diuretic Resistance
● Diuretic resistance  diminished or
loss of diuretic response before reach
the therapeutic goal of relief from
edema.
● Measuring diuretic efficacy or
resistance  weight loss, net fluid
loss, urine output after 40mg iv
furosemide and natriuresis
● No cut off or standard definition of
diuretic resistance
● Braking phenomena  diminished
diuretic induced natriuresis 
contributors to diuretic resistance
○ Hemodynamic braking
○ Neurohormonal braking
● Nephron Remodeling  determine
diuretic efficacy
● Add non loop diuretic overcome braking
phenomenon and nephron remodeling
augment natriuresis
Other medical therapies

Vasoactive and inotropic drugs Selective pulmonary vasodilator

used in RHF, clinical trial evidence has been successfully used for acute RHF where
lacking, most literature based upon cardio- PH is a major contributor, evidence in
centric optimization in advance HF patients CRS is still lacking
SUMMARY

Correlation of venous congestion

The heart and kidney have and renal dysfunction in HF which
complex bidirectional represents the significant influence
interlinks termed CRS from the right heart.

Decongestion is still the mainstay

Clinical assessment of extra-cellular fluid
strategy in HF with CRS and is
status remains important to keep the
clinically challenging. Prevention
balance between hypervolemia and
should be the most important goal.
dehydration.
THANKS!
Always listen to your heart!
It may on your left,
but it mostly always
RIGHT!