kardiorenal sendromlarıingilizcesunum

Cardiorenal ve Hepatorenal Syndromes

Dr. Türkay Akbaş

Düzce Üniversity, School of Medicine

Dep. of Internal Medicine, Division of ICU

No Conflict of Interest to Declare

Cardiorenal Syndromes

• Acute or chronic dysfunction in one organ induces acute or chronic dysfunction of the other

Acute/Chronic

• Kidney Heart

Ronco C. Intensive Care Med. 2008; 34:957–962

Classification

McCullough PA. Contrib Nephrol. 2013;2:82-98

Acute Cardiorenal Syndrome(Type 1)

• Acute hearth disease-worsening of renal

function (WRF)

(Cret ≥ 0.3 mg/dl 48 hr, cret > %50

increase/7 days)

• Patients with AHF/ACS: % 19-45 had

acute kidney injury (AKI)/ WRF

• Mortality predictor (short or long term)

• LOS, chronic kidney disease, readmission, cost↑

• Renal dysfunction severity correlates with mortality, ESRD

Ronco C. Eur Heart J. 2010;31:703-11


Etiology: Acute decompensated heart failure

• Acute coronary syndrome

• Postcardiotomy low cardiac output

• Valve diseases and PE

Risk factors: DM, HT, CKD (%60), elderly

• Admission with AHF, AMI

• Severe cardiac dysfunction (EF↓, pul. edema, arrhytmia

• High dose diuretic (furosemide > 100mg/day)

• Vasodilator /contrast material use

Type-1 - Pathophysiology

3 mechanisms

i. Low cardiac output, %20

ii. Venous congestion: Renal congestion due to increased

renal venous pressure determines the risk.

iii. RAAS and SSS activation: Decreased cardiac output and

renal blood flow: SVR increase

• Villi ischemia → local LPS production and endotoxemia

• Active inflammation

Virzi GM. Crit Care. 2014;18:201.

Ronco D. Heart Failure Clin. 2014;10: 251–280Cruz DN. Adv Chr Kid Dis. 2013;20:56-66

Decreased cardiac outputIncreased venous press.

Catheterisation and contrastFurosemide, ACE-I, ..

Benefit from loop diuretics, vasodilators (nitrate)


• Clinic: Decrease in furosemide response and then increase

in creatinine

• Sympathetic nervous system and RAAS activation secondary

furosemide → creatinine increase

• Hyponatremia: ↑ neurohormonal activation. Poor

prognosis

• ↑ natriuretic peptide, ↑ CVP / right atrial pressure and

pulm. congestion are risk factors for Type I CRS

Chronic Cardiorenal Syndrome(Type 1)

• Chronic heart disease → progressive CKD

Stage 3-5 CKD (GFR < 60 ml/min): % 45- 63

• Difficult to differentiate Type2-4

• Definition: CHF + CRF and

CHF underlies occurance or

progression of CKD


Chronic Cardiorenal Syndrome (Type 1)

• Congenital HF: renal dysfunction in %50, GFR < 60 ml/min in

%9 (3 x mortality)

• ACS → Left vent dysfunction → onset or progression of CKD

• CRS 2 CRS 1

• All and CV mortality high

• Readmission due to HF is predictor for mortality and CKD

Dimopoulos K. Circulation. 2008;117:2320–2328

McCullough PA. Contrib Nephrol . 2013;2:82-98

Acute Renocardiac Syndrome (Type 3)

• AKI: causing heart injury or dysfunction

progressing heart disease

• Insidance ? How many AKI patients will

have myocard injury?

• The time between AKI and heart injury?

• Rarely effects normal heart

• Myocard injury becomes obvious in patients with

subclinical heart disease when AKI develops



• ECG: Changes in QRS, PQ

waves

• ECHO: Left ventricular dilation/

hypertrophy, EF, relaxation

abnormalities…

Ronco D. Heart Failure Clin. 2014; 10: 251–280

Prototypical Condition

. Major surgery

. Postinflammatory GN

. Rhabdomyolysis

. Acute pyelonephritis

. Postobstructive uropaty

. Contrast induced AKI

. Drug induced AKI


• Mechanism? AKI may directly (inflammation) or

indirectly (acidosis, uremia…) produce an acute

heart event

• Experimental (animal) AKI studies (48 hours):

Systemic inflammation, increased leukocyte

infiltration and cytokine expression in heart,

increased myocardial apoptosis and vasoconstriction

Clementi A. Oxidative Medicine and Cellular Longevity, 2015, http://dx.doi.org/10.1155/2015/148082

Virzi GM. Crit Care. 2014;18:201.

Chronic Renocardiac Syndrome (Type 4)

• CKD: causing heart injury, disease or dysfunction.

• Cardiac mortality 10-20 times more, 50 % of all death due to CVD

• As CKD stage increases, all and CV mortality increases

• Histopathology: Left ventricular hypertrophy, cardiac

fibrosis (collagen-1, fibronectin, vimentin increment),

decreased capillary density, increased tissue calcification


Chronic Renocardiac Syndrome (Type 4)

Clinic: Systolic/diastolic dysfunction, chronic edema,

hosptalisation due HF, death (pump failure, sudden)

Microischemia due to increased left ventricular hypertropy

in contrast to decreased capillary density

Chest pain: correlates with ACS, HF and hospitalisation

ESRD + RRT: Cellular activation (T cells, heart macrophages)

and cytokine expression→ myocyte apoptosis + fibrosis

McCullough PA. Contrib Nephrol . 2013;2:82-98

Secondary Cardiorenal Syndrome (Tip 5)

• Involvement of two organs in

systemic diseases

• Acute/chronic

• Examples: Sepsis, DM, SLE,

sarcoidosis, amyloidosis,

Wegener granulomatosis,

cirrhosis


Sepsis - Cirrhosis

• Acute: Sepsis. Developes in hours to a few days

• Chronic: Cirrhosis. Takes weeks to months to develop.

Precipitating events (bleeding, infection…) can transition

to an acute deterioration in heart and kidney.

• Mechanism: Inflammation, RAAS, autonomic SS

dysfunction, HPA activation, maldistribution, endothelial

dysfunction

• Both organs have cellular, molecular and functional

changes.

Secondary Cardiorenal Syndrome (Tip 5)

• Sepsis: 11-64 % had AKI, 30-80 % had elevated

Troponin, ventricular dysfunction (septic

cardiomyopathy)

• Both are mortality predictors

• In AKI patients, the rate of heart involvement? Or

in septic cardiomyopathy, AKI rate ?

• ABY Cardiac dysfunction

Cirrhotic Cardiomyopathy

• Cardiac dysfunction in patients with cirrhosis characterized by impaired contractile responsiveness to stress, diastolic dysfunction and electrophysiological abnormalities in the absence of known cardiac disease

• Diastolic dysfun. → Systolic dysfun.→ left ventricular failure

• Chronotropic incompetence, prolonged QT

• Histopathology: Cardiac hypertrophy, fibrosis, subendotelial edema

• More insidious onset. Dysfunction develops slowly until a crucial point is reached and full decompensation occurs (infection, bleeding..)

Moller S. Dig Dis Sci. June 2015

DOI 10.1007/s10620-015-3752-3

Ronco D. Heart Failure Clin. 2014;10: 251–280

Enfeksiyon (SBP), kanama, parasentez

HRS - CRS• As the disease progresses, hyperdynamic cirrhotic heart can not

provide enough cardiac output (CO) to fill vascular beds: Hypovolemia → WRF

• Cardiac dysfunction is the main determinant of HRS development

• Patients with suppressed cardiac function have more HRS

• Lower CO in patients with cirrhosis who developed renal failure during a course of spontaneous bacterial peritonitis compared to those without renal failure. After resolution of the infection, patients with renal failure have lower CO.

• Data supporting the association between cardiac dysfunction and renal failure in cirrhosis, the so-called cardio-renal syndrome

Fede G. Ann Gastroenterol. 2015;28 (1):31-40Ronco D. Heart Failure Clin. 10 (2014) 251–280Ruiz-del-Arbol L. Hepatology. 2003;38:1210-1218

HRS Diagnostic Criteria1. Cirrhosis with ascites

2. Serum creatinine > 1.5 mg/dl

3. No improvement of serum creatinine (≤ 1.5 mg/dl )after at least 2 days with diuretic withdrawal and volume expansion with albumin (1 gr/kg, maximum 100 gr)

4. Absence of shock or nephrotoxic drug use

5. Absence of parenchymal kidney disease (proteinuria > 500 mg/day, >50 rbc/hpf, abnormal renal USG)

• HRS is a subtype of AKI in cirrhotic patients. A functional abnormality and severe intrarenal vasoconstriction exist.

• CO: low, normal, high. Shortly does not fill a need.Salerno F. Gut. 2007;56:1310-1318Wong F. Gut. 2011;60:702-709

CRS – Preventive Steps• Avoid contrast use

– < 30 ml for diagnosis, <100 ml catheterisation

• Avoid NSAID, thiozoldinedione, biguanide use

• Use isotonic fluids instead of colloid fluids

• Hydration (contrast material and cardiac surgery)

• Avoid hypotension

• Be careful when starting ACE-I in early phase of treat.

• Correct electrolyte and acid-base disturbances

• Exclude coronary diseases

• Treat the precipitating disease (Sepsis, cirrhosis, DM)

Treatment - Type 1 CRS

• Loop diuretic, ultrafiltration

• Hypotension: Norepineprine, left ventricular assist device

• Inotropic agents: Dobutamine, levosimendan

• Vasodilators: Dopamine, dobutamine, phosphodiesterase inhibitor

• Vasopressin antagonist

• Do not forget that excessive diuretic use cause AKI

• The same true for ACE-I and spironolactone

• Avoid hypotension during the first 48 hours of treatment

Treatment - Type 2 CRS

• ACE-I, ARB, β blocker, aldosterone: Decrease mortality

• Digoxin and loop diuretics: decrease symptoms, no effect on mortality

• Defibrillator : EF < %30 , long QRS, cardiac arrest, VT

• RRT

• Heart transplantation

• Worsening of renal function with treatment: Over diuresis, nephrotoxic drug use, persistent hypotension, renovascular diseases

Treatment - Type 3, 4 CRS

• Type 3: Treat underlying disease

– Avoid hypervolemia

– Correct electrolyte disorders

– Correct acid-base disturbances

– Hydration before and after contrast use

• Type 4: HT, DM and HL treatment, avoiding from hypervolemia, anemia treatment, Ca-P controlrevascularization

Treatment - Type 5

• Treat underlying disease

• SBP: Albumin (1.5 gr/kg-first day (maximum:150 gr), 1 mg/kg (maximum:100gr) 3th day

• HRS Tip 1: a-Terlipressin (0.5-2 mg/4-6 hour) + albumin (1 gr/kg first day, then 20-40 gr/day). Continue until the day of 15.

• b- Midodrine + octreotide + albumin

• c- Noradrenaline (0.5-3 mg/hour) + albumin

• d- TIPS

• Liver transplantation . Medical and TIPS increase waiting time for transplantation

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