Interorgan Crosstalk: Understanding Cardio-Pulmonary-Renal Interactions | Ten Points to Remember

Husain-Syed F, McCullough PA, Birk HW, et al.
Cardio-Pulmonary-Renal Interactions: A Multidisciplinary Approach. J Am Coll Cardiol 2015;65:2433-2448.

The following are 10 points to remember from a review on cardio-pulmonary-renal interactions:

  1. There are five subtypes of cardiorenal syndromes (CRS). Types 1 and 2 involve acute and chronic cardiovascular disease scenarios leading to acute kidney injury (AKI) or accelerated chronic kidney disease (CKD). Types 3 and 4 describe AKI and CKD, respectively, leading to heart failure. CRS type 5 describes a systemic insult to both the heart and the kidneys (e.g., sepsis).
  2. Pulmonary-renal syndromes represent different clinical entities. There may be a combination of diffuse alveolar hemorrhage on the basis of pulmonary capillaritis in conjunction with glomerulonephritis as well as acute respiratory distress syndrome (ARDS) associated with AKI in the absence of hematuria.
  3. Hypotension and fluid-responsive shock are not uncommon following intubation, and are a consequence of mechanical ventilation compressing the pulmonary vasculature, thereby increasing right ventricular afterload and diminishing cardiac output. Furthermore, mechanical ventilation is associated with pro-inflammatory effects that may contribute to AKI.
  4. Acute respiratory distress syndrome (ARDS) is defined by onset of lung failure within 1 week of onset of illness, and its hallmark is hypoxemia that cannot be explained by heart failure and in the presence of bilateral infiltrates on chest x-ray. In contrast to cardiogenic pulmonary edema, the resolution of edema in ARDS is often markedly impaired.
  5. Given the significance and prominence of interorgan crosstalk in heart failure, a TNM (Tumor-Node-Metastasis)-like method has been proposed for staging. This includes “H” for heart, “L” for lung, and “M” for impairment of other organs (including the kidney).
  6. AKI is common in acute decompensated heart failure, occurring in about to one-third of patients. It is an independent risk factor for length of stay, readmission, and mortality.
  7. While the mechanism of renal failure in heart failure may be related to renal hypoperfusion secondary to low-output failure, venous congestion is also likely to decrease renal perfusion pressure through increased renal edema.
  8. Heart failure with preserved ejection fraction accounts for over one-half of hospitalizations for heart failure. Activation of the renin-angiotensin-aldosterone system may be a common thread in cardiac, pulmonary, and renal disease associated with this entity. As the authors suggest, “The potential efficacy and anti-fibrotic role of mineralocorticoid receptor antagonists…merit further investigation” in the management of combined cardiopulmonary and renal impairment.
  9. Kidney disease may accelerate coronary artery disease through several mechanisms, and it is important to note that most patients with CKD rarely require renal replacement therapy and instead die prematurely of accelerated cardiovascular disease.
  10. Measurement of B-type natriuretic peptide (BNP) is an established tool for diagnosis, prognostication, and management of heart failure. However, elevated levels of BNP in the context of acute decompensated heart failure are also associated with an escalated risk of AKI.

Clinical Topics: Heart Failure and Cardiomyopathies, Vascular Medicine, Acute Heart Failure, Chronic Heart Failure, Heart Failure and Cardiac Biomarkers

Keywords: Acute Kidney Injury, Cardiac Output, Cardio-Renal Syndrome, Coronary Artery Disease, Edema, Glomerulonephritis, Heart Failure, Hematuria, Hyperemia, Hypotension, Intubation, Length of Stay, Mineralocorticoid Receptor Antagonists, Natriuretic Peptide, Brain, Neoplasms, Patient Readmission, Pulmonary Edema, Renal Insufficiency, Renal Insufficiency, Chronic, Renal Replacement Therapy, Renin-Angiotensin System, Respiration, Artificial, Respiratory Distress Syndrome, Adult, Risk Factors, Sepsis

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