Acid-Base Balance: Congestive Heart Failure

Writing III – Acid-Base Balance

Congestive heart failure (CHF) is caused by the inability of the heart to fill correctly, eject blood completely, or a combination of the two, which results in a decrease in cardiac output. Chronic hypertension (CH) is a constantly elevated blood pressure. Peripheral vascular disease (PVD) causes a restriction in blood circulation due to atherosclerosis, fatty deposits on the inner linings of the arteries that cause a blockage of blood flow; arteriosclerosis, loss of elasticity in the arteries themselves; or both. Restricted peripheral blood flow causes an increase in blood pressure because the heart would have to pump with more force to maintain proper cardiac output. Hypertension strains the filtration
membranes of the glomeruli in the kidneys. After prolonged hypertension, the filtration membrane can be damaged, decreasing the filtration ability in the kidneys, and allowing proteins and other large molecules to enter the filtrate. Congestive heart failure and peripheral vascular disease result in decreased blood flow to the kidneys, decreasing the glomerular filtration rate (GFR). Both damaged filtration membranes and decreased blood flow through the kidneys result in decreased filtration and decreased GFR. Eventually, any kidney under this sort of strain will require dialysis or kidney replacement. Congestive heart failure causes decreased cardiac output by decreasing the volume of blood ejected from the heart.
The resulting decreased blood flow to the lungs also decreases gas exchange in the alveoli. Decreased gas exchange can result in inadequately oxygenated blood. Incomplete ejection of blood during ventricular contraction can cause mitral valve prolapsed, allowing blood to backflow into the left atrium, which increases pressure in pulmonary veins, causing pulmonary edema. Excess fluid in the alveoli due to edema disrupts normal gas exchange in the lungs, causing shortness of breath. Peripheral vascular disease causes narrowing of peripheral blood vessels and a decrease in blood flow to the lungs. The restriction of peripheral blood flow causes an increase in blood pressure because the heart has to pump with more force to maintain the amount of blood circulating to the tissues and organs with every heartbeat. A decrease in cardiac output and in blood flow can cause the blood returning to the heart to back up in the tissues causing peripheral
edema. Patchy opacity and infiltrates on Robert’s radiograph indicate thickening of the lung tissue, which suggests inflammation. Inflammation in the lungs increases fluid permeability, so interstitial fluid can leak into the alveoli, resulting in pneumonitis. Prolonged pneumonitis causes a decrease in viable surface area in the lungs, decreasing gas exchange across the respiratory membrane. Because oxygen and carbon dioxide are exchanged through external respiration through the simple squamous epithelia and basement membranes of the alveoli and capillary bed, prolonged inflammation of the alveoli epithelium leads to increased partial pressure of carbon dioxide in the blood. Increased partial pressure of carbon dioxide in the blood leads to lower solubility of oxygen. Increased carbon dioxide in solution in the blood also leads to a decrease in blood pH levels, or respiratory acidosis. Based on his symptoms upon admittance, one would expect Robert’s blood glucose levels to be high, GFR to be low, blood pH to be low or acidic, partial pressure of carbon dioxide to be high, and urine pH to be acidic. Because CHF and PVD decreased blood flow to the kidneys and CH damaged the glomerular filtration membranes, he has a low GFR. Robert’s inability to regulate his blood glucose levels with insulin has led to prolonged elevated blood glucose levels, which damages the glomerular filtration membranes and can lead to deposits blocking filtration slits formed by podocytes. Opacity and infiltrates decrease gas exchange and increase carbon dioxide levels. Elevated carbon dioxide levels leads to the chemical formation of bicarbonate and hydrogen ions, which causes lower pH or more acidity. Bicarbonate ions are reabsorbed, but the hydrogen ions are excreted in the urine, causing acidic urine. Robert’s hematocrit and hemoglobin levels are low, which reduces the amount of oxygen transported to tissues. His sodium level is slightly lower than normal, potassium level is elevated, and chloride is low, all of which evidence inadequate water retention. GFR is one-third the normal range because of poor circulation. Glucose is six times the normal range, indicating improper reabsorption. Regularly monitored and maintained insulin shots would assist in cellular reabsorption. Creatinine is double the normal range, revealing Robert’s body has begun to break down lean muscle for energy due to his inability to utilize glucose properly. High levels of urea nitrogen, nearly three times the normal range, result from low GFR. His blood pH was 7.21, indicating acidosis. The partial pressures of carbon dioxide and oxygen are slightly elevated, indicating prolonged accelerated respiratory rate.
The lab found albumin, glucose, ketones, elevated red blood cells (RBC) (10-25>0-2), elevated white blood cells (WBC) (250>0-2), and a moderate level of bacteria in Robert’s urine, causing cloudiness. Finding such large molecules in his urine reveals significant kidney damage and moderate infection. High levels of ketones in the urine indicate further that Robert’s body is unable to utilize glucose for energy, as ketones are released when the body’s fat stores are converted to fuel. Continued diarrhea will lead to a further decrease in Robert’s blood pH by removing bicarbonate ions from his system faster than the pancreas can replenish the buffer, causing metabolic acidosis. The kidneys will attempt to correct the problem by reabsorbing more bicarbonate ions and secreting more hydrogen ions in urine, but decreased GFR prevents this mechanism from functioning properly. Chemoreceptors detect blood carbon dioxide levels, sending a signal to the respiratory center, on to the medulla oblongata, and finally to the lungs, which will attempt to increase blood pH by increasing expiration to blow off more carbon dioxide. Because the lungs are compromised by inflammation, however, the lungs are not able to compensate for Robert’s metabolic or respiratory acidosis. Hematocrit and hemoglobin levels dropped even more. Sodium, potassium, and chloride are all returned to the normal range, indicating restoration of proper fluid balance in the body. His creatinine level is still elevated, revealing continued renal distress. His urea nitrogen began to revert to normal range, but then jumped way up (higher than 1st admission), also indicating pending renal failure. Robert’s blood and urine pH continued to fall while carbon dioxide and oxygen levels continued to rise because his lungs and kidneys are still failing to correct his respiratory and metabolic acidosis. His albumin level was decreased, but still abnormal, showing continued failure of the kidney filtration membrane. His glucose levels were regulated properly and the ketone level found in the urine was reduced, but still abnormal. Bilirubin and hemoglobin in the urine indicate the excessive breakdown of RBC and failure of the kidney filtration membrane. Elevated bacteria count led to a seriously elevated WBC count in his blood and urine. Based on Robert’s symptoms and carbon dioxide levels, one should expect his respiratory rate to be increased and his bicarbonate ion levels to be decreased.
Hyperventilation, or increased respiratory rate, is attempting to correct his metabolic acidosis by expelling more carbon dioxide to allow the bicarbonate ion buffer system to kick in to raise blood pH. Also, the presence of large molecules in Robert’s urine indicate renal damage, at the very least, and even though many of his test levels returned to the normal range, upon 2nd admission to the hospital, his blood hemoglobin count continued to fall, creatinine level was still elevated, albumin level was above normal, urine ketone level was still above normal, and hemoglobin and bilirubin in his urine show RBC breakdown. Severe, prolonged acidosis ultimately led to complete pulmonary
failure.

Resources:
Adrogue, H. and Madias, N. (n.d.). Disorders of Water, Electrolytes and Acid-Base Balance. Retrieved from: http://www.kidneyatlas.org/book1/adk1_06.pdf.
Morse, H. et al. (2007). Acid-Base Balance, An Overview. Department of Pathology, College of Veterinary Medicine, University of Georgia, Athens, Georgia 30602-7388
Shaw, Patricia, ed. Fluids & Electrolytes Made Incredibly Easy! Springhouse, PA: Springhouse Publishing Co.,1997.