A 65 year old man presents with fatigue, shortness of breath, edema in the ankles, and distended neck veins. Upon further examination by the physician, he is also found to have a higher pulse (93 beats/min), low blood pressure (100/60mmHg), high respiratory rate (20 breaths/min), bilateral rales are heard in the lungs, and he is not running a temperature. He has a history of a myocardial infarction 4 months prior, and as treatment was prescribed a cardiac glycoside and a thiazide diuretic. The patient had blood work performed and his plasma sodium (130mEq/L), potassium (3mEq/L), bicarbonate (15mEq/L), and carbon dioxide (25mmHg) were all found to be low. His plasma creatinine (2.4mg/dL) was noted as being elevated (Table 1).
This patient’s myocardial infarction 4 months prior most likely has lead to a progressive worsening of his congestive heart failure (CHF). Congestive heart failure is characterized by the heart insufficiently distributing blood throughout the body (Widmaier, Raff, & Strang, 2008). Tissue death during the myocardial infarction would further diminish his heart’s ability to produce powerful contractions to supply the body with adequate cardiac output. As his heart’s pumping gets less effective over time, fluid builds up in the systemic and pulmonary circuits. Upon the physical examination, this was further concluded through the sound of rales in the lungs, characteristic of pulmonary edema, and swelling of the ankles, characteristic of systemic edema. The extracellular fluid volume in the patient is above normal as evidenced by his edema. In addition, distension of his neck vein is evidence of poor venous return and fluid back up in the systemic circuit.
The symptoms above are due to the heart’s inability to produce efficient cardiac output. This decrease in cardiac output, leads to a back-up of fluid in the left atria that continues to back into the pulmonary system causing the edema that is present. A diagnostic tool used to diagnose the increased left atrial pressure caused by the increased volume is the pulmonary capillary wedge pressure. This is performed by inserting a catheter into the branches of the pulmonary artery, which then detects the pressure present (Figure 1). This pressure is equal to the left atrial pressure, and in this case it was found to be elevated upon examination (Klabunde, 2007). The symptoms of pulmonary edema and rales at the base of the lungs are consistent with an increased pulmonary artery pressure. In addition, the patient is experiencing congestive heart failure that is affecting the right side of his heart. Systemic edema and distended neck veins support an increased right atrial pressure.
Although this patient presents with increased extracellular fluid volume, he has a decreased effective circulating volume (ECV). ECV is the volume of blood that is being pumped to supply the various tissues with oxygen and nutrients. This man’s congestive heart failure is leading to a decreased cardiac output, decreasing the ECV. This decrease in cardiac output is also evident by the low blood pressure (100/60). One way of confirming this decreased ECV is to test plasma renin levels. A decrease in ECV will signal the kidneys to release renin in order to increase aldosterone and sodium reabsorption, so therefore the patient should have increased levels (Figure 2) (Widmaier et al., 2008). In addition, the baroreceptor reflex will increase sympathetic stimulation to the heart in order to increase heart rate (93 beats/min), and constrict the vessels. He is being treated with a cardiac glycoside to try to increase contractility of the heart and therefore increase cardiac output and increase ECV. Cardiac glycosides work by inhibiting Na+/K+ pumps and increasing the plateau phase of contraction by increasing calcium levels (Klabunde, 2010).
Vasoconstriction of the arterioles and mesengial cells of the glomerular capillaries in addition to a decreased ECV will lead to a decrease in glomerular filtration rate (GFR)(DiBona, 1994). GFR is the amount of blood plasma filtered in the glomerular capillaries into Bowman’s space per unit time. There are three main factors that affect GFR; the net filtration pressure, the surface area available for filtration, and the membrane permeability. Creatinine is a good indicator of GFR because it is not reabsorbed and only minimally secreted. Creatinine is a waste product of muscle metabolism, which when plasma levels are elevated is indicative of a low GFR (Widmaier et al., 2008). In this patient, plasma creatinine levels are high (2.4 mg/dL) in response to a decreased GFR. Normal GFR values range from 97-137mL/min in men, but our patient has a severe decrease in GFR (approximately 29mL/min) due to his congestive heart failure affecting the overall functioning of his kidneys (Moses, 2009). Increased plasma creatinine levels as well as increased plasma BUN could also be used to confirm a diagnosis of decreased ECV (Moses, 2008).
In addition, his self-medication with Ibuprofen, was further compromising his condition. Ibuprofen acts to inhibit the enzyme that synthesizes prostaglandins. Prostaglandins normally lead to vasodilation of the afferent arteriole (DeMaria, 2010). Therefore, inhibiting prostaglandin secretion will decrease GFR due to a decreased afferent arteriole radius (Figure 3).
As previously mentioned, the renin-angiotensin-aldosterone system will most likely be activated in this patient to increase renin levels. In a healthy individual, aldosterone is the main factor controlling sodium reabsorption in the distal convoluted tubule and the cortical collecting duct. Renin will therefore increase aldosterone, which will work to increase sodium reabsorption. In addition the low blood pressure will be detected by baroreceptors that will signal to the posterior pituitary to release vasopressin, which stimulates the reabsorption of water in the collecting ducts. Although we have increased sodium reabsorption, the greater increase in water reabsorption is causing a decreased osmolarity (approximately 260mOsmol). The osmolarity, which is normally 300mOsmol, was approximated using two times the plasma concentration of sodium (Widmaier et al., 2008). Although the patient is absorbing sodium, he is likely hyponatremic and experiencing edema due to the fact that he is reabsorbing more water than sodium.
In addition to being hyponatremic, the patient is also hypokalemic. This can be attributed to two specific reasons, his medication a thiazide diuretic, and renin secretion. The thiazide diuretic inhibits sodium reabsorption by inhibiting the NaCl symport channels. It was meant to decrease the edema by decreasing sodium reabsorption, but will also cause an increase in potassium because the Na+/K+ pumps will be ineffective without sodium. Increased potassium will stimulate aldosterone secretion. Aldosterone then stimulates the exchange of sodium and potassium through the Na+/K+ pump to increase sodium reabsorption and increase potassium secretion (Widmaier et al., 2008). Renin secretion stimulated by the decrease in ECV, also leads to increased aldosterone. Both of these will create a continual cycle which leads to increased excretion of potassium and hypokalemia.
This patient’s lab results also showed low plasma bicarbonate and carbon dioxide. Using this information and the fact that the patient is suffering from CHF affecting his pulmonary system, we believe that the patient is experiencing metabolic acidosis. Experiencing dyspnea, the patient most likely has low oxygen levels creating the need to utilize anaerobic pathways for energy more often, which will generate excess lactic acid and hydrogen ions. According to the law of mass action and due to bicarbonate binding to buffer the excess H+, levels of bicarbonate will appear low in the blood plasma (Figure 4). In order to compensate for the metabolic acidosis affecting the kidney, the respiratory system will increase respiration rates to decrease CO2 as seen in our patient and help to decrease H+ (Widmaier et al., 2008). In addition, our patient will begin to secrete hydrogen ions in place of potassium in the kidneys as aldosterone continues to signal sodium reabsorption. The secretion of hydrogen will cause the urine to be acidic.
In conclusion, this patient is suffering from congestive heart failure as a result of a previous myocardial infarction. This patient presented with severe pulmonary and systemic edema, resulting in dyspnea and swelling of the ankles. This edema is due to an increased extracellular fluid volume that is a result of the heart failing to pump effectively. The decrease in cardiac output, results in a lowered ECV, manifested as a low blood pressure. The low blood pressure activated the renin-angiotensin-aldosterone system to increase sodium and water retention. In addition vasopressin secretion allowed for the increased reabsorption of water in an attempt to increase the effective circulating volume. The low blood pressure also caused a lower GFR. His situation was further compromised by taking Ibuprofen which further decreased the GFR. In addition to Ibuprofen, the patient was prescribed a thiazide diuretic to try to decrease extracellular fluid volume, although it further contributed to the development of hypokalemia. It is clear that the cardiovascular and renal systems are closely related as seen through the succession of this patient’s medical problems.
Table 1: Lab Results (Widmaier et al., 2008)
The patient was found to have low plasma sodium, potassium, bicarbonate, and carbon dioxide compared to the normal values. The patient’s plasma creatinine was found to be elevated compared to normal values. All of these values were used to give us insight into the functioning of the patient’s kidneys.
Figure 1: Pulmonary Capillary Wedge Pressure (Klabunde, 2007)
A diagnostic tool used to diagnose the increased left atrial pressure caused by the increased volume is the pulmonary capillary wedge pressure. This is performed by inserting a catheter into the branches of the pulmonary artery. The balloon at the tip is then inflated to determine the pulmonary pressure which is approximately equal to the left atrial pressure.
Figure 2: Response to a Low Effective Circulating Volume and Plasma Level (Widmaier et al., 2008) A decrease in plasma volume is sensed by the juxtaglomerular cells of the kidney which increase renin excretion in response. The increased renin causes increased levels of aldosterone, which acts on the cortical collecting duct to increase sodium and therefore water reabsorption. Figure 3: Afferent and Efferent Arteriole Control of GFR (Widmaier et al., 2008) H++ HCO3- <---> H2CO3<---> H2O + CO2 Figure 4: Law of Mass Action for Blood Buffering System In the blood, bicarbonate acts as a buffer. Bicarbonate will bind hydrogen ions to form carbonic acid. Carbonic acid can then either split into water and carbon dioxide or can again form bicarbonate and a hydrogen ion. In addition, water and carbon dioxide can react with the assistance of carbonic anhydrase to for carbonic acid. This system helps the body to regulate blood pH and maintain homeostasis.
Figure 2: Response to a Low Effective Circulating Volume and Plasma Level (Widmaier et al., 2008)
A decrease in plasma volume is sensed by the juxtaglomerular cells of the kidney which increase renin excretion in response. The increased renin causes increased levels of aldosterone, which acts on the cortical collecting duct to increase sodium and therefore water reabsorption.
Figure 3: Afferent and Efferent Arteriole Control of GFR (Widmaier et al., 2008)
H++ HCO3- <---> H2CO3<---> H2O + CO2
Figure 4: Law of Mass Action for Blood Buffering System
In the blood, bicarbonate acts as a buffer. Bicarbonate will bind hydrogen ions to form carbonic acid. Carbonic acid can then either split into water and carbon dioxide or can again form bicarbonate and a hydrogen ion. In addition, water and carbon dioxide can react with the assistance of carbonic anhydrase to for carbonic acid. This system helps the body to regulate blood pH and maintain homeostasis.
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