Which conditions are cardiovascular manifestations of alkalosis?

Respiratory Alkalosis

Alveolar hyperventilation decreases the Paco2 and increases the HCO3−/Paco2 ratio, thus increasing pH (alkalemia). Nonbicarbonate cellular buffers respond by titrating HCO3− down. Hypocapnia develops whenever a sufficiently strong ventilatory stimulus causes CO2 output in the lungs to exceed the metabolic production of CO2 by tissues. Plasma pH and HCO3− concentration vary approximately proportionately with Paco2 over a range from 40 to 15 mm Hg. The arterial [HCO3−] will decrease acutely approximately 2 mEq/L for each 10 mm Hg decrease in PCO2. The relationship between pH and Paco2 is about 0.01 pH unit/mm Hg.4

Beyond 2 to 6 hours, sustained hypocapnia is further compensated by renal response, a decrease in renal ammonium and titratable acid excretion and a reduction in filtered HCO3− reabsorption. The full expression of renal adaptation may take several days and depends on a normal volume status and renal function. The kidneys appear to respond directly to the lowered Paco2 rather than to the alkalemia per se, although both pH and PCO2 may be factors. With chronic respiratory alkalosis, a 1 mm Hg fall in Paco2 causes a 0.4 to 0.5 mEq/L drop in HCO3− and a 0.003 unit rise in pH, or the [HCO3−] will decrease 4 mEq/L for each 10 mm Hg decrease in Paco2.4 Chronic respiratory alkalosis is an exception to the general rule that physiologic compensation is never 100% efficient, since some patients with this acid-base disorder may exhibit a normal arterial pH and are, therefore, fully compensated.

The effects of respiratory alkalosis vary according to its duration and severity and the underlying disease. Acute respiratory alkalosis causes intracellular shifts of sodium, potassium, and phosphate and reduces ionized calcium by increasing the protein-bound fraction of calcium based on the acute pH changes. A rapid decline in Paco2 may cause dizziness, mental confusion, and seizures, even in the absence of hypoxemia, as a consequence of reduced cerebral blood flow. The cardiovascular effects of acute hypocapnia in the awake human are generally minimal, but in the anesthetized or mechanically ventilated patient, cardiac output and blood pressure may fall because of the depressant effects of anesthesia and positive pressure ventilation on heart rate, systemic resistance, and venous return. Cardiac rhythm disturbances may occur in patients with coronary artery disease as a result of changes in oxygen unloading by blood from a left shift in the hemoglobin-oxygen dissociation curve (Bohr effect). Hypocapnia-induced hypokalemia is usually minor.4

Respiratory Acidosis and Alkalosis

In perioperative medicine respiratory acid-base abnormalities are an uncommon complication of prolonged spontaneous breathing under anesthesia, inadequate mechanical ventilation (both acute respiratory acidosis) or excessive mechanical ventilation (respiratory alkalosis) (Table 48.4). Acute respiratory acidosis results from hypoventilation or increased dead space ventilation. Patients may manifest respiratory distress characterized by respiratory acidosis in the recovery room PACU or surgical ICU. Assessment begins with an examination of the patient’s breathing pattern (Fig. 48.8): slow shallow breathing indicates impaired respiratory drive, rapid shallow breathing suggests chest wall or lung pathology, and obstructed breathing signifies airway obstruction. Blood gas analysis of acute respiratory acidosis will reflect a dramatic fall in pH, an elevated PaCO2, and a slight rise in HCO3− (by 1 mEq/L [mmol/L] for every 10 mm Hg [or 1.2 kPa] rise in PaCO2). The BE should be zero. Respiratory acidosis as a complication of anesthesia is relatively common—excessive sedation (particularly opioids), partial neuromuscular blockade, intraoperative hypoventilation, pneumothorax, etc. It may also complicate CO2 insufflation during laparoscopy—the patients’ minute ventilation should be dynamically adjusted intraoperatively to maintain etCO2 levels near baseline.

For patients with COPD (or other causes of chronic respiratory failure), it is worthwhile, preoperatively, to calculate the baseline PaCO2 on a patient from the total CO2 on blood chemistry panel. As discussed earlier, the total CO2 (HCO3−) rises by 3 mEq/L (mmol/L) for every 10 mm Hg (1.3 kPa) rise in PaCO2. A patient, for example, with a baseline total CO2 of 33 mEq/L (mmol/L) would be expected to have a baseline PaCO2 of 70 mm Hg (9.3 kPa). For intraoperative management, the etCO2 should be maintained, if the patient is undergoing mechanical ventilation, between 3 and 5 mm Hg (0.5 –1 kPa) of baseline (the PaCO2-etCO2 gradient increases with age and nonsupine positioning).

If the patient is hypoventilating, perioperatively, the pH falls, the PaCO2 rises, but the rise in the total CO2 (HCO3−) is lower than expected. If this patient’s PaCO2, postoperatively, is 90 mm Hg (12 kPa) and the total CO2 (HCO3−) is35 mmol/L (mEq/L), then the patient has acute or chronic respiratory acidosis. This problem may be compounded by the patient’s lack of pulmonary reserve and the negative impact on the respiratory center by opioids and other anesthetic agents. Consideration should be given to administration of noninvasive ventilation to restore PaCO2 to what is normal for that patient.

How does alkalosis affect the cardiovascular system?

Which would the nurse claim is a cardiovascular manifestation of alkalosis?

What conditions diseases may result to alkalosis?

Which of the following are manifestations of metabolic alkalosis?