signs and symptoms of acid-base imbalances

Esme12, ASN, BSN, RN · Apr 19, 2012

There is no easy way to remember but to memorize. Most of the symptoms are very similar but causative factors vary.

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Symptoms are non-specific, and diagnosis can be difficult unless the patient presents with clear indications for arterial blood gas sampling. Symptoms may include chest pain, palpitations, headache, altered mental status such as severe anxiety due to hypoxia, decreased visual acuity, nausea, vomiting, abdominal pain, altered appetite (either loss of or increased) and weight loss(longer term), muscle weakness and bone pains. Those in metabolic acidosis may exhibit deep, rapid breathing called Kussmaul respirations which is classically associated with diabetic ketoacidosis. Rapid deep breaths increase the amount of carbon dioxide exhaled, thus lowering the serum carbon dioxide levels, resulting in some degree of compensation. Extreme acidosis leads to neurological and cardiac complications:

Neurological: lethargy, stupor, coma, seizures.
Cardiac: arrhythmias (ventricular tachycardia), decreased response to epinephrine; both lead to hypotension (low blood pressure).

Physical examination occasionally reveals signs of disease, but is otherwise normal.

http://www.nlm.nih.gov/medlineplus/ency/article/001181.htm

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Symptoms of metabolic alkalosis are not specific. Because hypokalemia is usually present, the patient may experience weakness, myalgia, polyuria, and cardiac arrhythmias.

Hypoventilation develops because of inhibition of the respiratory center in the medulla. Symptoms of hypokalemia (ekg, jitteriness, perioral tingling, muscle spasms) may be present.

The clinical history is helpful in establishing the etiology. Important points in the history include the following:

Vomiting or diarrhea - GI losses of HCl
Age of onset and family history of alkalosis - Familial disorders (eg, Bartter syndrome, which starts during childhood)
Renal failure - Alkali-loading alkalosis develops only when impairment of renal function occurs
Drug use (eg, loop or thiazide diuretics; licorice; tobacco chewing; carbenoxolone; fludrocortisone; glucocorticoids; antacids [and, magnesium hydroxide]; calcium carbonate)
Previous GI surgery(and, ileostomy)

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respiratory acidosis may occur due to a variety of etiologies, including the following:

Chronic obstructive pulmonary disease (COPD) – Emphysema, chronic bronchitis, severe asthma
- Neuromuscular diseases – Amyotrophic lateral sclerosis (ALS), diaphragm dysfunction and paralysis, Guillain-Barré syndrome, myasthenia gravis, muscular dystrophy, botulism
- Chest wall disorders – Severe kyphoscoliosis, status post thoracoplasty, flail chest, and, less commonly, ankylosing spondylitis, pectus excavatum,or pectus carinatum
- Obesity hypoventilation syndrome
- Obstructive sleep apnea
- Central nervous system (CNS) depression – Drugs (and, narcotics, barbiturates, benzodiazepines, other CNS depressants), neurological disorders (and, encephalitis, brainstem disease, trauma), primary alveolar hypoventilation, congenital central alveolar hypoventilation syndrome (Ondine curse)
- Other lung and airway diseases – Laryngeal and tracheal stenosis
- Lung-protective mechanical ventilation with permissive hypercapnia in the treatment of acute respiratory distress syndrome (These patients are typically heavily sedated and may require paralytic agents.)
  
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  The clinical manifestations of respiratory acidosis are often those of the underlying disorder. Manifestations vary depending on the severity of the disorder and on the rate of development of hypercapnia. Mild to moderate hypercapnia that develops slowly usually has minimal symptoms.
  
  Patients may be anxious and may complain of dyspnea. Some patients may have disturbed sleep and daytime hypersomnolence. As the partial arterial pressure of carbon dioxide (PaCO₂) increases, the anxiety may progress to delirium, and patients become progressively more confused, somnolent, and obtunded. This condition is sometimes referred to as carbon dioxide narcosis.
  
  Physical examination findings in patients with respiratory acidosis are usually nonspecific and are related to the underlying illness or the cause of the respiratory acidosis.
  Thoracic examination of patients with obstructive lung disease may demonstrate diffuse wheezing, hyperinflation (ie, barrel chest), decreased breath sounds, hyperresonance on percussion, and prolonged expiration. Rhonchi may also be heard.
  
  Cyanosis may be noted if accompanying hypoxemia is present. Digital clubbing may indicate the presence of a chronic respiratory tract disease or other organ system disorders.
  The patient's mental status may be depressed if severe elevations of PaCO₂ are present. Patients may have asterixis, myoclonus, and seizures.
  
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- Hyperventilation
- Clinical manifestations of respiratory alkalosis depend on its duration, its severity, and the underlying disease process. Note the following:
  
  The hyperventilation syndrome can mimic many conditions that are more serious. Symptoms may include paresthesias, circumoral numbness, chest pain or tightness, dyspnea, and tetany.
- - Acute onset of hypocapnia can cause cerebral vasoconstriction. Therefore, an acute decrease in PCO₂ reduces cerebral blood flow and can cause neurologic symptoms, including dizziness, mental confusion, syncope, and seizures; hypoxemia need not be present.
  - painful tingling in the hands and feet, numbness and sweating of the hands, and cerebral symptoms following voluntary hyperventilation.
Physical examination findings in patients with respiratory alkalosis are usually nonspecific and are related to the underlying illness or cause of the respiratory alkalosis. Note the following:
- Many patients with hyperventilation syndrome appear anxious and are frequently tachycardic. Understandably, tachypnea is a frequent finding.
- In acute hyperventilation, chest wall movement and breathing rate increase. In patients with chronic hyperventilation, these physical findings may not be obvious.
- Positive Chvostek and Trousseau signs (http://www.turner-white.com/pdf/hp_mar00_hypocal.pdf) may be elicited.
- Patients with underlying pulmonary disease may have signs suggestive of pulmonary disease, such as crackles and rhonchi. Cyanosis may be present if the patient is hypoxic.
- If the underlying pathology is neurology, the patient may have focal neurologic signs or a depressed level of consciousness.
- Cardiovascular effects of hypocapnia in healthy and alert patients are minimal, but in patients who are anesthetized, critically ill, or receiving mechanical ventilation, the effects can be more significant. Cardiac output and systemic blood pressure may fall
- Cardiac rhythm disturbances may occur because of increased tissue hypoxia .
Lengthy, I agree but it is just not a simple answer. Think of underlying mechanisms and associate specific disease to that section.
ie: Metabolic Acidosis: Diabetic Ketoacidosis/poisoning, antifreeze, aspirin
Metabolic Alkalosis: vomiting (puking hydrchloric acid)
Respiratory Acidosis: CO2 narcosis, paralysis, ALS,sleep apnea
Respiratory alkalosis: hyperventilation in anxiety

guest042302019, BSN, RN · Apr 20, 2012

I think it would to review your A&P book for compensatory mechanisms for Acid-Base Imbalances. While compensatory mechanisms won't entail all of the S/S of an imbalance, you'll be able to recognize some big ones. For instance, what happens to the RR during an acidic or basic situation. What happens to the pulse? What happens to the Pulse Ox? Usually questions will have VS data as well as other data. If you understand what happens to VS during imbalances, you are in really good shape. If you understand compensatory mechanisms, you'll recognize and foresee changes in VS and patient condition ultimately.