Respiratory Failure Clinical Presentation

Updated: Apr 07, 2020
  • Author: Ata Murat Kaynar, MD; Chief Editor: Michael R Pinsky, MD, CM, Dr(HC), FCCP, FAPS, MCCM  more...
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The diagnosis of acute or chronic respiratory failure begins with clinical suspicion of its presence. Confirmation of the diagnosis is based on arterial blood gas analysis (see Workup). Evaluation of an underlying cause must be initiated early, frequently in the presence of concurrent treatment for acute respiratory failure. The cause of respiratory failure is often evident after a careful history and physical examination.

Cardiogenic pulmonary edema usually develops in the context of a history of left ventricular dysfunction or valvular heart disease. A history of previous cardiac disease, recent symptoms of chest pain, paroxysmal nocturnal dyspnea, and orthopnea suggest cardiogenic pulmonary edema. Noncardiogenic edema (eg, acute respiratory distress syndrome [ARDS]) occurs in typical clinical contexts, such as sepsis, trauma, aspiration, pneumonia, pancreatitis, drug toxicity, and multiple transfusions.

A study by Canet et al, examining acute respiratory failure in kidney transplant recipients, determined that 200 of 6,819 kidney transplant recipients required admission to the intensive care unit (ICU) for acute respiratory failure, which was associated with high mortality and graft loss rates. [6] Early ICU admission and increased bacterial and Pneumocystis prophylaxis may improve outcomes.


Physical Examination

The signs and symptoms of acute respiratory failure reflect the underlying disease process and the associated hypoxemia or hypercapnia. Localized pulmonary findings reflecting the acute cause of hypoxemia (eg, pneumonia, pulmonary edema, asthma, or chronic obstructive pulmonary disease [COPD]), may be readily apparent. In patients with ARDS, the manifestations may be remote from the thorax, such as abdominal pain or long-bone fracture. Neurologic manifestations include restlessness, anxiety, confusion, seizures, or coma.

Asterixis may be observed with severe hypercapnia. Tachycardia and a variety of arrhythmias may result from hypoxemia and acidosis.

Cyanosis, a bluish color of skin and mucous membranes, indicates hypoxemia. Visible cyanosis typically is present when the concentration of deoxygenated hemoglobin in the capillaries or tissues is at least 5 g/dL.

Dyspnea, an uncomfortable sensation of breathing, often accompanies respiratory failure. Excessive respiratory effort, vagal receptors, and chemical stimuli (hypoxemia and/or hypercapnia) all may contribute to the sensation of dyspnea.

Both confusion and somnolence may occur in respiratory failure. Myoclonus and seizures may occur with severe hypoxemia. Polycythemia is a complication of long-standing hypoxemia.

Pulmonary hypertension frequently is present in chronic respiratory failure. Alveolar hypoxemia potentiated by hypercapnia causes pulmonary arteriolar constriction. If chronic, this is accompanied by hypertrophy and hyperplasia of the affected smooth muscles and narrowing of the pulmonary arterial bed. The increased pulmonary vascular resistance increases afterload of the right ventricle, which may induce right ventricular failure. This, in turn, causes enlargement of the liver and peripheral edema. The entire sequence is known as cor pulmonale.

Criteria for the diagnosis of ARDS include the following:

  • Clinical presentation - Tachypnea and dyspnea; crackles upon auscultation

  • Clinical setting - Direct insult (aspiration) or systemic process causing lung injury (sepsis)

  • Radiologic appearance - 3-quadrant or 4-quadrant alveolar flooding

  • Lung mechanics - Diminished compliance (< 40 mL/cm water)

  • Gas exchange - Severe hypoxia refractory to oxygen therapy (ratio of arterial oxygen tension to fractional concentration of oxygen in inspired gas [PaO2/FiO2] < 200)

  • Normal pulmonary vascular properties - Pulmonary capillary wedge pressure lower than 18 mm Hg



Complications of acute respiratory failure may be pulmonary, cardiovascular, gastrointestinal (GI), infectious, renal, or nutritional.

Common pulmonary complications of acute respiratory failure include pulmonary embolism, barotrauma, pulmonary fibrosis, and complications secondary to the use of mechanical devices. Patients are also prone to develop nosocomial pneumonia. Regular assessment should be performed by periodic radiographic chest monitoring. Pulmonary fibrosis may follow acute lung injury associated with ARDS. High oxygen concentrations and the use of large tidal volumes may worsen acute lung injury.

Common cardiovascular complications in patients with acute respiratory failure include hypotension, reduced cardiac output, arrhythmia, endocarditis, and acute myocardial infarction. These complications may be related to the underlying disease process, mechanical ventilation, or the use of pulmonary artery catheters.

The major GI complications associated with acute respiratory failure are hemorrhage, gastric distention, ileus, diarrhea, and pneumoperitoneum. Stress ulceration is common in patients with acute respiratory failure; the incidence can be reduced by routine use of antisecretory agents or mucosal protectants.

Nosocomial infections, such as pneumonia, urinary tract infections, and catheter-related sepsis, are frequent complications of acute respiratory failure. These usually occur with the use of mechanical devices. The incidence of nosocomial pneumonia is high and associated with significant mortality.

Acute renal failure and abnormalities of electrolytes and acid-base homeostasis are common in critically ill patients with respiratory failure. The development of acute renal failure in a patient with acute respiratory failure carries a poor prognosis and high mortality. The most common mechanisms of renal failure in this setting are renal hypoperfusion and the use of nephrotoxic drugs (including radiographic contrast material).

Nutritional complications include malnutrition and its effects on respiratory performance and complications related to administration of enteral or parenteral nutrition. Complications associated with nasogastric tubes, such as abdominal distention and diarrhea, also may occur. Complications of parenteral nutrition may be mechanical (resulting from catheter insertion), infectious, or metabolic (eg, hypoglycemia, electrolyte imbalance).