Three days after surgery for a perforated sigmoid diverticulitis with generalized peritonitis, a 56-year-old

man is noted to have a heart rate of 100/min, hemoglobin of 10 Gm/dL, and stroke volume of 50 ml.
Arterial blood gas analysis done while the patient is mechanically ventilated with an FiO2 of 1.0 and PEEP
of 10 cm H2O reveals: PaO2 = 100 mm Hg, arterial O2 saturation = 100%, pH = 7.30, PaCO2= 30 mEq/L, Be
= -10 mEq/L.
1. What is the pulmonary status of the patient?
2. Describe the existing acid-base imbalance
3. Calculate the oxygen delivery of the patient

Respiratory Compensatory Mechanisms

The respiratory system can compensate for metabolic acidosis or alkalosis by altering
alveolar ventilation. If carbon dioxide production is constant, the alveolar PCO2 is roughly
inversely proportional to the alveolar ventilation. In metabolic acidosis, the elevated blood
hydrogen ion concentration stimulates chemoreceptors, which, in turn, increase alveolar
ventilation, thus decreasing arterial PCO2 . This causes an increase in arterial pHa, returning it
toward normal. As the respiratory compensation for the metabolic acidosis occurs, in the form of
an increase in ventilation, the arterial PCO2 falls. The point representing blood pHa,Pa CO2 , and
bicarbonate concentration would then move a short distance along the lower than normal buffer
line until a new lower Pa CO2 is attained. This returns the arterial pH toward normal; complete
compensation does not occur. Of course, the respiratory compensation for metabolic acidosis
occurs almost simultaneously with the development of the acidosis. The compensation begins
to occur as the acidosis develops. Under most circumstances the cause of respiratory acidosis
or alkalosis is a dysfunction in the ventilatory control mechanism or the breathing apparatus
itself. Compensation for acidosis or alkalosis in these conditions must therefore come from
outside the respiratory system. The respiratory compensatory mechanism can operate very
rapidly (within minutes) to partially correct metabolic acidosis or alkalosis.

KEVIN N. RIVERA

2308093378

Section B

12/17/2014

1. PaO2 / FiO2 ratio is 100 mm Hg and means that the patient is currently experiencing severe
ARDS. The PaO 2 /FiO 2 is 100 mmHg on ventilators setting that include PEEP 5 cm H 2 O.
2. There is metabolic acidosis due to lactate production caused by severe Acute respiratory
distress syndrome. Metabolic acidosis can occur because of an increase in endogenous acid
production (such as lactate and ketoacids), loss of bicarbonate (as in diarrhea), or accumulation
of endogenous acids (as in renal failure). Lactic acidosis is one the most common causes of highAG acidosis in the ICU. An increase in plasma l -lactate is most commonly due to increased
production of lactate in setting of an imbalance in oxygen supply and demand at the tissue level
(type A). Thus type A lactic acidosis is thought to be caused by tissue hypoperfusion and/or
severe hypoxemia, although in recent years this view is thought to be an oversimplification.

3. Oxygen Delivery
CaO2 = (Hgb x SaO2 x 1.36) + (PaO2 x 0.0031)
= (10 Gm/dl x 1.00 ml/Gm x1.36) + (100 mmHg x 0.0031)
= 13.6 ml/dl + 0.31 ml/dl

CaO2 = 13.91 ml O2/dl

Q = HR x SV
= 100 beats/min x 50 ml/beat

Q = 5,000 ml/min or 5 L/min

DO2 = Q x CaO2 x 10
= 5 L/min x 13.91 ml O2/dl x 10 dl/L
DO2 = 695.50 ml O2/L