Page 420 - Clinical Small Animal Internal Medicine

388 Section 5 Critical Care Medicine

Hypercapneic Respiratory Failure pressures (e.g., removing ascites) or by pharmacologic
VetBooks.ir In acute hypercapneic respiratory failure, the primary means (e.g., methylxanthine administration). Maintaining
global cardiac output and mean arterial pressures should
goal is to reestablish adequate levels of alveolar ventila-
tion. If the underlying cause is reduced respiratory drive, be a primary goal.
When excessive mechanical loads are the proximate
then therapy should be aimed at increasing central drive cause of hypercapneic respiratory failure, the primary
by one or more of the following means:
goal is to restore loads on the respiratory system to
reversal of agents such as opioids which may be sup- more normal values. Intubation and temporary trache-
●
pressing central drive ostomy are essential means by which upper airway
administration of agents that may enhance/increase obstructions can be bypassed and airway patency
●
central drive such as doxapram restored. Having the necessary supplies and personnel
alleviation of elevated intracranial pressure if known immediately on hand is advised in cases where such
●
or suspected to be present with agents such as manni- measures seem likely to be required in the near future.
tol or hypertonic saline Permanent tracheostomy may be a suitable long‐term
enhancing elimination of agents suppressing central solution in dogs, but has been associated with poor
●
drive such as toxins or anesthetic agents. This may overall outcomes in cats in one study. Laryngeal paraly-
require fluid diuresis, short‐term ventilation, or extra- sis is another example of a cause that may be amenable
corporeal techniques such as hemodialysis. to surgical therapeutic approaches. While corticoster-
oids are advocated on occasion for the reduction of
If reduced ventilatory capacity is the underlying cause of upper airway edema, the empirical evidence for benefi-
hypercapneic respiratory failure then supportive meas- cial effects of this therapy remains quite limited.
ures may often play a larger role than specific therapies. Continuous positive airway pressure (CPAP) might be
Supplemental oxygen and/or mechanical ventilation (see of benefit in many cases of dynamic upper airway nar-
also Chapter 40) may be required until normal ventilatory rowing; however, more often than not, this therapy
capacity can be reestablished. In some cases, supportive requires general anesthesia in veterinary patients and
care may be required for a few days only (e.g., supportive thus offers less potential benefit over traditional posi-
care following removal of the tick in tick paralysis) and in tive pressure ventilation. Heated, humidified, high‐flow
others it may need to be provided for many weeks. nasal cannula oxygen therapy (HHHFNC) has compa-
Correction of metabolic myopathies and junctionopa- rable effects to nasal mask/pillow CPAP in human pedi-
thies due to hypokalemia or hypomagnesemia should be atrics. The author uses one such device (PrecisionFlow®,
addressed by rapid correction via parenteral supplemen- Vapotherm) in his practice to provide this form of ther-
tation. Antivenins, when available, may be appropriate apy although direct comparisons have not yet been
for hypercapneic respiratory failure syndromes second- made to other similar products and no specific recom-
ary to envenomations. Reduced ventilatory capacity due mendations are made here.
to cervical myelopathies may be amenable to surgical Excessive mechanical load due to low tissue compli-
treatment in many cases. Stabilization and decompres- ance may be addressed by reducing parenchymal inflam-
sion may speed the restoration of effective transmission mation and reducing extravascular lung water (edema).
of efferent signals to respiratory muscles. Toxic causes of Diuretic administration and maintaining a neutral or
reduced ventilatory capacity may on occasion have spe- negative fluid balance are advised in cardiogenic edema
cific therapies that may be employed to increase recovery states and in some noncardiogenic edema states.
rates. Organophosphate toxicity treated with atropine However, in patients on mechanical ventilation, the car-
and pralidoxime (2‐PAM) would be just one example. diovascular effects of high PEEP may preclude the clini-
Reducing metabolic rate and carbon dioxide production cian from keeping the patient as “dry” as one might
can help to bring ventilatory capacity and need closer to prefer. Reduced blood volume with high PEEP can often
adequacy. Addressing fever, preventing hyperthermia, lead to intolerably poor cardiac performance. In some
and controlling muscle tremors and seizures become noncardiogenic pulmonary edema states such as the
even more important goals than usual in this setting. acute respiratory distress syndrome, the use of diuretics
Lastly, the diaphragm is similar to cardiac muscle in remains controversial. In this setting, pulmonary vascu-
that maximal contractile strength is strongly dependent lar permeability may be increased to the point that
on adequate perfusion. Typical skeletal muscle is able diuretic therapy does little to reduce the rate of tran-
to maintain contractile strength in the face of reduced scapillary fluid flux and may lead to reductions in
perfusion to a larger degree. Diaphragmatic blood cardiac output with no discernible benefit. The patho-
flow may be improved by reducing intraabdominal physiology of neurogenic pulmonary edema is complex