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Effects of Mechanical ventilation on Lungs:

Among the potential adverse physiologic effects of positive-pressure ventilation


are decreased cardiac output, unintended respiratory alkalosis, increased
intracranial pressure, gastric distension, and impairment of hepatic and renal
function.
Effects of MEchanical ventilation on Heart:

During mechanical ventilation particularly when high PEEP or large tidal volumes
are employed, inspiration increases Ppl, decrease LV transmural pressure and
decreases LV afterload aiding in LV ejection even if arterial pressure also increases
(30). This is especially notable in patients with congestive heart failure

Positive pressure ventilation can reduce cardiac output which can result in
hypotension. The increased intrathoracic pressure decreases venous return and
right heart filling which may reduce cardiac output. It may also increase
pulmonary vascular resistance.
Atelectasis: This is collapse or closure of the lu...
Hyperventilation: Hyperventilation lowers PaC...
Ventilator Induced Lung Injury: Overdistension ...
Pneumonia: Ventilator-associated pneumonia ...

Barotrauma is tissue injury caused by a pressure-related change in body


compartment gas volume. Factors increasing risk of pulmonary barotrauma
include certain behaviors (eg, rapid ascent, breath-holding, breathing compressed
air) and lung disorders (eg, COPD [chronic obstructive pulmonary disease]).
.
Effect of Changes in Intrathoracic Pressure on Venous Return and Right Heart
Function
Intrathoracic pressure normally decreases during inspiration and spontaneous
ventilation. Systemic venous return depends on the pressure gradient between
the peripheral systemic veins (e.g., extrathoracic) and right atrium (e.g.,
intrathoracic). Blood flow into the thorax and right atrium (venous return)
increases during spontaneous inspiration. Right ventricular preload and stroke
volume increase, assuming normal contractile function (Starling effect) of the
heart. In contrast, intrathoracic pressure increases during inspiration and PPV,
thereby decreasing venous return to the right atrium. Right ventricular preload
and right ventricular stroke volume decrease, potentially resulting in a decrease in
cardiac output and arterial blood pressure (see Figure 17-10). The mean airway
pressure and therefore mean intrathoracic pressure are key factors determining
the impact of PPV on right ventricular preload and cardiac output.41 Ventilation
strategies that minimize PIP, PEEP, and the duration of inspiration reduce the
impact of ventilation on right ventricular performance.
Most mechanical ventilatory strategies used in horses have been shown to impact
cardiovascular performance.25 A pressure-targeted ventilatory mode in which the
PIP was adjusted to 20 cm H2O resulted in less depressant cardiovascular changes
than a PIP of 25 cm H2O. The horses with the latter changes had a significantly
lower PaCO2, which may have contributed to the differences in hemodynamic
outcome. PEEP values ranging from 5 to 30 cm H2O produced a negative effect on
cardiac output, systemic arterial pressures, and oxygen delivery.36 These later
findings suggest that impaired venous return produced by the increase in mean
intrathoracic pressure was responsible for the reduced cardiac output in
anesthetized horses.
The blood volume status of the horse affects the response to mechanical
ventilation. Specifically, the negative effects of PPV with or without PEEP are
greater in hypovolemic or vasodilated (endotoxic or septic) horses than in normal
normovolemic horses. Venous return and right ventricular preload increase
during inspiration because of the increase in intrathoracic pressure compresses
the vena cava and the right atrium. Right ventricular afterload increases because
pulmonary capillaries are compressed by the pressure generated in the alveoli
during inspiration, leading to a decrease in right ventricular ejection. The
inspiratory decrease in right ventricular output produces a decrease in left
ventricular filling and output a few heartbeats later during expiration.
Stabilization and replacement of the intravascular volume should be attempted
before anesthesia and minimizes the effects of PPV on right ventricular function.
Alternatively, if the horse is anesthetized and the cardiovascular effects of PPV
are profound (large cyclical variation in arterial pressure values during IPPV),
fluids should be administered, and inotropic support institute

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