Highlights of Unit 2 mechanical ventilation

Physiologic Effects of Mechanical Ventilation:

both hazards and positive effects of PPV & of negative pressure

ventilators

Airway pressures

• Spontaneous breathing results in a driving pressure of 0 - -5 = 5 cmH20

• At no point during quiet spontaneous breathing is the intrathoracic pressure positive

Airway pressures during PPV

• In the case of positive pressure ventilation [PPV], the pressure gradient is positive at the mouth and negative at the alveoli.

• The driving pressure is the difference between these two pressures.

• the intrapleural pressure will rise because the airway pressure has transmitted through the thin walls of the lung.

Cardiovascular effects of PPV• Positive airway pressure raises pressure in

thoracic cavity• Prevents the RA from sucking blood back into the

heart so the venous return is decreased• Less blood in heart- less blood out of the

ventricles so RV and LV both have decreased SV• Compression of pulmonary capillaries• Slows down blood return from head• Decreases Cardiac Output CO• Might decrease the myocardial perfusion

Who is more likely to suffer the effects of PPV on cardiovascular system?

• The person with hypotension • or with low blood volume

Who could benefit from the effects of PPV on the CV system?

• patient with congestive heart failure is helpful• need to push back the excess lung fluid• need to decrease the amount of blood

returning to the stressed heart, • so that the CO can actually rise with these

patients.

Effect of PPV on tissue delivery of oxygen

• 02 delivery = 02 content (cardiac output)– If decreases the CO ---decrease the delivery of 02

to the tissue– If PPV causes increased VD ventilation, the 02

content can go down

Lung Compliance and CO

• If the patient’s lungs have normal compliance, 50% of pressure in the lungs is transmitted to the thorax.

• • If the patient has stiff, low compliant lung, the

higher alveolar pressure may not transmit to the thorax.

reverse pulsus paradoxus

• status asthmaticus patients placed on PPV can have such excessive driving pressures that this dampens the systemic B/P

• decreased LV after load is so low that systemic BP changes significantly between inspiratory phase & expiratory phases.

Excessive VT and inappropriately high baseline pressures

• Excessive VT and inappropriately high baseline pressures [PEEP] will result in serious problems with CO and with myocardial perfusion.

Effects of PPV on hypoxemia

• alveolar recruitment, increases surface area for gas exchange so Pa02 rises

• as the alveolar C02 drops due to increased movement of gas into the lungs and collapsed alveoli re-inflate the PA02 rises.

PPV and hypoxemia with CHF

• As we increase the alveolar pressure with PEEP or CPAP, fluid is pushed back and Pa02 rises as more gas diffuses into the capillaries.

• As Pa02 rises, the Fi02 can be dropped to avoid 02 toxicity

Treatment of hypercapnea with PPV

VE rising decreases the PaC02.

• VT based on disease states:• 8-10 ml/Kg IBW normal lungs• 6-8 ml/kg IBW asthma• 5-8 ml/ kg IBW for ARDS & for COPD

• Keep Pplateau less than 30 cmH20.

PPV can increase V/Q

• Gas distribution to Zone I instead of Zone III• Pressure on pulmonary capillaries will

decrease Q in some areas and raise perfusion to under-inflated areas

• Increased Ventilation without perfusion results in increased VD—so PPV can increase VD/VT

PPV and acid pH

• If VE is too low, respiratory acidosis will result in increased Ventilatory demand

• Prolonged acidosis raises the serum potassium so hyperkalemia can cause cardiac arrhythmias

PPV and alkalosis

• If VE too high: • Prolonged alkalosis will drop the serum

potassium so that hypokalemia results- this can also effect the EKG

• Alters the Hb/02 affinity with shift to the left so that tissue oxygenation can be decreased

• High pH will drop the ventilatory drive and prolong weaning from mechanical ventilation

Time constants

• Time constant = RAW x C• we need at least 7 time constants for both I &

E.

PPV and excessive airway pressures

• PIP above 50 is associated with lung tissue trauma

• If increased RAW, check BBS for suctioning or need for bronchodilator

• Pplateau above 30-35 will cause sheer damage. Keep below 30, by decreasing the VT [usually too high for disease]

Mean airway pressures

• Increasing the PEEP will raise the mPAW

• Increasing the Ti will also raise the mPAW

• Increased airway pressures raise the FRC which can increase lung C and increase Pa02 but excessive FRC will only add to air trapping

Effects of PEEP

• PEEP can drop the Cardiac Output particularly in persons with good compliance

• PEEP can raise the FRC which may or may not have good effects– Low FRC associated with atelectasis –good– High FRC associated with asthma or COPD- bad

• Auto-PEEP created by prolonged Ti can result in air trapping and barotrauma

volutrauma.

• Excessive VT -- in the face of problems with gas distribution

Effect of PPV on VT

• If the patient’s parameters are based on pressure, the delivered VT will vary based on the patient’s compliance and RAW.

• If ventilation is based on a volume, the airway pressures will vary based due to changes in the patient’s compliance and RAW

Effect of PPV on WOB

• If WOB is not decreased, settings are wrong– WOB decreased because driving pressure is

increased by ventilator– Increased VE drops the PaC02 so ventilatory

drive drops– VD/VT decreased because VT is increased– Pa02 rises– If sensitivity set appropriately, there is little WOB

Inappropriate settings result in increased WOB

• inspiratory flow rate too low,• sensitivity not responsive to patient effort• failure to correct hypoxemia• failure to correct hypercapnia or acidosis. • if the level of auto-PEEP is interfering with

triggering a breath

Effect on ventilator muscles

• muscle atrophy within 72 hours in adults. • muscle mass and muscle fibers affected• resting muscle length increases [due to

increased FRC] results in decreased muscle strength,

• while alterations in the blood flow to the ventilatory muscles secondary to PPV just adds to the problem.

Ventilatory-associated pneumonia [VAP]

• VAP more an issue of artificial airways rather than ventilation– cuff pressures to prevent aspiration– oral care Q2 hours, – oral intubation– keeping the HOB

Effects on the kidneys

• When CO drops, the body shunts blood away from kidney so renal perfusion decreases

• Decreased perfusion decreased urine out put– less than 400 ml/day or 160ml/8 hours shift

serious– increases in BUN, creatinine , Potassium and

decreases in Na.– drug clearance may be affected

Serum inappropriate Anti-diuretic hormone [SIADH]

• baroreceptors located in the walls of the Aortic Arch and in the carotid arteries respond to decreases of LV pressures by sending a message that results in secretion of ADH so urine output decreases

Effects of negative pressure ventilation on the body

Major differences

• Negative airway pressures more nature, but also negative pressure on the outside of the thorax and on the abdominal cavity

• Immobility inside the device– always supine• Not effective ventilation in the face of

excessive secretions or other causes of increased RAW

• None-invasive so unable to protect airway

Negative pressure ventilation

• Pooling of venous blood in the abdomen can result in decreased CO

• If patient has paralysis, this can result in positional hypotension

• If person with Guilliam Barre or myotonic dystrophy may have increased cardiovascular instability– hard to get to patient for CPR

• Must decrease VE during nursing procedures

Problems with negative pressure ventilation

• Chest wall can-- over decades-- become deformed

• chest cuirass cover only the chest and not the abdomen so that there is less pooling of venous blood—but maybe less ventilation