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Causes of acute resp. acidosis
pulm. edema, pneumonia, aw disease, pleural effusions, chest wall abnormalities, neuromuscular disorders
There are two ways you could correct resp. acidosis in VV?
increase the vt to 12 ml/kg of ideal body weight, or if vt is already set at 12 ml/kg of ideal body weight, you could chg the f to correct high Co2
How could you correct resp. acidosis in PV?
increase or decrease the pressure to achieve Vt of 12 ml/kg IBW. then measure the exVt
Causes of Respiratory Alkalosis
hypoxia with compensated hyperventilation, meds, mech. vent., CNS disorders, anxiety, metabolic problems
How could you correct resp. alkalosis in PV?
decrease f then set pressure. When you get to a Vt of 12 ml/kg IBW, leave pressure setting there. bc in PV pressure and volume are directly measured
causes of metabolic acidosis
ketoacidosis, uremic acidosis, diarrhea, renal loss, lactic acidosis, toxins
If pure respiratory acidosis persists even after Va has been increased, the pt may have a problem with
increased deadspace can also occur when vent support reduces pulmonary blood flow to the lungs by causing
high alveolar pressure, such as application of high peep
hyperventilaiton reduces Co2 in the blood which is assc. with constriction of cerebral blood vessels and a
decrease in blood flow to the brain
For head injury's with increased ICP
do not recommend prophylactic hyperventilation (Paco2 <25 mmhg) during the 1st 24 hrs
Mild hyperventilation (Paco2 30-35 mmhg) may be used for
longer periods in situations in which increased ICP is refractory to standard txs of sedation, analgesia, neuromuscular block, cerebralspinal fluid drainage
Occasionally it becomes impossible to maintain normal vent. without risking
lung damage from high pressure and volumes
Pts with ARDS or Status asthmaticus and sometimes COPD, who require vent support are at risk for
With permissive hypercapnia you want to
sedate pt (b/c increased Co2 stimulates the drive to breath), let Co2 rise (>50 to 150 mm hg), PH fall ( >7.10 to 7.30), gradually rise not abruptly
Efforts to keep Paco2 near a pts normal might include
removing sources of mech. deadspace, increasing the f
When the decision is made to allow Paco2 to increase, the following may be used
Allow Co2 to increase and Ph to decrease with out changing rate or vol, avoid high vent pressure and maintain O2, administer sodium bicarb-THAM-or carbicarb to keep Ph > 7.25
PHY (permissive hyperventilation) is also contraindicated in
pts with closed head injury and ARDS; so you would want to change to PV, increase rate slightly to maintain PH, then let the Co2 rise
Circulatory effects with PHY
decreased MI contractility, arrythmias, vasodilation- which results in increased CO, pulmonary hypertension
Suctioning is performed
PRN, based on assessment of the pt (BS) and visibility examing the artificial aw ( if you can see it)
Acute CHF pts
often have pink frothy secretions that do not block the aw, so suctioning is not necessary. secretions will continue until the cause has been treated.
suctioning CHF pts with pulmonary edema will only worsen the
hypoxemia, which is commonly seen in these pts
Suctioning should be preceded and followed by
hyperoxygenation with 100% O2 for 30sec (before), then 1 min after
Complications with suctioning
can cause pt= discomfort, anxiety, coughing, bronchospasm, hemmorrhage, AW edema, ulceration of the mucosal wall (atelectasis), arrythmias, tachycardia, bradycardia
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