AcidBase, Resp Fail, Ventilation Flashcards

1
Q

Measures the acidity or alkalinity of a solution.

A

pH. 7.35-7.45. Large number of H+ means decreased pH, acidosis. Small number of H+ ions means increased pH, alkalosis.
Acid gives up H+, bases combine with acids.
Controlled in the body with the chemical buffers, respiratory control, renal regulation.

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2
Q

What are the three chemical buffer systems, which help to keep the pH relatively constant?

A

Carbonic acid-bicarbonate/ buffer system, the one we monitor clinically.
Phosphate buffer, esp in renal tubules.
Protein buffer system, which is the most plentiful.

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3
Q

Respiratory regulation of acid/base?

A

Makes changes quickly based on chemoreceptors in the medulla of the brain. Decreased pH means more acid and increased rate/depth. Increased pH means more alkaline and decreased rate/depth.

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4
Q

Regnal regulation of acid/base?

A

Kidneys make permanent adjustments. When acidosis occurs, H+ excreted in the urine: dumps H+ and holds bicarb. When alkalosis occurs, HCO3 excreted in urine: dumps bicarb and holds H+.

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5
Q

Abnormal increase in H+ ion concentration as a result of an accumulation of acid or a loss of base. Two causes?Abnormal condition caused by excess bicarb or a deficiency of acid. Causes?

A

Acidosis. Caused by either excess H+ or deficiency or bicarb. PaCO2 is high.
Alkalosis. Excess bicarb or deficiency of H+. PaCO2 is low.

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6
Q

Direct measurement of the partial pressure of CO2 in the blood. Indicates the effectiveness of breathing. Reflects the respiratory component of pH.

A

pCO2 or PaCO2. Inverse relationship to pH.
Normal is 35-45 mm Hg.
<35 is alkalotic. >45 is acidotic.

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7
Q

Measurement of the level of bicarbonate in the blood. Reflects the metabolic component of pH.

A

HCO3. Direct relationship to pH, moves with it.
Normal is 22-26 mm Hg.
<22 acidotic, >26 alkalotic

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8
Q

Steps for interpreting blood gases.

A
  1. pH: If compensated (and pCO2 or HCO3) look at whether it’s on the high or low end of normal. Use the number 7.4 to decide whether it’s alkalosis or acidosis.
  2. pCO2.
  3. pHCO3
  4. Match up the respiratory and/or metabolic component to the pH problem.
    You really only need the CO2 and HCO3 along with the pH to interpret ABG’s.
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9
Q

pH is in the normal range but the pCO2 and/or HCO3 are out of balance. Correction of abnormal pH.

A

Compensation. Lungs will compensate CO2 if the primary imbalance is metabolic. Kidneys will compensate if the primary imbalance is respiratory.
Acidosis: 7.35-7.39 compensated
Alkalosis: 7.40-7.45 compensated

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10
Q

The four acid/base disturbances?

A

Respiratory acidosis: High CO2, low pH
Respiratory alkalosis: Low CO2, high pH
Metabolic acidosis: High H+ or low HCO3, low pH
Metabolic alkalosis: Low H+ or high HCO3, high pH

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11
Q

A carbonic acid excess resulting from any situation that decreases the rate of pulmonary ventilation. Anything that decreases ventilation, perfusion, or diffusion. Compromise in blood flow and alveolar state. Etiology?

A

Respiratory acidosis. Damage to the resp center. Obstruction to the resp. passage: foreign body, inflammation, trauma, drowning, etc. Loss of lung surface for ventilation: pneumonia, COPD, scare tissue, fluid, mucous, etc. Weakness of the resp. muscles: muscular dystrophy, paralyzed, etc. Severe resp. depression: opioids, sedation. In chronic the pH stays within normal cause the kidneys are compensating.

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12
Q

S/s of resp acidosis? Interventions?

A

Decreased pH and increased pCO2. Visual disturbances. headaches, decreased arterial O2, confusion, nervous system s/s because cerebral blood vessels dilate. Most important: Restlessness/agitation, confusion, drowsiness, coma. Nervous s/s cause CO2 and H+ causes the blood vessels to dilate.
Recognize inadequate ventilation early so interventions can be begun. Correct the cause.

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13
Q

A carbonic acid deficit, decreased pCO2. Etiology?

A

Respiratory alkalosis. Caused by excessive pulmonary ventilation or any condition that increases the respiratory rate (anxiety, O2 deficit, pain, etc), like hyperventilation.

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14
Q

Interventions and s/s for respiratory alkalosis?

A

Increased pH and decreased pCO2, can cause cerebral vasoconstriction. Lightheadedness, numbness and tingling of the lips, fingers, and toes, tachycardia, muscle weakness, confusion, syncope. May have hypokalemia, Ca levels drop. Treat the underlying cause.

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15
Q

A bicarbonate deficit that occurs when excess acids are added or bicarbonate is lost. Etiology?

A

Metabolic acidosis.
Loss of bicarb: vomiting, diarrhea. Renal failure: kidney fails to release H+ or retain HCO3. DKA: ketones (acid) made from metabolization of protein for fuel, compensatory hyperventilation/Kussmaul. Salicylate intoxication. Starvation or hypothyroidism: ketones. Shock: decreased perfusion due to lowered BP switches cells to anaerobic metabolism which makes lactic acid. Adrenal insufficiency. Hypothyroidism. Hypoaldosteronism. K+ sparing diuretics.

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16
Q

S/s and interventions for metabolic acidosis?

A

Decreased pH, decreased HCO3. Headache, mental dullness, Kussmaul respirations: rapid and deep. Diminished muscle tone and deep tendon reflexes due to hypercalcemia. Reduced excitability of nerve cells depresses the CNS. Confusion, cerebral vessels dilate.
Treat cause, fluid and electrolyte replacement, dialysis. Sodium bicarb, only used if underlying cause cannot be solved quickly. Can throw the pt into alkalosis.

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17
Q

Bicarb excess that occurs when an excessive amount of acid is lost from the body or when an increased amount of bicarb is added PO or IV. Etiology?

A

Metabolic alkalosis. Loss of hydrochloric acid from the stomach, loss of K+. Ingestion of large amounts of bicarb or antacids. Excessive administration of bicarb. Diuretic therapy. Mineralocorticoids, Cushing’s, aldosteronism.

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18
Q

S/s and treatment for metabolic alkalosis?

A

Increased in pH and increase in HCO3. Mental confusion, dizziness, numbness, tingling of toes and fingers, muscle twitching, tetany, seizures.
Treat underlying problem. Fluid and electrolyte replacement. Diamox which will increase excretion rate of bicarb from the kidneys.

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19
Q

A sudden, life-threatening deterioration of the gas exchange function of the lung and indicates failure of the lungs to provide adequate oxygenation or ventilation for the blood. Classified by ABG.

A

Acute respiratory failure. PaO2 <50 mm HG. PCO2 >50 with pH <7.35. Three categories are ventilatory, oxygenation, and combined ventilatory/oxygenation failure. S/s of hypoxemia, hypercapnia, and pH acidosis.

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20
Q

Not enough air moving in and out of the lungs. Mechanical failure in nature. Unable to maintain normal PaCO2.

A

(resp) Ventilatory failure.

Extrapulmonary and intrapulmonary types

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21
Q

Air is moving but no oxygenation is taking place. Unable to maintain normal PaO2. Causes?

A

(resp) Oxygenation failure. Normally a problem with the blood, can’t carry O2 or oxygenated blood can’t perfuse. Low atmospheric O2 concentration, pneumonia, CHF, pulmonary embolism, ARDS, abnormal hgb, hypovolemic shock, hypoventilation.

22
Q

Ventilation/oxygenation mismatch?

A

Hypoventilation.
Pulmonary embolism: Hypoxia rt perfusion problem. Tachypnea keeps the pCO2 normal or low, but pO2 continues to decrease. They’re breathing faster/harder to get O2 but only blows off CO2.

23
Q

Extrapulmonary ventilatory failure?

A

Extrapulmonary: Neuromuscular disorder, diaphragm dysfunction, spinal cord injury, CNS dysfunction, kyphoscoliosis, morbid obesity, sleep apnea, obstruction, constriction, external pressure. Tend to be related to diaphragm use, muscular disorders, or external pressure.

24
Q

Intrapulmonary ventilatory failure?

A

Airway disease like COPD and asthma. Ventilation/perfusion (V/Q) mismatch like pneumothorax and interstitial fibrosis. Airway resistance or obstruction. Lung compliance.

25
Q

Ventilation/perfusion(Q) ratio mismatch? Three types in the old ppt? Two in the new?

A
Dead space: area wherein perfusion is blocked but ventilation (alveoli gas exchange) still occurs. Crackles can sometimes be heard with a PE due to blood flow that’s backing up in that area and stagnant. PE, shock. 
Shunting: perfusion is flowing, ventilation decreases in alveoli. The blood that is returning to the heart has not picked up oxygen. Fluid overload is a common cause, prevents the stuff crossing the membrane of the alveoli. Pneumonia, atelectasis
Silent unit (old ppt): perfusion and ventilation are blocked/limited together. Pneumothorax, ARDS
26
Q

S/s of hypoxemia?

A

PaO2 <50 mm Hg. Restlessness, agitation, dyspnea (the 1st), tachycardia, tachypnea, tachycardia, orthopnea. apprehension, confusion, cyanosis, HTN, dyshrythmia, metabolic acidosis, labored breathing. CO2 moves across membranes easier. So early alkalosis due to tachypnea, and late acidosis due to fatigue and decreased breathing (guppy breath)

27
Q

S/s of hypercapnia?

A

PCO2 >50-60ish mm Hg with low pH. Dyspnea, tachycardia, HTN, drowsiness, coma, systemic vasodilation, HF, resp acidosis, seizures, headache. Papilledema (increased ICP leads to swelling of the optic nerve).

28
Q

Interventions for acute resp failure?

A

Treat the underlying cause! Support ventilation and gas exchange. O2 therapy, decrease anxiety, energy conservation to minimize O2 demand. Breathing control, deep breathing and pursed lip. Positioning, mostly good lung down. Mechanical ventilation. Meds: bronchodilators, antibiotics, anti-inflammatories, diuretics if needed. Restore gas exchange.

29
Q

Indications for endotracheal intubation?

A

Glasgow under 8 intubate! Airway protection and to keep it patent, as in the case of burns, spinal cord injuries, obstructions, etc. Need for mechanical ventilation, not doin well on BIPAP. Allows deeper suctioning. Provide positive pressure or high O2 concentration. Bypass airway obstruction. Facilitate pulmonary hygiene: pulmonary toilet, flushing out the lungs

30
Q

Goals of care for mechanical/endotracheal intubation?

A

Endotracheal is short-term, 14-21 days. Maintain patent airway, decrease work of breathing, don’t allow resp muscles to become weak, monitor ABG’s, provide ventilation and O2. Removes secretions via suctioning to improve oxygenation. Prevents complications.

31
Q

Preparation for intubation?

A

Emergent situation in which no consent is required. Explain procedure. May require sedation: must lie flat which can make breathing more difficult, pt may be combative. Oral care. Attempts no longer than 30 seconds, must maintain oxygenation, use AMBU bag. Stabilize endotracheal tube, verify placement

32
Q

Role of the nurse during intubation?

A

Monitoring the pt during procedure, AMBU bag. First priority is breathing and O2, so stabilize airway first (oral airway) as well as vitals and continuous monitoring. Education. Suction, making sure they’re clear of secretions both before and after. Sedation (paralytics, analgesics), especially because anxiety makes it difficult to intubate. Preparation. Gathering equipment, including code cart.

33
Q

Immediate care after intubation?

A

Assess tube placement. Prevent dislodging with securing with tape (note cm marking in case tube moves), sedation, and restraints as a last resort. Oral/ET tube suctioning. Communication.

34
Q

Assessing tube placement for intubations?

A

Exhaled end tidal CO2, litmus paper attachment (fastest way to check). Breath sounds and equal chest expansion, should be bilateral. (Tube could go too far into the bronchioles, typically the right side because the right main stem is shorter). CXR, most definitive. About 2-3 cm above the carina, radio-opaque marking. Make sure to monitor for gastric distention.

35
Q

Indications for mechanical ventilation?

A

Temporary life support for a reversible condition, hopefully less than 2wks. Life-long if they have something like a progressive neuromuscular disease. Diaphragm may be weak, so they need support daily. Hypoxemia, progressive alveolar hypoventilation. Resp acidosis to blow off CO2. Resp support after surgery (smokers, elderly, COPD, etc)

36
Q

Type of mechanical ventilation commonly used as first primary mode. Pt receives same set tidal volume on each breath, minimum RR set, but can breathe faster than the rate wherein pt starts a breath and full volume delivered. Tidal volume and back-up rate preset.

A

Assist control ventilation. If client does not trigger breath, then the ventilator will deliver a breath, back up RR. Advantage in that the client controls the rate of breathing to an extent. Pt workload decreased. Disadvantage in that increased RR leads to hyperventilation and then resp alkalosis.

37
Q

Used as primary ventilator mode or weaning mode. Minimum RR set. Pt can breathe faster than minimum rate with its tidal. Client breathes independently in addition to the designated number of volume controlled assisted breaths. Doesn’t help with own breaths.

A

SIMV. Spontaneous breathing between ventilator breaths at clients own rate and tidal volume. A set tidal volume must be met intermittently. Allows pt to increase the work of breathing to help wean and get muscles stronger.
When the pt takes their own spontaneous breath the tidal volume is not delivered.

38
Q

FIO2, tidal volume, and rate?

A

FIO2: fraction of inspired O2. Percentage of O2 being delivered. O2 concentration. 21% (room air) to 100%.
Tidal volume: VT. Amount of breath that is delivered, based on weight. Volume of air delivered with each breath.
Rate: IMV. Breath per minute.

39
Q

Peak airway (inspiratory) pressure?

A

Amount of pressure required to deliver breaths and set tidal volume. Alarm sounds if pressure changes too much. Can change if pt condition changes. Needing more PIP can indicate the lungs are getting worse and are less compliant.

40
Q

Air pressure delivered at the end of expiration. Provides more time for O2 to get back to the capillary and back to the heart. Same as at the end of BIPAP. Treatment for persistent hypoxemia.

A

Positive end-expiratory pressure, PEEP. Keeps the alveoli open between breaths, decreases the work of breathing, improves oxygenation and ventilation. Maximum is 20.

41
Q

Complications of PEEP?

A

Hypotension, pressure impedes the flow of blood back to the heart (decreased volume return). Barotrauma, the pressure causes the trauma. Pneumothorax, the blebs burst, can lead to a collapsed lung.

42
Q

CPAP?

A

Continuous positive airway pressure that eases the work of breathing. Positive pressure during the entire respiratory cycle, both inspiration and expiration. Keeps a patent airway. Must have spontaneous reparations and a tight-fitting mask.

43
Q

BIPAP?

A

Continuous positive airway pressure with increased pressure during inspiration and decreased during expiration that eases the work of breathing. More assistance on inhalation than on CPAP. Can be used as a rescue ventilator. Must have spontaneous reparations and a tight-fitting mask.

44
Q

Indications and contraindications for CPAP/BIPAP?

A

Indications are sleep apnea, reparatory fatigue/exacerbations, post-extubation, temporary respiratory emergency, comfort, palliative treatment.
Contraindications are decreased LOC (inability to protect airway), n/v, need for frequent PO meds/feeding/oral access. Inability to establish mask seal. Severe respiratory distress. Swallowing impairment.

45
Q

Nursing care of the pt with non-invasive positive pressure vent?

A

Assess pt’s response: Vs, RR, lung sounds, ABG’s, and O2 sats. Breathing pattern, tolerating or fighting the ventilator. Any need for suctioning.
Nursing goals: evaluate response to respiratory assistance, manage system safely, prevent complications. Ambu at bedside for if ventilation fails. Sedation. Nutrition, 1.5-2 times the calories. Communication.

46
Q

Closed suctioning that allows suctioning without disconnecting the ventilator.

A

In-line suction. Benefits are a continuation of O2 supply, the stability of the PEEP, a reduced incidence of ventilator-associated pneumonia (VAP).

47
Q

Sounds when the PIP alarm reaches the set limit. Stops trying to force air in because it realizes it’s too hard to get the air in. Causes?

A

High pressure alarm. Caused by increased amount of secretions, coughing, gagging, biting the tube, anxiety, fighting the ventilator, wheezing, bronchospasm, pneumothorax, airway displaced, obstruction in the tubing, decreased compliance of the lung or collapse.
Check pt first and vent second! Ambu at bedside

48
Q

Low pressure vent alarms?

A

Low exhaled volume sounds the alarm, it relaxes it’s too easy to get the tidal volume in. Leak in the circuit prevents breath from being delivered. Cuff leak occurs in the ET or trach tube. Pt. extubated self. If the pt can talk there’s a leak.

49
Q

Complications of ventilation?

A

Cardiac: hypotension, fluid retention. Pulmonary: Barotrauma, blebs, ventilator dependence. GI: stress ulcer, malnutrition. Immune: risk for infection because of secretions, pneumonia. Muscle: atrophy, immobility.

50
Q

How might respiratory failure be signaled in patients with COPD?

A

May only be signaled by a drop in ABG’s and clinical deterioration. Acute drop in O2 of 10 or more.
Chronic COPD has a chronically low PaO2, increased PaCO2, normal and compensated pH. 90% SoO2 is okay for COPD.

51
Q

Complications of noninvasive positive pressure ventilation?

A

Nasal and face skin breakdown. Nasal dryness and congestion. Eye irritation from air leaking under the mask. Risk for aspiration if the air goes into the stomach and causes contents to come back up

52
Q

Ventilator bundle?

A

HOB 35-45. Oral care q2-4hrs with q12hr or daily chlorohexidine mouthwash. Sedation assessment for readiness/sedation vacation. Peptic ulcer prophylaxis. DVT prophylaxis.