NUR 425 Exam 3

Treatment of pulmonary infections

IV antibiotics

Potential complications of CPAP

If respiratory depression, hypoventilation and hypoxia can result. - Patient anxiety while off sedation

Respiratory Problem: acidosis (↓pH)

kidneys reabsorb HCO3 + ↑excretion of hydrogen = ↑HCO3 formed in renal tubule = ↑HCO3 retained in the blood = ↑ pH

What is hypoxemia?

lack of oxygen in arterial blood

What is hypoxia?

lack of oxygen to tissues

Nursing tasks during ET tube placement

- preparing the supplies - getting the patient positioned for intubation- often removing the headboard - administering medications and monitoring the patient during this procedure

Metabolic alkalosis causes:

- profuse vomiting - massive blood transfusions due to citrate in them - GI suctioning - K wasting diuretics, such as Lasix-Bumex - overuse of antacids or Tums, mylanta

Respiratory alkalosis Treatments:

- purse-lip breathing or breathing into paper bag - anti-anxiety agents - normal altitudes - reducing fever - reduce ventilation rate if on mechanical ventilation

Nursing Priorities for pressure support

-Patient must be awake enough to breathe on own

Nursing Priorities for AC

-Watch for tachypnea -monitor for s/s of volutrauma/barotrauma

Nursing Priorities for SIMV

-can be a weaning mode if the RR is low - patient will need to be strong and awake enough to take any needed extra breaths

Potential complications of pressure support

If respiratory depression, hypoventilation and hypoxia can result. - Patient anxiety while off sedation - Potential respiratory Alkalosis if tachypnea (getting assistance with every breath)

Monro Kellie Hypothesis

If the VOLUME of one increases, then a reciprocal decrease in one or both of the others must occur

Respiratory acidosis causes:

- hypoventilation related to depressant drug overdose - COPD - ETOH intoxication - not fully awake post-surgical procedure - airway obstruction, neuromuscular disease - chest trauma - pulmonary edema

ABG reads: pH: 7.50 PaCO2: 38 HCO3: 28

"Metabolic Alkalosis" - 7.50 is out of normal range not "fully compensated" by lungs because... - CO2 is normal didn't try to compensate ("uncompensated") -> "Uncompensated Metabolic Alkalosis"

ABG reads: pH: 7.28 PaCO2: 52 HCO3: 25

"Respiratory Acidosis" - 7.28 is out of normal range not "fully compensated" by kidneys because... - HCO3 is normal didn't try to compensate ("uncompensated") -> "Uncompensated Respiratory Acidosis"

Respiratory System

(Changes in CO2) - Moderate- Effects within minutes, max effect in 24h, more sustainable but not long term

Renal System

(Changes in H+ and HCO3-) - Slowest- Effects take days, but more sustainable

Failure of ventilation:

(hypercapnia) - Difficulty moving their lungs (get O2 in and CO2 out) - PaCO2 >45 in combination with academia - the patient may have healthy lungs, they just can't move them enough

Failure of oxygenation:

(hypoxemic) - Can't get oxygen from the alveolus into the blood stream - PaO2 < 60 mm Hg when receiving an inspired O2 concentration >60%.

Buffer System

(proteins, ions etc absorb/release H+) - Fastest- immediate, but low threshold

Testing for Respiratory alkalosis

- ABGs - Serum electrolytes to detect metabolic disorders that could be causing compensatory - hypokalemia, hypocalciemia - 12-lead ECG - Toxicology screening for salicylate poisoning.

Medication Agents Used in mechanically ventilated patients

- Analgesics(morphine & fentanyl) - Sedatives (midazolam, propofol, dexmetetomidine ) - Neuromuscular blocking agents cause chemical paralysis (pancuronium, vecuronium, rocuronium, neostigmine) - Facilitates synchrony with the ventilator (let the ventilator do all the work) *Remember, there are no sedative or analgesic properties associated with neuromuscular blocking agents!

Hyperventilation (too deep/fast) Often caused by

- Anxiety (due to...?) - Pain - Mechanical ventilator causing hyperventilation (requiring patient to breathe too fast/deep)

Acute Respiratory Failure Drug Therapy

- Bronchodilators (Albuterol) - Corticosteroids - Diuretics, nitrates if heart failure present - IV antibiotics - Benzodiazepines - Opioids

Metabolic acidosis causes:

- DKA - ASA OD - Shock states - sepsis - diarrhea - renal failure

Reasons for HIGH Mechanical Ventilator Alarms

- Decreased lung compliance - Biting on oral ETT - Copious thick secretions in airway - Condensation in circuitry tubing - Right mainstem bronchus intubation - Coughing, gagging - Bronchospasm - Equipment failure

What causes hypoventilation?

- Drug OD - neuromuscular disorders - chest wall abnormalities - too many narcotics or anesthesia post op - rate, Tv, or PEEP setting on vent too low

Complications of intubation

- Esophageal intubation - Right mainstem intubation - Structural injury during procedure - Unplanned extubation - Damage to structures (laryngeal, trachea, vocal cords) - Laryngospasm - Aspiration - Infection

Buffers:

- Fastest-acting system - Primary regulator, but cannot maintain pH without Respiratory & renal systems - Change strong acids to weaker acids - Bind acids to neutralize their effect

Causes of IICP: CSF

- Hydrocephalus due to blockage of CSF outflow - CSF absorption blocked (due to SAH or infection) - Excess CSF production

How do CO2 and HCO3 Affect pH?

- Hydrogen and Bicarbonate join to make carbonic acid - Carbonic acid becomes water and Carbon dioxide (Reversible process) H+ + HCO3- H2CO3 H2O + CO2 ↑ HCO3 = BASE ↓ HCO3= ACID ↑ CO2 = ACID ↓ CO2= BASE

Metabolic acidosis Treatments:

- IV sodium bicarbonate - hemodialysis - manage blood sugars - OD protocols - antibiotics - anti-diarrhea agents

Respiratory acidosis Treatments:

- Incentive Spirometer - NG tube with charcoal if OD - bronchodilators or corticosteroids if COPD - reversal agent such as Narcan or Romazicon - TCDB (turn, cough, deep breathe) - increase O2, PEEP, Vt, and ventilation rate if on mechanical ventilation

Causes of IICP: Cerebral edema

- Infectious neurological processes, such as; meningitis, viral encephalitis, Guillain-Barre Syndrome - Hydrocephalus - Scalp lacerations that become infected - Brain treatment, such as radiation therapy - Stroke (ischemic)

Causes of IICP: BLOOD

- Intracranial hemorrhage *Closed head injuries/head trauma/skull fractures *Stroke (hemorrhagic) - Increased blood flow *HTN *Vasodilation: *(Hypercapnea and hypoxia causes cerebral vasodilation) *(Increased oxygen demands (body triggers an increase in CBF to augment O2 supply) -- Fever, pain, physical activity, shivering, seizures) - Obstruction of outflow (impaired venous return) *Hyperflexion, hyperextension, rotation of neck, tight tracheotomy ties, tumor/abcess compressing venous structures *Increased intraabdominal or intrathoracic pressure (pushes back against venous outflow)

Renal System Compensation

- Kidneys relate to HCO3 (bicarbonate) levels: normal 22-26 mm Hg - Bicarbonate assesses the metabolic components of Acid base balance - Compensation: usually begins within 24 hours (slower than the lungs but more sustainable )

Possible interventions for Respiratory Acidosis:

- Maintain airway and oxygenation prepare for possible mechanical ventilation - Monitor respiratory pattern/sounds, vital signs, cardiac rhythm, neuro changes ABGs, serum electrolytes - Medications: bronchodilators, antibiotics, sedation/narcotic reversal - Pulmonary toilet, tracheal suctioning - Fluid status - Safety and education

Goals of Acute Respiratory Failure

- Maintain patent airway - Optimize O2 delivery - Minimize O2 demand - Treat cause - Prevent complications

Nursing Priorities for CPAP

- Patient must be awake enough to breathe on own and strong enough to take deep breaths A final weaning mode -patient may have anxiety

Synchronized Intermittent Mandatory Ventilation (SIMV)

- Preset # of breaths and tidal volume (Vt) - In between "mandatory" (preset) breaths, the patient may initiate spontaneous breaths- but these are NOT supported (unlike AC) - Volume of spontaneous breaths VARIES (whatever the patient does) - Considered a weaning mode - Helps to prevent respiratory muscle weakness, because patient contributes more WOB - Risk of hypoventilation (what if the patient doesn't take any extra breaths?)

Assist/Control Ventilation (A/C)

- Preset # of breaths and tidal volume (Vt) - Patient may trigger additional breaths-considered a weaning mode - Vt of spontaneous breaths DOES NOT vary- Ventilator supports ALL breaths (set RR and patient-triggered breaths) with the set Vt - Ventilator performs most of the WOB - Useful in normal respiratory drive but weak or unable to exert WOB - Risk of hyperventilation and respiratory alkalosis - Patient takes an extra breath? The ventilator will assist with that breath by controlling the amount of volume

V/Q mismatch: pulmonary embolus

- Pulmonary embolus reduces blood flow-less blood gets to alveoli to receive O2 - one example of VQ mismatch is when the V is fine but the Q is not. - So the ventilation is effective and the alveoli are moving well- but we have a perfusion problem- we can't get that blood to the alveolus. - This type of VQ mismatch - where we have bad perfusion is most commonly caused by a pulmonary embolism. - So you can see- there's plenty of oxygen sitting in that alveolus- ready to be diffused into the bloodstream- but we have a big clot blocking the blood from even getting there

Clinical Manifestations of failure of oxygenation:

- Rapid, shallow breathing pattern - Tripod position - Pursed-lip breathing - Dyspnea - Retractions - Paradoxic breathing - Diaphoresis - Prolonged hypoxemia: Aerobic metabolism lactic acidosis - Abnormal breath sounds

Failure to Wean off of mechanical ventilation

- Respiratory rate > 35 or < 8 breaths per minute - Low spontaneous tidal volumes < 5 mL/kg - Labored respirations and use of accessory muscles - Poor ABGs or sats (< 90%) during weaning process - Tachycardia and HTN - Dysrhythmias: PVCs - ST-segment elevation not present prior to weaning - Decreased LOC - Increased WOB to point of exhaustion - Agitation, Anxiety - Diaphoresis

Respiratory System Compensation

- Second line of defense against imbalance - Twice as effective as Chemical buffer system - Responds within minutes to pH changes - Only temporary

Proning

- Shifts perfusion to the anterior portion from posterior bases with improved ventilation (alters V/Q ratio) - Moves lung tissue to anterior chest - Considered if PaO2/FiO2 ratio below 100 - Need to be careful of pressure points - Protect corneas by lubricating and taping eyes closed - Have basin or towel for all secretions from nose and mouth and provide moisture barrier

Respiratory acidosis compensation:

- To compensate, the kidneys conserve bicarbonate and secrete increased concentrations of hydrogen ion into the urine - During acute respiratory acidosis, the renal compensatory mechanisms begin to operate within 24 hours - Until the renal mechanisms have an effect, the serum bicarbonate level will usually be normal

Reasons for LOW Mechanical Ventilator Alarms

- Tube disconnected - ET tube displaced - Low tracheal cuff pressure - Ventilator malfunction - Leak in circuitry

Readiness to Wean off mechanical ventilation

- Underlying cause for mechanical ventilation is resolved/resolving - Hemodynamically stable; adequate cardiac output to provide tissue perfusion - Adequate respiratory muscle strength RR < 30 PaO2 > or= 80mmHg - Minimal secretions - Acceptable vital signs - Alert/awake and spontaneously breathing - Acceptable chest x-ray and ABGs - Adequate oxygenation without a HIGH FiO2 (> 50% ) and/or HIGH PEEP (> 8 cm H2O) - Absence of any factors that impair weaning-infection, anemia, fever, sleep deprivation, pain, abdominal distention - Mental readiness - Minimal need for medications that cause respiratory depression

Metabolic alkalosis Treatments:

- anti-emetics - stop GI suctioning - stop bicarbonate or antacid use - stop diuretics-switch to K sparing (spironolactone) hydrochloric acid infusion (RARE)

Causes of Intrapulmonary Shunting

- atrial or ventricular defects - atelectasis - pneumonia - pulmonary edema

Respiratory alkalosis Medication causes:

- catecholamines - nicotine - salicylates - xanthines (aminophylline)

Upper airway:

- conducts gas to and from lower airway (includes nasal cavity and pharynx) - food and air pass through here

Respiratory alkalosis causes:

- hyperventilation - anxiety - high altitudes - pregnancy - fever - hypoxia - PE-initial

Your patient is now only speaking to you in one-word sentences and doesn't look up when you come in the room. Which of the following are signs of respiratory distress? (SELECT ALL THAT APPLY) 1. Diaphoresis 2. HR: 120 3. Auscultating scattered crackles in the bases of his lungs 4. BP: 160/95 5. RR: 12 6. ABG shows a PaO2 of 80mmHg

1, 2,4 - Diaphoresis he's working too hard to breathe (remember, if he looks like he's working out, something is wrong!) - HR: 120 another sign that he's working too hard- this is his sympathetic nervous system responding - BP: 160/95 another sign that he's working too hard- this is his sympathetic nervous system responding

The patient has been successfully intubated but the tube is not properly secured. What complication(s) could occur? (SELECT ALL THAT APPLY) 1. Inadvertent extubation 2. Right Mainstem intubation 3. Laryngeal trauma 4. Breaking of teeth

1,2,3 - Inadvertent extubation an unsecured tube is more likely to come out accidentally - Right Mainstem intubation an unsecured tube is more likely to slip down - and the right mainstem is the more straight bronchus- thus, more likely for the tube to enter the right mainstem than the left. - Laryngeal trauma an unsecured tube could come out with the cuff inflated, so an inflated cuff pushing against the larynx as the tube comes out could cause trauma.

Two days later, your patient is doing much better. His pneumonia is resolving, his chest x-ray is improved, and he appears to be taking some of his own breaths when you look at the ventilator. The physician asks if he is ready to wean. Which of these indicate that he is ready? (SELECT ALL THAT APPLY) 1. He holds up 2 fingers when you ask him to 2. He is on continuous norepinephrine and vasopressin 3. His WBC count is normal 4. He becomes aggressive during sedation vacations 5. His heart rate is 130

1,3 - He holds up 2 fingers when you ask him to mentally ready, follows commands - His WBC count is normal a sign that the underlying problem is resolving

Your patient is intubated successfully. How do you know this likely true? (SELECT ALL THAT APPLY) 1. His oxygen saturations go from 90% to 98% 2. His Chest X-ray shows the tip of the ETT at the carina 3. You hear loud bubbling when you auscultate the stomach 4. You observe bilateral chest rise when breaths are delivered 5. You observe "purple" in the CO2 detector

1,4 - His oxygen saturations go from 90% to 98% obvious and immediate improvements in O2 saturations can indicate the patient is successfully intubated- but it is not how we confirm placement - You observe bilateral chest rise when breaths are delivered yes, we want to see both sides rise indicating that the ETT is placed so we can ventilate both lungs

CHECK ALL THAT APPLY: Which of the following are the 5 characteristics of ARDS? 1. Dyspnea 2. Myasthenia Gravis 3. Refractory hypoxemia 4. Cyanosis 5. Dense pulmonary infiltrates on CXR 6. Decreased pulmonary compliance 7. Non-cardiac pulmonary edema 8. Chest pain

1,4,6,7,8

Alan is a 17-year-old male who comes to the clinic with c/o feeling "bad," fatigue, constant thirst, and frequent urination. Focused assessment reveals rapid deep respirations (rate 28) with a fruity breath odor. A capillary blood glucose is 484 mg/dL. 1. What type of acid-base imbalance would you expect Alan to have? 2.What is causing it? 3. What type of compensation would you expect or not expect? Explain 4. What will Alan's ABGs look like? 5. What is the treatment?

1. Metabolic acidosis 2. - Breakdown of fats for energy secondary to lack of insulin and subsequent inability to utilize glucose for energy. - Ketones are an acid byproduct of fat breakdown. 3. - The deep, rapid respiratory rate (Kussmaul respirations) demonstrate respiratory compensation—may be partial or full, depending on longevity of the hyperglycemia 4. - A diabetic ketoacidosis is a metabolic acidosis indicated by a pH <7.35 and a HCO3− <20 mEq/L. - The PCO2 will be within the normal range if the acidosis is uncompensated but will be <35 mm Hg if compensation has occurred. - The PaO2 will not be affected. 5. - Administration of insulin to promote normal glucose metabolism and administration of fluids and electrolytes to replace those lost because of the hyperglycemia

Anthony is a 54-year-old male with a history of nausea and vomiting for the past week. He has been self-medicating himself with baking soda to control his abdominal discomfort. 1. What type of acid-base imbalance would you expect Anthony to have? 2. What is causing it? 3. What type of compensation would you expect or not expect? Explain 4. What will Anthony's ABGs look like? 5. What is the treatment?

1. Metabolic alkalosis 2. Loss of gastric acid and excess bicarbonate with baking soda ingestion 3. - There is limited compensation for metabolic alkalosis. - The kidneys can respond by increasing excretion of bicarbonate. - The respiratory system can respond by decreasing respirations, but once the carbon dioxide level increases, stimulation of chemoreceptors results in increased ventilation 4. - The metabolic alkalosis in this case would be reflected by a pH >7.45 and a HCO3− >30 mEq/L. - Because of the duration of this condition, compensation may be indicated by a PCO2 >45 mm Hg. 5. - Determine the underlying cause of the vomiting if possible, and stop the use of baking soda (sodium bicarbonate). - Antiemetic drugs and nasogastric intubation may help relieve the vomiting, and IV replacement of fluids and electrolytes may be necessary.

Jeri is a 22-year-old female who has been on a 3-day party binge. Her friends bring her to the ED after being unable to awaken her. Assessment reveals shallow respirations with a rate of 8/min, diminished breath sounds, and decreased level of consciousness. 1. What type of acid-base imbalance would you expect Jeri to have? 2. What is causing it? 3. What type of compensation would you expect or not expect? Explain 4. What would Jeri's ABGs look like? 5. What is the treatment?

1. Respiratory acidosis 2. Hypoventilation secondary to alcohol ingestion 3. - Compensation might be noted if the respiratory depression has been present for 24 hours or more: - The HCO3− may be elevated as the result of renal compensation. - If her respiratory depression has lasted less than 24 hours, there will not yet be any renal compensation 4. - Respiratory acidosis reflected by pH <7.35 and PCO2 >45 mm Hg. The HCO3 will be normal (20-30 mEq/L) if her respiratory depression has lasted less than 24 hours; - if longer than 24 hours, the HCO3 may be elevated as the result of compensation. - The PaO2 may be <80 mm Hg because of respiratory depression leading to hypoxemia 5. - Determine the cause of the respiratory depression. - If induced by opioids or benzodiazepines, treat with appropriate antagonists. - If induced by alcohol or other CNS depressants, breathing must be stimulated until the effects of drugs have worn off. - Mechanical ventilation may be necessary to increase respiratory rate and depth, increasing oxygenation and promoting excretion of carbon dioxide

Mayna is an 18-year-old female who presents to the ED after a sexual assault. She is hysterical and in severe emotional distress. Her BP is 140/96, heart rate 104, respiratory rate 38, and oxygen saturation 96%. Lung sounds are clear. 1. What type of acid-base imbalance would you expect Mayna to have? 2. What is causing it? 3. What type of compensation would you expect or not expect? Explain 4. What do Mayna's ABGs look like? 5. What is the treatment?

1. Respiratory alkalosis 2. Hyperventilation secondary to anxiety and hysteria 3. - None at this point—compensation would not be occurring yet in this acute event - However, buffering of acute respiratory alkalosis may occur with shifting of bicarbonate (HCO3-) into cells in exchange for Cl- - It would take several days for renal compensation to occur 4. - Respiratory alkalosis indicated by pH >7.45 and PCO2 <35 mm Hg. - The HCO3− will be normal (20-30 mEq/L) because compensation will not occur in this acute event 5. - Relieve her anxiety and coax her to take slow breaths. - Carbon dioxide may be administered by mask, or she may be asked to breathe into a paper bag placed over her nose and mouth.

Your patient has a MAP of 70 and an ICP of 20. What is an appropriate nursing intervention? 1. Continue to monitor, this is normal 2. Take measures to decrease the ICP 3. Take measures to decrease the MAP 4. Take measures to increase the ICP

2 - This patient has a CPP of 50 (70- 20). So because the CPP is low, we need to address the abnormal number. - In this case, the ICP is too high, so we need to reduce that counter pressure - that ICP- to improve CPP

A 61 year old male is receiving Pancuronium, Fentanyl, and Propofol while on the ventilator. You assess the patient's Train of Four and see the patient's hand twitch four times. Which of the following is the most appropriate nursing action? 1. Turn down the Pancuronium 2. Turn up the Pancuronium 3. Turn off the Pancuronium 4. Leave the Pancuronium at this rate

2 - the purpose of pancuronium is to paralyze our patient. - We want them to be appropriately paralyzed by showing us 2 twitches in response to receiving four impulses. - However, this patient has just twitched in response to all of the impulses- he is not paralyzed enough and we need to titrate the pancuronium up according to protocol

Your patient has just been placed on the Rot-a-prone for ARDS. Which of the following are appropriate nursing considerations? (Select all that apply) 1. Ensure the patient is taken off sedation every 30 minutes to assess neurologic function 2. Ensure pressure points such as shoulders, knees, heels, forehead, are covered with pressure relief pads or duoderm 3. Ensure the patient is appropriately sedated 4. Lubricate and gently tape the eyes closed 5. Place an ice pack on the eyes when the patient is supine 6. Ensure the patient's IV tubing is as short as possible so that no one trips on it 7. Monitor the patient's oxygenation status very closely when they are supine.

2,3,4,5,7

Normal HCO3

22-26 mEq/L

The physician states she would like to intubate the patient. You position the patient in a sniffing position at the head of the bed and provide the physician with supplies. You then announce that you have administered neuromuscular blocking agents, sedation, and analgesia. She begins to attempt the first intubation. What should you do first? 1. Document the patient's vital signs 2. Assist with visualizing the vocal cords 3. Announce changes in the patient's oxygen saturation 4. Auscultate both lungs

3 - correct, we need to have our eyes on the monitor and inform the team of changes

Your patient has just begun his first CPAP trial: CPAP, PEEP: 5, FiO2: 40%. After 8 minutes, his vital signs are: BP: 140/85, HR: 145, SaO2: 92%, RR: 35, T: 37.6. His wife is now at the bedside and asks what is going on. Which statement is most appropriate? 1. He is trying to breathe on his own, but it appears he is not doing a very good job. We will need to sedate him more. 2. He is breathing on his own- which is a lot of work, but this is normal. We will wait a bit longer. 3. He is trying to breathe on his own, but it appears he is working too hard. We will need to stop the trial. 4. He is breathing with some support from the ventilator. As long as he triggers breaths, he will get support from the ventilator

3 - he is working too hard and we do not need to drag this out any more. He needs more support from the ventilator

Your patient has just been intubated with the diagnosis of ARDS. You recognize the following is TRUE about suctioning 1. Suctioning is used purely for patient comfort 2. Suctioning should be done q2hours on schedule 3. Suctioning is appropriate when the patient is showing signs of hypoxia or copious secretions 4. Patients on a mechanical ventilator should be able to cough up all of their own secretions- suctioning is only for an emergency

3 - very uncomfortable and we do not want to routinely suction without assessing whether the patient needs suctioning

A 61 year old male is receiving Pancuronium, Fentanyl, and Propofol while on the ventilator. You walk in the room and the patient's BP is 200/130, heart rate is 154, and the patient is diaphoretic. You look at the ventilator screen and see no issues, you see that the patient's oxygen saturations are 98%. What is the most appropriate nursing action? 1. Turn up the Pancuronium 2. Turn down the Pancuronium 3. Turn up the Propofol 4. Turn down the Propofol

3 - your patient is having a sympathetic response- he is panicking - It is likely that he is paralyzed but too awake - Increasing his sedation is a key humane comfort measure in this case

You are caring for a 69 year old male with pneumonia who was just admitted from the ED. Which of the following symptoms indicate early respiratory failure? 1. Face appears purple 2. Feet are cold to the touch 3. He keeps trying to get out of bed 4. He does not respond when you call his name

3 - he is restless and confused- due to poor oxygenation of his brain

Normal PaCO2

35-45 mm Hg

Considering this ABG, pH: 7.29; CO2: 65; HCO3: 25; PaO2: 58 The physician asks you what you recommend. Which statement is most correct? 1. This patient needs sodium bicarbonate 2. This patient needs to breathe into a paper bag 3. This patient needs a non-rebreather mask 4. This patient needs to be intubated and mechanically ventilated

4 - correct, a high CO2 indicates a failure of ventilation, we need to help this patient ventilate!

Metabolic alkalosis (base bicarbonate excess) occurs when?

A loss of acid (prolonged vomiting or gastric suction) or a gain in HCO3− (e.g., ingestion of baking soda) occurs. - Renal excretion of HCO3− occurs in response to metabolic alkalosis

Normal Intracranial Pressure

5-15 mm Hg

PaO2 is 50 and FiO2 is .70 Determine if patient is in ARDS

50/.7=71.43 less than 200 so patient is in ARDS

Normal CPP

60-100mmHg

Normal pH:

7.35-7.45

Patients A and B are both on mechanical ventilatory support. Patient A is receiving an FiO2 of 70% and patient B is receiving an FiO2 of 30% Which statement about these patients is most accurate?

70% of the air being delivered to patient B is NOT oxygen

Which of the following is a normal CPP value?

80

Normal PaO2

80-100 mm Hg

Which of the following is a normal ICP value?

9

Acidosis pH:

< 7.35 Death: 6.8 and less

Alkalosis pH:

> 7.45 Death: 7.8+

Normal SaO2

> 95%

The rate of V usually = Q resulting in

A V/Q ratio of 1

Which of the following values is associated with "alkalosis"? (SELECT ALL THAT APPLY) a. ph: 7.5 b. CO2: 30 c. HCO3: 20 d. CO2: 45 e. HCO3: 45

A,B,E

Tests for Metabolic Acidosis:

ABG and labs - Serum potassium (usually elevated as H+ move into the cells and potassium moves out. - Blood glucose and serum ketones (elevated with Diabetic Ketoacidosis) - Plasma Lactate levels (high with lactic acidosis due to tissue hypoxia)

Testing for Metabolic alkalosis:

ABG, ECG Monitor: - Vitals (slow , shallow RR - compensation), ECG (electrolytes), BP (hypotension) Labs: - Potassium (hypo), Calcium (hypo), chloride (hypo), bicarb (hyper) Neuro Assessment: - muscle twitching, weakness, tetany, hyperactive reflexes, numbness/tingling in fingers, toes, & mouth. Apathy, confusion, seizure, stupor, coma Medication cause: - antacids corticosteroids, Na bicarbonate, thiazide, loop diuretics GI: - Hypokalemia, anorexia, N/V

Pupillary response from IICP

If the oculomotor nerve (CN III) is compressed, the pupil on the affected side (ipsilateral) becomes larger until it fully dilates. - If ICP continues to increase, both pupils dilate

According to the Monro Kellie Hypothesis, which of the following is true?

If the volume of the brain increases, the blood and/or CSF must decrease

Drawing an ABG

Specimen comes from arterial blood; - thus the A Can be a direct stick to the artery - (radial, brachial, or femoral) If frequent ABG's needed - an Arterial Line is usually placed Allow a minimum of 20 minutes after suctioning - (suction time < 15 seconds), vent or oxygenation changes to obtain an ABG

Settings:

The specifics of that relationship - example: speed, type of car, shoes

Modes:

The ventilator's "Relationship" with the patient - example: driving, walking

Example of low hemoglobin level:

GI bleed

Purpose of the respiratory system:

Gas exchange - (O2 in and CO2 out)

Normal gas exchange unit in the lung

Gas exchange occurs across the alveolus membrane - O2 and CO2 diffuse across it in 0.25 seconds

Kidneys impact pH with

HCO3

Low pH: Acidemia ->

High PCO2 (resp. acidosis) Low PCO2 (metabolic acidosis)

Causes of Failure of ventilation

Airflow obstruction/Air trapping - Asthma, COPD, Cystic fibrosis Chest wall abnormalities (limiting lung expansion) - Trauma (Flail chest, rib fractures) - Kyphoscoliosis, severe obesity Respiratory depression - CNS Depression, head injury (esp. brain stem) - Opioids, sedatives Muscle weakness/paralysis - Spinal cord injury - Guillain-Barre, Myasthenia gravis, MS, - Toxin exposure - Muscle wasting/atrophy

Work of Breathing

Amount of effort required for the maintenance of a given level of ventilation - ↑ WOB ↑energy needed ↑ O2 needed - Normally: ↑CO2 stimulates respiration - (in COPD pts ↓O2 better stimulant to breathe)

Tidal Volume (Vt)

Amount of gas (in mL) to be delivered with each breath. Based upon IDEAL body weight. 8-10 mL/kg ideal body weight Example: 70 kg patient should receive between 560 to 700 mL

Metabolic acidosis occurs when?

An acid other than carbonic acid accumulates in the body or when bicarbonate is lost in body fluids. - Ketoacid accumulation in diabetic ketoacidosis and lactic acid accumulation with shock are examples of acid accumulation. - Severe diarrhea results in loss of bicarbonate. - In renal disease, the kidneys lose their ability to reabsorb bicarbonate and secrete hydrogen ions.

PaCO2:

How much CO2 is in the blood? Did enough/too much CO2 get "blown off" by the lungs or is it building up?

HCO3:

How much bicarbonate is in the blood? How are the kidneys working? Is there a metabolic issue?

Your brain's thermostat!

Hypothalamus Our patients with brain injury may have trouble controlling body temperature - High temperatures increased metabolic demand

A patient's ABG results include pH 7.31, PaCO2 50 mm Hg, PaO2 51 mm Hg, and HCO3 28 mEq/L. Oxygen is administered at 2 L/min, and the patient is placed in high-Fowler's position. An hour later, the ABGs are repeated with results of pH 7.36, PaCO2 40 mm Hg, PaO2 60 mm Hg, and HCO3 24 mEq/L. What is most important for the nurse to do? A. Increase the oxygen flow rate to 4 L/min. B. Document the findings in the patient's record. C. Reposition the patient in a semi-Fowler's position. D. Prepare the patient for endotracheal intubation and mechanical ventilation.

Answer: A Rationale: - The initial arterial blood gas (ABG) report indicates partially compensated respiratory acidosis with moderate hypoxemia. - The next ABG results indicate improvement, but the hypoxemia continues (Pao2 remains low). - The patient should receive a higher concentration of oxygen to treat hypoxemia.

If the PaO2 is 60 mm Hg and the FiO2 is 0.6, the PaO2/FiO2 ratio is: A. 100 B. 1000 C. 360 D. 3600

Answer: A. Show the math: 60/0.6 = 100. This patient would be in severe ARDS, since it's less than 200.

Which patient is at highest risk for hypoxemic respiratory failure? A. A patient who has respiratory muscle paralysis B. A patient who has fractured ribs and a flail chest C. A patient who has a massive pulmonary embolism D. A patient who has slow breathing from a drug overdose

Answer: C Rationale: - Hypoxemic respiratory failure is also referred to as oxygenation failure because the primary problem is inadequate O2 transfer between the alveoli and the pulmonary capillary bed. - A massive pulmonary embolism is an example of a cause of hypoxemic respiratory failure. - Sedative overdose, respiratory muscle paralysis, and flail chest are examples of hypercapnic respiratory failure. - Hypercapnic respiratory failure is also referred to as ventilatory failure because the primary problem is insufficient CO2 removal.

A patient with severe chronic lung disease is hospitalized with respiratory distress. Which finding would suggest to the nurse that the patient has developed rapid decompensation? A. An SpO2 of 86% B. A blood pH of 7.33 C. Agitation or confusion D. PaCO2 increases from 48 to 55 mm Hg

Answer: C Rationale: - It is especially important to monitor specific and nonspecific signs of respiratory failure in patients with chronic lung disease because a small change can cause significant decompensation. - Immediately report any change in mental status, such as agitation, combative behavior, confusion, or decreased level of consciousness.

When assessing a patient with sepsis, which finding would alert the nurse to the onset of acute respiratory distress syndrome (ARDS)? A. Use of accessory muscles of respiration B. ABGs of pH 7.33, Paco2 48 mm Hg, and Pao2 80 mm Hg C. PaO2/FiO2 ratio of 340 D. PaO2 remains below 55 regardless of administration of 90% oxygen

Answer: D - One of the cardinal signs of ARDS is refractory hypoxemia. - This patient received a lot of oxygen (90%) but it did not improve the patient's oxygen saturation.

A patient has the following ABG results: pH 7.48, PaO2 86 mm Hg, PaCO2 44 mm Hg, HCO3− 29 mEq/L. When assessing the patient, the nurse would expect the patient to have A. Muscle cramping B. Warm, flushed skin C. Respiratory rate of 36 D. Blood pressure of 94/52

Answer: a Rationale: - The patient is experiencing metabolic alkalosis (elevated pH and elevated HCO3− ). - Clinical manifestations of metabolic alkalosis include hypertonic muscles and cramping and reduced respiratory rate. - Hypotension and warm, flushed skin may occur with respiratory acidosis

A patient with an acid-base imbalance has an altered potassium level. The nurse recognizes that the potassium level is altered because A. Potassium is returned to extracellular fluid when metabolic acidosis is corrected. B. Hyperkalemia causes an alkalosis that results in potassium being shifted into the cells. C. Acidosis causes hydrogen ions in the blood to be exchanged for potassium from the cells. D. In alkalosis, potassium is shifted into extracellular fluid to bind excessive bicarbonate.

Answer: c Rationale: - Changes in pH (hydrogen ion concentration) will affect potassium balance. - In acidosis, hydrogen ions accumulate in the intracellular fluid (ICF), and potassium shifts out of the cell to the extracellular fluid to maintain a balance of cations across the cell membrane. - In alkalosis, ICF levels of hydrogen diminish, and potassium shifts into the cell. - If a deficit of H+ occurs in the extracellular fluid, potassium will shift into the cell. - Acidosis is associated with hyperkalemia, and alkalosis is associated with hypokalemia

Arterial blood gas and chest x-ray for Respiratory Acidosis:

Arterial Blood Gas: - pH typically below 7.35 mm Hg - PaCO2 above 45 mm Hg - HCO3 normal (22-26 mm Hg) in acute cases; chronic maybe >26 mm Hg Chest X-ray - often pinpoints a cause - Pulmonary edema - Pneumonia - COPD - Pneumothorax

Mechanical Ventilator Malfunction

Assess alarm settings (volume, pressure limits, and apnea) and ordered settings If suspected ventilator equipment failure or problem VENTILATE your patient with 100% O2 Ambu (BVM) bagging-collaborate with RT until their arrival Mechanical malfunction is rare, if in doubt CHANGE out machine

Volume Controlled Modes of PPV

Assist/Control Ventilation (A/C) Synchronized Intermittent Mandatory Ventilation (SIMV)

Acute Respiratory Distress Syndrome (ARDS) can be best defined as _____________________________. A. Sudden life-threatening deterioration of gas exchange in the lungs B. Non-cardiac pulmonary edema with increasing hypoxemia despite treatment with O2 C. Sudden life-threatening pulmonary edema that causes a deterioration of gas exchange despite treatment with O2

B

Lower airway:

Larynx: - narrowest part of conducting airways, contains vocal cords, is covered by the epiglottis Glottis: - passage through vocal cords Trachea: - warms, humidifies, and filters air- cilia propel mucous and foreign material up through the airway R&L mainstem: - right bronchus is shorter wider, and straighter than the left - Bifurcation: carina

Which could be a cause of increased intracranial pressure? (SELECT ALL THAT APPLY) a. hip extension b. hydrocephalus c. reduced outflow of blood from the brain d. pain e. anxiety

B,C,D,E

Which of the following places a patient at risk for a state of acidosis? (SELECT ALL THAT APPLY) a. A patient with severe anxiety b. A patient rescued from a drowning c. A patient who consumed an entire bottle of Tums d. A patient with severe diarrhea e. A patient with kidney failure

B,D,E

When do you suction and endotracheal tube?

Only done when clinically indicated: - Increased inspiratory pressures - Adventitious lung sounds - Coughing - Decreased O2 saturations (SpO2) - Copious secretions

Why would kidney failure cause metabolic acidosis?

Because the kidneys were supposed to get rid of hydrogen ion and didn't. - Now we have H+ and HCO3- -- which leads to H2CO3 (carbonic acid) - The more hydrogen ion circulating in the blood, the more hydrogen ion can bind with HCO3 and create carbonic acid more acidmetabolic acidosis

Reduction of severe anxiety, pain, and agitation

Benzodiazepines Opioids

In general, respiratory alkalosis is due to what?

Breathing too quickly and/or deeply

Relief of bronchospasm

Bronchodilators (Albuterol)

How do our bodies NORMALLY regulate acids and bases?

Buffer System Respiratory System Renal System

Metabolic Acidosis Multiple potential causes

Build up of acid (eg. due to poor perfusion, organ failure, altered metabolism) - Shock- lactic acid build up - Renal failure- uric acid build up - DKA- accumulation of ketoacids Intoxication (ASA overdose) Bicarbonate deficit/loss - Diarrhea (↓ PaHCO3-)

Signs & Symptoms of Increased Intracranial Pressure

Change in LOC, vision, reflexes, and vital signs Cushing's Triad: a late sign of IICP - ( Systolic Hypertension with widening pulse pressure, BRADYCARDIA, irregular respiratory pattern) ICP > 15 mm Hg Increasing and persistent HEADACHE Vomiting (oftentimes, projectile)

Hypoventilation (too slow/shallow) often caused by

CNS depression - Drugs (sedatives, opioids), alcohol, brainstem injury Pulmonary disease - COPD, PE, Pneumonia, pulmonary edema Respiratory muscle weakness - Paralysis, fatigue

Lungs impact pH with

CO2

Respiratory Acidosis

CO2 is being retained in the lungs (CO2 levels increase) Hypoventilation (too slow/shallow) (↑PaCO2)

Calculate this patient's CPP and determine what nursing intervention is indicated MAP: 72 ICP: 20

CPP is 52, measures to reduce ICP are indicated

Calculate this patient's CPP and determine what nursing intervention is indicated MAP: 50 ICP: 5

CPP: 45 Administer prescribed norepinephrine

MAP: 55 ICP: 5 Determine CPP

CPP: 55-5= 50 CPP: 75-5= 70

MAP: 75 ICP: 22 Determine CPP

CPP: 75-22 = 53 CPP: 75-10=65

Treating Acute Respiratory Failure (Collaborative Care):

CXR, ABG, CBC, ECG Sputum and blood Cx Oxygen delivery and ventilatory support - Tolerated by the patient - Maintain PaO2 >55, SaO2>90 at lowest O2 concentration possible - Oxygen delivery devices *Noninvasive: NC, simple mask, venti mask, NRM, CPAP, BIPAP *Invasive: Endotracheal tube, tracheostomy Ventilatory support - Positive Pressure Ventilation (PPV) *CPAP, BIPAP (noninvasive) *Invasive Mechanical ventilation (ETT, Trach) Suctioning, positioning, hydration, effective coughing (airway clearance)

Endotracheal tube placement

Can be done in a low stress environment or a high stress environment - For example, maybe before a planned surgery on a stable patient- sounds low stress. - Or maybe a patient who has been having a hard time breathing, oxygen saturations are in the 70's, the patient's respiratory rate is 45, their last ABG looked absolutely terrible- that sounds like a high stress situation

Which of the following is the body's first line of defense against an acid-base imbalance?

Chemical and protein buffers

Abnormal Respiratory Patterns: A sign of IICP

Cheyne-Stokes CNS Hyperventilation Apneustic Cluster Ataxic

Example of low cardiac output:

Congestive heart failure

Pressure Controlled Modes

Continuous Positive Airway Pressure (CPAP) Pressure Support Ventilation (PS or PSV)

Continuous Positive Airway Pressure (CPAP) Invasive or Non-Invasive

Continuous positive airway pressure throughout respiratory cycle to a patient who is spontaneously breathing That's it! No respiratory rate, no tidal volume, no support for any breaths...so what does our patient have to do on their own? Via ventilator (invasive ) or via nasal pillow, mouth/nose mask, or face mask-must have tight seal (non-invasive) (next slide) Similar to PEEP when provided invasively...

Treatment for Metabolic alkalosis:

Correct acid base imbalance - Dc Thiazide diuretics and NG suction - Antiemetics - Acetazolamide (Diamox) to increase secretion of bicarb by kidneys - O2 is hypoxia - Seizure precautions - Replace electrolytes - Irrigate NG with saline to prevent electrolyte loss

Resistance

Opposition to the flow of gases in the airways, due to airway diameter (narrow, mucous), length (short or long), and flow rate of gases - anything opposing flow of gas

Treatments for for Metabolic Acidosis:

Correct the acidosis addressing the symptoms and the underlying cause - Respiratory compensation typically first line intervention including mechanical ventilation if needed. - Diabetes: rapid acting insulin to reverse DKA and drive potassium back into the cell - Monitor potassium levels - levels will drop as acidosis is corrected so need to monitor for hypokalemia as well - Monitor and correct all electrolytes, BUN, CR - Sodium bicarbonate to neutralize - Fluid replacement - Dialysis with renal failure or toxicities - Antibiotics for infections - Antidiarrheal - Monitor vitals, ECG (hyperkalemia can cause VT/VF) - Assess and monitor neuro - Position to promote chest expansion Encourage compensatory mechanisms - Increased CO2 excretion by lungs -> Kussmaul respirations (deep and rapid)

Treatment for Respiratory alkalosis

Correct underlying disorder: - detect and remove salicylate or other drugs, reduce fever, - treat sepsis - Oxygen therapy - Anxiety medication - Breathe into bag for hyperventilation - Adjust ventilator settings (decrease RR and TV) in on vent - Monitor vitals, neuro or cardiac changes, abnormal labs, ABG

Reduction of airway inflammation

Corticosteroids

A nurse is assessing a female client with multiple trauma who is at risk for developing acute respiratory distress syndrome. The nurse assesses for which earliest sign of acute respiratory distress syndrome? A. Bilateral wheezing B. Inspiratory crackles C. Intercostal retractions D. Increased respiratory rate

D

Examples of health problems that lead to imbalance:

DM COPD Kidney disease GI Disturbances

Injury/Exudative Phase of ARDS

Damage to alveolar-capillary membrane causes increased capillary permeability leading to pulmonary edema Decreased lung compliance (stiff lungs)

ETT Suctioning Complications

Decreases PaO2 and O2 sats (SpO2) May cause ECG arrhythmias (PVCs etc) Increases arterial blood pressure (ABP) Increases ICP (intracranial pressure) Causes bronchospasm May cause tracheal hemorrhage May cause tracheal wall damage Predisposed to noscomial pneumonia

Oscillatory Ventilation

Delivers low tidal volume at very fast rate (300-420 bpm) - Used in patients with noncompliant lungs (such as ARDS) who remain hypoxemic despite conventional and advanced ventilation - Used to treat refractory respiratory failure - Close monitoring essential - Sedation and paralysis indicated

Clinical Manifestations of failure of ventilation:

Dependent on extent of PaO2 or PaCO2 changes - acute or chronic, ability to compensate. Early signs: - Change in mental status, fatigue, restlessness - Anxiety (SNS response): tachycardia, tachypnea, mild HTN - Morning headache

Sedation considerations for SIMV

Depends if this is a weaning mode- usually sedated, but may need to have respiratory drive to trigger own breaths

Early Signs of ARDS

Difficulty Breathing: - Dyspnea, tachypnea, cough, restlessness Lung sounds: - normal or fine, scattered crackles ABG: - mild hypoxemia, respiratory alkalosis CXR: - normal or scattered infiltrates

Later Signs of ARDS

Difficulty Breathing: - Tachycardia, diaphoresis, changes in mental status, cyanosis, and pallor - Increasing WOB Lung sounds: - Diffuse crackles, coarse crackles ABG: - Hypoxemia despite increased FIO2 CXR: - Bilateral, extensive diffuse infiltrates

Causes of Failure of oxygenation:

Difficulty getting the blood to the alveolus - Pulmonary embolus - Shock/hypotension (reduced flow to PA) Difficulty getting enough oxygen to cross the space between the alveolus and the capillary - Alveolar injury - Pneumonia - Toxic inhalation - ARDS - Diffusion limitation

Reduction of pulmonary congestion

Diuretics, nitrates if heart failure present

What does artificial breathing look like today?

Don't create a vacuum, have to push the air in (opposite of normal respirations) "Positive pressure ventilation" - A machine can "PUSH" the air in rather than it getting "sucked" in naturally - Inspiration: Causes intrathoracic pressures to increase - Expiration: happens passively

Causes of Diffusion Defect

Due to any pathologic changes in the membrane structure such as: - ARDs - COPD - CF - granuloma - interstitial edema - proliferation of connective tissue

What happens when patient triggers own breath on pressure support?

Each triggered breath is supported with set amount of pressure

Different ways our patients can fail to oxygenate

Hypoventilation - so if our failure is to oxygenate- to get oxygen into the blood- the problem could be that our patient is simply not breathing enough - they are hypoventilating V/Q Mismatch - the V stands for ventilation and the q stands for perfusion - any mismatch in ventilation and perfusion - either not good ventilation or bad blood flow- now we're not going to be able to get oxygen into the bloodstream as well - we have failure to oxygenate - naturally happens in our upper airways- we have great ventilation and movement of air in our upper airway- near the apex of our lungs- but our blood flow is not as great- the density of capillaries is lower Diffusion limitation - this is referring to that space between the capillary and the alveolus. - We need those two to have good contact- we need the oxygen from the alveolus to get into that capillary and into the bloodstream- but in diffusion limitation, that space between the alveolus and the capillary is thickened or damaged. - So that normal pathway of oxygen is limited.

Treating Ventilator Associated Pneumonia (VAP)

Elevate head-of-bed 30 to 45 degrees (prevent aspiration) Hand washing (prevent infection) Interrupt sedation each day to assess readiness to wean from ventilator Prophylaxis for deep vein thrombosis (DVT) Prophylaxis for peptic ulcer disease (PUD) Meticulous oral care Q2 hours

Post Extubation

Endotracheal cuff is deflated prior to removal during inspiration-plan for secretions - Suction secretions before deflating cuff (can dump secretions into lungs) - Towel, more suction, O2 Assess for: - Stridor or hoarseness - Gag reflex prior to feeding-if client coughs with water then stop-refer to ST or RD for gag swallow test (dysphagia/aspiration) - Signs of respiratory distress - Changes in vital signs - Low oxygen saturations - Restlessness, increased WOB and diaphoresis

Endotracheal Tube (ETT) Patency

Endotracheal suctioning - Closed (in-line suctioning) - Open (sterile catheter suctioning)

Primary Disturbance Examples

Example 1: - PH 7.14 PaCO2 51 HCO3 24 Example 2: - PH 7.21 PaCO2 40 HCO3 16 Example 3: - PH 7.50 PaCO2 30 HCO3 25 Example 4: - PH 7.61 PaCO2 40 HCO3 42

Mixed or Combined Examples

Example 1: - PH 7.68 PaCO2 24 HCO3 36 Example 2: - PH 7.11 PaCO2 58 HCO3 18 Example 3: - PH 7.62 PaCO2 30 HCO3 30 Example 4: - PH 7.51 PaCO2 26 HCO3 32

Respiratory Alkalosis

Excessive CO2 is removed by the lungs (CO2 levels drop) Hyperventilation (too deep/fast) (↓ PaCO2)

3 Classifications of respiratory failure:

Failure of ventilation Failure of oxygenation Failure of BOTH ventilation and oxygenation

Hypoventilation

Failure of ventilation - Not breathing enough Not getting enough O2 to begin with - Low O2 coming in, low O2 diffuses into blood

Example settings for CPAP

FiO2 40% PEEP 5

Example settings for pressure support:

FiO2 40% PEEP 5 PS: 7cmH2O

Example settings for SIMV:

FiO2 40% PEEP: 5 Vt: 450 RR: 8 If SIMV with PS: FiO2: 40% PEEP: 5 Vt: 450 RR: 8 PS: 10

Example settings for AC:

FiO2: 40% PEEP: 5 Vt: 450 RR: 8

CPAP example settings:

FiO2: 40% PEEP: 5cmH20

Proliferative/Reparative of ARDS

Fibrin matrix forms progressive hypoxemia

What to do for Respiratory Acidosis

Focus to improve ventilation and lower PaCO2 level and correct underlying cause if possible

FiO2-fraction of inspired oxygen

Fraction or percent of oxygen (O2) delivered to the patient Varies from .21 (21%) to 1.00 (100%)

ABG results are as follows: pH 7.20 PaCO2 28 mm Hg PaO2 81 mm Hg HCO3- 18 mEq/L Describe a patient who would have these ABGs, including history, assessment, and treatment.

In this case, the decreased pH and decreased HCO3− indicate a metabolic acidosis. - The decreased PaCO2 reflects compensation for the acidosis. Metabolic acidosis most commonly occurs in uncontrolled diabetes, but may also be caused by lactic acidosis, starvation, severe diarrhea, renal failure, or shock. Assessment findings may include drowsiness and confusion leading to coma; deep, rapid respirations (compensation); hypotension and arrhythmias; warm, dry, flushed skin; and nausea, vomiting, and abdominal pain. Determination of the underlying cause is necessary to treat the acidosis. - Diabetic acidosis is treated with insulin to normalize glucose metabolism, and carbohydrate (glucose) is provided in the case of starvation. - Dialysis may be used to treat renal failure, and other underlying causes are treated as appropriate.

ABG results are as follows: pH 7.50 PaCO2 28 mm Hg PaO2 85 mm Hg HCO3- 24 mEq/L Describe a patient who would have these ABGs, including history, assessment, and treatment.

In this case, the increased pH and decreased PaCO2 indicate a respiratory alkalosis. - The normal HCO3− reflects no compensation for the alkalosis. Respiratory alkalosis most commonly occurs with hypoxemia from acute pulmonary disorders. - Anxiety, CNS disorders, and mechanical over-ventilation also increase the ventilation rate, leading to respiratory alkalosis. Assessment findings may include tingling and numbness of the fingers, restlessness, hyperreflexia, tetany, headache, dizziness, confusion, tachycardia, dysrhythmias, nausea, vomiting, and epigastric pain. Determination of the underlying cause is necessary to treat the alkalosis. - Having the patient rebreathe into a paper bag can increase CO2 retention and thus decrease the pH. - Correction of hypoxemia with oxygen therapy and bronchodilators can also be useful.

A 55 year old male with a brain tumor is hypoxic and hypercarbic (high CO2), what is he at risk for?

Increased ICP due to cerebral vasodilation

Causes of IICP

Increases in brain volume, cerebral blood volume, or CSF volume Cerebral edema (numerous types) Brain mass, tumor, abscess, contusions BLOOD CSF

Intracranial Pressure Compliance:

Increases in one of those 3 other 1 or 2 have to decrease - CSF? displaced into subarachnoid space - Blood? vasodilation/constriction; displaced into venous sinuses - Both? - Blood and CSF can only be displaced so much... - Brain tissue? Herniation (moves from high pressure to low pressure area

Pathophysiology of ARDS (phases):

Injury/Exudative Phase Proliferative/Reparative Fibrotic Phase

VAP Bundle

Interventions that are geared towards reducing VAP - elevating the head of bed to 30-45 degrees - a daily break from sedation to increase neurological stimulation and possibly exercising the breathing muscles- this is often called a "sedation vacation" - PUD prophylaxis - DVT prophylaxis

In regards to acid-base imbalance, what does "compensation" mean?

It is the body's attempt to correct the acid-base imbalance

Proper cuff inflation for intubation

Just enough to create seal - Prevent air leak *the cuff prevents air from sneaking back out the tracheal and allows all of the air delivered through that ETT to go down into the lungs. If air is allowed to go back around that tube and out the mouth, we call that an "air leak". - Decrease risk of pulmonary aspiration *when we're not intubated, we swallow oral secretions- without even thinking of it. However, we've bypassed this person's epigolottis, their normal eating and breathing mechanisms- so they can't swallow anymore! Thus, all of these secretions could get dumped into the lungs- however, this cuff also prevents much of this Excessive pressure (overinflation) - Tracheal ischemia - Necrosis, erosion of surrounding tissue - Cuff rupture (too tight) Check policy. Who measures & how often? - resp. therapist

Positive End Expiratory Pressure (PEEP)

Keeps alveoli open at end of expiration and increases Functional Residual Capacity Positive airway pressure to mechanically assisted breaths - PEEP is constant

pH between 7.4-7.45 "normal, but on the basic side of 7.4" CO2 -> "acid" HCO3 -> "base"

Kidneys are causing the problem, lungs are helping and Brought the pH back within normal range- fully compensating "FULLY compensated metabolic alkalosis"

Respiratory Problem: alkalosis (↑pH)

Kidneys excrete HCO3 and retain hydrogen= ↑urine alkaline + ↓ HCO3 in blood = ↓pH

Intrapulmonary Shunting

Large amount of blood returning to left side of heart that has not engaged in gas exchange causes low PaO2 (hypoxemia) -> leads to alveolus collapse - Higher levels of oxygen will not be helpful, because blood is being shunted away from the lungs

Types of devices for ICP Monitoring

Location (eg. Epidural, Subdural, Subarachnoid) Purpose - Trend an ICP waveform only -> fiberoptic catheter or subarachnoid bolt or screw - Drain CSF and trend ICP waveform ->Ventriculostomy/External ventricular Drain(EVD) ->catheter that can trend ICP and drain CSF if necessary

Metabolic Alkalosis

Loss of acid - Stomach acid: NGT suctioning/vomiting - Drugs causing hypokalemia (eg. Thiazide diuretics) -> causes body to release aldosterone -> triggers retention of potassium in exchange for excreting H+ ions acid loss Bicarbonate excess - Antacid overdose - Over-administration of NaHCO3 (↑ PaHCO3-)

High pH: Alkalemia ->

Low PCO2 (resp. alkalosis) High PCO2 (metabolic alkalosis)

Examples of O2/CO2 problems and ventilator settings:

Low PaO2 and high CO2 - (not getting enough O2, not getting rid of CO2 - things aren't moving! - increase the Respiratory Rate) High PaO2 and high CO2 - (getting too much O2, not getting rid of CO2 - need to turn down FiO2 and increase the Respiratory Rate)

pH between 7.35-7.4 "normal, but on acid side of 7.4" CO2 -> "acid" HCO3 -> "base"

Lungs are causing the problem, kidneys are helping and brought the pH back within normal range- fully compensating! "FULLY compensated respiratory acidosis"

Fibrotic Phase of ARDS

Lungs become fibrotic, reduced functional residual capacity, narrowing airways

Equation to determine CPP

MAP - ICP = CPP

Which of the following is the correct formula for calculating CPP?

MAP-ICP=CPP

ARDS Treatments

Maintain airway: - Endotracheal tube Optimize oxygen delivery: - High PEEP, High Frequency Oscillatory Ventilation (HFOV), Rot-a-prone bed Minimize oxygen demand: - Reduce metabolic demand (stress, fevers, pain) Treat the cause: - Sputum cultures/antibiotics, sepsis, multiple organ dysfunction Prevent complications: - VAP, hypoxia (tissue and organ damage), decubitus ulcers (from rot-a-prone bed)

What is the key of intubation?

Maintaining a secure and stable airway! - Assess - Assess - Assess - And maintain Sedation for client's on Mechanical Ventilation when NOT weaning!

Giving medications prior to ET tube placement

Many times these patients will be provided sedation, analgesia, and even a neuromuscular blocking agent-a paralytic- prior to having this large tube placed down their airway. - We will often be responsible for administering these medications and clearly announcing them to the physician who will be intubating. - Timing is key- think about it-You don't want to give a sedative or a paralytic if the physician isn't ready to intubate! - You'll be looking at an apneic patient and a team that may not be ready to breathe for the patient

Compliance

Measure of stretch or distensibility of the lungs-high compliance indicates EASE in stretching verses low compliance indicates difficulty stretching, such as a client with COPD or ARDS who have "non-compliant" lungs

What imbalance is this? pH 7.18 PaCO2 38 mm Hg PaO2 70 mm Hg HCO3- 15 mEq/L

Metabolic acidosis pH is low. PaCO2 is normal. HCO3− is low. - By using the ROME mnemonic, the metabolic component (HCO3−) is going in the same direction as the pH—thus the patient has metabolic acidosis. - Because the CO2 is normal, there is no compensation.

What imbalance is this? pH 7.28 PaCO2 28 mm Hg PaO2 70 mm Hg HCO3- 18 mEq/L

Metabolic acidosis, partially compensated pH is low. PaCO2 is low. HCO3− is low. - By using the ROME mnemonic, the metabolic component (HCO2) is going in the same direction as the pH—thus the patient has metabolic acidosis. - Because the PaCO2 is also low but the pH is not yet back to normal, there is partial compensation.

What imbalance is this? pH 7.58 PaCO2 35 mm Hg PaO2 75 mm Hg HCO3- 50 mEq/L

Metabolic alkalosis pH is high. PaCO2 is normal. HCO3− is high. - By using the ROME mnemonic, the metabolic component (HCO2) is going in the same direction as the pH—thus the patient has metabolic alkalosis. - Because the PaCO2 is normal, there is no compensation.

Sedation considerations for pressure support

Minimal- patient must be awake enough to trigger breaths on own - this is a weaning mode

There are only 2 types of "mixed" or "combined" disturbances:

Mixed Acidosis Mixed Alkalosis

What is the nurse's responsibility related to intubation?

Monitor the patient's SaO2 and alert the team of any complications during intubation attempts

Immediate Nursing Assessment for intubated patients

Monitor ventilation with BVM Assess oxygenation by SaO2 Suction when necessary Watch the clock with intubation attempts! Preliminary Assessment of ETT Placement - Observe chest for symmetrical rise & fall - Auscultate lungs bilaterally - Auscultate over the stomach - CO2 detector Secure the tube & identify 'cm' placement Inflate the cuff via pilot balloon

Sedation considerations for AC

Most likely- patient will be slightly more comfortable because they can take own breaths, but still need sedation for comfort to avoid tachypnea

Diffusion

Movement of O2 and CO2 at the capillary membrane level. - Diffusion is the movement of gases from an area of higher to lower pressure - (driven by pressure gradients)

Ventilation

Movement of gases O2 and CO2 in and out of the aveoli

Your patient is a 62 year old male with history of COPD, recently diagnosed with pneumonia and respiratory distress, he was just intubated. He is alert and following commands while on the ventilator but appears exhausted. The physician is discussing with you what ventilator mode to put the patient on. She mentions SIMV and CPAP. Which mode is best, why?

NOT CPAP -> patient is too tired to initiate his own breaths, need a respiratory rate setting SIMV -> YES- patient will have a set rate and volume but can take his own breaths

Treatment/interventions for respiratory acidosis due to hypoventilation:

Need to Breathe more (increase RR and depth) -CNS depression? Narcan/reduce sedation -Intubate or change existing ventilator settings (↑RR and/or size of each breath) -Suctioning, bronchodilators -Treat pneumonia/pneumothorax

Treatment/interventions for respiratory alkalosis due to hyperventilation:

Need to breathe less (decrease RR and depth) -CNS stimulation --anxiety/pain/fever/drugs (nicotine, catecholamines)? Analgesia, anxiolytics, antipyretics, stop or reverse drugs -Need to retain CO2 (can breathe into a paper bag) -Change existing ventilator settings (↓ RR and/or size of each breath)

Treatment/interventions for metabolic acidosis due to acid build up/bicarbonate loss:

Need to excrete acid/retain bicarbonate (monitor for hypokalemia as acidosis is corrected) -Administer Sodium Bicarbonate -Encourage Kussmaul respirations (natural compensation)- can also do this with mechanical ventilator -Antidiarrheal (Diarrhea) -Dialysis (renal failure) -Insulin (DKA)

Treatment/interventions for metabolic alkalosis due to bicarbonate build up/acid loss:

Need to excrete bicarbonate/retain acids -D/C drugs causing imbalance (antacids, thiazide diuretics) -D/C NGT suction -Antiemetics -Acetazolamide (Diamox)

Sedation considerations for CPAP

No sedation (or minimal sedation in some cases)

What happens when patient triggers own breath with CPAP?

No volume or pressure assistance- volume and frequency is up to the patient

What does normal breathing look like?

Normal breathing= negative pressure ventilation

Respiratory Failure

Occurs due to a disease state (not a disease in itself) - ARF in ARDS - COPD - asthma - pneumonia - VAP

Bronchial breath sounds over the lung periphery:

Often result from lung consolidation that is seen with pneumonia

Partial Compensations

One system is causing the disturbance- one system is TRYING to compensate. Both PaCO2 and HCO3 are abnormal! - You just have to figure out which one is abnormal because it's causing the problem and which one is abnormal because it's trying to fix the problem - HOW? Which abnormal value "matches" the pH? pH is still abnormal (it has only "partially" compensated) - Movement of all values, but either the PCO2 or HCO3 is MATCHING the PH - The other value is moving in the OPPOSITE DIRECTION attempting to compensate, but it's a partial compensation because the PH is NOT in normal range

Medications for the patient with IICP

Osmotic Diuretics (eg. Mannitol) - Causes diuresis by increasing osmolarity within the nephron decreases cerebral edema Hypertonic Saline (eg. 3% NaCl) - Pulls fluid out of interstitial space and into the intravascular space decreases cerebral edema - WARNING: must infuse SLOWLY and through a central line (see hospital protocol)- often around 30mL/hour - Monitor Na levels Antiseizure drugs (eg. Phenytoin/ Dilantin) - Seizures increase metabolic demand Corticosteroids (eg. Dexamethasone) - Reduce swelling (brain tumors, cerebral edema)

Mixed Acidosis

PH < 7.35 PaCO2 > 45 HCO3 < 22 - pH is acidic, everything is abnormal/acidic - Patient has a metabolic problem AND a respiratory problem (both causing acidosis) - No one is trying to compensate- they are both causing the disturbance! - example: a patient in cardiopulmonary arrest

Mixed Alkalosis

PH > 7.45 PaCO2 < 35 HCO3 > 26 - pH is basic, everything is abnormal/alkalotic - Patient has a metabolic problem AND a respiratory problem (both causing alkalosis) - No one is trying to compensate- they are both causing the disturbance! - example: a patient who is hyperventilating because of postoperative pain and losing acid secondary to nasogastric suctioning

Pressure Ventilator Modes: Issues

PRESSURE setting - Lungs with low compliance will reach the set pressure setting much sooner than compliant lungs - Why is this a problem? - The same amount of pressure might inflate a compliant lung, but only meet resistance in a lung with low compliance

Respiratory Failure based upon ABGs (room air):

PaO2 < 60 mm Hg when receiving an inspired O2 concentration >60%. (Hypoxemic) PaCO2 > 45 mm Hg (Hypercapnic) pH ≤ 7.35 (Hypercapnea has caused acidosis)

What happens when patient triggers own breath on SIMV?

Patient determines volume of the breaths they trigger on their own

Early signs of ARDS:

Patient is responding to lung injury working hard to get enough O2! • Tachypnea respiratory alkalosis • Normal CXR at first • Early hypoxia: restlessness, altered LOC, disorientation, increased HR and Temperature • Refractory hypoxemia (O2 saturations do not improve even if you give oxygen)

Ventilator Associated Pneumonia (VAP)

Pneumonia that occurs 48 hours or more after ETT intubation - ETT bypasses normal airway defenses (cilia) - Purulent sputum, fever, elevated WBCs, crackles or rhonchi --> CXR reviewed for signs of pneumonia

ICP Management & Care

Positioning - HOB to facilitate outflow but promote CPP - prevent neck flexion Skin Care Prevention of infection and/or hemorrhage Pain Management/Reduce Anxiety Psychosocial Issues Decrease environmental stimuli Decrease causes that raise ICP - metabolic demand (fever, seizures, shivering) - Stress - Suctioning (keep to <10 seconds at a time) - Abdominal distension Assess neurological status frequently Safety considerations: - Seizure precautions? - Restraints? Keep normotensive, hydrated, and nutritionally adequate Family? - Allow involvement as appropriate (watch ICP/CPP) Maintain normal intracranial pressure (ICP), cerebral blood flow (CBF) and cerebral perfusion pressure (CPP) Watch for SECONDARY brain injury (developed after primary injury- we can prevent this with close ICP monitoring and early intervention)

Late sign of IICP

Posturing - Decorticate Abnormal flexion - Decerebrate: Abnormal extension

Pleural friction rub

Presence of pneumonia that has involved the pleura

Which of the following is true about pressure versus volume modes?

Pressure modes deliver breaths with a set amount of pressure measured in cmH20

ICP Monitoring

Pressure signal coming from within the cranium that needs to be transduced - Requires a device bored into the patient's skull - Requires Pressure Line device set up (different than with hemodynamics - no "pressure bag" at 300mmHg needed!) Indications: GCS score of 3-8 (out of 15) - Used to assess response to therapy or augment neuro assessment

Pressure Support (PS)

Pressure support can be BOTH a setting and pressure mode Example PS as a setting (added on to SIMV- providing help with spontaneous breaths): - SIMV: RR 14 Vt: 500mL PS 10 cmH2O FiO2 50% PEEP: 5cmH20 - Patient is in SIMV, but instead of their extra breaths being unsupported by the ventilator (Regular SIMV), they get 10cmH20 support (SIMV with a PS setting) Example PS as a mode (All the ventilator is doing is supporting breaths the patient takes on their own): - PS: PS 10 cmH2O FiO2 50% PEEP: 5cmH20 - Missing settings: No RR, No Vt- just help with breaths the patient triggers on their own!) - Patient must be spontaneously breathing if used as a MODE- otherwise they will not get ANY breaths!

Example of hypoventilation

RR of 6 - would result in our patient not taking in enough air overall- and that's going to mean that we're also not taking in enough oxygen

Your patient's tube is secured and connected to the mechanical ventilator. The physician orders the following mode and settings: SIMV RR: 12 Vt: 450 PEEP: 5cmH20 FiO2: 40% Describe what will happen in this ventilator mode. (short answer)

RR: 12 -> the ventilator will guarantee that the patient receives 12 breaths a minute, but if the patient decides to take any more breaths over 12, the ventilator will not help them- thus, the tidal volume will be a natural volume, not a pre-set volume delivered by the ventilator Vt: 450 -> guaranteed volume for 12 breaths a minute PEEP: 5cmH20 amount of pressure constantly provided to keep the alveoli open FiO2: 40% -> amount of air delivered to the patient that is oxygen. Room air is 21%.

Compensated respiratory alkalosis is what?

Rare - In acute respiratory alkalosis, aggressive treatment of the causes of hypoxemia is essential and usually does not allow time for compensation to occur. - Some buffering may occur with shifting of bicarbonate (HCO3-) into cells in exchange for Cl- - In chronic respiratory alkalosis that occurs with pulmonary fibrosis or CNS disorders, compensation may include renal excretion of bicarbonate.

ICP Monitoring: Nursing Considerations

Reduce risk of/monitor signs of Infection - Assess insertion site and drainage for signs of infection Assess brain perfusion - CPP? - Neurological assessment - Increased ICP? - Reduce risk for IICP Ventricular Drains - Physician orders: *Closed, intermittent, continuous *Height ("open at 10cmH20") - Evaluate CSF drainage and document *Color/Characteristics *Amount Pressure lines need to be leveled at the appropriate reference point! - Phlebostatic axis ICP-> leveled at the Foramen of Monro (tragus of the ear)

Compensation: How do the lungs help our bodies handle an acid base imbalance?

Regulates CO2: normal levels 35-45 mm Hg Metabolic Acidosis Problem: (↓pH) - triggers Hyperventilation (↑rate and depth of RR) = ↓CO2 = ↑pH Metabolic Alkalosis Problem: (↑pH ) - triggers Hypoventilation (↓rate and depth of RR) = ↑CO2 = ↓pH

Abnormal ABGs:

Remember, there is a "disturbance" and sometimes compensation

Pressure support settings: (a mode and setting)

Respirations Is this a setting? - NO - Patient must trigger every breath on their own Volume Is this a setting? - NO Pressure Support Is this a setting? - yes - specific amount of pressure will be provided with each breath triggered by the patient PEEP Is this a setting? - yes FiO2 - yes

CPAP settings

Respirations Is this a setting? - NO - Patient takes own breaths Volume Is this a setting? - NO Pressure Support Is this a setting? - NO PEEP Is this a setting? - yes FiO2 - yes

AC settings

Respirations Is this a setting? - Yes Volume Is this a setting? - yes Pressure Support Is this a setting? - no PEEP Is this a setting? - yes FiO2 - yes

SIMV settings

Respirations Is this a setting? - Yes Volume Is this a setting? - yes Pressure Support Is this a setting? - not usually - however, PS can be added on to SIMV where triggered breaths are actually supported with set pressure PEEP Is this a setting? - yes FiO2 - yes

Increased PaCO2 and decreased PaO2 -> Which acid-base disturbance would present?

Respiratory acidosis

What imbalance is this? pH 7.33 PaCO2 67 mm Hg PaO2 47 mm Hg HCO3− 37 mEq/L

Respiratory acidosis, partially compensated pH is low. PaCO2 is high. HCO3− is high. - By using the ROME (Respiratory Opposite Metabolic Equal) mnemonic, the respiratory component (PaCO2) is going in the opposite direction as the pH—thus, the patient has respiratory acidosis. - Because the HCO3− is elevated, the patient is partially compensating.

What imbalance is this? pH 7.60 PaCO2 30 mm Hg PaO2 60 mm Hg HCO3- 22 mEq/L

Respiratory alkalosis pH is high. PaCO2 is low. HCO3− is normal. - By using the ROME mnemonic, the respiratory component (PaCO2) is going in the opposite direction as the pH—thus the patient has respiratory alkalosis. - Because the HCO3− is normal, there is no compensation.

Compensation:

Sometimes the other system tries to help out The system (renal or respiratory) that does not have a disturbance may try to correct the disturbance (think: "who is trying to fix the problem?" "which system is NOT causing the problem?") - Example: Metabolic disturbance causing acidosis? Lungs try to help bring the pH back to normal (more alkalotic) - Example: Respiratory disturbance causing alkalosis? Kidneys try to help by bringing the pH back to normal (more acidic)

Mechanical Ventilation: Complications > 3 days is considered long-term Associated with increased complications and poor outcomes

Right mainstem bronchus intubation - the tube could migrate down past the carina and potentially slip into the easiest place- the right mainstem Unplanned extubation; ETT malposition/extubation Laryngeal/tracheal injury; Damage to oral/nasal mucosa Oxygen toxicity - When the partial pressure- or total amount of oxygen- in our blood stream gets too high, your patient develops hyperoxia where your patient experiences a large amount of reactive oxygen - these reactive oxygen begin to cause pulmonary toxicity and can cause the lining of the alveoli - if our patient has an FiO2 over 50% but is still not oxygenating well, we look into increasing PEEP instead of just cranking up the FiO2--- putting our patients at risk for oxygen toxicity Acid-Base Disturbances Psychosocial concerns: stress, anxiety,& depression Peptic Ulcer Disease (PUD) - this stress, paired with impaired splanchnic perfusion, mucosal damage, and other factors, our patients are also placed at risk Hemodynamic compromise; PEEP causing decreased CO/BP - when we increase pressure to inflate the lungs, we increase the pressure up against the heart - It's pretty hard to fill up if something is squishing you and pushing you down - if your heart can't fill up, it isn't going to pump out very much blood either - thus, A lower cardiac output and lower blood pressure

Intracranial Pressure

Rigid cranial vault + 3 non-compressible contents: blood, brain tissue, CSF

Potential complications of the patient with an External Ventricular Drain (EVD)

Risk for rapid outflow of CSF (risk for herniation, ventricular collapse) Infection, subdural hematoma Inaccurate readings inappropriate interventions patient complications

Confirm Placement for intubation

STAT CXR after intubation - Tip of ETT should be 3-4 cm above the carina for adults Assess daily CXR on ventilated clients for ETT position Document size of ETT Document placement (depth of ETT) by confirming cm at lip Document ventilator settings Time for an ABG?

Interpretation of ABGs

STEP 1: - Look at each number and label STEP 2: - Evaluate oxygenation STEP 3: - Determine acid-base status - Evaluate the pH STEP 4: - Determine the primary cause of the acid base status (respiratory or metabolic) same direction as pH-(MATCHES pH) STEP 5: - Determine compensation

Comparing AC and SIMV

Settings: RR: 12 Vt: 400mL FiO2: 40% PEEP: 5 AC: patient can take a 13th + breath- and it will be supported with 400mL - Patient: RR: 12 or more Vt: always 400mL SIMV: patient can take a 13th + breath- but they won't get any help from the ventilator - Patient: RR: 12 or more Vt: 12 breaths will be 400mL, any extra breaths will be whatever the patient is able to do on their own

Cardinal signs of ARDS

Severe refractory hypoxemia - ("stubborn hypoxia" - low PaO2 and SaO2 despite increasing oxygen administration) "White out" CXR - represents fluid in the lungs Abnormalities related to the mechanical ventilator: - Increasing use of PEEP (Positive End Expiratory Pressure) *pressure needed to keep alveoli open) - Increasing PIP levels (peak inspiratory pressure) *how much resistance the ventilator is encountering when it tries to deliver breaths

Short-Term Weaning Trials

Short duration-usually 30 minutes to 2 hours with periods of rest Change the mode and settings so that the patient does more work! - SIMV vs. AC (both can be weaning modes if the RR is lowered) - Pressure Support (now the patient has to trigger all breaths, but they get some support with each breath) - CPAP (now the patient has to trigger every breath- and they don't get any extra support with each breath) T-Piece trials strengthens respiratory muscles (no pressure, just humidified FiO2 and a secure airway!)

Example of tissue hypoxia:

Some conditions prevent tissues from using O2 despite availability - cyanide or carbon monoxide poisoning

Disturbance:

Something is wrong - Either a metabolic source or a respiratory source- causing either acidosis or alkalosis (think: "who is at fault?" "which system caused this pH problem?") - Sometimes the disturbance comes from both metabolic and respiratory sources!

Nursing Care of the patient with an External Ventricular Drain (EVD)

Strict Aseptic Technique during dressing changes Signage or other alerts that the patient has EVD Reassess level of transducer with any position change Position changes with the drain CLOSED To review an accurate ICP signal - EVD should be closed for at least 6 minutes before the waveform is considered "accurate" - Stopcock allowing signal from EVD to monitor - Evaluate for causes of inaccurate ICP waveform: improper level, bubbles in the tubing, CSF leaks, kinks in tubing, obstructions Monitor and manage ICP

Patient Data to Monitor when on mechanical ventilation

TOTAL Respiratory Rate (RR) - How many did the patient take on their own? Peak Inspiratory Pressure (PIP): maximum pressure that occurs during inspiration - Increases with airway resistance Tidal Volume - Is the full Vt getting in? - Safety mechanism on the ventilator to stop forcing volume in if too much pressure encountered - How big of a breath can the patient take on their own? - How big of a breath did that amount of pressure create? Oxygen saturation ABGs Look at your patient!

What is PEEP?

The amount of pressure delivered at the end of exhalation aimed at keeping the alveoli open

Respiratory rate or (f)

The frequency (f) of breaths set to be delivered by the ventilator - Number of breaths set to be delivered each minute - Usually between 12-20 breaths/minute physiological rate - Based on patient's condition: ABGs, SpO2, chest x-ray, any acid-base disturbances

To compensate for metabolic acidosis:

The kidneys attempt to excrete additional acid and the lungs increase CO2 excretion. - The patient often develops Kussmaul respirations (deep, rapid breathing). - If metabolic acidosis is present, calculating the anion gap can help determine the source of metabolic acidosis. - The anion gap is the difference between the measured serum cations and anions in ECF. - You calculate an anion gap by using the following formula: Anion Gap = Na+ - (HCO3− + Cl −) - A normal anion gap is 8 to 12 mmol/L. - The anion gap increases in metabolic acidosis associated with acid gain (e.g., lactic acidosis, diabetic ketoacidosis), but is normal in metabolic acidosis caused by bicarbonate loss (e.g., diarrhea)

To compensate for metabolic alkalosis:

The lung's compensatory response is limited. - The respiratory rate decreases in order to increase plasma CO2. - However, once hypoxemia occurs or plasma CO2 reaches a certain level, stimulation of chemoreceptors increases respirations

Increased Intracranial Pressure

The pressure exerted by brain tissue, blood, and cerebrospinal fluid against the inside of the skull - Pressure of 20 mm Hg or > persisting for 5 minutes or longer

Cerebral Perfusion Pressure (CPP)

The pressure required to perfuse the brain - MOST IMPORTANT SINGLE FACTOR IN MAINTAINING BRAIN HEALTH

Diffusion Defect

There is a problem with diffusion OR the gas movement from an area of high conc to low concentration. - Time to cross the capillary membrane is prolonged and it's thickened - Gas movement from area of high concentration to low DD due to increased interstitial fluid - HYPERCAPNIA is a LATE SIGN of DD - O2 needs to move across a membrane- if the membrane is too thick or full of fluid, O2 exchange is more difficult or "defective"

ABG results are as follows: pH 7.57 PaCO2 46 mm Hg PaO2 87 mm Hg HCO3- 38 mEq/L Describe a patient who would have these ABGs, including history, assessment, and treatment

These ABG results indicate a metabolic alkalosis: the pH and HCO3− are elevated. - The slightly elevated PaCO2 indicates some compensation for the alkalosis. The history of a patient with metabolic alkalosis may include severe vomiting or excessive gastric suctioning, diuretic therapy, potassium deficit, excessive intake of sodium bicarbonate (baking soda), or excessive mineralocorticoid therapy. Assessment findings may include nervousness and confusion, tachycardia and dysrhythmias, nausea and vomiting, tremors, hypertonic muscles, tetany, and tingling of the fingers and toes. As in all acid-base imbalances, determination and treatment of the underlying cause is necessary. - The potassium that is lost in an alkalosis must be replaced to prevent dysrhythmias, and contributing drugs must be discontinued. - Vomiting with bicarbonate is treated as in previous case analysis.

ABG results are as follows: pH 7.36 PaCO2 58 mm Hg PaO2 50 mm Hg HCO3- 33 mEq/L Describe a patient who would have these ABGs, including history, assessment, and treatment

These ABGs indicate a hypercapnic respiratory failure indicated by decreased PaO2 and increased PaCO2. - Elevated HCO3− and (low) normal pH indicate compensation of a respiratory acidosis. Common causes of hypercapnic respiratory failure include any of the obstructive respiratory diseases (asthma, cystic fibrosis, COPD), CNS-induced respiratory depression such as head injury, spinal cord injury, brainstem infarction, sedative and narcotic overdose, and neuromuscular diseases such as myasthenia gravis, ALS, Guillain-Barré syndrome, and multiple sclerosis. Assessment findings include dyspnea, decreased respiratory rate or increased shallow respirations, and decreased tidal volume. - Cerebral symptoms include disorientation and progressive somnolence. - The patient may also have tachycardia, bounding pulse, arrhythmias, and hypertension. Treatment of the underlying condition is necessary. - In addition, oxygen therapy, mobilization of secretions, positive-pressure ventilation, and drug therapy are used. - Commonly used drugs include bronchodilators, corticosteroids, diuretics, antibiotics, sedatives, and analgesics.

ABG results are as follows: pH 7.39 PaCO2 38 mm Hg PaO2 44 mm Hg HCO3- 24 mEq/L Describe a patient who would have these ABGs, including history, assessment, and treatment.

These ABGs indicate a hypoxemic respiratory failure because all ABGs are within normal range except for the PaO2. Patients experiencing hypoxemic respiratory failure may include those with pneumonia, shock, pulmonary embolism, acute respiratory distress syndrome, or pulmonary edema. - The patient's history would include an underlying organ damage or assault. Respiratory symptoms include dyspnea, tachypnea, accessory muscle use, and late cyanosis. - The patient may experience decreased level of consciousness, restlessness, tachycardia, and late arrhythmias and hypotension. In addition to treating the underlying cause, oxygen therapy and mobilization of secretions are used to correct the hypoxemia. - Positive-pressure ventilation via endotracheal intubation may be necessary. - Maintaining adequate cardiac output with IV fluids and medications is also necessary

ABG results are as follows: pH 7.20 PaCO2 58 mm Hg PaO2 59 mm Hg HCO3- 24 mEq/L Describe a patient who would have these ABGs, including history, assessment, and treatment

These ABGs reflect an uncompensated respiratory acidosis with hypoxemia. - This could occur with a respiratory infection causing an exacerbation in a patient with COPD. The hypoxemia may be reflected by restlessness, confusion, or stupor. Respiratory and cardiac findings could include rapid, shallow breathing, rhonchi, crackles, diminished breath sounds, increased work of breathing with use of accessory muscles, orthopnea, tachycardia, and arrhythmias. Treatment includes treatment of any underlying respiratory infections, bronchodilator therapy, corticosteroids, hydration therapy, chest PT and postural drainage, breathing exercises, low-flow oxygen therapy, and mechanical ventilation if the patient continues to deteriorate

The respiratory therapist will commonly inflate what is called the "cuff." What does this mean?

This is basically a little balloon near the bottom of the ETT that prevents air from escaping out the mouth. - Since the cuff itself is way down in the trachea, we can't tell if it's underinflated or overinflated without something called the "pilot balloon" and this is a little balloon that hangs outside the patient's mouth- it has a tube connected to that cuff and basically gives us an idea of how inflated that balloon is

The amount of air in milliliters to be delivered with each breath describes which ventilator setting?

Tidal Volume

Ventilator Settings

Tidal Volume (Vt) Pressure Support (PS or PSV) FiO2-fraction of inspired oxygen Respiratory rate or (f) Positive End Expiratory Pressure (PEEP)

Monitor ventilation and oxygenation (DO NOT hyperventilate)

Too much CO2 vasodilation IICP Too low CO2 vasoconstriction cerebral tissue ischemia

Volutrauma & Barotrauma

Too much pressure/too much volume? Volutrauma: When a large Vt is used to ventilate noncompliant lungs - Movement of fluids and proteins into alveolar spaces Barotrauma: Increased airway pressure distends the lungs and could rupture alveoli - Eg. High PEEP - Air can escape to interstitium, possible pneumothorax Bottom line: damage to the alveoli

4 Primary Acid-Base Disturbances All of the uncompensated states!

Uncompensated Respiratory Acidosis Uncompensated Metabolic Acidosis Uncompensated Respiratory Alkalosis Uncompensated Metabolic Alkalosis - pH is abnormal - One system is causing the disturbance (abnormal) - One system is doing nothing/not compensating (normal)

The patient's first ABG comes back after being in this SIMV mode. Interpret the results and make a recommendation to the healthcare team. (short answer) pH: 7.31 CO2: 50 HCO3:25 PaO2: 70

Uncompensated respiratory acidosis with hypoxia. - This patient has a failure to ventilate causing failure to oxygenate. - We need to either increase the respiratory rate setting for this SIMV mode or change the patient to Assist Control mode (both answers would be appropriate).

The patient is changed from SIMV to AC mode ventilation: AC; RR: 15; Vt: 500; PEEP: 5; FiO2: 50% He appears a little bit anxious when you walk in the room. You review the ABG results from approximately 20 minutes after the ventilator mode change. Interpret these results and make a recommendation to the healthcare team (short answer) pH: 7.50 CO2: 30 HCO3: 24 PaO2: 110

Uncompensated respiratory alkalosis with hyperoxia. - This patient is hyperventilating. - We could reduce the respiratory rate setting which can reduce hyperventilation. - However, if the patient is triggering a lot of breaths on his own due to anxiety, each of those breaths is getting 500cc of tidal volume (causing hyperventilation). - Therefore, in that case we would consider sedating the patient more. - We could also change him back to SIMV so that every triggered breath is not supported with the full volume. - All of these are potential strategies and should be discussed as options with the healthcare team.

Before and During Paralyzing a patient: Train of Four (TOF) Peripheral Nerve Stimulation

Used when patients are given a neuromuscular blocking agent (NMB) ie paralytic IV drip Testing their personal neuro muscular activation (like a vital sign, everyone is a little different) Machine delivers 4 impulses of electricity, watch the patient for a response (4 "twitches")

Volume Ventilator Modes: Issues

VOLUME setting - Lungs with low compliance- forcing in a volume of air - Potential high pressure - If the lungs have low compliance, then you could cause trauma when trying to "force" an amount of air that won't fit.

Gas exchange is dependent upon:

Ventilation = movement of gas Perfusion = blood flow

IICP and the ICU

Ventilation and/or oxygenation problems - What does hypercapnia and/or hypoxia cause? Position Changes Decreased Venous Return from Head Increased Metabolic Rate Stress

What happens when patient triggers own breath on AC?

Ventilator assists and controls the volume of the breath (all provided breaths and any breaths the patient triggers on their own)

Benefits of Pressure Modes

Ventilator set to allow air flow until preset pressure is reached: Popular mode!! Vt is variable-similar to normal breathing Peak inspiratory pressure (PIP) can be better controlled-TOP concern (high PIP can cause pneumothorax, barotrauma etc) However, there are risks of hypoventilation and respiratory acidosis - What if the pressure we're providing isn't strong enough to deliver a good breath?

Nurse's job after the ET tube is placed:

Verify that the ETT is in the correct place- meaning we are ventilating both lungs, not just one, and we're not ventilating the stomach - listen to both lungs- and often, to make sure the ETT is in the right place, we can quickly listen to the wrong place- the stomach. - If we hear loud bubbling when we bag the patient, we're in the wrong spot. - Time to take the tube out, ventilate the patient, and reattempt the intubation. - A CO2 detector or even capnography can be connected to the endotracheal tube to determine if the tube is in the lungs as well

2 Types of PPV

Volume targeted ventilation Pressure targeted ventilation

Example A/C Settings:

Vt 700 RR 12 FiO2 45% PEEP 5cmH20 - If patient does not initiate any effort? Will still receive 700 mL 12 times per minute - However, if patient can trigger spontaneous breath-will ALWAYS receive 700 mL Vt with own breathes

Example SIMV Settings:

Vt 700 RR 12 FiO2 45% PEEP 5cmH20 - Patient receives Vt 700 mL 12 breaths per minute with 45% FiO2 - Any spontaneous breaths above 12 times per minute-the Vt VARIES (still get 45% FiO2)

What is the nurse's job if the ET tube is placed correctly and functioning well?

We have bilateral chest rise, oxygen saturations are 94%, and we're feeling good about this intubation - the tube needs to be secured. - Just because it's in the right place now does not mean that it couldn't move. - So it needs to be secured to the patient- but we also need to see WHERE it's secured- therefore you'll see these little markings on the ETT itself so that we can identify how deep the tube should be for this specific patient. - This is something you as the nurse need to document in the chart- for example, size 7 ETT taped 22 centimeters at the lip. - For example- and the next nurse should be able to walk in the room and look at the tube- sure enough the patient's lip is touching the tube at the little 22 mark

Effects of PEEP on alveoli

When patient has enough PEEP -> their alveoli are inflated - it essentially pushes our alveoli closer to that ever-so-important blood supply to exchange gases- remember, that's why we're breathing in the first place- we need good communication with the bloodflow

Full Compensation

When the pH is normal because the compensatory mechanism has successfully corrected the imbalance. - *The critical indicator of 7.40 will need to be used. - (pH is normal, all other values abnormal, one is causing the problem, one is trying to fix the problem) Ex: pH: 7.33 CO2: 50 HCO3: 30 -> "fully compensated respiratory acidosis"

Uncompensated (Acute)

When the pH is out of normal range and the compensatory mechanism has not taken effect. - (only 2 abnormal values, no attempt to compensate with 3rd value) Ex: pH: 7.25 CO2: 50 HCO3: 25 -> "uncompensated respiratory acidosis

Partially Compensated

When the pH is still out of normal range but the compensatory mechanism has begun to take effect. - (all values abnormal, one is causing the problem, one is trying to fix the problem) Ex: pH: 7.25 CO2: 50 HCO3: 30 -> "partially compensated respiratory acidosis"

V/Q Mismatch

When we have a ventilation problem- say pulmonary edema- we call this type of VQ mismatch "shunting"- so in a sense. - Shunting occurs when you have blood flowing but it doesn't participating in any gas exchange Shunt is a type of VQ mismatch where blood is flowing (we have our Q) but there is a ventilation issue- but what about when our lungs are just fine (we have a good "V") but our perfusion is a problem. - So an example of this would be a pulmonary embolism. - Where a patient's actual lungs and lung movement is just fine- but we can't get bloodflow to those oxygen rich lungs. - This is another type of VQ mismatch- now we have a Q- or a perfusion problem- where the Q is not matching with the V

Respiratory alkalosis is carbonic acid deficit that occurs when?

With hyperventilation, or an increase in respiratory rate or volume. - The primary cause of respiratory alkalosis is hypoxemia from acute pulmonary disorders. - Hyperventilation can occur as a physiologic response to metabolic acidosis and increased metabolic demands (e.g., fever). - Pain, anxiety, and some CNS disorders can increase respirations without a physiologic need. - Pain, anxiety, and CNS disorders can increase the ventilation rate. - Hyperventilation "blows off" CO2, leading to a decreased carbonic acid concentration in the blood and an increased pH.

CO2 Detector (AKA: ETCO2 Detector) for intubation

YELLOW means YES PURPLE means PROBLEM

CO2 is an

acid (regulated by the lungs)

Cerebral Blood Flow (CBF):

amount of blood (mL) passing through 100g of brain tissue

SaO2 is the

amount of oxygen bound in the hemoglobin and it's your pulse oximetry. - This is expressed as a percentage.

The cranium

an inexpandable VAULT

Absent or diminished breath sounds May indicate:

atelectasis or pleural effusion

HCO3 is a

base (regulated by the kidneys)

Homeostasis

crucial to sustain life

Buffer system can't maintain pH without

good kidney and lung function

SaO2:

how much oxygen is attached to the hemoglobin? ("oxyhemoglobin")

PaO2:

how much oxygen is in the blood

Hypoxemia leads to

hypoxia

Decerebrate: Abnormal extension

indicative of a brainstem or midbrain lesion.

Pressure targeted ventilation

deliver a set pressure with each breath - Tidal volume (Vt) varies with changes in compliance and resistance - Pressure is measured in cm H2O - Goal is to ventilate alveoli with minimal pressure - Constant monitoring required to prevent hyperinflation and hypoventilation

Volume targeted ventilation

deliver a set volume with each breath - Tidal volume (Vt) is set - Pressures vary based on client's airway/lung compliance and resistance

Decorticate Abnormal flexion

indicative of a cerebral lesion

Acid Base Imbalance

just a symptom of disease- not a disease itself

As the CO2 rises or HCO3 falls, the pH becomes

more acidic

As the CO2 falls or HCO3 rises, the pH becomes

more alkalotic

Causes/treatments for metabolic problems:

must TREAT THE UNDERLYING CAUSE!!

The relationship between the PaO2 and SaO2 is the

oxyhemoglobin disassociation curve

Uncompensated acidosis:

pH <7.35

Only difference between partial and full compensation?

pH falls within 7.35-7.45!

The healthcare team decides to get an ABG on your patient. Interpret the results: pH: 7.29 CO2: 65 HCO3: 25 PaO2: 58

pH: 7.29 -> acid (Acidosis) CO2: 65 -> acid (Respiratory) HCO3: 25 -> normal (uncompensated) PaO2: 58 -> low (qualifies as respiratory failure since it's below 60mmHg "Uncompensated Respiratory Acidosis with hypoxia"!!!

If a [pH, HCO3-, H+, CO2, Respiratory rate] were basic, would it be high or low?

pH: ↑ HCO3-: ↑ RR/depth: ↑ CO2: ↓

ABG's of uncompensated metabolic alkalosis:

pH: ↑ PaCO2: normal HCO3: ↑

ABG's of uncompensated respiratory alkalosis:

pH: ↑ PaCO2: ↓ HCO3: normal

If a [pH, HCO3-, H+, CO2, Respiratory rate] were acidic, would it be high or low?

pH: ↓ HCO3-: ↓ RR/depth: ↓ CO2: ↑

ABG's of uncompensated metabolic acidosis:

pH: ↓ PaCO2: normal HCO3: ↓

ABG's of uncompensated respiratory acidosis:

pH: ↓ PaCO2: ↑ HCO3: normal

PaCO2 =

partial pressure of CO2 in arterial blood - Monitored through Arterial Blood Gases

PaO2 is the

partial pressure of oxygen dissolved in the arterial blood plasma. - A measurement of oxygen in the arterial blood. - PaO2 on ABGs

How does the ventilator deliver a breath?

pressure or volume

Example of V/Q mismatch

pulmonary edema pulmonary embolus

Crackles May indicate:

pulmonary edema and COPD

Examples of diffusion limitations or diffusion defect:

pulmonary fibrosis or even interstitial edema - makes the oxygen's journey from alveolus to capillary much more difficult

Acute Respiratory Distress Syndrome (ARDS)

sudden, progressive form of Acute Respiratory Failure - PaO2/FiO2 ratio of less than 200 mmHg (if less than 200, than patient has ARDS) - Starts with damage to alveolar-capillary membrane - Increased capillary permeability allows fluid to fill the alveoli - 50% mortality rate (based upon if the person has mild, moderate, or severe ARDS)

SIRS =

systemic inflammatory response syndrome

The partial pressure of the alveolar O2 is approximately equal to what?

the PaO2

Pressure Support (PS or PSV)

the amount of pressure in centimeters water that will be delivered to the patient with each breath - volume setting: 500mL, 600 mL, 450 mL - pressure support setting: 10cmH20, 12cmH20

Autoregulation

the process by which the brain maintains its perfusion pressure over a wide range of systemic pressures. - Highly dependent upon MAP - Keep MAP between 70 to 90 mm Hg - OTHERWISE DECOMPENSATION OCCURS??

Causes/treatments respiratory acidosis:

the same for all types of respiratory acidosis, whether it be uncompensated, partially, or fully compensated states!!

Resp failure occurs when?

there is failure of ventilation, oxygenation and/or perfusion or a combination of all 3

What is the nurse's job during ET tube placement?

very closely assessing oxygenation on the monitor. - Frankly you need to be bold and speak up if you notice an attempt is taking too long and the patient's oxygen saturation is dropping- it's time to stop with this attempt and get the bag valve mask back on the patient and bring their oxygen saturations back up

Potential complications of SIMV

volutrauma/barotrauma -hypoventilation if patient doesn't take enough breaths on their own and the respiratory rate setting is too low

Potential complications for AC

volutrauma/barotrauma -respiratory alkalosis if patient is tachypneic (all extra breaths will be assisted)

Failure of Oxygenation

we're looking at an issue where not enough oxygen is getting to the blood- we have a failure to oxygenate

Respiratory acidosis (carbonic acid excess) occurs when?

whenever there is hypoventilation. - Hypoventilation results in a buildup of carbon dioxide, resulting in an accumulation of carbonic acid in the blood - Carbonic acid dissociates, liberating hydrogen ions, and there is a decrease in pH. - If carbon dioxide is not eliminated from the blood, acidosis results from the accumulation of carbonic acid.

FIBROTIC PHASE

• 2-3 weeks after onset • Fibrosis obliterates the alveoli, bronchioles, and interstitium • Lungs become fibrotic decreased functional residual capacity • narrowing airways & resistance to airflow • Inflammatory mediators can begin to cause damage to capillaries throughout the body- widespread edema and MODS

Continued worsening ARDS: what does our pt. look like?

• Central cyanosis • Lungs less compliant ventilation even more difficult hypoventilation respiratory acidosis • Lactic acid buildup from anaerobic metabolism and workload metabolic acidosis • Fluid in alveoli (pulmonary edema) crackles, rhonchi • Chest x-ray: early spots of "ground glass opacities" - later- "white out" chest x-ray

As ARDS Progresses: what does our pt. look like?

• Dyspnea becomes more severe • Intercostal and sternal retractions • Increased WOB

PROLIFERATIVE/REPARATIVE PHASE

• Happens 4-21 days after onset • Pulmonary edema resolves but replaced by a fibrin matrix progressive hypoxemia

INJURY/EXUDATIVE PHASE

• Uncontrolled inflammation inflammatory mediators mediators damage pulmonary capillary endothelium • Inflammatory mediators damage alveolar-capillary membrane increased capillary membrane permeability fluids, protein, blood cells leak from capillary beds to alveoli pulmonary edema pulmonary hypertension • Pulmonary edema leads to V/Q mismatch • Production of surfactant is stopped • Lungs less compliant decreased ventilation • Work of breathing increases • Refractory hypoxemia

Respiratory Disturbance: Renal System compensates by...

↑PaCO2 (resp. acidosis/↓pH): kidneys retain HCO3, excrete H+ = ↑ HCO3= ↑pH ↓PaCO2 (resp. alkalosis/ ↑pH): kidneys excrete HCO3, retain H+ = ↓ HOC3= ↓pH

Metabolic disturbance: Respiratory system compensates by...

↓ HOC3 (metabolic acidosis/↓pH): Lungs ↑ventilation to blow off CO2 = ↓CO2= ↑pH ↑ HCO3 (metabolic alkalosis/ ↑pH ): Lungs ↓ ventilation to retain CO2 = ↑CO2 =↓pH