nur.324review for final exam 2012-part 1

7/31/2019 Nur.324Review for Final Exam 2012-Part 1

http://slidepdf.com/reader/full/nur324review-for-final-exam-2012-part-1 1/86

NUR 324 Review

•

NUR 324 review is graphics intensive, sothere are 2 PowerPoint files for the review.

• Use this one as a PowerPoint slide show

presentation, so that the questions andanswers come up one at a time, not justas a print out for ECG review and others.

• There are website addresses imbeddedthat can only be clicked for direct accesswhen in slide show view.



Contents of this PPT• ECG review - slides 3- 22• ABG review - slides 23 – 25•

Acute renal failure – slides 26 – 31• Renal diet – slide 32• Peritoneal dialysis – slide 33 – 37 (the type of dialysis a nurse

at bedside will most likely do)

•

HD AV Access – slide 38 – 40 (must prepare patient, protectsite, and teach)

• Other renal – slides 41 – 43• Hematological – slides 44 – 58•

Respiratory – tracheostomy slide 59• Laryngeal – slide 60-66• Intubation, mechanical ventilation – slides 67 - 77• ARDS – slides 78 & 79•

Bioterrorism – slides 80-86



Electrical basics

30

0

15

0

10

075

60

50

ECG paper moves at 25 mm/secSmall black square = _____ sec.

Larger Aqua block = _____ sec.(5 little squares)

Each 25 little squares = 5 bigger blocks = 1 second

Rate calculations based on beats/minute1. 6 sec X 10, 2. 300/# blocks, 3. 1500/ # sq



ECG Analysis• Rhythm

–

Regular (normal) vs Irregular • Rate (normal 60-100)

– 3 ways to calculate

• P-waves – Are they present? – Shape? One for every QRS?

• P-R interval (normal .12-.20 seconds)• QRS complex (normal < .12 sec.)• Q-T interval (less than half the R-R

interval)



Normal Sinus Rhythm

30

0

15

0

10

075

60

50

Rhythm::Rate:P wavesPR:QRS:



Normal Sinus Rhythm

30

0

15

0

10

075

60

50

Rhythm::Rate:P wavesPR:QRS:

PR QTQRS

Normalrate

Look closely to see were PR, QRS, & QT are measured.



Six second ECG Simulator http://www.skillstat.com/Flash/ECGSim531.html

Good source for practice rhythms

• Rate: 13 x 10 = 130 or # big blocks: >2 (150 bpm)but less than 3 (100 bpm)

• Rate: between 100-150, so Sinus Tachycardia• Treat the cause

Six second ECG Simulator http://www.skillstat.com/Flash/ECGSim531.html

http://www.skillstat.com/Flash/ECGSim531.html

http://www.skillstat.com/Flash/ECGSim531.html



• Regular rhythm, rate: 70, P-waves before eachQRS, PR: >.12, but <.20, QRS: narrow (<.12)

• Normal sinus rhythm



• Irregular because of two beats•

T-wave left of arrows is bigger,• Hiding p wave• Sinus Rhythm with PAC’s (premature atrial

contractions)



• Atrial Flutter



• Irregular rhythm• Rate?• 5 beats x 10 = 50 beats per minute

• Atrial Fibrillation



• Junctional Rhythm (will not be on exam)



Fun way to review Rhythms

• The Heartbeat Dance

• http://www.youtube.com/watch?v=x5oq4ErAm

http://www.youtube.com/watch?v=x5oq4ErAmW0

http://www.youtube.com/watch?v=x5oq4ErAmW0



•

Irregular because of what?• Sinus Rhythm with unifocal PVC’s• How many PVC’s per minute?

•

Works the same way as beats/minute• 2 x 10 = 20 What treatment needed?• > 6 bpm antiarrhythmic drip



• Sinus rhythm with multifocal PVC’s



• Ventricular Tachycardia• Treatment?

• Defibrillation (asap)• CPR & ACLS otherwise



•

NOTE: this wave is not flat• Ventricular Fibrillation (Fine V-fib)

• Treatment: Defibrillation, CPR & ACLS



• This wave is considered flat

• Asystole• Treatment: CPR



Blocks next

• Regular, P wave with every QRS, PR:>.20, QRS narrow

• First degree heart block• Treatment: observe if asymptomatic



• Regular, P wave with every QRS, butseveral P waves without a QRS

• PR: <.20, QRS narrow

• Second degree Heart Block, Type 2• Treatment: Too slow, Atropine & pacemaker



• Regular P wave with every QRS,•

PR: varies(<.20, >.20, >.20, > last, drops QRS)

• QRS narrow, but irregular • Second degree Heart Block, Type 1

(Wenkebach)• Treatment: rate & symptom based,•

If too slow or low BP: Atropine• May have temporary pacemaker



Arterial Blood Gases

pH pCO2 HCO3

Respiratory Acidosis Normal

Respiratory Alkalosis Normal

Metabolic Acidosis Normal

Metabolic Alkalosis Normal

2323

This is the part you learned in NUR 222. But what about compensation?The next 2 slides will summarize the changes, butREMEMBER: if the arrows for pCO2 and HCO3 go the same direction,there is compensation happening, either partial (pH still abnormal) or

full (pH back to normal).

Students may find the ABG Tic-Tac-Toe helpfulhttp://www.youtube.com/watch?v=_OpvyEIlFj8&feature=relate

http://www.youtube.com/watch?v=_OpvyEIlFj8&feature=related

http://www.youtube.com/watch?v=_OpvyEIlFj8&feature=related



Metabolic: Arterial Blood Gases

2424

Respiratory

(Lung buffer)

pCO2 pH HCO3 Metabolic

(problem area)(normal) normal ↓↓

(< 7.35)↓

(<22)

UncompensatedMetabolic Acidosis

slight alkalosis ↓(< 35)

↓(closer tonormal)

↓(unchanged)

PartialCompensation

Metabolic Acidosis

more alkalosis tobalance resp.

↓(< 35)

Normal(7.35-7.45)

↓(unchanged)

FullyCompensated

Metabolic Acidosis

(normal) normal ↑↑(>7.45)

↑(>26)

UncompensatedMetabolic Alkalosis

slight acidosis ↑(>45) ↑ ↑(unchanged) PartialCompensationMetabolic Alkalosis

more acidosis tobalance resp.

↑(>45)

Normal(7.35-7.45)

↑(unchanged)

FullyCompensated

Metabolic Alkalosis



Respiratory: Arterial BloodGases

2525

Respiratory

(Lung problem)

pCO2 pH HCO3 Metabolic

(kidney buffer)Uncompensated

Respiratory Acidosis↑

(< 35)↓↓

(< 7.35)

normal (normal)

PartialCompensation

Respiratory Acidosis

↑(unchanged)

↓(closer tonormal)

↑(>26)

slight alkalosis

FullyCompensated

Respiratory Acidosis

↑(unchanged)

Normal(7.35-7.45)

↑(>26)

more alkalosis tobalance resp.

UncompensatedRespiratory Alkalosis

↓(>45)

↑↑(>7.45)

Normal (normal)

PartialCompensationRespiratory Alkalosis

↓(unchanged) ↑ ↓(<22) slight acidosis

FullyCompensated

Respiratory Alkalosis

↓(unchanged)

Normal(7.35-7.45)

↓(<22)

more acidosis tobalance resp.



Acute Glomerulonephritis

• 70% of adults recover fully• Treatment:

– Penicillin DOC (if allergic-erythromycin) – Bed rest until urine clears, BP is back to normal

and BUN/Cr WNL. –

Restriction of Na if HTN or CHF or edema ispresent.

– Cautious Intake based on Output (calculatefluid replacement carefully.)

•

Complications: CHF, Pul. Edema,Hypertensive encephalopathy. – If rapid deterioration, do plasmaphereis, give

steroids, antibiotics may be utilized and mayrequire dialysis if progresses to renal failure

A t R l F il



Acute Renal Failure• Etiology and Risk Factors (prevention is best treatment)

–

Prerenal (renal ischemia)• volume depletion, fluid shifts(3rd spacing)decreased CO, decreased PVR and renal vascular obstruction

– Intrarenal• Acute Tubular Necrosis (ATN) 75% (drugs, dyes),

Trauma(blunt), severe muscle exertion(rhabdomylosis), genetic conditions,glomerulonephritis & vascular lesions

– Postrenal• obstuctions like calculi, tumors, prostate

enlargement, spinal cord injury, pelvic trauma andsurgical accidents

– McCance, Table 36-11, p. 1389 (UA compared)

A t l f il Ph



Acute renal failure: Phases (IV E 2)

• I. Oliguric-anuric phase –

last 1-8 weeks, usually 8-14 days• #1 symptom - decreased urine output

– UOP under 400 ml/24 hours (600-700 ml/day inelderly)

–

Fluid vol. excess edema, wt gain, HTN and CHF – Elevated Urine Na+ and protein – Hyperkalemia - EKG shows tall peaked T waves

• increase BUN/Creatinineazotemia (uremic syndrome)

• anemia (due to decreased hematopoiesis)

weak



Acute Renal Failure• II. Diuretic Phase

–

mark the recovery of nephrons and their ability toexcrete urine.

– UOP as much as 1- 2 liters /day dehydration

– is still azotemic (BUN decreases, Cr still high) –

25% of deaths in this phase• III. Recovery Phase

– improved renal function, may last 3 months to ayear.

–

Kidneys are able to concentrate urine again. – Often some residual effects, but can have

complete recovery.

Acute Renal Failure



Acute Renal Failure• Measures to lower K+ in 2-3 hours (K+ < 6):•

1. Sodium Polystyrene sulfonate(Kayexalate) – administered by mouth or as a retention enema. – cation exchange resin (sodium for potassium)

therapy that removes 1 MEQ of K+ per gram of drug – mixed in water and sorbitrol to produce osmotic

diuresis (and diarrhea to remove K+ from body).•

2. Dietary restrictions: – daily K+ intake is limited to 40 to 60 meq

Ac te Renal Fail re



Acute Renal Failure• Measures to lower K+ in 30-60 minutes (K+ >6.5):• 1. Hypertonic glucose (D50W) and insulin IV

– K+ moves into the cells with the glucose in the presence of insulin (H+ ions move out of cells).

• 2. Sodium bicarb IV – to correct the underlying acidosis and cause a shift of K+

into the cells (H+ ions move out of cells).• 3. Dialysis

– Hemodialysis can bring K+ levels to normal within 1-2 hoursand correct the acidosis. Peritoneal dialysis takes 4-8 hoursto achieve the same effect.

---------------------------------------------------------------------------------------------------------------------------

• Calcium gluconate IV – generally used in advanced cardiac toxicity. Calcium

antagonizes the cardiac effects of K+ to protect the heart.

CRF N i i l C id i



CRF: Nutritional Considerations• Fluid: urine output plus 500ml/24 hours

–

very cautious and balanced I & O• Protein: 1gm/kg(40-50gm/day think limited- high quality)

• Calories: 35-40 Kcal/kg estimated dry weight(approx. 2000-2500KCal/day)

• Carbohydrates: unlimited intake of sugarsand starches; bread and cereals limited dueto protein limit.

•

Need MVI, but no Iron unless low• Phosphate binders with meals (Phoslo)• Antihypertensive meds, adjust all meds for

renal doses

P it l Di l i C li ti



Peritoneal Dialysis: Complications• Infection of exit site

–

staph aureus or staph epidermidis – red, tender and drainage treat with antibiotics

• Peritonitis – due to contamination of the solution or tubing –

signs include cloudy peritoneal fluid, WBC countgreater than 100 cells per micro liter (cells/mL)

– may have diffuse abd pain, nausea and vomiting,diarrhea, abd distension and hyperactive bowel

sounds. – Fever or no fever. – Usually staph aureus or epidermidis-treat with

antibiotics. May need cath removed.

Peritoneal Dialysis: Complications



• Abdominal pain –

not severe but common – caused by: low pH of the Dialysate. – Also could be due to peritonitis, intra-

peritoneal irritation (usually subsides in 1-2

weeks after dialysis started) – If the tip touches the bladder, bowel or

peritoneum pain will occur • remedy is easy - reposition the tube.

– Rapid infusion of dialysate causes referredpain to the shoulder

• remedy is easy - decrease the rate of infusion.





• Outflow problems – kinks may be in the tube itself, or piece of

omentum, or catheter migration out of the pelvicregion;

– after time if outflow problem-may be due to a fullcolon—remedy is an enema!

• Hernias – due to continued intra-abdominal pressures – especially multi- parous women and elderly men. – After surgical repair healing, can return to PD

• Low back pain – due to increased abdominal pressure – treat with orthopedic binder





• Bleeding –

first exchange pink or slightly bloody(due to trauma). – Gross bleeding indicates injury to the abdominal wall.

• Pulmonary complications – atelectasis, pneumonia, bronchitis due to repeated

upward displacement of the diaphragm. – Frequent position changes and TCDB are important.

• Protein loss – protein, amino acids and polypeptides( 9-12g/day) are

lost in dialyzing fluid. – With peritonitis get a 40g/day loss!





• Encapsulating sclerosing peritonitis and

loss of ultra filtration – thick fibrous membrane surrounds and

compresses bowel –

Small Bowel Obstruction and strangulationoccur – Must change to hemodialysis


A D i AV Fi t l



Access Devices: AV Fistula

• Complications of fistula:• Thrombosis (may need anticoagulation

or surgery to remove the clot)• Infection (usually due to staph aureus)•

Aneurysm formation (due to repeatedcannulation-may need surgical repair)

• Ischemia (cold fingers to gangrene-dueto decreased arterial flow-occurs in very

small numbers of clients) – Steal syndrome




Access Devices: AV Fistula• No BP or needle sticks in the fistula arm

– Arms may be “protected” when CRF develops• Assess patency by palpate for a thrill or

auscultation for a bruit.• Avoid compression of fistula loose dressing•

Inspect site for infection• Need to use the arm to prevent clotting,

Assess movement by pt wiggling fingersimmediately post op

• Elevate the arm on pillow until swelling isdown; no slings, no ice.




Access Devices: AV Fistula• Teach

–

to assess patency by palpating for a thrill (or auscultation for a bruit). – to avoid compression of fistula by tight clothing,

or carry objects with arm bent, and not to lie onthe site.

– to inspect site for infection – To protect arm from HCP: No BP or needle

sticks in the fistula arm –

To continue to use the arm to prevent clotting – ball squeezing 5-7 days after surgery (after

swelling is gone)



Renal Arterial: Surgery• RA stenosis:

– Try percutaneous transluminal renalangioplasty (PTRA) & stenting

• Stenosis may reoccur (antiplatlet medsgiven) or PTRA may be contraindicated

• Improvement in 2/3 of cases; home in 24-48hrs.

– Aortorenal bypass:• use autogenous vascular graft•

Severe HTN expected for 48 hrs – mustmonitor and treat aggresively



Obstructive Disorders: Urinary Calculi (IV C1)

• Etiology and risk factors – Urinary stasis and supersaturation

• Pathophysiology: based on stone types – Calcium, oxalate, struvite, uric acid, cystine,

xanthine• Clinical manifestations (see Fig. 34-4)

– PAIN (spasm, colic, peristalsis, radiates down) –

Obstruction (hydronephrosis) – Tissue trauma (hemorrhage) – Infection

A Review of Diagnostic Studies &



A. Review of Diagnostic Studies &B. Critically Analyze values

•

Complete Blood Count(Black, Tables 74-4 & 74-5, p

2000)

– RBC, Hgb, Hct – WBC (blast = immature)

–

Differential: (%) – Granulocytes:

• Neutrophils (Segs, Bands)

• Eosonophils

• Basophils – Monocytes Macrophage – Lymphocytes (B, T, NK)

A. Review of Diagnostic Studies &



gB. Critically Analyze values

• Platelets –

Regulate blood flow (can cause vasospasm) – Activate & aggregate to form platelet plug – Activate clotting cascade to stabilize clot – Initiate repair (clot retraction & dissolution)

•

Coagulation factors & studies (Table 74-7, p. 2002) – Fibrinogen, Fibrin split products, Fibrin degradation

(FDP) – PT/INR & PTT – Clotting factors (V, VIII, IX) – Bleeding time – dDimer

Leukemia: Diagnosis



Leukemia: Diagnosis• CBC

– decrease in RBC – decreased platelets – low-normal or high WBC – Positive leukemic blast cells on peripheral smear

•

Bone marrow aspiration – key diagnostic tool. (Adults: aspirate thesternum)

– Painful, with slight risk of infection with thisprocedure.

– Shows: increase #s and > % blast cells types.• Lumbar puncture (chronic disease)

– CNS involvement

Leukemia: Treatment



Leukemia: Treatment• Major aim of initial treatment:

– achieve a primary remission that lasts withoutrelapse

– A remission means the absence of detectableleukemic cells in the marrow

– A relapse is the reappearance of leukemia cells inthe marrow

• If a patient has a remission but relapses, asecond remission is possible, but much more

difficult• with each relapse, remission is shorter.

Polycythemia Vera (U it III C3)



Polycythemia Vera (Unit III C3)

•

Relentless overproduction of erythrocytes abnormally high number of RBC’s inwhole blood

• Areas were common in WV, frequently

relatives

• Clinical Manifestations – Hypervolemia & Hyperviscosity (poor blood

flow) – Hypercoagulable!! – Diagnostic Tests:

• Hgb 18 gm/dl or over • RBC 6 mil/mm3

Polycythemia Vera



Polycythemia Vera• Medical/Nursing Management•

Assessment for:Headache, Plethora, Dyspnea, Thrombosis,Spleenomegaly, Parasthesias, Tendency to bleed(nosebleeds, etc)

Treatment: Phlebotomy to decrease volume and viscosity

May repeat weekly until levels improve (high normal)

Infectious Mononucleosis (D1)



Infectious Mononucleosis (D1)

• Etiology: herpesvirus or Epstein-Barr • Pathophysiology: viral, thought to be spread

by the oro-pharygeal route• Clinical Manifestations:

–

painful enlargement of lymph nodes, sorethroat, fatigue, headache, malaise, myalgias,fever, pharyngitis

– 10-15% get a maculo-papular rash; – Can get splenic enlargement – if mono severe, splenic rupture due to WBC

invasion of the spleen

Mononucleosis



Mononucleosis• Diagnosis:

–

physical assessment and physical findings; – Lab: WBC 12-20,000 (50% are lymphocytes

and monocytes and 10-20% are large,atypical lymphocytes.

–

Mono spot is a blood test, detects anti-EBVantibodies

• + in 50% 1st week and 90% in the 4th week

• Treatment: – Symptom based: increase fluid intake, rest,

analgesics (NSAIDS) and antipyretics, gargle, – Long, slow convalescence (fatigue can last 6

months)

Hemophilias (E1)



Hemophilias (E1)

• Hemophilia is a group of bleeding disorders wherethere is a deficiency of clotting factors.

–

More common in men (1:10,000 in the US) – About 80% inherited pattern is X recessive

linked gene. – Example how to deterime offspring results –

Xh = hemophilia gene, Xo = normal – Father hemophilia, mother carrier

Father/Mother Xh Xo

Xh XhXhFemale hemophilia

XhXoFemale carrier

Y XhYMale hemophilia

XoYNormal male

Disseminated Intravascular



Disseminated Intravascular Coagulation (DIC) (III F)

•

Complication of pathologic conditions – hypoxia, acidosis, shock, systemic disease like

congenital heart, gram negative sepsis, etc.• An inappropriate systemic activation of the

normal clotting mechanisms.• Clinical Manifestations

– onset acute, days to hours after onset of illness – If it rapidly develops, usually pt will bleed from 3

unrelated areas• IV sites, a-line, surgical wounds, eyes, nose, gums,• development of purpura, petechiae and hematomas

Disseminated Intravascular



Disseminated Intravascular Coagulation (DIC) (III F)

•

Complication of pathologic conditions – hypoxia, acidosis, shock, systemic disease like

congenital heart, gram negative sepsis, etc.• An inappropriate systemic activation of the

normal clotting mechanisms.• Clinical Manifestations

– onset acute, days to hours after onset of illness – If it rapidly develops, usually pt will bleed from 3

unrelated areas• IV sites, a-line, surgical wounds, eyes, nose, gums,• development of purpura, petechiae and hematomas

DIC di ti t t



DIC: diagnostic tests (Table 75-7, p. 2036)

•

Bleeding time > 7min• Platelets <100,000• Plasma fibrinogen

less than <195mg/dl

• Fibrin degradation

product > 10 mcg/ml• Activated Partial

Thromboplastin Time(aPTT) greater than

36 sec.

• Prothrombin Time(PT) prolonged (highINR)

• One stage factor

assays (Coag.System – slide 53)

• Factor II < 25mcg/ml;•

Factor V < 50%,• Factor VII < 65%• Factor X < 45%•

Factor XIII reduced

DIC: Medical & Nursing Management



DIC: Medical & Nursing Management

• ID cause and treat it•

Establish homeostasis – Phase I: concern is thrombosis, so give heparin

IV – Phase II: Replace lost blood components

(platelets, FFP, Give clotting factors)• Supportive therapy

– Assess all body systems (vigilant) – Monitor & quantify blood loss & replacement – Draw & monitor labs (especially after

treatments) – Prevent further injury – Intense emotional support to client & family

Si kl C ll A i P th



Sickle Cell Anemia: Patho• Increased “sickle” rates when:

– Hypoxia, acute illness, dehydration and other conditions.

• Sickle cells are rigid – clump up and obstruct the blood or slow blood

flow – ischemia and possible infarction of an organ

– PAIN, SWELLING AND FEVER!!•

Symptoms are secondary to hemolysis andVaso-occlusive Crisis• Diagnosis occurs in childhood as discussed in Peds course

Sickle Cell Anemia



Sickle Cell Anemia• Manifestations in Adults:• See Table 75-6 in Black text (p. 2024)

• Chronic hemolytic Anemia (hgb 7-10) – Patient looks jaundiced – heart rate is elevated, flow murmur and enlarged

heart, arrhythmias and heart failure may ensue• Vaso-occlusive crisis

– Severe pain – Hand-foot syndrome with ulcers

•

Aplastic, Hemolytic or Sequestration Crisis• Acute Chest Syndrome – highest mortality

– Emboli & infarction to lungs ARDS death

Sickle Cell Anemia: Treatment



Sickle Cell Anemia: Treatment

• Pain: treat aggressively! –

Morphine IV q1-2 hrs or PCA pumps – taper dose over 24-48 hrs – NSAIDS & oral opiates at home

• Prevent infection &/or Treat infections earlyand aggressively (broad spectrum antibiotics)Maintain hydration, electrolytes, blood

May need blood transfusion

•

Maintain oxygenation: avoid hypoxia• Bed rest during crisis:

– decreases O2 consumption



Potential Problems Associated with aTracheostomy

• Potential complications – Airway obstruction – Infection –

Tracheal dilation – Accidental decannulation – Tracheal wall necrosis – Subcutaneous emphysema –

Tracheal dilation and stenosis – Tracheomalacia



Cancer of the Larynx

• Benign Tumors of the Larynx:Papillomas (viral wart-like growth-polyps)

•

Cancer of the Larynx – Clinical Manifestations – Intrinsic-(hoarseness) – Extrinsic (burning pain with ingestion of

citrus juices & hot fluids) – Late (pain that radiates to ear)

Cancer of the Larynx



Cancer of the Larynx• Medical management

– Radiation and chemotherapy• Surgical management

– Laser • used for small lesions of the vocal cords• leaves voice intact

–

Partial• takes one cord and sometimes part of the second cord• removes ½ of the larynx-preserves the voice (also called

“vertical partial laryngectomy)• Another form of partial is the “supraglottic” removes the

superior larynx, false cords and base of the tongue – true cords are left intact so voice is preserved

• This procedure requires temporary trach.



Surgical Interventions• Total Laryngectomy

-done with largetumors that are fixedon the cords-larynx

and cords areremoved-have apermanent trach—novoice-must work withalternative forms of communication-teaching essential

POST OP CARE



POST-OP CARE

• Continuous assessment and monitoring of patient and trach tube.

• Keep trach opening patent• Semi fowlers is essential to facilitate

ventilation, promote drainage andminimize edema

• Assess for complications

POST-OP CARE



POST OP CARE• Maintain a patent airway•

Semi fowlers (45 degrees at least)• Monitor resp rate and depth• Monitor pulse for increases• No meds that decrease resp• TCDB• Suctioning and humidified O2 (trach collar)• Enteral feedings and IV therapy•

Care of stoma, suture lines and drains(hemovac)

• Monitor for rupture of carotid artery

POST OP CARE



POST-OP CARE

• Nutrition-usually TF for 2-3 days• Clear liquids to progressive as tolerated• Assess swallowing to assure safety• Same measures as aspiration risk•

Oral care every 2 hours and prn• Assess total protein and albumin• Communication and speech rehab-

–

Assist pt. With alternative form of comm-yes/no ?; magic slate or flash cards,esophageal speech and electro-larynx speechare possibilities

Rehabilitation



Rehabilitation• Essential

–

works with speech pathologist to affectchange in alternative communication.

• Discharge teaching for patient and family – trach care, signs of complications, nutrition

and pain management• Refer to support groups

– like Lost Chord Club for social support.

•

Client education box – swallowing look in Black (2009)



Who needs intubation?• Patient unable to maintain normal gas exchange• Progressive deterioration of the patient’s

condition: – worsening of ABG’s, –

signs of hypoxemia, – changes in chest x-ray such as infiltrates, patchy white-

outs

• Respiratory arrest; Respiratory insufficiency;

airway obstruction; persons requiring surgery(many need).

6767



Confirming ETT placement

• How do we confirm the endotracheal tubeis in place????

• A. Auscultation of lung sounds• B. Use of the end-tidal CO2 monitor • C. Chest x-ray

6868



MV: Ventilator Mechanics



MV: Ventilator Mechanics

Positive pressure ventilators•

1. Volume cycled (controlled) ***** – deliver a breath until a pre-set volume is achieved – Tidal volume, rate, flow are pre-set, – pressure varies (Alarm limits)

• 2. Pressure cycled **** – deliver the breath until a pre-set pressure is

reached in the patient airway – Pressure limit, rate, and flow pre-set, – Volume varies

•

3. High Frequency Ventilation – Deliver small tidal volumes at very rapid rates to

exchange gas in lungs with minimal distentionpressures (limit damage to the lung)

7070



Adjuncts

• PEEP – Positive endexpiratory pressureapplied during MV

•

CPAP – Continuous positive airwaypressure is applied to a client withspontaneous respiration

•

Pressure support (PS) – Increasedpositive pressure applied during inspirationfor intubated clients (ventilator weaning)

7171

Mechanical Ventilators and



Analgesics• In hemo-dynamically stable patients:• Analgesics (for pain relief)

– Morphine and Fentanyl (sublimaze) opioids• Sedatives (sedation effect)

– benzodiazepines like Ativan and Versed•

Neuroleptics (sedation) – Haldol: good sedation with minimal resp depression

• Anesthetic agents (sedation) – Propofol (Diprovan) “milk of anesthesia” –

given by constant infusion – short onset of action and short acting drug – cause hypotension-use with caution if unstable

7272

Modes of Ventilation



Modes of Ventilation• Control –

– Preset volume delivered at a preset rate.Circuit is closed in between these mandatorybreaths. Patient must be apneic or paralyzedor they fight the ventilator.

• Assist/Control – – Preset volume delivered for each patient

inspiratory effort (of set amount). If pt fails to

initiate a minimum # of bpm, the vent willinitiate the breaths at the preset rate.

7373



Modes of Ventilation

• Pressure Support Ventilation – – Preset positive pressure is initiated by the

patient’s inspiratory effort –

TV and rate is patient controlled (minimal levelalarm set) – Augments or assists spontaneous breathing

efforts

–

Frequently combined with CPAP

7575



Alarms•

Alarms set on the ventilator alert the nurse to theneeds of the patient• NEVER TURN OFF ALARMS! (pause, reset OK)• The prudent nurse will:

– Check the patient –

Check the circuit – Check the ventilator settings – Check alarm limits when the ventilator alarms.

• Common causes of high pressure alarms:

7676

Al



Alarms

• Common causes of low alarms

*Never turn off alarms!

See Bridge to Critical Care, p 1644

7777

ARDS: findings



ARDS: findings• Hypoxemia unresponsive to oxygen therapy

(PaCO2 of over 60, pO2 less than 50 with FiO2

higher than 50%)• Diffuse bilateral alveolar infiltrates seen on chest x-

ray without heart disease (non-cardiac pulmonaryedema)

• Worsening crackles• Eventual metabolic acidosis because of the

increased work of breathing and cellular hypoxia• Fluffy infiltrates, or “Patchy white-outs” seen on

Chest

x-ray• If not reversed resp acidosis, further hypoxemia,

hypotension, decreased cardiac output and deathoccurs.

Management of ARDS



g• Early detection and treatment interventions: treat cause (if known)

to reverse process, oxygen therapy•

Resp support with intubation, mechanical ventilation and PEEP;• may “prone”- Read evidence based practice, Black (2008) page

1656 -Prone positioning of adults.• [Nursing history lesson: an ICU RN on nights started doing this with

her patients and they got better instead of dying. She then went onto design and sell a special support that assisted in the turningprocess (and made lots of money) until the roto-bed came out (nowKCI gets the big money and a physician has to order the bed to getinsurance to pay for it, since it could be a nursing action.]

Bi t i



Bioterrorism

• Used to intimidate a government or harm largenumbers of people for political or socialobjectives

• Biological agents used during wartime are used

to produce large numbers of casualties over awide geographical area

• Biological weapons are any agents configuredon groups of people with the intent to harm or

kill. Bioterrorists use these agents for thispurpose – often with motives unknown

BIOLOGICAL WEAPONS



BIOLOGICAL WEAPONS

• Easy to acquire and deploy• Invisible and odorless• Most people wouldn’t know they were

exposed until after they become ill• Most s/s mimic the flu• Mass illness and death produced by

aerosolized weapons

BIOLOGICAL WEAPONS



BIOLOGICAL WEAPONS

• >50 bacteria, viruses or toxins that can be usedin an attack

• Vaccines are available for only 12 or 13 of these•

The 6 most likely to be used, and of greatestconcern – “Critical Agents” are smallpox,anthrax, plague, tularemia, botulinum toxin andpathogens causing viral hemorrhagic fevers(Ebola & Marburg)

ANTHRAX



ANTHRAX

• Diagnosed by blood cultures, nasalswabs and chest xrays

• Treatment is with Cipro or Doxycycline•

Prophylaxis is 60 days of antibiotics• Anthrax vaccine available but supplies are

severely limited•

Mortality rate >90%

PLAGUE



PLAGUE

• Leads to shock, multiorgan failure & DIC• Few labs have tests to confirm plague• Treatment is with streptomycin sulfate,

gentamicin, tetracycline and doxycycline• A vaccine is available but probably

wouldn’t protect in an attack situation• Mortality close to 100% if not treated

within 24 hours of symptom onset

TULAREMIA



TULAREMIA

• Presents as an atypical pneumonia• Incubation 3 to 5 days• S/S: fever, chills, rigors, myalgias,

anorexia, sore throat & headache• Chest xrays & serological assays

diagnose•

Treatment is aminoglycosides x 10 days• 35% mortality untreated

BOTULINUM TOXIN



BOTULINUM TOXIN

• S/S progress to skeletal muscle weaknessthen paralysis that is symmetrical,descending and progressive often leadingto respiratory failure

• Diagnosis made on clinical circumstances• Treatment is supportive care and passive

immunization with an antitoxin•

All seven toxins have an antitoxin

nur.324review for final exam 2012-part 1

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