Critical Care Nursing08.31.12 GoldenArwanna

A specialty within nursing which deals specifically with human responses to life threatening problems

Scope of CCN1. Critically ill patient – Acute

conditions MI, Stroke, pulmonary embolism, hemorrhage, bleeding tendencies, multiple organ failure, hypokalemia, HGB2,

2. CCN3. CCN environment – stepdown units

(similar to IC)

History Nightingale developed the idea of

clustering the most acutely ill patients in 1800

1960s- ECG, arterial, CVPs Coronary care units for MI were

developed 1920- ICU became a standard

globally Progressive care units (stepdown) Rapid response teams (RRT) has

three members (CCN, RT, CCP or APN)

ACCN standards: healthy environment

1. Skilled communication2. True collaboration3. Effective decision making4. Appropriate staffing5. Meaningful recognition6. Authentic leadership

Critical Nurse

Greater clinical expertise and maturity

Critical thinking ability Assertiveness Client management skills (med-surg) Genuine, humane, compassionate

attitude Intelligent decision-making Coordinator of the health care team

- Health related goals to regain or maintain biological and psychological wellness. This may include ensuring a peaceful death

- Has understanding of ethical and legal principles to protect nurses from lawsuits.

- Cares for patient and family

- Indepth knowledge in Anatomy and Physiology, pathology, advance assessment and advanced bioltechnology

- Use of total care model

Reasons for admission to ICU:1. Physiologically unstable (respi,

cardio, neuro)2. At risk for serious complications3. Requires intensive and complicated

nursing support

Common problems:- Nutrition - Anxiety (stigma)- Pain- Impaired communication- Sensory perceptual problems

(sensory overload – equipment)- Sleep problems

Assessment:

*Glasgow Coma Scale – patients with low scores (3-4) have high mortality and poor prognosis for cognitive recovery compared

Sterna rub by eye opening, cries during pain assessment, moves body resisting the painful stimulus – 10

*PQRST scheme for pain: Pattern – how oftenPrecipitating and PalliatingQuality – type of pain (throbbing, stabbing, sharp, dull)Region – radiatingSeverity – pain rating, visual pain analogueTime – duration, time of the day

*AVPU Mnemonic (LOC)A – AlertV – VerbalP – PainfulU – Unconscious

*AMPLE MnemonicA – AllergiesM – MedicationP – Past Medical HistoryL – Last food intakeE – events preceding the injury

*ABCDE MnemonicA – airwayB – breathingC – circulationD – disabilityE – Expose and evaluate

*CRAMS scaleC – circulationR – respirationA – abdomenM – motorS – speechLess than 8 indicates major trauma, above 8 indicates minor trauma

S1 – AV valves close (5th ICS LMC or PMI)S2 – diastolic, Pulmonic and aortic semilunar valve closure (2nd ICS L/R SB)

Abnormal heart sounds

S3 – after S2, L/R SB, use bell of stethoscope, regurgitation`S4 – increased resistance to ventricular filling (CHF, CAD, aortic stenosis, heard after S1Splitting of heart sounds (split S2: Lub T-Dub)

- Aortic valve closes significantly earlier than the pulmonic valve

- Caused by the delay in the closure of the right-sided valves

- Indicates pulmonary stenosis, R/L bundle branch block, RV failure, atrial/septal defect

Systolic Murmur- A blowing, swooshing sound upon

auscultation- Reflect turbulent blood flow- Heard through abnormal valves

Laboratory Examinations:

Ultrasound (2d echocardiogram) Coronary angiography Electrocardiogram Serum studies

Serum Markers/ Cardiac enzymes released due to myocardial damage:

Elevated CK (Creatinine kinase and CK MB, MM, BB)

o Increased in 3-6 hours after onset of chest pain, peak in 12-18 hrs. return to normal level in 3-4 days

Elevated LDH (Lactate Dehydrogenase) – increased 14-24 hpurs after the onset of chest pain, peak within 48-72 hours. Return to normal level in 7-14 days.

o LDH 1,2 – kidneys, heart, RBC (1:1)

o LDH 3 –specific in lungo LDH4, 5 – skeletal muscles

and kindneys Elevated troponin T (similar to

CKMB) – thin filaments of the myocardium

o Troponin C – not sensitive and specific to MI

o Troponin T – 50% sensitivity after 4 hours onset of chest pain, 75% after 6 hours, 100% after 12 hours

o Troponin I – after a few hours of onset 96%

Increase AST (aspartate transaminase) within several hours peak within 12-18 hpurs. Return normal within 3-4 hours, this is also in the liver, kidney, brain

C-reactive protein (CRP) – peaks several days later, produced by liver, and indicative of atherosclerotic plaques, associated with MI, stroke, non-specific

Myeloperoxidase (a Leukocyte enzyme)

o Predictive of AMI even in clients without elevations in Troponin T

o Predicts MI dev’t 30-60 days before MI

Leukocytosis – appears 2nd dat after AMI (response to necrosis) disappears in 1 week

Erythrocyte Sedimentation Rate (ESR) – rises within a week and remains elevated for a month or longer

Hematocrit – elevated due to hemoconcentration, normalizes after 1 week

ABG shows rise in pHo Response to stress; decreased

pHo K to be assessed

Other diagnostic examinations:

Stress test/ exercise tolerance test – dne after acute stages to evaluate ECG changes, medical therapy, and identify those for referral for invasive therapy,

o 20 mmHg systolic stop the stress test

o Fatigue and dyspnea stopo Equipment is broken stopo No caffeine, smoking before

stress test Scans – Thallium and MUGA

(Multiple Gated Acquisition)o Thallium 201, should be

absorbed into the cells – gamma radiation (if not absorbed a cold spot will be seen)

o Technetium 99 Sestamibi – absorbed by ischemic cells (hot spot)

o Explain that client will experience nausea.

Cardiac Catheterization – to determine the extent and location of obstruction of coronary arteries

allows to identify those who can benefit from PTCA or CABG

Hemodynamic Parameters

- Intra-arterial blood pressure- Central venous pressure- Pulmonary artery pressure- Cardiac output- Venous oxygen saturation

Central Venous Pressure – pressures inside atria

- Indicated for significant fluid volume alterations (hypervolemia and hypovolemia)

- Assesses diuresis- Complications:

o Injuryo Bleeding o Infectiono Catheter occlusiono Cannulation of central vein,

hemothorax and pneumothorax

- Options: o Subclaviano Internal jugular o Femoral

- Trendelenburg position decreases the risk of air embolism

- NV: 4-12 cm H20- Nurses responsibilities:

o Consent is securedo Explain the procedureo Trendelenburg positiono Assist during the procedureo Instruct to deep breathe and

holdo Maintain sterility

- Increases in cardiogenic shock and Right ventricle infarction

Cardiac output = Stroke volume x Heart Rate- Determined with a quadruple lumen

(thermodilution) pulmonary catheter and bedside computer

- NV: 4-8 L/min- Stroke volume = EDV – ESV

NV: 60-100 mL/ beat

Intra-arterial blood pressure – direct measurement of BP by use of an arterial catheter

- Catheter is connected to a high pressure tubing to a transducer and continuous flush system with heparinized NSS

- Viewed as waveforms or digital movement

- NV: Sys – 80-90 mmHgDias – 60-65 mmHg

Pulmonary artery pressure- Uses Swan Ganz catheter- Pulmonary wedge pressure- NV:

o Sys 15-25 mmHgo Dias 8-10 mmHgo Cap wedge 8-12 mmHg

Venous oxygen saturation – NV: 60-80%- Reflects the amount of oxygen left in

the blood

ABG Monitoring

R – RespiratoryO – oppositeM – metabolicE – equal

NV:pH 7.35-3.45PaCo2 35-45 mmHgHCo3 22-26

Basic ECG Interpretation

Myocardial Cells – working or mechanical cells

- Contain contractile filaments

Pacemaker cells – specialized cells of the electrical conduction system

- Responsible for spontaneous generation and conduction of electrical impulses

- Exitability- Contractility- Automaticity- Conductivity

A visual representation of the electrical activity of the heart reflected by changes in the electrical potential at the skin surface

Types:- Standard leads – 12 leads- Telemetry monitoring – 3-5 leads- Holter monitoring – continuous

portable

Purposes:- Evaluate effects of systemic related

diseases (renal/pulmonary)- To aid in confirming definite

diagnosis or as a differential diagnosis (MI, Angina, pericarditis)

- MI = 12 leads (helps determine if there is infarction by visualizations of significant changes in cardiac waveforms)

- To guide appropriate or more definitive therapy (Electrolyte replacement)

- Insertion if temp/permanent pacemakers

Each EKG should include identifying information:1. Client’s name and ID number2. Location, time, date of recording3. Client’s age, sex, cardiac and non-

cardiac medications currently being taken.

4. Height, weight BP5. Clinical diagnosis and current

clinical status6. Any unusual positioning of the client

during the recording

7. If present, thoracic deformities, respiratory distress or muscle tremors

Holter monitor – used in patients with possible ischemia

o Wear upon arising and remove before sleeping

o 24-hour log

AV node has the capacity to block electrical impulses

Limb Leads Electrodes are placed on the:

o Right armo Left armo Right lego Left lego Wrists/ ankles, ante-cubital

area, thighs, femoral

Chest Leads V1 – 4th ICS R SB V2 – 4th ICS L SB V3 – in between V2 and V4 V4 – 5th ICS LMCL V5 – 5th ICS anterior axillary line V6 – 5th ICS mid axillary line

Cable connections - Before you attach the electrodes,

know whether the cable used is American or European cables. Improper placement can give incorrect ECG recordings

3 – lead ECG Monitors the standard leads I, II, III Lead II is commonly called the

monitoring lead. It provides info if the HR, regularity, conduction time and and ectopic beats. Mi is best validated by a 12-lead EKF

5 wire cable

15 - lead ECG

Includes 12 lead ECG plus V4R – 5th ICS at RMCL V8 - posterior 5th ICS left

midscapular area V9 – directly between V8 and SC at

5th ICS

Components of ECG tracing

Characteristics:Wave – a deflection either positive of negative away from the isoelectric lineComplex – several wavesSegment – a straight line between waves and complexesInterval – a segment and a wave

Isoelectric line – imaginary straight line, used to determine + or - deflection

P-QRS-T (view 2)

P wave – will tell you the activity of the SA node

- Will tell you electrical activities in the atria

- First wave seen- Small rounded upright- Indicates atrial depolarization

(results to contraction)

QRS complex- 3 deflections following P waves- Ventricular depolarization- Q wave: 1st negative deflection- R waveL 1st positive deflection- S wave – 2nd negative deflection- Normal: 0.06-0.10 s

T wave – relaxation of ventricles

P-R interval – distance between the start of the P wave to the beginning of thw QRS intervalN Va,ies: 0.12 – 0.20s’

T Wave - runded, upright wave following QRS cmplex

- Indicates ventricular repolarization

Sinus Tachycardia

- Rhythm: regular- Heart rate: 101 – 150 - P waves: rounded, precede each QRS

complex, alike- PR interval: 0.12 – 0.20 s- QRS interval: 006-1.10 s- If rate is >150bpm it is SVT or Atrial

tachycardia- Caused by increased metabolism

(fever), thyroid problems, caffeine intake, exercise, stress, anxiety

- Determine cause and treat

Atrial Rhythms Above 150 bpm Not SA node P waves change in

appearance or are not seen at times Regular or irregular rhythms

Atrial Flutter- Rhythm: atrial rhythm regular,

ventricular rhythm regular or irregular depending on consistency of AV conduction of impulses

- Heart rate: ventricular rate varies above 150

- P waves: flutter or F waves with saw-tooth pattern

- PR interval: none measurable- QRS complex 0.06-0.10 secs- Tx: Vagal maneuvers – decreases

heart rate (e.g. valsalva maneuver, rectal temp, coughing out, carotid massage)

o Cardioversion and meds

Atrial Fibrillation- Rhythm: grossly or irregularly

irregular- Heart rate: atrial rate not measurable,

ventricular rate under 100 is controlled response, >100 is rapid ventricular response

- P waves: no identifiable P waves- PR interval: none can be measured

because no P waves are seen- QRS complex: 0.06-0.10 s- Clots may be formed

Junctional rhythms

Rate: 40-60 bpm

P waves: absent, flat or depressed Rhythm: regular

Configuration: P waves flat, absent or inverted, QRS and T waves seen

Rhythm – regular (from AV nodes) Rate: 40-60 bpm QRS: 0.06-0.10

Accelerated Junctional Rhythms: Configuration: P waves flat, absent

or inverted, QRS and T waves seen Rhythm – regular (from AV nodes) Rate: 40-60 bpm QRS: 0.06-0.10

Junctional Tachycardia: Configuration: P waves flat, absent

or inverted, QRS and T waves seen Rhythm – regular (from AV nodes) Rate: 101-180 bpm QRS: 0.06-0.10

Heart Blocks Blockage is at the AV node P wave is normal. AV node blocks

impulse. Impulse not transmitted to BofH and PF. No transmission. No depolarization. No contraction. No SV. No BP.

Treatment: Pacemaker

1st degree AV block Configuration: P, QRS complex and

T wave seen PR interval prolonged Rhythm – regular Rate: may vary

2nd Degree AV Block (Mobitz I or Wenkebach)

P waves, QRS complex, and T waves seen

Rhythm – regularly irregular Normal or slow Progressive lengthening of the P-R

interval until a QRS complex is dropped (dropped beat)

2nd Degree AV block (Mobitz II orn Non-Wenkebach)

Configuration: P waves and QRS waves at times unpaired

Rhythm – slow Rate: normal or slow Constant lengthened P-R interval

until a QRS complex is dropped

3rd degree AV block (complete heart block) Configuration: P waves unrelated,

QRS generated by ventricles Rhythm – regular Rate: slow Complete heart block: no atrial

impulses pass through the AV, so AV node creates impulse thus rate is junctional.

Ventricular rhythms – death forming arrhythmias

Ventricular tachycardia Rhythm: usually irrefular, may have

some irregularity Heart rate: 150-250 ventricular bpm,

slow VT is below 150 bpm P waves: absent PR interval: none QRS complex: greater than 0.11 s V tach + pulse, tx is cardioversion

and meds Vtach without pulse, tx is defib and

meds

Ventricular fibrillation Rhythm: chaotic and extremely

irregular Heart rate: not measurable P waves: none PR interval: none QRS complex: none CPR, defib, meds

Asystole Rhythm: none Heart rate: none P waves: none PR interval: none QRS complex: none Tx is epinephrine Cardiac standstill or flatline

Pulseless electrical activity Monitor shows identifiable rhythm

but no pulse is detected Rhythm may be sinus, atrial,

junctional or ventricular Electromechanical dissociation Any rhythm without a pulse other

than vfib, vtach, and asystole CPR

Common Cardiovascular Conditions:

Ischemia - assoc. with CAD- Happens due to loss of oxygen and

nutrients to myocardial tissue due to poor coronary blood flow

- Risk factors:o Heredityo Age (above 40)o Sex and gender

More in men and women with contraceptives

o Race More in African

Americans- Modifiable/ Controllable Risk

Factors:o Dieto Habit/lifestyleo Contributing:

Obesity, stress response, DM

o Lipid Profiles (LDL, HDL)o Coronary artery spasm

associated with atherosclerosis or from an unknown cause.

Control of CADA - for aspirin and anti-anginal therapyB - for beta-blocker therapy and BP controlC – for cigarettes and cholesterolD – diet and diabetesE – for education and exercise

Triansient Ischemic Attack- Decreased blood supply through

partially occluded coronary arteries- Precipitating factors:

1. Temperature change2. Exercise3. Heavy meals4. Emotions5. Sexual intercourse6. Valsalva maneuver (carotid

massage, recta; stimulation, sterna rub) increases intrathoracic pressure

7. Smoking causes central vasoconstriction

8. Stimulants (coffee, flush it with water when palpitation occurs)

9. PTCA, CABG (coronary artery bypass graft), stress tests

Characteristics

- Pain or chest discomfort: burning suffocating, squeezing or crushing tightness

o Radiates: left arm, neck, jaw or shoulder blade

- Clenching fist or rubbing left arm: n/v, fainting, sweating, and cool extremities are noted when you touch the patient (mamugnaw then makuyapan)

STABLE (CHRONIC) ANGINA- Manageable- Physical exertion, emotional stress,

or cold weather- Stable pattern of onset, duration and

severity and relieving factorsPain

- Mild to severe and lasts for 1 to 5 mins

- ST segment depression, T wave inversion relieved by rest and sublingual NTG, or both

UNSTABLE ANGINA- Preinfarction/ crescendo/ intermittent

coronary syndrome- Unpredictable degree of exertion or

emotion that occur at night- Patient may wake up with sinus

tachycardia and pain, no changes in ECG

Medical emergency:- Progressive, prolonged, or frequent

angina with increasing severity- Pain lasts for 30 mins and above- Not completely relieved with NTG

Morphine SO4

PRINZMETAL’S ANGINA- Chest pain of longer duration- May occur at rest- Happen between midnight and 8am- Occlusions in coronary artery

associated with elevation of ST segment in the EKG

Treatment:- NTG - Calcium channel blockers are most

effective- Goal: vasodilation and reduction of

myocardial oxygen demands

Nitrglycerin: most frequently recommended drug for angina

Administration

- Check vital signs (BP)- Sublingually(tablet) given x3q5mins

(if pain doesn’t go away after the 3 doses, bring patient to hospital) spray: one spray sublingual

- Vital signs after each dosage (hold if BP is <90 – 100mmGh, or if HR is 50)

- Activity of NTG: burning sensation- Common side effect: headache due

to central vasodilation (tell patient to remain in bed, get the BP)

- Pain is relieved 45 seconds to 5 mins sublingually

Nursing care- Nitrates (short acting) nitroglycerin

SL (spray or tablet)Guidelines:

- Stop any activity right away- Retain saliva- Note burning sensation- Potency: 3-6 months- Inactivated b light, heat, and time

(wrap drug in paper)

NTG Patch: (long-acting) Nitrol; Nitrodisk- On patients chest and is rotated every

now and then Guidelines

- Use gloves- Use in non-hairy areas- Rotate- Avoid heat/ defibrillation- Worn 12 hours in the body during

waking hours

ACUTE MYOCARDIAL INFARCTIONDefinition: necrosis of the myocardial cells

- Loss of functional myocardium effects heart ability to maintain effective cardiac output

- Life-threatening event- Most common cause, fat plaque,

blood clot

Pathophysiologic changes- Ulceration or rupture of complicated

atherosclerosic lesion- Clot occludes vessel in myocardium

distal to obstruction- Prolonged ischemia (>20 -45 mins):

irreversible hypoxemia damage- Anaerobic metabolisms: H+ ions and

lactic acid - Pain and discomfort; heart failure

- Common site at anterior wall of left ventricle ( most important chamber of the heart)

- STEMI: ST segment elevation myocardial infarction (MI 30 mins or less)

- NSTEMI: prolonged MI

Types:- Zone of ischemia

o Outer region of the myocardium; composed of viable cells: ECG- (T wave inversion) there should be ST segment depression plus inverted or depressed P wave

o Progress to zone of injury if not addressed

- Zone of injuryo IZ is surrounded by injured

but still potentially viable tissue: ECG (elevated ST segment)

o Potentially viable tissueo Progress to zone of infarction

if not managed- Zone of infarction

o Area of cellular death and muscle necrosis in the myocardium: ECG (pathologic Q waves: q wave should not be more than .04 in the time factor of ECG; if Q wave is 25% more than the height of R wave)

Depth of Infarction

Subendocardial or non-O-wave infarction (innermost part)

1. Subendocardial tissue2. Within 20 minutes of injury3. S-T segment depression with small

infarct4. Ischemia- T wave inversion possible5. Reversible

*if chest pain, O2 dayunIntramural infarction (middle part)

1. Myocardium2. Associated with frequent angina

pectoris3. Injury- 30-45 mins4. Reparable

Transmural infarction or O-wave infarction1. All layers of myocardium to

epicardium

2. Within 1-6 hours3. Prominent Q wave4. Irreversible

PAIN: Classic Manifestation- Greater than 15 to 20 mins- Rest and NTG ineffective- Sudden and not associated with

activity- Crushing and severe, heavy or

squeezing sensation- Location: center of chest and may

radiate atypical chest pain: CC: indigestion heartburn, n/v

- No chest discomfort for 25% of clients with acute MI

Laboratory Tests- Cardiac serum markers: myoglobin,

myeloperoxidase, C-reactive proteins, troponin T or i

- Increased leuko in CBC, increased ESR (inflammation)

- ABGs (acidosis)- Electrocardiography:

o T wave inversiono Elevation of S-T Segmento Formation of Q waves

- Echocardiography (anatomy assessment)

o Transesophageal echocardiography (like endoscopy with Doppler, views the back part of the heart)

- C- cardiography (echocardiograms: shows functional and non functional tissues)

- A- abg’s- S- serum markers- E- electrocardiogram

Nursing Dx’s- Acute pain- Ineffective tissue perfusion: 12 lead

ECG- Ineffective coping: overuse of denial

may interfere with learning and compliance

- Fear

Nursing Interventions- Relief of pain: MONA is the guide

of treatment of clients with chest pain.M- Morphine sulfate (dilates blood vessels of heart

O- oxygen therapyN- nitrates, NTG for vasodilation for coronary arteriesA- Aspirin antiplatelets

- Measures to maintain cardiac parameters

o Cardiac monitoring (LeadII)o Report changes in LOC heart/

lung sounds for backflow and result to pulmonary congestion (crackles)

o Pulses and CRT <3 secondso JVD assessment: semi-

fowler’s position, use o PAWD is less than 18 mmHg

– volume depletion if more than 18 mmHg – pulmo congestion or cardiogenic shock

o MIO: assess whether there is increase/decrease for possible retention of fluids/ blood

o Decreased ADL (provide rest periods) order is complete bed rest

o Stool softeners: valsalva maneuver

- Promote measures to maintain adequate 02 and carbon dioxide changes

o 02 administration ; caution in COPD

o Pulse oximetryo ABG resultso Monitor secretions: coughing

and suctioning o Intubation PRN: if O2 sat is

below 70%

- Fibrinolyticso Within 1-3 hours from onset

of symptoms o SE: bleeding, allergic

reaction, fever, n/v, hypotension

o Precautions: reperfusion dysrythmias

o Common complication for patients with MI: dysrythmias

o Antidote: aminocaproic acido Time 0: the last time patient

was seen no0rmal, the 1-3 hours will start then.

Types: aminocaproic acida. Streptokinaseb. Urokinasec. Morphine sulfate: analgesicsd. ACE inhibitors: vasodilatione. Beta adrenergic blockers:

decrease contractility; decrease O2 demand; increase coronary blood flow

f. Calcium channel blockersg. Antidysrhthmic drugs: lidocaineh. Anticoagulants (heparin,

warfarin, Coumadin)a. Heparin: SQ: avoid

massage (increase absorption and create hematoma), aspirin (cause bleeding), same site, alcohol, pressure; rotate sites, you may not use alcohol when you cleanse the site

b. Warfarin: avoid aspirin, green leafy vegetables (Vit. K: antidote for warfarin), watch for signs of bleeding

i. Antidotes:1. Heparin:

rotamine2. Warfarin:

vitamin K Other Medical Interventions

1. Percutaneous transluminal coronary angioplasty(PTCA)

2. Laser revascularization3. Intracoronary stents: placement of a

tubular mesh or coil spring device: risk for rupture of veins and risk for infection due to placement of foreign stent

4. Intra-aortic balloon pump (IABP): inflation of a balloon in the coronary artery during diastole and deflated during systole:

5. Coronary artery bypass graft (CABG): conduit through anastomosing of the saphenous vein or internal mammary artery

Potential Complications: 1. Dysrhythmias: fibrillation is the most

common2. Heart failure3. Cardiogenic shock: due to massive

left ventricular failure

4. Ventricular aneurysm: a healing necrotic tissue can cause thinning and weakening of the ventricular wall

5. Pericarditis: inflammatory response to MI

6. Dressler’s syndrome: aka: post- Mi syndrome; late pericardities, precordial pain, friction rub, fever, pleuritis and/or pleural effusion

a. Give steroids and supplemental oxygen

7. Pulmonary embolism8. Ventricular septal rupture9. Papillary muscle rupture

Acute Respiratory Distress Syndrome- Edema inside alveolus

1. Hypoxemia – PO2 below 50 mmHg2. Hypercapnia- PCO2 above 45

mmHgOccurs in a person with previous respiratory

Causes:1. COPD2. Pneumonia3. Tuberculosis4. Contusion5. Aspiration6. Inhaled toxins7. Pulmonary embolism

Internal causes:

Sepsis, Anaphylaxis, uremia, drug overdose, hypervolemia, shock and massive blood transfusion- causes vasoconstriction that may increase hydrostatic pressure, DIC

Phases of ARDS:1. Exudative – leakage if fluid from

capillaries within 24 hours due to capillary damage from inflammation, leading to alveolar damage

2. Proliferative – 7-10 days (destruction of type 1 and 2 pneumocytes - by leukotrines, macrophages, proteases) decreased surfactant production, atelectasis, intrapulmonary shunting, V/Q mismatch, decreased lung compliance

3. Fibrinolytic – 2-3 weeks, irreversible deposition of fibrin in the lung with

hyaline membrane formation, decreased FRC

Hallmark: hypoxemia even with supplemental oxygen

Nursing plans and interventions:

1. Maintain client on ventilator with correct settings

2. Provide care for either an oral airway or tracheostomy (suctioning prn)

3. Monitor breath sounds for pneumothorax especially when positive and expiratory pressure (PEEP) is used (5-10 cm of water)

4. Provide emotional support to decrease anxiety and allow ventilator to “work the lung”

5. Monitor the ff:- Hemodynamics- ABG- Vital organ status: CNS LOC, renal,

CO- F/E balance- Metabolic status

Medical Management- Artificial surfactant (survanta/

beractant) * through ET tube- Nitric oxide – pulmonary vasodilator- Dobutamine/Dopamine – for fluid

instability - Steroids – inflamm- Antibiotics- Ventilator support with PEEP

SHOCK- Widespread serious reduction of

tissue perfusion (lack of oxygen and nutrients)

1. Hypovolemic shock: circulating blood volume; decrease blood volume dec venous return dec filling pressure dec. stroke volume dec. cardiac output dec. tissue perfusion

a. High Pulse rateb. High heart ratec. Low BP: low circulating

blood volume2. Cardiogenic shock: shock wherein

the problem is on the patient’s heart. 4-5L blood volume capacity of the heart. Those with MI.

a. Heart is not able to pump out blood or contract properly

b. Ineffective pump dec. stroke volume dec. cardiac output dec. tissue perfusion

3. Neurogenic shock: motor-vehicular accidents; or any injury involving the spinal cord; blood vessels will remain vasodilated due to problems in the spinal cord; BP will remain low even though circulating and cardiac fluids are normal

4. Anaphylactic and septic shock: increase in capillary permeability which results to release of plasma to outside environment resulting to inflammatory responses; septic: due to infections

Shock will SNACH your life away

S- septicN- neurogenicA- anaphylacticC- cardiogenicH- hypovolemic

Nursing Assessment

Skin Changes- Cool clammy ( warm skin in

vasogenic and early shock)- Diaphoresis- Pale

Fluid Status (acute tubular necrosis)- Urine output decreases or an

imbalance between intake and output occurs

- Abnormal CVP (<4 cm of H20)- Urine specific gravity >1.020

(indicates hypovolemia)

Nursing Dxs1. Fluid volume deficit2. Decreased cardiac output3. Altered thought processes4. Anxiety (family and individual)

Nursing Plans and Interventions1. Monitor arterial pressure

a. Monitor vital signs and arrhythmias (q15mins) or PRN depending on stability

b. Assess urine every hour to maintain at least 30 ml/hr

2. Military Anti Shock Trousers (MAST) patient is made to wear the pants compressing the legs in such a

way that the blood vessels are pressed so that the blood is brought t to the central area than the distant extremities, IABP, external counterpulsation devise (compresses during diastole to return the blood to central circulation)

5. Administer fluids as prescribed by provider: blood colloids, or electrolyte solutions until designated CVP is reached

6. Place client in modified Trendelenberg’s position

7. Administer medications IV until perfusion improves in muscles and subcutaneous tissues

HINT: if cardiogenic shock exists with the presence of pulmonary edema, i.e. from pump failure, position client to REDUCE venous return (high Fowler’s and legs down) in order to decrease venous return further to the left ventricle. The next organ affected after the brain after shock would be the kidneys

Drugs of Choice for shock1. Digitalis preparations:

a. Increase contractility of the heart muscle

2. Vasoconstrictors (Dopamine)a. Generalized vasoconstriction

to provide more available blood to the heart to help maintain cardiac output.

b. Increases BP

If patient loses fluids- Whole blood: to replace large

volume loss- Packed RBC: for moderate blood

loss improve O2- carrying capacity without adding excessive volume

- Autotransfusion (trauma): Hct. Rises about 4% and Hgb rises about 1 Gm% for each unit of packed RBC