Critical Care Nursing 08.31.

12 GoldenArwanna
A specialty within nursing which deals specifically with human responses to life threatening problems Scope of CCN 1. Critically ill patient Acute conditions MI, Stroke, pulmonary embolism, hemorrhage, bleeding tendencies, multiple organ failure, hypokalemia, HGB2, 2. CCN 3. 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. 2. 3. 4. 5. 6. Skilled communication True collaboration Effective decision making Appropriate staffing Meaningful recognition Authentic leadership -

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 complications 3. 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

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

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

*PQRST scheme for pain: Pattern how often Precipitating and Palliating Quality type of pain (throbbing, stabbing, sharp, dull) Region radiating Severity pain rating, visual pain analogue Time duration, time of the day *AVPU Mnemonic (LOC) A Alert V Verbal P Painful U Unconscious *AMPLE Mnemonic A Allergies M Medication P Past Medical History L Last food intake E events preceding the injury *ABCDE Mnemonic A airway B breathing C circulation D disability E Expose and evaluate *CRAMS scale C circulation R respiration A abdomen M motor S speech Less 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 S1 Splitting of heart sounds (split S2: Lub TDub)

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 lung o 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 devt 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 pH o Response to stress; decreased pH o K to be assessed

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

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 stop o Equipment is broken stop o 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

Central Venous Pressure pressures inside atria - Indicated for significant fluid volume alterations (hypervolemia and hypovolemia) - Assesses diuresis - Complications: o Injury o Bleeding o Infection o Catheter occlusion o Cannulation of central vein, hemothorax and pneumothorax - Options: o Subclavian o Internal jugular o Femoral - Trendelenburg position decreases the risk of air embolism - NV: 4-12 cm H20 - Nurses responsibilities: o Consent is secured o Explain the procedure o Trendelenburg position o Assist during the procedure o Instruct to deep breathe and hold o 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 mmHg Dias 60-65 mmHg

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. Clients name and ID number 2. Location, time, date of recording 3. Clients age, sex, cardiac and noncardiac medications currently being taken. 4. Height, weight BP 5. Clinical diagnosis and current clinical status 6. Any unusual positioning of the client during the recording 7. If present, thoracic deformities, respiratory distress or muscle tremors

Pulmonary artery pressure - Uses Swan Ganz catheter - Pulmonary wedge pressure - NV: o Sys 15-25 mmHg o Dias 8-10 mmHg o Cap wedge 8-12 mmHg Venous oxygen saturation NV: 60-80% - Reflects the amount of oxygen left in the blood

ABG Monitoring R Respiratory O opposite M metabolic E equal NV: pH 7.35-3.45 PaCo2 35-45 mmHg HCo3 22-26

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

Wave a deflection either positive of negative away from the isoelectric line Complex several waves Segment a straight line between waves and complexes Interval 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 interval N Va,ies: 0.12 0.20s T Wave - runded, upright wave following QRS cmplex - Indicates ventricular repolarization

Limb Leads Electrodes are placed on the: o Right arm o Left arm o Right leg o Left leg o 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:

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

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 NonWenkebach) 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

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

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 Heredity o 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 Diet o Habit/lifestyle o Contributing: Obesity, stress response, DM o Lipid Profiles (LDL, HDL) o Coronary artery spasm associated with atherosclerosis or from an unknown cause. Control of CAD A - for aspirin and anti-anginal therapy B - for beta-blocker therapy and BP control C for cigarettes and cholesterol D diet and diabetes E for education and exercise Triansient Ischemic Attack - Decreased blood supply through partially occluded coronary arteries - Precipitating factors: 1. Temperature change 2. Exercise 3. Heavy meals 4. Emotions 5. Sexual intercourse 6. 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 factors Pain - 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 PRINZMETALS 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 doesnt 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 INFARCTION Definition: 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

2. Within 1-6 hours 3. Prominent Q wave 4. 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 inversion o Elevation of S-T Segment o 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- abgs - S- serum markers - E- electrocardiogram Nursing Dxs - 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

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 injury o IZ is surrounded by injured but still potentially viable tissue: ECG (elevated ST segment) o Potentially viable tissue o 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 tissue 2. Within 20 minutes of injury 3. S-T segment depression with small infarct 4. Ischemia- T wave inversion possible 5. Reversible *if chest pain, O2 dayun Intramural infarction (middle part) 1. Myocardium 2. Associated with frequent angina pectoris 3. Injury- 30-45 mins 4. Reparable Transmural infarction or O-wave infarction 1. All layers of myocardium to epicardium

O- oxygen therapy N- nitrates, NTG for vasodilation for coronary arteries A- 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 seconds o JVD assessment: semifowlers 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 oximetry o ABG results o Monitor secretions: coughing and suctioning o Intubation PRN: if O2 sat is below 70% Fibrinolytics o 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 acid o Time 0: the last time patient was seen no0rmal, the 1-3 hours will start then. Types: aminocaproic acid

Streptokinase Urokinase Morphine sulfate: analgesics ACE inhibitors: vasodilation Beta adrenergic blockers: decrease contractility; decrease O2 demand; increase coronary blood flow f. Calcium channel blockers g. Antidysrhthmic drugs: lidocaine h. 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: rotamine 2. Warfarin: vitamin K Other Medical Interventions 1. Percutaneous transluminal coronary angioplasty(PTCA) 2. Laser revascularization 3. 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 common 2. Heart failure 3. Cardiogenic shock: due to massive left ventricular failure 4. Ventricular aneurysm: a healing necrotic tissue can cause thinning

a. b. c. d. e.

5. 6.

7. 8. 9.

and weakening of the ventricular wall Pericarditis: inflammatory response to MI Dresslers syndrome: aka: post- Mi syndrome; late pericardities, precordial pain, friction rub, fever, pleuritis and/or pleural effusion a. Give steroids and supplemental oxygen Pulmonary embolism Ventricular septal rupture Papillary muscle rupture

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 rate b. High heart rate c. Low BP: low circulating blood volume 2. Cardiogenic shock: shock wherein the problem is on the patients 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

Acute Respiratory Distress Syndrome - Edema inside alveolus 1. Hypoxemia PO2 below 50 mmHg 2. Hypercapnia- PCO2 above 45 mmHg Occurs in a person with previous respiratory Causes: 1. COPD 2. Pneumonia 3. Tuberculosis 4. Contusion 5. Aspiration 6. Inhaled toxins 7. 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

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- septic N- neurogenic A- anaphylactic C- cardiogenic H- 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 Dxs 1. Fluid volume deficit 2. Decreased cardiac output 3. Altered thought processes 4. Anxiety (family and individual) Nursing Plans and Interventions 1. 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 Trendelenbergs 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 Fowlers 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 shock 1. 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