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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
CAD.A blowing. R/L bundle branch block. MM. visual pain analogue Time – duration. this is also in the liver. peak in 12-18 hrs.Sterna rub by eye opening. aortic stenosis. use bell of stethoscope. regurgitation` S4 – increased resistance to ventricular filling (CHF. Return to normal level in 7-14 days. return to normal level in 3-4 days Elevated LDH (Lactate Dehydrogenase) – increased 14-24 hpurs after the onset of chest pain. dull) Region – radiating Severity – pain rating.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.Reflect turbulent blood flow . Return normal within 3-4 hours. atrial/septal defect Systolic Murmur . cries during pain assessment. Pulmonic and aortic semilunar valve closure (2nd ICS L/R SB) Abnormal heart sounds S3 – after S2. sharp. 75% after 6 hours. o LDH 1. BB) o Increased in 3-6 hours after onset of chest pain. RV failure.2 – kidneys. swooshing sound upon auscultation . kidney. heart. brain . peak within 48-72 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.Indicates pulmonary stenosis.Caused by the delay in the closure of the right-sided valves . above 8 indicates minor trauma S1 – AV valves close (5th ICS LMC or PMI) S2 – diastolic. heard after S1 Splitting of heart sounds (split S2: Lub TDub) Aortic valve closes significantly earlier than the pulmonic valve . 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. stabbing. RBC (1:1) o LDH 3 –specific in lung o LDH4. 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. moves body resisting the painful stimulus – 10 *PQRST scheme for pain: Pattern – how often Precipitating and Palliating Quality – type of pain (throbbing. L/R SB.
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. medical therapy. and indicative of atherosclerotic plaques.Indicated for significant fluid volume alterations (hypervolemia and hypovolemia) .NV: 4-12 cm H20 . associated with MI.Trendelenburg position decreases the risk of air embolism .Assesses diuresis . 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.NV: 4-8 L/min . 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. smoking before stress test Scans – Thallium and MUGA (Multiple Gated Acquisition) o Thallium 201.Increases in cardiogenic shock and Right ventricle infarction Cardiac output = Stroke volume x Heart Rate . stroke. o 20 mmHg systolic stop the stress test o Fatigue and dyspnea stop o Equipment is broken stop o No caffeine.Options: o Subclavian o Internal jugular o Femoral .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 . produced by liver. hemothorax and pneumothorax .Complications: o Injury o Bleeding o Infection o Catheter occlusion o Cannulation of central vein. and identify those for referral for invasive therapy.Stroke volume = EDV – ESV NV: 60-100 mL/ beat Intra-arterial blood pressure – direct measurement of BP by use of an arterial catheter . C-reactive protein (CRP) – peaks several days later.Determined with a quadruple lumen (thermodilution) pulmonary catheter and bedside computer .Catheter is connected to a high pressure tubing to a transducer and . Cardiac Catheterization – to determine the extent and location of obstruction of coronary arteries Central Venous Pressure – pressures inside atria . normalizes after 1 week ABG shows rise in pH o Response to stress.
pericarditis) .Automaticity . Angina. weight BP 5. Client’s age. If present.Reflects the amount of oxygen left in the blood ABG Monitoring R – Respiratory O – opposite M – metabolic E – equal NV: pH 7. Any unusual positioning of the client during the recording 7.Evaluate effects of systemic related diseases (renal/pulmonary) .- 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 .Pulmonary wedge pressure .Insertion if temp/permanent pacemakers Each EKG should include identifying information: 1.To aid in confirming definite diagnosis or as a differential diagnosis (MI. cardiac and noncardiac medications currently being taken.Responsible for spontaneous generation and conduction of electrical impulses . 4.45 PaCo2 35-45 mmHg HCo3 22-26 .Holter monitoring – continuous portable Purposes: . thoracic deformities. Clinical diagnosis and current clinical status 6.Uses Swan Ganz catheter . Client’s name and ID number 2.MI = 12 leads (helps determine if there is infarction by visualizations of significant changes in cardiac waveforms) .35-3.NV: o Sys 15-25 mmHg o Dias 8-10 mmHg o Cap wedge 8-12 mmHg Venous oxygen saturation – NV: 60-80% . Height.Exitability . date of recording 3.Contractility .Standard leads – 12 leads .Telemetry monitoring – 3-5 leads .Conductivity A visual representation of the electrical activity of the heart reflected by changes in the electrical potential at the skin surface Types: .To guide appropriate or more definitive therapy (Electrolyte replacement) . respiratory distress or muscle tremors Pulmonary artery pressure . time. sex. Location.
Q wave: 1st negative deflection .12 – 0.posterior 5th ICS left midscapular area V9 – directly between V8 and SC at 5th ICS Components of ECG tracing Characteristics: . upright wave following QRS cmplex .R waveL 1st positive deflection .Small rounded upright . regularity. thighs. II.Indicates atrial depolarization (results to contraction) QRS complex . ante-cubital area. It provides info if the HR. III Lead II is commonly called the monitoring lead. know whether the cable used is American or European cables.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. 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.Normal: 0. conduction time and and ectopic beats.20s’ T Wave .First wave seen .lead ECG Includes 12 lead ECG plus V4R – 5th ICS at RMCL V8 . Mi is best validated by a 12-lead EKF 5 wire cable 15 .Before you attach the electrodes. Improper placement can give incorrect ECG recordings 3 – lead ECG Monitors the standard leads I.runded.Will tell you electrical activities in the atria .Ventricular depolarization .3 deflections following P waves . used to determine + or .S wave – 2nd negative deflection .deflection P-QRS-T (view 2) P wave – will tell you the activity of the SA node .ies: 0.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.06-0. 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 .
06-0.06-0. stress. No SV.Heart rate: atrial rate not measurable.P waves: no identifiable P waves . QRS and T waves seen Rhythm – regular (from AV nodes) Rate: 101-180 bpm QRS: 0. QRS complex and T wave seen PR interval prolonged Rhythm – regular Rate: may vary 2nd Degree AV Block (Mobitz I or Wenkebach) P waves.PR interval: none can be measured because no P waves are seen .Sinus Tachycardia Rhythm: regular Heart rate: 101 – 150 P waves: rounded.10 Heart Blocks Blockage is at the AV node P wave is normal. ventricular rhythm regular or irregular depending on consistency of AV conduction of impulses . AV node blocks impulse. QRS and T waves seen Rhythm – regular (from AV nodes) Rate: 40-60 bpm QRS: 0. QRS and T waves seen Rhythm – regular (from AV nodes) Rate: 40-60 bpm QRS: 0. valsalva maneuver. No depolarization. exercise. absent or inverted.20 s QRS interval: 006-1. caffeine intake.10 secs . No contraction.g. ventricular rate under 100 is controlled response. precede each QRS complex. No BP.Heart rate: ventricular rate varies above 150 .10 s . coughing out.P waves: flutter or F waves with saw-tooth pattern .06-0.06-0. 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 . flat or depressed Rhythm: regular . carotid massage) o Cardioversion and meds Atrial Fibrillation .PR interval: none measurable .Clots may be formed Junctional rhythms Rate: 40-60 bpm P waves: absent. >100 is rapid ventricular response .12 – 0. alike PR interval: 0.Rhythm: grossly or irregularly irregular . No transmission.Rhythm: atrial rhythm regular.10 Junctional Tachycardia: Configuration: P waves flat. thyroid problems.Tx: Vagal maneuvers – decreases heart rate (e. rectal temp. Treatment: Pacemaker 1st degree AV block Configuration: P. anxiety Determine cause and treat Configuration: P waves flat.QRS complex 0.10 s If rate is >150bpm it is SVT or Atrial tachycardia Caused by increased metabolism (fever).06-0. absent or inverted. absent or inverted.QRS complex: 0. QRS complex.10 Accelerated Junctional Rhythms: Configuration: P waves flat. Impulse not transmitted to BofH and PF.
sterna rub) increases intrathoracic pressure 7. Ventricular rhythms – death forming arrhythmias Ventricular tachycardia Rhythm: usually irrefular.assoc. Smoking causes central vasoconstriction 8. so AV node creates impulse thus rate is junctional. junctional or ventricular Electromechanical dissociation Any rhythm without a pulse other than vfib. with CAD . Stimulants (coffee.for beta-blocker therapy and BP control C – for cigarettes and cholesterol D – diet and diabetes E – for education and exercise Triansient Ischemic Attack . Emotions 5. Sexual intercourse 6.11 s V tach + pulse. may have some irregularity Heart rate: 150-250 ventricular bpm.3rd degree AV block (complete heart block) Configuration: P waves unrelated. Heavy meals 4. DM o Lipid Profiles (LDL. Control of CAD A . Temperature change 2. defib. atrial. slow VT is below 150 bpm P waves: absent PR interval: none QRS complex: greater than 0. tx is cardioversion and meds Vtach without pulse.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 . and asystole CPR Common Cardiovascular Conditions: Ischemia . CABG (coronary artery bypass graft). Exercise 3. 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.Modifiable/ Controllable Risk Factors: o Diet o Habit/lifestyle o Contributing: Obesity. recta.Precipitating factors: 1. HDL) o Coronary artery spasm associated with atherosclerosis or from an unknown cause.Decreased blood supply through partially occluded coronary arteries . QRS generated by ventricles Rhythm – regular Rate: slow Complete heart block: no atrial impulses pass through the AV. stress tests . 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. flush it with water when palpitation occurs) 9.for aspirin and anti-anginal therapy B . vtach. stimulation. Valsalva maneuver (carotid massage. PTCA. stress response.
Loss of functional myocardium effects heart ability to maintain effective cardiac output .Anaerobic metabolisms: H+ ions and lactic acid . fainting. and cool extremities are noted when you touch the patient (mamugnaw then makuyapan) STABLE (CHRONIC) ANGINA .Not completely relieved with NTG Morphine SO4 PRINZMETAL’S ANGINA .Clot occludes vessel in myocardium distal to obstruction . heat.Stable pattern of onset. emotional stress.Calcium channel blockers are most effective . or both UNSTABLE ANGINA .Physical exertion. bring patient to hospital) spray: one spray sublingual .May occur at rest .Prolonged ischemia (>20 -45 mins): irreversible hypoxemia damage .Mild to severe and lasts for 1 to 5 mins . duration and severity and relieving factors Pain .Manageable .Ulceration or rupture of complicated atherosclerosic lesion .Stop any activity right away .Occlusions in coronary artery associated with elevation of ST segment in the EKG Treatment: . squeezing or crushing tightness o Radiates: left arm.Potency: 3-6 months .Check vital signs (BP) .On patients chest and is rotated every now and then Guidelines .Most common cause.Goal: vasodilation and reduction of myocardial oxygen demands Nitrglycerin: most frequently recommended drug for angina Administration .Clenching fist or rubbing left arm: n/v.Preinfarction/ crescendo/ intermittent coronary syndrome . no changes in ECG Medical emergency: .Rotate . neck.Note burning sensation .Happen between midnight and 8am . or if HR is 50) . blood clot Pathophysiologic changes .Inactivated b light.Pain lasts for 30 mins and above . sweating.Avoid heat/ defibrillation .Sublingually(tablet) given x3q5mins (if pain doesn’t go away after the 3 doses.Nitrates (short acting) nitroglycerin SL (spray or tablet) Guidelines: .Use gloves . jaw or shoulder blade .ST segment depression.Progressive.Patient may wake up with sinus tachycardia and pain.Vital signs after each dosage (hold if BP is <90 – 100mmGh. T wave inversion relieved by rest and sublingual NTG.Pain is relieved 45 seconds to 5 mins sublingually Nursing care .Characteristics . and time (wrap drug in paper) NTG Patch: (long-acting) Nitrol.Life-threatening event .Chest pain of longer duration .Worn 12 hours in the body during waking hours ACUTE MYOCARDIAL INFARCTION Definition: necrosis of the myocardial cells .Unpredictable degree of exertion or emotion that occur at night . Nitrodisk .Common side effect: headache due to central vasodilation (tell patient to remain in bed.NTG . fat plaque. get the BP) . or cold weather .Pain or chest discomfort: burning suffocating. prolonged. or frequent angina with increasing severity .Retain saliva .Activity of NTG: burning sensation .Use in non-hairy areas .
A.Echocardiography (anatomy assessment) o Transesophageal echocardiography (like endoscopy with Doppler.Crushing and severe.(T wave inversion) there should be ST segment depression plus inverted or depressed P wave o Progress to zone of injury if not addressed . Prominent Q wave 4. views the back part of the heart) .ABGs (acidosis) .Electrocardiography: o T wave inversion o Elevation of S-T Segment o Formation of Q waves .Rest and NTG ineffective .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 . heavy or squeezing sensation .04 in the time factor of ECG.Acute pain .Zone of ischemia o Outer region of the myocardium. composed of viable cells: ECG. Ischemia.Greater than 15 to 20 mins .S. Injury. Subendocardial tissue 2.serum markers .- - - Pain and discomfort. Irreversible PAIN: Classic Manifestation . Reversible *if chest pain.T wave inversion possible 5. All layers of myocardium to epicardium .Sudden and not associated with activity . if Q wave is 25% more than the height of R wave) Depth of Infarction Subendocardial or non-O-wave infarction (innermost part) 1.C. Associated with frequent angina pectoris 3.30-45 mins 4. 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. S-T segment depression with small infarct 4. Within 20 minutes of injury 3. n/v .Location: center of chest and may radiate atypical chest pain: CC: indigestion heartburn.Fear Nursing Interventions .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 . myeloperoxidase.Ineffective coping: overuse of denial may interfere with learning and compliance . M. troponin T or i .electrocardiogram Nursing Dx’s . Within 1-6 hours 3. Reparable Transmural infarction or O-wave infarction 1. increased ESR (inflammation) .abg’s .Increased leuko in CBC.cardiography (echocardiograms: shows functional and non functional tissues) .Relief of pain: MONA is the guide of treatment of clients with chest pain.Morphine sulfate (dilates blood vessels of heart Types: . Myocardium 2.Ineffective tissue perfusion: 12 lead ECG . O2 dayun Intramural infarction (middle part) 1.Cardiac serum markers: myoglobin. C-reactive proteins.E.No chest discomfort for 25% of clients with acute MI Laboratory Tests .
Anticoagulants (heparin. 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. Heparin: SQ: avoid massage (increase absorption and create hematoma). Coumadin) a.oxygen therapy N. warfarin. increase coronary blood flow f. 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. NTG for vasodilation for coronary arteries A. allergic reaction. alcohol. c. same site. fever. Types: aminocaproic acid - - Streptokinase Urokinase Morphine sulfate: analgesics ACE inhibitors: vasodilation Beta adrenergic blockers: decrease contractility. .O. Ventricular aneurysm: a healing necrotic tissue can cause thinning a. Calcium channel blockers g. aspirin (cause bleeding). green leafy vegetables (Vit. Antidotes: 1. 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. Antidysrhthmic drugs: lidocaine h. K: antidote for warfarin). Coronary artery bypass graft (CABG): conduit through anastomosing of the saphenous vein or internal mammary artery Potential Complications: 1. decrease O2 demand. b. Cardiogenic shock: due to massive left ventricular failure 4. e. Dysrhythmias: fibrillation is the most common 2. pressure. Warfarin: vitamin K Other Medical Interventions 1.nitrates. 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 . you may not use alcohol when you cleanse the site b. rotate sites. watch for signs of bleeding i. Heart failure 3. n/v. the 1-3 hours will start then. d.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: semifowler’s position. Heparin: rotamine 2. Intra-aortic balloon pump (IABP): inflation of a balloon in the coronary artery during diastole and deflated during systole: 5. Percutaneous transluminal coronary angioplasty(PTCA) 2. Warfarin: avoid aspirin. Laser revascularization 3.
macrophages.Widespread serious reduction of tissue perfusion (lack of oxygen and nutrients) 1. Monitor breath sounds for pneumothorax especially when positive and expiratory pressure (PEEP) is used (5-10 cm of water) 4. leading to alveolar damage 2. Low BP: low circulating blood volume 2. High heart rate c. and weakening of the ventricular wall Pericarditis: inflammatory response to MI Dressler’s syndrome: aka: post. stroke volume dec. late pericardities. 7. irreversible deposition of fibrin in the lung with hyaline membrane formation.Steroids – inflamm .ABG . precordial pain.Metabolic status Medical Management . Ineffective pump dec. decreased FRC . 4-5L blood volume capacity of the heart. Monitor the ff: . Those with MI. Pulmonary embolism Internal causes: Sepsis. Provide emotional support to decrease anxiety and allow ventilator to “work the lung” 5. CO . decrease blood volume dec venous return dec filling pressure dec. atelectasis.Nitric oxide – pulmonary vasodilator . Hypovolemic shock: circulating blood volume. Hypoxemia – PO2 below 50 mmHg 2.Vital organ status: CNS LOC.PCO2 above 45 mmHg Occurs in a person with previous respiratory Causes: 1. 6. 8. DIC Phases of ARDS: 1.Ventilator support with PEEP SHOCK . friction rub.Dobutamine/Dopamine – for fluid instability .Mi syndrome. Contusion 5. fever.Edema inside alveolus 1. hypervolemia.causes vasoconstriction that may increase hydrostatic pressure. pleuritis and/or pleural effusion a. cardiac Acute Respiratory Distress Syndrome . Hypercapnia. Pneumonia 3.by leukotrines. COPD 2. Anaphylaxis. Maintain client on ventilator with correct settings 2. renal. shock and massive blood transfusion. Exudative – leakage if fluid from capillaries within 24 hours due to capillary damage from inflammation. a. drug overdose.Artificial surfactant (survanta/ beractant) * through ET tube .Hemodynamics . intrapulmonary shunting. 9. Heart is not able to pump out blood or contract properly b. decreased lung compliance 3. V/Q mismatch.F/E balance . cardiac output dec.Antibiotics . Tuberculosis 4. Give steroids and supplemental oxygen Pulmonary embolism Ventricular septal rupture Papillary muscle rupture Hallmark: hypoxemia even with supplemental oxygen Nursing plans and interventions: 1. Cardiogenic shock: shock wherein the problem is on the patient’s heart. High Pulse rate b.5. tissue perfusion a. stroke volume dec. Provide care for either an oral airway or tracheostomy (suctioning prn) 3. Proliferative – 7-10 days (destruction of type 1 and 2 pneumocytes . Aspiration 6. Fibrinolytic – 2-3 weeks. proteases) decreased surfactant production. uremia. Inhaled toxins 7.
Fluid volume deficit 2. or any injury involving the spinal cord. Generalized vasoconstriction to provide more available blood to the heart to help maintain cardiac output.neurogenic A. Increases BP If patient loses fluids . Monitor arterial pressure a. Anxiety (family and individual) Nursing Plans and Interventions 1. Altered thought processes 4. from pump failure. Administer fluids as prescribed by provider: blood colloids.Urine specific gravity >1. Monitor vital signs and arrhythmias (q15mins) or PRN depending on stability b. IABP. or electrolyte solutions until designated CVP is reached 6.Cool clammy ( warm skin in vasogenic and early shock) . septic: due to infections Shock will SNACH your life away S. The next organ affected after the brain after shock would be the kidneys Drugs of Choice for shock 1.Pale Fluid Status (acute tubular necrosis) .hypovolemic Nursing Assessment Skin Changes . Anaphylactic and septic shock: increase in capillary permeability which results to release of plasma to outside environment resulting to inflammatory responses.cardiogenic H. Place client in modified Trendelenberg’s position 7. Rises about 4% and Hgb rises about 1 Gm% for each unit of packed RBC . Decreased cardiac output 3. external counterpulsation devise (compresses during diastole to return the blood to central circulation) 5. BP will remain low even though circulating and cardiac fluids are normal 4.Autotransfusion (trauma): Hct. Assess urine every hour to maintain at least 30 ml/hr 2. tissue perfusion 3. Administer medications IV until perfusion improves in muscles and subcutaneous tissues HINT: if cardiogenic shock exists with the presence of pulmonary edema. Neurogenic shock: motor-vehicular accidents.septic N.output dec.Urine output decreases or an imbalance between intake and output occurs .e. Vasoconstrictors (Dopamine) a.Diaphoresis . 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. Digitalis preparations: a.020 (indicates hypovolemia) Nursing Dxs 1. blood vessels will remain vasodilated due to problems in the spinal cord.anaphylactic C. Increase contractility of the heart muscle 2.carrying capacity without adding excessive volume . i. position client to REDUCE venous return (high Fowler’s and legs down) in order to decrease venous return further to the left ventricle. b.Packed RBC: for moderate blood loss improve O2.Whole blood: to replace large volume loss .Abnormal CVP (<4 cm of H20) .
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