• Describe the effects of shock, SIRS, MODS on the major body

systems.-
o decreased perfusion to systems (hypoperfusion) causes
them to shut down (failure) • Determine the medical management of the patient with MODS.-
• MODS- Multiple Organ Dysfunction Syndrome o Ventilatory support
• Identify measures that can be taken to prevent/limit the occurrence o Pharmacology- same as septic shock
of MODS.- o Nutrition
o Aggressive infection control= decrease risk for o Dialysis
nosocomial infections o Blood and blood products
o Prevent progression of SIRS—MODS  Nsg interventions:
 Vigilant assessments of all systems and ongoing • Multisystem patient assessment
monitoring • Maintain vent support
• Relate the precipitating factors of MODS to its incidence and • Maintain patent airway
mortality.- • Monitor CV & renal status
o Increases with # of systems affected • Maintain fluid and med admin (Septic
• Pathophysiology- shock)
o Sepsis • Monitor tissue perfusion
o Reduced circulating volume • Prevent further systemic sepsis
o Reduced oxygenation and tissue perfusion • Prevent aspiration of gastric contents
• Assess a pt with MODS- • Maintain nutritional support
o Assess all systems  Nsg. Dx:
o Clinical manifestations: o Decreased CO
 Sepsis o decreased tissue perfusion
 Shock  DIC (Disseminated Intravascular Coagulation)
 Resp failure o Abnormally initiated & accelerated clotting leads to
 Noncardiogenic pulmonary edema uncontrollable hemorrhage
 Altered cerebral function  Pathophysiology of DIC-
 Myocardial dysfunction o Abundant intravascular thrombin
 Liver dysfunction o Inactivated antithrombins
 Anasarca o Clot lysis
 Paralytic ileus o Unable to form clot at injury site
 GI bleeding o Thus predisposing to hemorrhage
 Acute renal failure  Precipatory factors-
• Dx Procedures: o Multisystem organ failure
 o Shock state o IV site- check apply pressure @ least 10 mins
o Neoplasia o I/O QH
o Obstetric conditions o Blood products
o Trauma o Weigh drsg’s
o Assess GI/ GU bleeding
 Clinical Manifestations- no well defined sequence of events o Serial blood results
o Abnormal bleeding s hx  All systems assessment
o Weakness, malaise  Prevention & recognition of hemorrhage or
o Fever thrombotic complications
o Bleeding and thrombic sx’s  Monitor lab values
o Resp and GI sx’s  Provide comfort
o Acute renal failure  Maintain nutrition
o Decreased systemic tissue perfusion  Monitor fluids at electrolyte
o Multisystem organ failure  I/O
 Dx studies findings  Assure pt. safety
o Bleeding clotting times (not reliable  Provide emotional &psychological support
o Fibrin splitting product (FSP)  Comfort
o D-dimer Pulmonary Problems
o CBC Arterial Blood Gas Disturbances
 Medical Mgmt- no bleeding-no therapy  Maintenance of Acid-base balance
o Tx underlying factors o Hydrogen
o Fluid replacement o Bicarb
o Blood transfusion o Base: acid ratio
o Pharmacology- (Chronic DIC no anticoagulants) o Norm arterial pH
 Heparin (controversial) o Compensation measures
 Amicar (inhibits fibrinlysis)  Arterial Blood Gas analysis
 Nsg Dx: o pH
o Potential for injury o PaCO2
o Fluid vol. deficit o HCO3
o Decreased tissue perfusion o Base excess/base deficit
o Decreased CO o PaO2
 Nsg. Interventions o Oxygen saturation
o Don’t scrub bleeding areas  Acid-Base imbalance
o Complete bed rest o Respiratory Acidosis
 o Respiratory Alkalosis o Hypoxemia
o Metabolic Acidosis o Hypoxia
o Metabolic Alkalosis o Hypocarbia/hypercapnia
 Nsg. Dx: o Acute
o Impaired airway clearance o chronic
o Alteration in resp. fxn  Precipitating Factors
o Chronic airway obstruction
o Restrictive defects
o Neuromuscular defects
o Respiratory center depression
 Nsg. Interventions  Clinical manifestations
o Resp assessment o Primary disease
o ABG analysis o Hypoxia
o Airway clearance o Hypercapnia
o Promotion of ventilation o Respiratory acidosis
 Acute Respiratory Failure- either hypoxemia (type 1) o Hypoxemia
or Hypercapnia (type 2)  Dyspnea
 Tidal volume= amt of air in & out during norm breathing  Tachypnea
(500)  Prolonged expiration
 PaO2 & PaCO2 determine the definition of Resp. Failure  Intercostal muscle retraction
o Major threat of resp failure is inability of lungs to  Use of accessory muscles
meet the O2 demands of tissues  Paradoxical movements
 In mins to hrs  Agitation, disorientation, delirium,
 Decrease PaO2 (sudden of rapid) + restlessness, combative behavior, confusion
 Increase PaCO2 = implies serious  Decrease LOC
condition  Tachycardia
 Labs:  HTN
• PaO2 < 50  Cool, clammy, and diaphoretic
• PaCO2 > 50  Arrhythmias (late)
• pH < 7.25  Hypotension (late)
• === ARF  Cyanosis (late)
 Gradual changes= compensation can occur (kidney)  Coma (late)
 Compensatory failure = resp. failure o Hypercapnia
 Pathophysiology  Dyspnea
  Decreased RR c shallow respirations o Alteration in respiratory fxn
 Decreased tidal volume o Impaired gas exchange
 AM h/a  Nsg Interventions
 Disorientation o Assess resp status
 Arrhythmias o I/O
 HTN o Labs: ABG, H/H, lytes
 Tachycardia o Monitor pulse ox
 Bounding pulse o VS
 Muscle weakness o Sputum
 Decreased DTR o BGM during steroid therapy
 Pursed-lip breathing o O2
 Tripod position o Monitor vent status
 Coma (late) o Suction PRN
 Tremor, seizures (late) o TC & DB
o CPT
o Postural drainage
 Dx studies o Semi/ high fowlers
o H&P o Monitor chest tube systems
o ABG o Meds:
o CXR  Analgesics- MS
o CBC w dif  Anesthetic- Diprivan
o Lung scan (V/Q)  Antianxiety – Ativan
o Sputum study  Antibiotics
o PFT  Anticoagulants- heparin
o Bronchoscopy  Bronchodilators- Albuterol, Atrovent
 Medical Mgmt  Diuretics
o CPT  Histamine blockers- Pepcid
o Postural drainage  Steroids
o Chest tube  Neuromuscular blocking agents- “ium”
o Increase caloric, increase protein Pavulon, Norcuron
o Decrease fluids  Sedatives- to calm
o O2, intubation, vent  Acute Respiratory Distress Syndrome (ARDS)-
o Manage secretions alveoli get coated=no gas exchange (hallmark sign= no gas
 Nsg. Dx exchange regardless of O2 therapy)
 Precipitating factors  CXR= “white out”
o Tissue hypoperfusion  Clinical Manifestations
o Tissue injury o Dyspnea
o Acute disease process o Tachypnea
o Infection o Cough
o aspiration o Restlessness
 Incidence and mortality o Rales/ Rhonchi
 Pathophysiology- o Altered LOC
o Noncardiogenic pulmonary edema o Decrease O2 sat
o Atelectasis  Medical Mgmt
o Hypoxia o Preventive measure
o Hypercapnia o Vent support
o Alteration in ABG’s o Fluid balance (swan-ganz)
 3 Phases- o Positioning (PRONE) debatable
o Injury or Exudative Phase o Pharmacology-
 1-7 days p initial insult  Bronchodilators- Albuterol
 Influx of neutrophils and macrophages cause  Epinephrine
damage to endothelium  Aminophylline
 Alveolar fluid accumulates  Diprivan- Propofol (sedative)
 Nsg interventions
o Airway maintenance
o Vent support
o Reparative of Proliferative Phase o Safety
 1-2 wks p o Hydration/ nutrition
 Influx of granulocytes, monocytes, & o Mobility needs
lymphocytes o Pt. teaching
 Attempting to repair damage o Labs- H/H, WBC, pt, ptt, INR
 Progression may be resolved or continue to o I/O, CVP
fibrosis o Suction PRN
o Fibrotic Phase o Bed rest- prone
 2-3 wks o Fluid restriction
 Diffuse scarring and fibrosis o Reposition Q2H
 Decreased lung compliance o CPT
 Hypoxemia due to thickened walls o High fowlers
 Pulmonary HTN (increased fluid)
 o TPN or eternal feedings  Dx Procedures
o Daily weights o H&P
o Encourage feedings o Labs; blood
 Nsg dx: o CXR
o Impaired gas exchange o VQ Scan (radiopaque substance)
o Impaired airway clearance o Pulmonary angiography
 Pulmonary Emboli-undisolved mass that travels In the o ECG
bloodstream  Medical Mgmt
 Pathophysiology o Prevention (sequentials, activity)
o Thrombus formation o Anticoagulant therapy
o Thrombus fragmentation or dislodgement o Fibrinolytic therapy/ thrombolytics
o Increased pulmonary circulatory resistance o O2 therapy/ Vent support
 Precipitating Factors o Bed rest
o Hypercoagulability of blood o Pain relief
o Altered integrity of blood Bessel wall o Iv route for drugs and fluids
o Venous stasis- bed rest, obesity, varicose veins, post-  Surgical Mgmt
op, long periods of sitting and standing o Interruptions of the IVC
 Clinical Manifestations o Pulmonary embolectomy
o Alteration in resp fxn o Intracaval “umbrella” (Greenfield filter)
 Sudden onset of dyspnea  Does not dissolve can be dislodged
 Tachypnea  Nsg Dx:
o Altered gas exchange o Impaired gas exchange
 anxiety o pain
o Signs of vital organ compensation  Nsg Interventions
o Right heart failure o Resp & CV assessments
o Reduced CO o ABG analysis
 Tachycardia o Monitor hypoxemia
 Pleuritic chest pain o Maintenance of O2 delivery
 Cough o Pain control
 Hemoptysis o Hydration
 Crackles o Monitor labs
 Fever o Pt teaching
 Accentuation of pulmonic heart sound Chest Trauma-
 Sudden change in mental status Blunt Trauma
 o Body is struck by a blunt object o Pharmacology
o Contrecoup Trauma o Thoracentesis
 Type of blunt trauma o Pericardiocentesis
 Cause by impact of parts of the body o Chest tubes
against other objects  Surgical Mgmt
Penetrating Trauma o Pneumonectomy/ post op care
o Foreign body impales or passes thru the body tissues o thoracotomy
 Types  Nsg Dx
o Rib fx o Impaired gas exchange
o Sternal fx o Alteration in resp fxn
o Flail chest  Nsg Interventions
o Pneumothorax o Resp assessment
o Pleural contusion o Airway maintenance
o Myocardial contusion o Promotion of adequate ventilation
o Cardiac tamponade o Maintenance of chest tube drainage systems
 Precipitating Factors o Pt education
o Motor vehicle accidents
o Falls
o Recreational activities Pneumothorax
o Crush injuries
o Violent acts • Air in the pleural space
o Role of substance abuse • Complete or partial
 Clinical manifestations • Types
o Airway obstruction o Closed Pneumothorax
o Impaired breathing o Open Pneumothorax
o Circulatory impairment  Should be covered with a vented dressing
o Altered LOC (secured on 3 side)
o Unstable cervical spine
 Dx procedures o Tension Pneumothorax
o H&P  Rapid accumulation of air into pleural space
o X-ray causing severely high intrapleural pressures with
o ABG analysis tension on the heart and great vessels
o CT scan  Caused by open or closed Pneumothorax
 Medical Mgmt  Medical emergency that effects both resp and
o Vent support circulatory systems
 o Hemothorax • Reexpand lung and ensure adequate oxygenation
 Blood
o Chylothorax Chest Tubes
 Lymphatic fluid in pleural space due to leak in If intrapleural pressure becomes equal to atmospheric pressure the lungs
thoracic duct will collapse
• Clinical Manifestations • 2-3 ICS to remove air
o Small: mild tachycardia, dyspnea • 8-9 ICS to remove blood and fluid
o Large: resp distress (shallow, rapid resps, dyspnea, and air Pleural Drainage
hunger), chest pain, cough (with or without Hemoptysis), • 3 compartments
no breath sounds over affected area 1. Collection chamber
o Tension Pneumothorax: sever resp distress, tachycardia,  Fluid and air from chest cavity
and hypotension, mediastinal displacement occurs, and 2. Water-seal chamber
trachea shifts to unaffected side  Contains 2cm of H2O- acts of one-way valve
• Care  Initial bubbling of air is seen
o Depends on severity  Intermittent bubbling can be seen during
o If stable may not need tx exhalation, coughing, or sneezing
o Can be aspirated with large bore needle  Fluctuations or “tidaling” will be seen, if not
o Heimlich valve may be used either lungs have reexpanded or there is a kink or
o Chest tube (most definitive) obstruction in tubing
Fractured Ribs 3. Suction control chamber
• Clinical manifestations:  Controlled suction
o Pain at injury site  Wet or dry
o Splints affected area • Mgmt:
o Shallow breaths o Keep tubing straight and coiled
• Treatment o Al connections tight
o Decrease pain to increase resp affects o Maintain appropriate H2O levels
• o Mark measurement of drainage
Flail Chest o Observe for bubbling in water-seal chamber and tidaling
• Results from multiple fib fx o Constant and continuously bubbling needs to be checked
• Affected area moves paradoxically to the intact portion of the chest o Monitor pt’s clinical status
during respiration (opposite) o Never elevate drainage system
• Usually apparent, rapid shallow breaths, tachycardia o Encourage DB often
• TX: ventilation, humidified O2, careful administration of o Check position of drainage system often
crystalloid o Don’t milk or strip tubing
o Don’t clamp unless performing certain procedures
• Complications o Blood glucose
o Malposition most common o Serum electrolytes
o reexpansion pulmonary edema o CBC
o infection o Cardiac cath (possible)
• Removal o Physical assessment
o CXR to determine removal o CPT (possible)
o Suction D/C and gravity drainage for a period of time • Post-op Care
o Clamped for period of time o Impaired gas exchange
o Bear down and exhale during removal o Ineffective breathing pattern
o CXR done after removal o Anxiety
Pleural Effusion
• Collections of fluid in pleural space
Chest Surgery • Type can be determined by Thoracentesis
• Lobectomy= removal of one lobe of lung • Emphyema = pleural effusion that contains pus
• Pneumonectomy= entire lung • Clinical manifestations
• Segmental resection = one or more lung segments o Progressive dyspnea
• Wedge resection = small localized lesion that occupies only part of o Decreased movement of the chest wall on affected side
a segment o May have Pleuritic pain
• Decortication= removal of stripping of thick, fibrous membrane o Dullness to percussion
from visceral pleura o Absent or diminished breath sounds
• Exploratory thoracotomy = incision into thorax to view injured or o Emphyema= s/a, also fever, night sweats, cough, and
bleeding tissues weight loss
• Thoracotomy not involving lungs = incision into thorax for surgery • Thoracentesis
on other organs o Sit on edge of bed and lean forward over the bedside table
• Thorascopy (endoscopic thoracotomy) = 1-4 1in incisions thru
camera is introduced as well as other instruments and suction • Care
• Pre-op care o Tx underlying cause
o Baseline data
o PFT’s Pleurisy
o CXR • Inflammation of pleura
o ECG • Classified as dry (fibrinous) or wet (serofibrinous)
o ABG’s • Shallow rapid breathing
o BUN • May have pleural friction rub
o Serum Creatinine
• Pain
• Tx o underlying cause • Other tx for pulmonary HTN
• Pain relief o Vasodilators
• Analgesics and lying on or splinting affected side o Calcium channel blockers
o Anticoagulants
Atelectasis
• Collapsed, airless alveoli Sarcoidosis
• Deep breaths are important to prevent • Chronic multisystem granulomatous disease of unknown cause
• Most pts get well s tx
Cor Pulmonale • Corticosteroids can relieve sx’s
• Enlargement of right ventricle secondary to disease of the lung,
thorax, or pulmonary circulation Pulmonary HTN
• Pulmonary HTN usually preexisting condition in this pt • Primary (PPH)
• May be present c or s overt cardiac failure o Mean PAP > 25 mm Hg @ rest
• Most common cause is COPD • Secondary
• Clinical manifestations o Tx underlying cause
o Dyspnea • Clinical manifestations
o Chronic productive cough o Dyspnea on exertion and fatigue
o Wheezing o Exertional chest pain
o Retrosternal or substernal pain o Dizziness
o Fatigue o Exertional syncope
o If heart failure accompanies: o Sx’ RT inability of CO to increase in response to increase
 Peripheral edema demand
 Weight gain o Increase workload of right ventricle causing hypertrophy
 Distended neck veins (cor pulmonale)
 Full, bounding pulse • DX
 Enlarged liver o ECG
• Care o CXR
• Tx underlying cause o Echocardiogram
o Right cardiac cath(if doubt) to measure PAP
• Long-term low flow O2 (to correct hypoxemia)
• Care
• Fix any fluid, electrolyte, and acid-base imbalances
• No cure only relief from sx’s
• Diuretics and low Na diet
• Diuretics
• Bronchodilator if underlying resp problem
• Anticoagulant therapy
• Dig if left sided heart failure
• Vasodilators calcium channel blockers- ADALAT, CARDIZEM
• Epoprostenol (Flolan) promotes pulmonary vasodilation and
reduces pul. Vascular resistance

Pharmacology
Adrenergic (adrenergic agonist, sympathomimetics)
• Stimulate the SNS
• Mimic Epi and norepinepherine
• Alpha1
o Increase contraction
o Vasoconstriction
o Mydriasis (dilates pupils)
o Decrease salivary gland production
o Increase contraction of bladder and ejaculation
1. Alpha2
o Inhibits norepinepherine
o Dilates blood vessels
o Produces hypotension
o Decreases gastric mobility and tone
2. Beta1
o Increase HR
 o Increase contraction
o Increase rennin secretion (increase BP) Cholinergic
3. Beta2 • Stimulate PSNS (parasympathetic)
o Bronchodilates • Urecholine
o GI and uterine relaxation • Reglan
o Increase in blood sugar
o Increase blood flow to skeletal muscles
• Catecholamine’s Anticholinergics (antispasmodics)
o Produce a sympathomimetic response • Decrease in GI mobility, salivation, pupil dilation, increase pulse
o Epi, norepi, dopamine, dobutamine (synthetic) rate
• Decreased bladder contraction, and rigidity and tremors
• Can cause increased intraocular pressure= not for glaucoma
o Atropine
1. Epinephrine  Used for pre-op (decrease salivation)
a. promotes CNS, cardiac stimulation, and bronchodilation  Treat peptic ulcers
2. Albuterol  Increase HR
a. Selective beta2 o Propantheline bromide (Pro-banthine)
b. Bronchodilation
 Decrease gI secretions and spasms
c. High doses may affect beta 1 (increase HR)
3. Isoproterenol Hydrochloride (Isuprel)
a. Beta 1 and beta 2
Antihistamines
b. Increase HR & Bronchodilation
c. Severe tachycardia may occur if used excessively • Anticholinergics (type)
4. Clonidine (Catapres) and Methydopa (Aldomet) • Scopolamine (Transderm Scop)
a. Selective alpha 2 o Placed behind the ear for motion sickness
b. Used for HTN • Dimenhydrinate (Dramamine)
• Cyclizine (Marezine)
• Meclizine hydrochloride (Bonine)
Adrenergic Blockers (Antagonists or sympatholytics)
1. Alpha adnergic blockers
a. Can cause orthostatic hypotension and tachycardia
b. vasodilation
2. Beta adnergic blockers – “lol”
Volume Expanders
a. HR Four classifications of IV solutions
b. Some also cause bronchoconstriction 1. Crystalloids
a. Dextrose
 b. Saline • Monitor VS
c. Lactated Ringers • UOP
2. Colloids (Volume expanders) • Daily weights
a. Dextran solutions
• S/sx’s of fluid volume deficit
• Has no products that carry O2
• S/sx’s of fluid volume overload
• Dextran 40 interferes c platelet fxn and can prolong
• Daily lab values
bleeding
b. Amino acids • Check IV site
c. Hetastarch
• Lasts more than 24 hrs but can persist for wks in the
body
• Isotonic Drugs Used For Shock (Emergency)
• Decrease platelet and hematocrit values
• Contraindicated with CHF, bleeding disorders, and 1. Dopamine
a. Sympathomimetic (SNS, Epi)
renal dysfunction
b. Tx of hypotension shock NOT caused by
d. Plassmanate
HYPOVOLEMIA
• Commercially prepared protein substance
c. Doses 2-10 mcg/kg/min = increase contractility, Increase
• Used instead of plasma or albumin to replace body HR, vasoconstriction
protein d. Doses 10 and above= vasoconstriction
3. Blood and Blood Products e. Sodium bicarb will inactivate (don’t use in same line)
a. Whole Blood 2. Dobutamine
• Should not be used to tx anemia unless severe a. Sympathomimetic c beta 1
• Elevates Hgb by 0.5-1g b. Increase contractility
b. Packed Red Blood Cells (PRBC) c. Increase HR
• Contains whole blood s plasma d. No vasoconstrictive effects (but may mildly vasodilate)
• Decreased chance of circulatory overload compared 3. Norepinepherine
with whole blood a. Extremely potent vasoconstrictor
• Elevates Hct by 3 points b. Not for Hypovolemic pts
c. Plasma 4. Epinephrine
d. Albumin a. Tx anaphylactic shock
4. Lipids b. Bronchodilation
a. Fat emulsion solution c. Vasoconstriction
b. Usually indicated when IV therapy last longer than 5 days 5. Albuterol
a. Beta adnergic bronchodilator
Nursing Interventions for Fluid Administration b. Wheezing may become pronounced= indicating
therapeutic response
6. Diphehydramine Hydrochloride
a. Antihistamine
b. Often administered with Epi for anaphylaxis
c. Tx histamine-induced tissue swelling and pruritis
d. Adverse: drowsiness, sedation, confusion, vertigo,
excitability, hypotension, tachycardia, GI disturbances,
and dry mouth
7. Dextrose 50%
a. Insulin shock
b. Usually given IV bolus
c. Phlebitis can occur (so central is best)
d. UOP and blood glucose monitored closely
8. Glucagon
a. Insulin shock
b. SQ, IM, or IV
c. Adverse effects : N/V

Antihistamines
• H1 blockers or H1 antagonists
• Prevents histamine response by competing for receptors sites
• H1 receptor = smooth muscle constriction
• H2 receptor = increase in gastric secretions (cause peptic ulcers)
• 1st generation
o Cause drowsiness, dry mouth, and other Anticholinergics
effects
o Diphenhydramine (Benadryl)
• 2nd generation
o Little or no sedating effects
o Cetirizine (Zyrtec)
o Fexofenadine (Allegra)
o Loratadine (Claritin
o Azelastine (Astelin, Optivar)