unit 2 Flashcards
pulmonary embolism
collection of matter that enters venous circulation and lodges in the pulmonary vessel
large emboli obstruct pulmonary blood flow
reduced gas exchange reduced oxygenation pulmonary tissue hypoxia decreased perfusion potential death
cause of pulmonary embolism
inappropriate blood clotting forms a DVT in vein in legs or pelvis
risk factors for pulmonary embolism
prolonged immobility central venous catheters surgery obesity advancing age conditions that increase blood clotting history of thromboembolism pregnancy estrogen therapy cancer trauma smoking
Pulmonary embolism prevention
passive and active ROM turn cough and deep breath Ted hose prevent compression in popliteal space avoid constricting clothing asses appropriateness of anticoagulant therapy frequent physical assessment of circulation patient and family teaching encourage smoking cessation
manifestations of pulmonary embolism
dyspnea pleuritic chest pain on inspiration crackles or clear wheezes or rub dry or productive cough; hemoptysis tachycardia low grade fever JVD syncope cyanotic diaphoresis hypotension abnormal heart sounds shock and death
psychosocial assessment for pulmonary embolism
anxiety restlessness fear "impending doom" change LOC
lab assessment for pulmonary embolism
respiratory alkalosis low PaCO2 followed by metabolic acidosis Low SaO2 Metabolic panel troponin BNP d-Dimer
Imagining assessment pulmonary assessment
pulmonary angiography
C1-PA
Chest x-ray
Nursing diagnosis related to pulmonary embolism
Hypoxemia r/t mismatch of lunch perfusion and alveolar gas exchange
Hypotension r/t inadequate circulation to left ventricle
Potential for inadequate clotting and bleeding r/t anticoagulants therapy
Anxiety r/t hypoxemia and life threatening life
interventions for pulmonary embolism
elevate HOB apply oxygen call Rapid response reassurance telemetry continuous pulse oximeter Maintain adequate venous access assess respiratory and cardiac every 30 minutes Administer prescribed anticoagulants: heparin, lovenox, fibrinolytics, warfin, Revesing agents
aPTT, PTT
measure heparin therapy
common range: 20-30 seconds
therapeutic range: 1.5-2.5 times normal value
PT (prothrombin time)
measures effectiveness’s of Coumadin
NR: 11-12.5 seconds
TR: 1.5-2.0 times normal value
INR
CR: 0.8-11
TR for PE: 2.5-3.0
TR: for recurrent PE: 3.0-4.5
Managing hypotension
IV fluid therapy ( crystalloid solution)
ECG and hemodynamic monitor
Monitor effectiveness of IF therapy( I&O, skin turgor)
DRug therapy and vassopressors; dopamine; levophed; dobutamine; nitroprusside
VS
Minimize bleeding
assess for evidence of bleeding every 2 hours check emesis, stool, urine for blood asses IV every 4 hours Avoid IM injections apply ice to sites of trauma use electrical razors use soft bristled toothbrush avoid nose blowing supportive shoes hold pressure on IV site for 10 minutes after removing monitor labs
Home management of pulmonary embolism
self-assessment of respiratory status self-assessment of cardiac assessment of lower extremities bleeding precautions change in LOC assess family to assume care
thoracic trauma
first emergency approach to all chest injuries in BAC (breathing, airway, circulation)
rapid assessment and treatment of life threatening conditions
pulmonary contusion
car crashes life threatening respiratory occur hemorrhage and edema in alveoli hypoxia and dyspnea
Notes to take on pulmonary contusion
bruising over chest cough tachycardia tachypnea decreased breath sounds wheezes or crackles
Pulmonary contusion x-ray
may be normal at first then develop over several days
Rib fractures
blunt force
pain on movement and splints the affected side
1st and 2nd ribs flail chest
poor prognosis
Focus of treatment with rib fractures
analgesics to reduce pain so they can deep breath
flail chest
blunt chest trauma
high speed car crashes
CPR
Flail chest
fractures of at least 2 neighboring ribs in 2 or more places
causes paradoxical chest wall movement
Asses for paradoxical chest movement
dyspnea cyanotic tachycardia increased work of breathing hypotension
flail chest interventions
humidified oxygen pain management deep breathing with positioning deep breathing and coughing tracheal suctioning Mechanical ventilation ABG's Monitor VS, fluid and electrolyte balances SaO2
pneumothorax
any injury that allows air to enter the pleural space increases chest pressure reduces vital capacity blunt chest trauma or medical procedure can be opened or closed
pneumothorax assessment findings
reduced breath sounds hyperresonance on percussion lack of chest wall movement deviation of trachea away from side of injury pleuritic pain tachypnea subcutaneous emphysema
pneumothorax interventions
chest x-ray chest tube pain control pulmonary hygiene continuous assessment for impending respiratory failure
tension pneumothorax
air leak in the lung or chest wall
causes collapse of affected lung
air entering pleural cavity on inspiration
air does not leave on expiration
air under pressure collapses blood vessels and decreases blood return
causes of tension pneumothorax
blunt chest trauma
mechanical ventilation
chest tubes
insertion of central venous access devices
assessment findings of tension pneumothorax
asymmetry of thorax tracheal movement from midline toward the unaffected side extreme respiratory distress absence of breath sounds distended neck veins cyanosis hyper tympanic sound on percussion hemodynamic instability ABG's reveal hypoxia and respiratory alkalosis chest x-ray
tension pneumothorax emergency management
needle thoracotomy with large bore needle inserted in 2nd intercostal space midclavicular chest tube in fourth intercostal space pain control pulmonary hygiene psychosocial interventions
hemothorax
penetrating injuries
bleeding from injury to lung tissue or fractured ribs or sternum
bleeding from trauma to heart, great vessels, or intercostal arteries
assessment findings of hemothorax
decreased breath sounds
percussion on affected side is dull
chest x-ray
hemothorax interventions
remove blood chest tubes serial chest x-rays aggressive pain management frequent VS accurate I&O fluid replacement surgical management open thoracotomy mechanical ventilation
chest tubes
drain air, blood or fluid from pleural space
placed in pleural space to allow re expansion and prevents air and fluid from re-entering
has water seal compartment to ensure that air does not enter the patient
Chest tubes are used for
after thoracic surgery
pneumothorax
hemothorax
palliative treatment of lung cancer or HF
chest tubes placement and care
tip of tube placed near front lung apex
tip of tube is placed on side near base of lung
insertion sites are protected with airtight dressing
approx. 6 feet into patients chest
3 parts of the drainage system on chest tubes
water seal chamber
collection chamber
suction regulator
chest tube chamber #1
collects fluid draining from patient and is checked hourly x24 hours
chest tube chamber #2
water seal that prevents air from reentering the patients pleural space
causes gently bubbling
keep filled with 2 cm of water
bubbling will stop once chest tube removed
blocked or kinked can cause bubbling to stop
excessive bubbling means an air leak
Chest tube chamber #3
suction control
Management of chest tubes drainage system
maintain patency sterility of drainage system keep manipulation of tubing frequent respiratory assessment pain management
Acute Coronary Syndrome
Unstable angina Last longer than 15 minutes May not be relieved by rest of NTG ST elevation but not troponin or CK-MB changes Untreated may lead to MI
Unstable angina
Chest pain
Discomfort that occurs at rest or with exception
Causes severe activity limitation
Acute myocardial infarction
Ischemia lead to injury and necrosis of myocardial tissue
80-90% occluded
Myocardial infarction
Myocardial tissue abruptly
Severely deprived of oxygen
NSTEMI (Non ST Elevation)
ST segment and T wave changes on 12 lead indicating myocardial ischemia
Enzyme elevate over 3-12 hours
STEMI (ST elevation MI)
ST elevation in 2 contiguous leads on 12 lead ECG
Cause by plaque rupture
Complete occlusion of coronary artery
Acute MI
Evolves over several hours
Hypoxemia from ischemia
Increased oxygen demand may cause life-threatening ventricular dysrhythmias
Acute MI Extent of infarction depends on
Collateral circulation
Metabolism
Workload demands
Acute MI timeframe
At 6 hours tissue blue and swollen
48 hours infarction area gray and yellow striped
8-10 days granulation tissue develops
3 months thin, firm scar formation causes ventricular remodeling
LAD. Acute MI
Left. Anterior or septal MI
Highest mortality rate
Ventricular dysrhymaias
Circumflex Acute MI
Left lateral ventricle
Possible posterior wall
SA node and AV node
Sinus dysrhythmias
RCA Acute MI
SA and AV nodes
Right ventricle and inferior portion of LV
Right sided MI
Atherosclerosis nonmodification risk factors
Age
Gender
Family history
Ethnic background
Atherosclerosis modifiable risk factors
Elevated serum lipid levels Smoking/tobacco use Limited physical activity Hypertension Diabetes mellitus Obesity Excessive alcohol Excessive stress/ poor coping skills
Hypoxemia from ischemia
Acidosis and electrolyte imbalances
Metabolic Syndrome (Syndrome X) Indicators of Risk Factors
Additional risk factor for CVD
Hypertension: either BP of 130/85 or higher or taking HTN meds
Decreased HDL; high LDL: either HDL,45 (men) or than 160 (men) or 135 (women) or taking antichlosterol meds
Elevated FBS: either 100 or higher or taking anti diabetic drugs
Large waist size: 40 inches or greater (men) or 35 inches for women; excessive abdominal fat causing central obesity
Patient Centered Collaborative Care
History: presenting symptoms
Physical assessment: assessment, VS, pain, symptoms
Psychosocial: denial, fear, anxiety, anger, depression,
Laboratory: troponins, CK-MB, chemistries
Radiology: chest X-Ray
12 lead ECG within 10 minutes
Immediate assessment
Labs
ECG
Patients wait before presenting so loss of 4-6 hours window
“Time is tissue”
Managing ACute pain
MONA
(morphine, oxygen, NTG, aspirin)
IV access X2
Improving cardiopulmonary tissue perfusion
Adequate cardiac output
Normal sinus rhythm and VS within normal limits
90 minutes from door to intervention
Monitoring for and Managing heart failure
Decreased CO due to ventricular dysfunction
Rupture of the intraventricular septum
Killip Classification of heart failure
Class I: absent crackles and S3
ClassII: crackles in lower half of lung and possible S3
Class III: crackles more than halfway up the lung and frequent pulmonary edema
Class IV: cardio genie shock!!!!
Drug therapy for ACS
ASpirin: recommended; chewing 4 baby aspirins; or chew 325 mg tab X1
Glycoproteins inhibitors: IV; decreased dosage with fibrolytics
Beta-adrenergic blocking agents: Metoprolol; decrease size of infarction;
ACEI’s and ARBS: given within 48 hours of ACS; prevent ventricular remodeling
CCB: promotes vasodilation and myocardial perfusion; NOT indicated after AMI; helps with angina
Thrombolytic therapy: dissolves thrombi in coronary arteries ; restore myocardial blood flow
Tissue plasminogen activator: IV (activase)
Reteplase: IV (retavase)
Tenecteplasae: IV push (TNK)
Thrombolytics
Most effective within 6 hours of coronary event
Indicated for CP > 30 minutes duration unrelieved by NTG indications of STEMI by ECG
Start within 30 minutes of Ed admission
Absolute contraindications to Thrombolytic therapy
Prior intracranial hemorrhage Cerebral vascular lesion Malignant intracranial neoplasm Ischemic stroke within last 3 months Suspected aortic dissection Active bleeding Significant CHT or facial trauma in last 3 months
Relative contraindications to Thrombolytic therapy
History of HTN History of ischemic stroke, dementia Traumatic CPR or major surgery writhing last 3 weeks No compressible vascular punctures Prior allergic reaction to strepto Pregnancy Active peptic ulcer Current use of INR
Percutaneous coronary intervention
Reopen clotted coronary artery
Restore perfusion writhin 2-3 hours of onset
Indications that artery has re-perfused
Abrupt cessation of pain
Sudden onset of ventricular dysrhythmias
Resolution of ST segment depression/ elevation or T wave inversion
A peak at 12 hours of markers of MI damage
Post thrombolytics
Heparin infusion for 3-5 days
APTT usually 1.5-2.5
Enoxaparin IV
Coronary Artery Bypass Graft
Open heart surgical procedure
Replace occluded artery
Arterectomy or stent placement
Angiography to remove plaque
Maintain potency of coronary artery
Hemodynamic Monitoring
Swan Ganz catheters
CVP
PAWP
RAP
Treatment of cardiogenic shock
Assessment
Fluids
Drug
Oxygen
Troponin values
CPK-MB values
3-5%
Troponin values
Book
CPK-MB values
Book
Improving gas exchange
Ventilation assistance Monitor respiratory rate q 1-4 hours Auscultate breath sounds q 4-8 hours Position in high fowlers Maintain oxygen saturation of 90%
Drugs to reduce afterload
ACE inhibitors
ARB
Human BNP
Interventions that reduce preload
Diuretics
Venous vasodilators
Drugs that enhance contractility
Digoxin
Beta blockers
Managing pulmonary edema
Early signs: crackles, dyspnea at rest, disorietnation, confusion High fowlers position Oxygen therapy Nitro Rapid-acting diuretics IV morphine sulfate Continual assessment
Assessment for valvular heart disease
Sudden illness Ask about attacks of rheumatic fever, infective endocarditis, ask about possibility of IV drug abuse Chest x-ray ECG Stress test
Nonsurgical managment of valvular heart disease
Rest Drug therapy: Diuretics Beta blockers Dig Oxygen Nitrates Vasodilators Anticoagulants
Surgical management of valvular heart disease
Reparative procedures Balloon valvuloplasty Open commissurotomy Mitral valve annuloplasty Replacement procedures
Infective endocarditis risk factors
IV drug abusers
Valve replacement recipients
Systemic infections
Structural cardiac defects
Manifestations of endocarditis
Murmur Heart failure Arterial embolization Splenic infarction Neurologic changes Petechiae Splinter hemorrhages
nonsurgical Management of endocarditis
Antimicrobials
Activites balanced with adequate rest
Surgical management of endocarditis
Removal of infected valve
Repair or removal of congenital shunts
Repair of injured valves and chordae tendineae
Draining of abscesses in heart or elsewhere
Assessment of pericarditis
Substernal precordial pain
Radiating to left side of neck, shoulder, or back
Grating, oppressive pain, aggravated by breathing, coughing, swallowing
Pain worsened by supine position
Relieved by sitting up and leaning forward
Pericardial friction rub
Interventions for pericarditis
NSAIDs
Antibiotics for bacterial form
Pericardiectomy
Pericardial effusion
Puts patient at risk for cardiac tamponade Cardiac tamponade findings: JVD Paradoxical pulse Decreased CO Muffled heart sounds Circulatory collapse
Rheumatic carditis
From upper respiratory tract infection with group A beta hemolytic streptococci
Inflammation in all layers of heart
Ashoff bodies
Clinial manifestations of rheumatic carditis
Tachycardia Cardimegaly New or changed murmur Pericardial friction rub Precordial pain Changed in ECG Indications of heart failure Existing streptococcal infeection
Cardiomyopathy
Chronic disease of caridac muscle
Cardiomyopathy nonsurgical management
Diuretics Vasodilation agents Cariac glycosides Toxin exposure avoidance Alcohol avoidance
To decrease high potassium (hyperkalemia) do what
Insulin and dextrose
Right MI do not give
A nitro drip
Automaticity
Cardiac cells to generate an electrical impulse spontaneously and repetitively
Excitability
Non-pacemaker cells to respond to an electrical impulse
Depolarize
Conductivity
Ability to send an electrical stimulus from cell membrane to cell membrane
Contractility
Atrial and ventricular muscle cells to shorten their fiber length
Mechanical
SA node
Electrical impulses 60-100 bpm
Primary pacemaker
P wave on ECG
(Atrioventricular) AV node
PR segment on ECG
Contraction known as atrial kick
Bundle of His
Right and left bundle branch system
QRS on the ECG
Purkinje cells
Responsible for rapid conduction of electrical impulses throughout ventricles
Leading to ventricular depolarization
Ventricular muscle contraction
Depolarization
Negatively charged cells
And develop a positive charge
P wave
Atrial depolarization
PR segment
Impulse to travel through AV node
Pr interval
Atrial depolarization
QRS complex
Ventricular depolarization
QRS duration
Depolarization of both ventricles
ST segment
Ventricular repolarization
T wave
Ventricular repolarization
QT interval
Total time
ECG rhythm analysis
Heart rate (slow, normal, fast)
Heart rhythm (regular, irregular)
Analyze P waves (present before each QRS)
Measure PR interval (0.12-0.20 Sec)
Measure QRS (after each P wave, less than or equal to 0.12 sec)
Q-T interval (less than or equal to 0.40 sec)
Interpret rhythm
First degree atrioventricular block
All sinus impulses eventually reach ventricles
Sinus bradycardia
HR less than 60 bpm
Patient centered care for sinus bradycardia
Maintain perfusion and CO
Assess LOC and patient tolerance
Atropine
Pacemaker
Atropine
IV bolus Repeated every 3-5 minutes Assess urinary retention Dry mouth Glaucoma
Sinus tachycardia
HR greater than 100 bpm
SNS stimulation or PSN inhibition
Patient collaborative care for sinus tachycardia
Maintain perfusion and CO Assess dehydration Hypovolemia Infection HF MI Urinary output Assess emotional status , medications
Supraventricular tachycardia
HR 100-280bpm
170 for adults
Terminated suddenly with or without intervention
Interventions for supraventricular tachycardia
Vagal maneuvers: strain like having a BM
Carotid massage: only doctors can do those
Adenosine: push this medication fast alongwith flushing fast
If does not work can do two more times
Put arm over arm
Atrial fibrillation
Atrial fibrosis Loss of muscle mass Cardiac decreases 20-30% 350-450bpm No clear P waves
Atrial fibrillation is common in
Hypertension
Heart failure
Coronary artery disease
COPD
Atrial fibrillation patient centered care
Risk for PE, VTE Antidysrhythmic drugs Cardioversion Percutaneous radiofrequency catheter ablation Biventricular pacing Maze procedure All on anticoagulant
Atrial flutter
220-350bpm
Saw tooth appearance
One-half of atrial beats are blocked at AV junction
Calcium channel blockers
Cardioversion
Synchronized countershock
Cardioversion used for
Emergencies for unstable patients
Ventricular
Supraventricular tachydysrhythmias
Stable tachydysrhythmias resistant to medical therapies
Ventricular dysrhythmias
Life-threatening
Do not get oxygenated blood to vital organs
Premature ventricular complexes
Early ventricular complexes followed by a pause
Unifocal or multifocal
Common causes of premature ventricular complexes
MI Age CHF COPD Anemia or hypoxia Stress Caffeine Nicotine Infection Hypokalemia Hypomagnesium
Ventricular tachycardia
Repetitive firing of irritable ventricular ectopic focus
140-180 bpm
May last longer than 15-30 seconds
Causes of ventricular tachycardia
Muscle ischemia MI Valvular disease HF Drug toxicity Hypomagnesium Hypokalemia
Ventricular fibrillation
Electrical chaos in ventricles
Lethal dysrhythmias
Shock them
CPR
Ventricular asystole
Complete absence of any ventricular rhythm
Dead
Not shockable
CPR
CPR manegment
Maintain airway
Ventilate with mouth-to-mask device
Start chest compressions
Defibrillation
Depolarizes critical mass of myocardium simultaneously
Stops and allows sinus node to regain control of heart
