test 2 Flashcards
(106 cards)
1
Q
Pulmonary embolism
A
Collection of particulate matter that enters venous circulation and lodges in the pulmonary vessel.
2
Q
Large emboli obstructs pulmonary blood flow
A
Reduced gas exchange, oxygenation
Pulmonary tissue hypoxia
Decreased perfusion
Potential death
3
Q
PE Cause
A
Inappropriate blood clotting forms a venous thromboembolism in vein or legs, pelvis
4
Q
Risk factors for PE
A
Prolonged immobility Central venous catheters Surgery Obesity Advanced age History Pregnancy, estrogen therapy, contraceptive therapy Cancer Trauma Smoking
5
Q
Prevention of PE
A
Start PROM, AROM ambulate Ted hose Prevent compression in popliteal space Avoid constricting clothing Change patient every 2 hours Frequent physical assessment of circulation Patient/family teaching Encourage smoking cessation
6
Q
PE physical assessment
A
Displeasure Pleuritic chest pain on inspiration Auscultation: crackles or clear, hemoptysis Tachycardia, low grade fever JVD syncope Cyanosis, diaphoreses Hypotension Abnormal heart sound Shock and death
7
Q
PE Signs
A
Tachypnea, crackles Pleural friction rub Tachycardia Petechia over chest and axillae Anxiety, restlessness, fear of impending doom
8
Q
Assessment of PE
A
Pulmonary angiography
CT-PA
chest x-ray
9
Q
Nursing diagnosis PE
A
Hypodermic r/t mismatch of lung perfusion and alveolar gas exchange
Hypotension r/t inadequate circulation to left ventricle
Potential for inadequate clotting and bleeding r/t anticoagulant or fibrinolytic therapy
Anxiety r/t hypoxemia and life threatening illness
10
Q
PE intervention
A
Elevate the HOB, apply o2, call RRT
Reassurance
Telemetry and continuous pulse ox
Maintain adequate venous access
Assess respiratory and cardiac status at least every 30 min
Administer prescribed anticoagulants
Heparin,lovenox, fibrinolytic a, warfarin
Reversing agents heparin-protamine sulfate
Warfarin-vitamin k
11
Q
PE Laboratory
A
aPTT, PTT
*measures heparin therapy
*common range:20-30 sec
* therapeutic range:1.5-2.5 times normal value
PT, prothrombin time
*measures effectiveness or Coumadin therapy
*normal range: 11-12.5 sec
*therapeutic range: 1.5-2.0 times normal range
INR
* common range
* therapeutic range for PE 2.5-3.0, 3.0 -4.5 for recurrent PE
12
Q
Managing hypotension
A
Iv fluid Ecg monitor I&O Drug therapy and vasopressors Vitals
13
Q
PTT, aPTT
A
Normal 20-30 seconds
PE 1.5-2.5 times normal value
Therapeutic times:means that the clotting time is increased from normal but this increase is indicated in the case of PE
Prolonged times: patients with PE >75 sec indicates the pt is at risk for serious bleeding. Heparin is usually stopped until PTT is normal
14
Q
PT
A
Normal range 11-12.5 sec
PE 1.5-2.0 times the normal
Therapeutic: pro time is increased from normal but this increase is indicated in the case of PE
Prolonged: at risk for bleeding, warfarin decreased or stopped until it is normal
15
Q
INR
A
Normal 0.8-1.1
Therapeutic:INR is increased from normal but the increase is indicated in the case of PE
Prolonged: at risk for bleeding, stop warfarin, instructed to eat food in vitamin k
16
Q
Minimize bleeding
A
Have antidote available
Asses for bleeding every 2 hours
Check emissions, stools and urine for blood
Avoid im injection, apply ice to site of trauma avoid nose blowing, use soft tooth brush and electric razor
Hold pressure on needle stick for 10 minutes
Monitor lab
17
Q
The client diagnosed with dvt suddenly complains of chest pain and feeling of impending doom.
A
Pulmonary embolus
18
Q
Nurse is preparing to administer warfarin an oral anticoagulant to a client diagnoses with a PE. which data should the nurse questions?
A
INR is 5
19
Q
Client is suspected of having a PE, which diagnostic test confirms the diagnosis?
A
Plasma d-dimmer
20
Q
Which nurse intervention should the nurse implement for a client diagnose with PE who is undergoing thrombolytic therapy
A
Keep protamine sulfate readily
Assess for overt and covert signs of bleeding
Avoid invasive procedures and injections
Ad mister stool softeners
21
Q
Thoracic trauma
A
First emergency approach to all chest injuries is BAC
Breathing, airway, circulation, a rapid assessment and treatment of life threatening conditions
22
Q
Pulmonary contusion
A
Occurs most often by rapid deceleration during car crashes
Potential life threatening
Respiratory Failure can develop
Hemorrhage and edema in and between alveoli reducing lung movement and available area for gas exchange
May present or develop hypoxia and dyspnea over time
Note brushing over chest , cough, tachycardia, Tachypnea, a auscultate decreased breath sounds wheezing or crackles
23
Q
Pulmonary contusion management
A
Maintenon of ventilation and oxygen.
Provide o2, give it fluids and place patient in a moderate fowler so position. When side lying the good lung down position
24
Q
Rib fracture
A
Often results of blunt force trauma to the chest
Increase the risk for deep chest injury such as pulmonary contusion, pneumothorax and hemothorax
Presents with pain on movement and splints the affected side
Pre existing lung conditions increase the risk for atelectasis and pneumonia
Fx of 1st or 2nd ribs, frail chest, multiple rib fractures and low expired volumes [15mg] have poor prognosis
Focus of treatment is analgesics to reduce pain and promote normal ventilation
25
Frail chest
Results of blunt force trauma
Fractures of a leas two neighboring ribs in two or more places causing paradoxical chest wall movement
Assess for paradoxical chest movements, dyspnea, cyanosis, tachycardia, increased work of beating and hypotension
26
Frail chest interventions
Humidified oxygen, pain management, promote deep breathing with positioning, encourage deep breathing and coughing, tracheal auctioning
Mechanical ventilation with peep for respiratory failure or shock
ABG and vital capacity monitoring while ventilated
Monitor vitals fluid and electrolyte balances pain sa02
Offer psychosocial due to fear anxiety and pain
27
Pneumothorax
Any injury that allows air to enter the pleural space, increase chest pressure and reduces vital capacity(lung collapse)
Often caused y blunt chest trauma or medical procedure
Can be open or closed
-reduced breath sounds on auscultation on affected side
-Hyperresonance on percussion
-Lack off chest wall movement on affected side
-deviation of trachea away from side of injury
-pleuritic pain, Tachypnea and subcutaneous emphysema
28
Pneumothorax interventions
```
Chest X-ray
Chest tube
Pain control
Pulmonary hygiene
Continuous assessment for impeding respirator failure
```
29
Tension pneumothorax
Rapidly developing and life threatening complication of blunt chest trauma resulting from an air leak in the lung or chest wall
-cause complete collapse of affected side
-air entering pleural cavity upon inspiration does not exit upon expiration
-air under pressure collapses blood vessels and decreases blood return
-without prompt detection and treatment, quickly becomes fatal
Cause: blunt force trauma, mechanical ventilation with PEEP, chest tubes, insertion of central venous access devices
30
Tension pneumothorax finding
Asymmetry of the thorax
Tracheal movement away from midline toward the unaffected side
Extreme respiratory distress
Absence of breath sounds on one side
Distended neck veins
Cyanosis
Hyper tympanic sounds on percussion over the affected side
Hemodynamics instability
Abg reveal hypoxia and respiratory alkalosis
Chest X-ray reveal collapsed lung and shifting of internal organs away from affected side
31
Tension pneumothorax treatment
Needle thoracostomy with large bore needle inserted in 2nd intercostal space midclavicular line of affected side
Chest tube in forth intercostal space to water seal
Pain control
Pulmonary hygiene
Psychosocial
32
Hemothorax
Common after blunt chest trauma or penetrating injuries
-simple or massive
-bleeding from injury to lung tissue
-bleeding from trauma to heart, great vessels or intercostal arteries
Finding:
Respiratory distress with decreased breath sounds on affected side
Percussion on affected side is dull
Blood in plural space
33
Hemothorax management
```
Redoing blood to improve breathing and recent infection
Chest tube to drain
Chest X-ray
Pain management
Vital signs I&O
Transfusion and fluid replacement
Open thoracostomy for large initial blood or persistent bleeding
Mechanical ventilation
```
34
Automaticity
(Pacing function) is the ability of cardiac cells to generate an electrical impulse spontaneously and repetitively
35
Excitability
Ability of non-pacemaker heart cells to respond to an electrical impulse that begins in pacemaker cells and to depolarize
36
Depolarization
Occurs when the normally negatively charged cells within the heart muscle develop a positive charge
37
Conductivity
The ability to send an electrical stimulus from cell membrane to cell membrane
38
Contractility
The ability of atrial and ventricular muscle cells to shorten their fiber length in response to electrical stimulation, causing sufficient pressure to push blood forward through the heart
(Mechanical activity of the heart)
39
P wave
representing atrial depolarization
40
PR segment
Represents the time requires for the impulse to travel through the AV node, where it is delayed , and though the bundle of HIS, bundle branches, and purkinje fiber network, just before ventricular depolarization
41
PR interval
Represents the time requires for atrial depolarization as well as impulse travel through the conduction system and purkinje fiber network, inclusive of the p wave and PR segment
Measures from the beginning of the P wave to the end of the PR segment
Normal measure 0.12-0.20 seconds five small blocks
42
QRS complex
Ventricular depolarization and is measured from the beginning of the Q(or R) wave to the end of the S wave
43
QRS Duration
Measures from the beginning of the QRS complex to the Jpoint(the junction where the QRS complex ends and the ST segment begins
Normal measured from 0.04-0.12 seconds up to 3 small blocks
44
ST segment
Represents early ventricular repolarization
45
QT interval
The total time required for ventricular depolarization and repolarization and is measured from the beginning of the QRS complex to the end of the T wave.
The interval varies with the patients age, gender and changes with the heart rate, lengthening with slower heart rates and shortening with faster for rates
46
Normal sinus rhythm
Rate: 60-100
Rhythm: regular
P waves: present, consistent configuration, one p wave before each QRS complex
PR interval: 0.12-0.20 seconds and constant
QRS duration: 0.04-0.20 seconds and constant
47
Chest tube
A drain placed in the pleural space, allows lung re-expansion. Also prevents air and fluid from returning to the chest.
The drainage system consist of one or more chest tubes or drains, a collection container placed below the chest level and a water seal to keep air from entering the chest.
Nursing care for a chest tube to ensure the integrity of the system, promote comfort ensure chest tube patency and prevent complications
48
Stationary chest tube drainage
Use a water seal mechanism that acts as a one way valve to prevent air or liquid from moving back into the chest cavity
The tubes from the patient are connected to the 1st chamber, this chamber is the drainage collection chamber
The 2nd chamber is the water seal o prevent sit from moving back up the tubing system and into the chest.
The 3rd chamber when suction is applied is the suction regulator
49
Chest tube bubbling
The bumbling of the water in the water seal chamber indicates air drainage from the patient, bubbling is seen when the patient exhales, coughs or sneezes. When the air is the pleural space has been removed, bubbling stops.
A blocked or kinked chest tube also can cause bubbling to stop.
Excessive bubbling in the water seal chamber(2nd) may indicate an air leak
Check the water seal chamber for unexpected bubbling created by an air leak in the system. Bubbling is normal during forceful expiration since or coughing because air in the chest is being expelled. Continuous bubbling indicates an air leak.
With PRESCRIPTION gently apply a padded clamp briefs on the drainage tubing close to the occlusive dressing, if bubbling stops the sir eat may be at the chest tube insertion see or within the chest requiring physician intervention. Bubbling that does not stop when a padded clamp is applied indicated that the air eat is between that clamp and the drainage system
50
Manage chest tube
Ensure the dressing around the use is tight
| Access for difficulty breathing check alignment of trachea
51
Electrophysiology
Electrical activity of the heart
Automaticity:(pacing function) is the ability of cardiac cells to generate an electrical impulse spontaneously and repetitively
Excitability: is the ability of non-pacemaker heart cells to respond to an electrical impulse that begins in pacemakers cells and to depolarize.
Depolarization:occurs hen the normally negatively charged cells within the heart muscle develop a positive charge
Conductivity is the ability to send an electrical stimulus from cell membrane to cell membrane
Mechanical of the heart
Contractillity: ability of the of atrial and ventricular muscle cells to shorten their fiber length in response to electrical stimulation, causing sufficient pressure to push blood forward through the heart
52
Cardiac conduction system
SA node: electrical impulses 60-100 beats/min, p wave on ecg
AV node: PR segment on ecg, contraction (atrial kick)
Bundle of HIS: right bundle branch system, left bundle branch system
53
Complexes
The p wave is a deflection representing atrial depolarization
Pr segment is the isometric line from the end of the p wave to the beginning of the QRS complex, when the electrical impulse is traveling through the AV node
PR intervals measured from the beginning of the P wave to the end of the PR segment
QRS duration it is measured from the beginning of the QRS complex to the J point( the junction where the QRS complex ends and the ST segment begins) normal 0.04-0.12seconds up to 3 small boxes
T wave follows the st segment and represents ventricular depolarization
54
ECG rhythm analysis
Determine heart rate (slow, normal, fast)
Determine heart rhythm (regular or irregular)
Analyze P waves (presence, before every QRS, deflection)
Measure PR interval (0.12 sec-0.20 sec)
Measure QRS (after each p wave, shape &measure size, less than or equal to 0.12 sec)
Q-T interval: less than or equal to 0.40 sec)
Interpret rhythm
55
Normal sinus rhythm
Is the rhythm originating from the sinoatrial node.
Rae:60-100 beats/min
Rhythm: present
P waves: present, consistent configuration one p wave before each QRS complex
PR interval:0.12-0.20 sec and constant
QRS:0.04-0.10 sec and constant
56
Patient s with tachydysrhythmias
```
May have palpating
Chest discomfort
Restlessness and anxiety
Pale, cool skin
Syncope
```
57
Class 111 antidysrhythmics
Length the absolute refractory period and prolong repolariztion and the action potential duration and prolong the action potential duration of ischemic cells. Amiodarone and covert are used to treat or prevent VT, VF
58
CLASS IV
Calcium channel blockers, verapamil, cardiazem used to treat SVT, AF to slow ventricular response
Slow the flow of calcium into the cell during depolarizations, thereby depressing the automaticity of the SA and AV nodes decreasing the heart rates and prolonging the AV nodal refractory period and conduction
59
Amiodarone
Used for AF, PAF,PSVT, life treating ventricular dysrhythmias
Stay with patient and monitor HR and BP
Report any weakness,tremors,difficulty with ambulate on.shortness of breath, cough, pain and fever use sunscreen
Bradycardia, hypotension
60
Digoxin
Used for CHF, AF, atrial flutter, PSVT
Assess apical heart rate for 1 min before each dose
Assess for sudden increase in heart rate
Report nausea, vomiting, diarrhea
61
Atropine
Used for bradycardia
Monitor heart rate and rhythm chest pain after admin, assess for urinary retention and dry mouth, avoid in patient with glaucoma
62
Sinus bradycardia
HR less than 60 BPM
Excessive Vagal stimulation to the heart causes a decreased rate of sinus node discharge. It may result from carotid sinus massage, vomiting, auctioning, Vagal maneuvers, ocular pressure or pain
May only have decreased pulse rate.
Maintain perfusion and CO, assess LOC, VS and tolerance
ADMIN ATROPINE
Syncope
Dizziness and weakness
Confusion
Hypotension, diaphoreses shortness of breath
Chest pain
63
Sinus tachycardia
```
HR greater than 100 BP
Increases cardiac output ad BP
SNS stimulation or PSN inhibition
Maintain perfusion and CO
Assess for dehydration, hypovolemia, infection, HF, MI, urinary output
Fever increase HR
```
64
PAC
Occurs when atrial tissue becomes irritable. This ectopic focus firs an impulse before the next sinus impulse is due. The premature p wave may not always be clearly visible because it can be hidden in the preceding T wave. A PAC is usually followed by a pause.
The cause of atrial irritability include
Stress, fatigue, anxiety, inflammation, infection, caffeine, nicotine or alcohol. Drugs, epi,
65
SVT
Rapid stimulation of atrial tissue at a rate of 100-280 BPM
Paroxysmal SVT rhythm is intermittent, terminated suddenly with our without intervention
Intervention: Vagal maneuvers, carotid massage, drug therapy. Adenosine-restart the heart 6 mg FAST followed by normal saline fast repeat 2 x to total 12mg
66
AFIB
Most common
Associated with atrial fibrosis and loss of muscle mass
Common in heart disease such as hypertension, heart failur, COD, COPD
Cardiac output can decrease by as much as 20-30% due to loss of atrial kick
Increases with age
HTN, previous MI, TIA, COA, diabetes heart failure and mitral valve diseases
Treatment is to slow the ventricular conduction calcium channel blockers cardiazem, more difficult amiodarone
67
AFIB cont
```
Patient centered care
Risk for PE, VTE
Antidysrhythmics drugs
Cardio erosion
Percutaneous radofrequency Cather ablation
Bi-ventricular
Maze procedure
```
68
Atrial flutter
Re-errant tachydysrhythmias that produces flutter waves at rates between 220-350-BPM
Gives saw tooth appearance
Cardio version, ccbs
69
Cardioversion
Synchronized counter shock
Used in emergencies for unstable ventricular/superventricular tachydyrshythmias
Used electively for unstable tachydyrshythmias resistant to medical therapies
70
Ventricular dysrhythmias
Are life threatening than atrial because the left ventricle pumps oxygenated blood through the body to perfume vital organ and other tissues
71
Pvc
Results of increase irritability of ventricular cells
Ventricles quiver consuming tremendous amount of o2
. There is no cardiac output or pulse rhythm no perfusion, fatal if not cared for in 3-5 min
72
V tach
Occurs with repetitive firing of an irritable ventricular ectopic focus usually at 140-180bmp
May be intermittent or sustained
Wide, bizarre QRS complex caused by rent rant cycle of electrical activity within the ventricle
Causes include muscle ischemia, mi valvular disease, HF drug toxicity, hypo magnesium hypo kalmia
73
Self help
Patients at risk for vasovagal attacks causing bradydysrhythmias:avoid doing Hingis that stimulate the vagus nerve, such as raising your arms above your head, applying pressure on your eyes, bearing down or strain gin during a bowel movement and stimulating gag reflex
Patient with premature beats: take mess, report affects, stop smoking, avoid caffeine, or alcohol. Learn ways to manage stress.
Patients with ischemic HD: treat angina prompt, see dr if chest pain is not relieved with nitro
Patients at risk for potassium:know the symptoms, eat foods high in K such as tomatoes, beans, prunes, avocados, bananas, strawberries and lettuce. Take supplements.
74
Hemodynamics monitoring
Pa Cather allows for assessment of cardiac function and fluid volume PAP/PAWP elevated with left heart failure
75
Improving gas exchange
```
Promoting oxygenation and gas exchange
Ventilation assistance
Monitor resp rate 1-4 HR
Auscultate breath sounds every 4-8 HR
Position in high fowler if patient dyspneic
Maintain o2 90%
```
76
Improving cardiac pump effectiveness
Preload
After load
Contractility
Hemodynamics regulation
77
Drugs used to reduce afterload
ACE inhibitors:suppress the renin-angiotensin system which is activated in response to decreased renal blood flow, prevent conversion of Angio-1 to angio-2 resulting in arterial dilation and increased stroke volume. Also block aldosterone which prevents sodium and water retention thus decreasing fluid overload
ARB
Human BNP :lowers pulmonary capillary wedge pressure and improves renal glomerular
78
Interventions that reduce preload
National therapy
Drug therapy:reducing sodium and water retention to decrease workload of heart
Diuretics:enhance renal excretion of sodium and water by reducing circulation blood volume, decreasing preload and reducing systemic and pulmonary congestion
Venous vasodilators: nitrate, returning venous vasculature to a more normal capacity, decreasing the volume of blood returning to the heart, improving left ventricle function
79
Drugs that enhance contractility
Intropic drug: digoxin, benefits increased contractility, reduce Heart rate,slowing conduction through the atrioventricular node, inhibition of sympathetic activity while enhancing parasympathic activity
Beta andrenergic blockers:
80
Pulmonary edema
```
Crackles
Dyspnea at rest
Disorientation
Tachycardia
Hyper/hypotention
Reduced cardiac output
Cough
Pvc
Anxiety
Restlessness
Lethargy
```
81
Preventing or managing PE
```
Assess for early signs
High fowlers position
O2
Nitro
Rapid-acting diuretics
IV morphine
Continual assessment
```
82
Valvular heart disease
```
Mitral stenosis
Mitral regurgitation
Mitral valve prolapse
Aortic stenosis
Aortic regurgitation
Assess sudden illness or slowing developing symptoms
Ask about attacks of rheumatic fever, endocarditis, IV drug use
Chest X-ray, ecg, stress test
```
83
Right sided heart failure
```
Jugular distinction
Enlarged live and spleen
Anorexia, nausea
Dependent edema
Distended abdomen
Swollen hands and fingers
Polyuri at night
Weight gain
Increased or decreased BP
```
84
Left sided heart failure
```
Fatigue
Weakness
Confusion restlessness
Dizziness
Tachycardia, palpitation
Cool extremities
Hacking cough
Dyspnea
Crackles
Froth pink tinged sputum
Tachypnea
```
85
Valvular heart disease
Mitral stenosis: from rheumatic carditis with causes valve thinking.Fatigue,Dyspnea, Neck vein distention,Pitting edema, A fib
mitral regurgitation: prevent the mitral valve from closing completely during systole. Fatigue, dyspnea, palpating,a-fib, pitting edema
Mitral valve prolapse: atypical chest ain ,dis sines, palpating,atrial tachycardia
Aortic stenosis: most common carina valve dysfunction in US disease of wear and tear. Dyspnea, angina, fatigue, syncope,
Aortic regurtaion: valve legs so not close, palpating,dyspnea, Angie fatigue
86
Infective endocarditis
Microbial infection of the endocardium
Primarily in patients IV drugs, valve replacement and systemic infection . Portal of entry rash, lesions, oral cavity, infection, surgery.
Manifestation: murmur, HF, arterial embolization, splenic infarction
Antimicrobials, activities balanced with adequate rest
Surgery remove infected valve, shuts, repair, draining of abscess in heart
87
Pericarditis
Inflammation or alteration of the pericardium
Infected organism post MI
Radiating to left side of neck, shoulder, back
Grating oppressive pain,
Pain worsened by supine position received by sitting up and leaning forward
Intervention NSAIDS, antibiotics
88
Rheumatic carditis
```
Sensitivity response that develops after an upper respiratory tract infection with group a strep
Tachycardia
Cardiomegaly
New or changed murmur
Pre cordial pain
```
89
Cardiomyopathy
Subacute or chronic disease or cardiac muscle dilated cardiomyopathy, hypertrophic cardiomyopathy
Restrictive right ventricular cardiomyopathy
Diuretics, vasodilation agents, cardiac glycosides
Toxin exposure avoidance
Alcohol avoidance
90
CAD
Single largest killer of American men and women in all ethic groups.
Coronary arteries diseased, causing decreased function of the myocardium, resulting in decreased perfusion to vital organs and tissue. Results in ischemia and infarction of myocardial tissue
Included stable and unstable angina.it affects the arteries that provide blood, o2, and nutrients to the myocardium.
91
Chronic stable angina pectoris
Angina pectoris: chest pain caused by a temporary imbalance between the coronary arteries ability to supply oxygen and the cardiac muscles demand for oxygen
Ischemia:lack of oxygen that occurs with angina is limited in duration and does not cause per ant damage of myocardial tissue
Chronic sable angina: chest discomfort that occurs with moderation to prolong exertion in a pattern hat familiar to the patient
92
Acute coronary syndrome
Patients who have unstable angina or an acute myocardial infarction
Atherosclerotic plaque in coronary artery ruptures causing platelet aggregation, thrombus formation and vasoconstriction
Classified in three categories according to ST-segment elevation on ECG and serum troponin markers STEMI, nonSTEMI, unstable angina
93
ACU
Unstable angina: chest pain or discomfort that occurs at rest or with excretion and causes severe activity limitation
May last longer than 15 min and may not be relieved by rest or NTG
Untreated may lead to MI
94
Acute MI
Myocardial infarction: myocardial tissue abruptly and severely deprived of o2 blood flow 80- 90 %
Ischemia leads to injury and necrosis
95
Acute MI
Dynamic process-evolves over several hours
Hypodermic form ischemia: acidosis and electrolyte imbalance
Increased o2 demand may cause lie threading vfib
Extent of infarction depends on 1-collateral circulation 2-metabolism and 3 workload demands on myocardium
Timeframes:6 hours tissue blue and swollen: 48 hours infected area and grey/yellow stripped 8-10 days granulation develops 3 months thin firm scar formation causes ventricular remodeling
96
MI response
Conakry artery involved determines manifestations of event and structures affected by infracted area
LAD, left anterior or septal MI: highest mortality rate, Ventriculars dysrhythmia
Circumflex-left lateral ventricle: possible posterior wall, SA node and AV node, sinus rhythm
RCA-SA, AV, nodes:right ventricle sand inferior portion of LV right sided failure
97
Atherosclerosis risk factors
Non Modifiable: age, gender, family history, ethnic background
Modifiable: lipid levels, smoking, exercise,hypertension,diabetes,obesity, alcohol,stress
98
Metabolic syndrome (syndrome x)
Risk factor for cardiovascular disease
Indicator of risk factors need to have 3 to be considered
Hypertension - either BP 130/85 /^ or taking anti hypertensive drugs
Decreased HDL- either HDL-C
99
Patient centered care
History- dependent upon presenting symptoms
Physical assessment- rapid assessment or vital signs, pain and symptoms
Psychosocial:denial, fear, anxiety, anger, depression
Lab-troponin,ck-mb, chemistry
X-ray
12 lead ecg within 10 min
100
Planning and implantation syndrome x
Assessment remember time is an issue, most people wait 4-6 window
Manage acute pain: MONA-morphine,o2,NTG,aspirin) IV access x2
Adequate cardiac output 90 minuet door to intervention
Patient and family
Identify dysthymia- identify, assess, evaluate
Monitor and mange HF:
101
Killing classification
Class 1: absent crackle and s3
Class 2: crackles in lower half of the lung fields and possible s3
Class 3: crackles more than halfway up the lung field and frequent pulmonary edema
Class 4 : cardiogenic shock
102
Drugs for ACS
Aspirin:81 mg x4 baby or chew 325 mg
Glycoproteins:reopro given to decrease douse with fibrin
Beta-adrengic blockers:decrease the size of infarct,occurrence,ventricular dysrhythmias heart can perform more work without ischemia
Ace and arb:given within 48 hrs to prevent ventricular remodeling
Calcium channel blockers: promote vasodilation and MI perfusion
thrombolytic: dissolve thrombin
103
Contraindication
Absolute: prior hem orange, cerebral vascular lesion, malignant intracranial neoplasm, stroke, active bleeding
Relative: HTN, stoke, traumatic CPR, pregnancy, active ulcer
104
Cardiogenic shock
Necrosis of more than 40% of the left ventricle occurs.
Common cause of heart damage
Patients have stuttering pattern of chest pain, resulting in piecemeal extensions of the ACS
Monitor and report tachycardia, hypotension, systolic BP less than 90 or 30 less than the patients baseline
Urine output less than 0.5-1
Cold, clammy skin
Agitation, restlessness confusion
Pulmonary congestion
Tachypnea
Continuing chest discomfort
Poor myocardial contractility
High venous pressure leads t fluid extravasation and edema
Despite normal or high BP organs are poorly perfumed due to reduction in blood flow
Sympathetic over activity leads to vasoconstriction in order to maintain BP
105
Treat cardiogenic shock
Relieve pain and decrease myocardial o2 requirements through preload and afterload reduction
IV morphine used to decrease pulmonary congestion and pain
Fluids dopamine drip to increase heart no diuretic or beta
On back take care of family experience b vitamins
106
Hemodynamics monitoring
Invasive system used to give information about vascular capacity, blood volume, pump effectiveness and tissue perfusion. It directly measure pressure in the heart and great vessels
Catheter with infusion system
