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Care test 1

Terms in this set (108)

What medication do use for MI?
MONA B
M - morphine
O - Oxygen
N - Nitroglycerin
A - Aspirin
B - Beta blocker
Why is morphine used for?
Decrease pain and to suppress sympathetic activity and vasodilator
Why is oxygen used?
Increase oxygen supply
What is nitroglycerin used for?
Vasodilator (Decrease preload & workload on heart and decrease o2 demand)
What is Aspirin used for?
Antiplatelet
What is Beta Blocker used for?
-Decrease myocardial o2 demand by decreasing decreasing force of contraction
-Slows HR/impulse conduction
-Slowed HR increase fill time and increase CA perfusion
-Decrease BP to decrease afterload
Biggest thing with heart pt in monitoring at home
Weight (Fluid retention)
What else is included in nursing care for heart pt?
-Manage low sodium (2g a day)
-Daily weight
-I&O
-Diuretics
Most common type of cardiovascular disease and accounts for the majority of these deaths
Coronary artery disease (CAD)
What is the major cause of CAD? and what happens?
Atherosclerosis
-Lipid deposits within intimate of artery
-Endothelial injury and inflammation
What is C-reactive protein
Protein produced by liver, non specific marker of inflammation

Better is HsCRP (more sensitive but inflammation can be from somewhere else)
What is the non modifiable risk factors for CAD?
-Age
-Gender
-Ethnicity
-Family history
-Genetic predisposition
(White middle aged men)
Modifiable risk factors for CAD
-Hypertension (>140/90 or >130/80 if diabetes or CKD
-Elevated lipid levels (Cholesterol >200 and Triglyceride >150)
- Tobacco use (increase catecholamine release, increase LDL and oxygen radicals, carbon monoxide, decrease HDL)
-Second hand smoke
-Psychologic states (type A personality, depression, stress)
-Homocysteine level (breakdown of essential amino acid methionine)
-Substance abuse
-Physical inactivity (30 min/5x a week)
-Obesity
-Diabetes
- Metabolic syndrome
Prevention of CAD
-Control cholesterol abnormalities
-Physical activity
-Smoking cessation
-Managing HTN
-Managing DM
Diets for CAD
-Decrease saturated fats and cholesterol
-Increase complex carb and fiber
-Decrease red meat, egg yolks, and whole milk
-Increase Omega-3 fatty acid
Physical fitness for CAD formula
FITT
F-frequency (how often
I-Intensity (how hard)
T-Type (isotonic)
T- time (how long)

30 mins/most days plus weight training 2 days a week
Medication for CAD
*Fibric acid derivative (Lopid) Decrease triglyercide and increase HDL, GI side effects
*Bile acid sequestrants-increase conversion of cholesterol to bile acid, GI side effects
*Ezetimibe (Zetia) - Decreae absorption of dietary and biliary cholesterol
-Statins (inhibit cholesterol synthesis, decrease LDL increase HDL, monitor for liver damage and myopathy)
*Niacin (Lowers LDL & triglyceride by inhibiting synthesis, increase HDL, Flushing, pruritus, GI side effects and orthostatic hypotension)
-ASA
-Clopidogrel (Plavix) -can be used for high risk women who are intolerant of ASA
What is Angina?
Chest pain from reversible myocardial ischemia
-occurs when arteries are blocked 75% or more
-Hypoxic within 10 seconds of occlusion
-Viable for 20 mins
When you think of chest pain, what systems do you think of?
1. Cardiovascular
2. Pulmonary
3. GI (timing when eating)
4. Musculoskeletal
What kind of pain is angina?
-Pressure/ache
- Squeezing, heavy, choking, or suffocating sensation
-Rarely sharp or stabbing
-Indigestion or burning
-Various locations (substernal, neck radiating to jaw, shoulder and down the arms, between shoulder blades)
Signs and symptoms of Angina
-Mild indigestion to choking or heavy sensation in the upper chest
-Feeling of apprehension, impending doom
-Poorly localized and may be fed deep (retrosternal area) inner aspects of upper arms (L>R)
-Diabetes may not feel pain
Chronic stable angina
-Intermittent chest pain that occurs over a long period with the same pattern of onset, duration, and intensity of symptoms
-5-15 min duration
-ST segment depression and/or T-wave inversion
-Control with drugs
Silent ischemia
-occurs in the absence of any subjective symptoms
-Associated with diabetic neuropathy
-Confirmed by ECG changes
Goal of collaborative care for chronic stable angina
Decrease O2 demand and/or increase O2 supply
Drugs for chronic stable angina
-Short acting nitrates (dilate peripheral and coronary blood vessels - flushing, HA, dizziness, orthostatic hypotension)
-Nitroglycerin (HA, Hypotension, tachycardia, syncope)
-Long-acting nitrates (to reduce angina incidence, 8 hour nitrate free period every day)
Other drugs for chronic stable angina
-ACE inhibitors (for lower risk pt, vasodilation and reduce blood volume, prevent or reverse ventricular remodeling)*weight gain, depression, sexual dysfunction, no to asthma/diabetic pt
- Calcium channel blocker - prinzmetal angina (systemic vasodilator, decreased myocardial contractility and coronary vasodilator)
-Sodium current inhibitor - Ranolazine/Ranexa (prolongs QT internal, dizziness, nausea, constipation, and general weakness)
Diagnostic studies for chronic stable angina
-Chest x-ray
-Lab studies
-12-lead ECG
-Calcium-score screening heart scan
-Echocardiogram
-Exercise stress test
-Pharmacologic nuclear imaging
Acute intervention for chronic stable angina
1. Position Pt semi fowler unless contradicted and administer supplemental o2
2. Assess vital signs
3. Obtain a 12-lead ECG
4. Provide prompt pain relief first with a nitrate followed by an opioid analgesic if needed
5. Ausculate heart and breath sound (Pt may have pale, cool clammy skin)
*May reveal an atrial (S4) or a ventricular (S3) gallop.
Cardiac catheterization/coronary angiography
(For pt with increasing symptoms or w/ significant amount of myocardium that is ischemic under stress, provides images of the coronary circulation and identify the location and severity of any blockage)
-Visualize blockage (diagnostic)
-Open blockages (interventional)
*Percutaneous coronary intervention (PCI) if coronary blockage is amenable to intervention
*Balloon angioplasty (inflatable balloon tip, atherosclerotic plaque is compressed, vessel dilation)
*Stent (treat abrupt or threaten abrupt closure and restenosis)
Nursing care for chronic angina
-Balance rest w/ activity to reduce ep of angina
-Follow prescribed exercise program
-Extreme temp (esp cold) may induce angina
-Stress reduction
-OTC meds - anything that inc HR, BP
-Stop smoking
-Diet low sat fat, high fiber, low in calories if weight loss
-Maintain BP, Glucose
-Carry NTG at all times, take other meds as prescribed
Chronic stable angina and ACS subjective data
-Family history
-Indigestion/heartburn;N&V
-Urinary urgency/frequency
-Straining at stool
-Palpitations, dyspnea, dizziness, weakness
-Chest pain
-Stress, depression, anger, anxiety
-Health history (CAD, chest pain, heart failure, HTN, diabetes, anemia, hyperlipidemia)
-Drugs
-History of present illness
Chronic stable angina and ACS objective data
-Anxious, fearful, restless, distressed
-Cool, clammy, pale skin
-Tachycardia or bradycardia
-Pulsus alternans (change in respiration)
-Pulse deficit
-Dysrhthmias
-S3, S4, increase or decrease Bp, murmur
Unstable angina
Chest pain that is new in onset, occurs at rest or has a worsening pattern
-Increase in frequency
-Unpredictable
-Medical emergency
-Symptoms in women may be vague (Fatigue, SOB, indigestion and anxiety)
*Change in QRS complex, ST segment and T wave caused by ischemia and infaraction
STEMI vs UA or NSTEMI
STEMI - more extensive MI that is associated with prolonged and complete coronary occlusion and the development of a pathologic Q wave on the ECG
UA or NSTEMI - transient thrombosis or incomplete coronary occlusion, don't develop pathologic Q wave
Acute myocardial infarction
-Caused by complete obstruction of coronary artery with fibrous clot
-Causes myocardial ischemia distal to clot
-Depresses myocardial contractility causes risk of death from dysrthmias
-Ischemia lasting more than 20 mins results in death of tissue
Myocardial infarction pain
-Severe immobilizing chest pain not relieved by rest, position change or nitrate administration
-Heaviness. pressure, tightness, burning, constriction, crushing
-Substernal, retrosternal, epigastric
-More common in AM
-Atypical in women, elderly
-No pain if cardiac neuropathy (diabetic)
-Older pt may experience confusion, SOB, pulmonary edema, dizziness or a dysrhythmia
Clinical manifestation of Myocardial infaraction
-Pain
- Catecholamine release - stimulation of SNS (vasoconstriction of peripheral blood vessel, skin: ashen clammy, cool to touch)
- CV (initially increase HR and BP, then decrease BP secondary to CO, crackles, JVD, abnormal heart sounds, holosystolic murmur - septal defect, papillary muscle rupture/valve dysfunction)
-N&V
-Fever (up to 100.4 F in first 24 hrs. inflammatory process)
Healing process of MI
-10-14 days after MI, scar tissue still weak
-Myocardium vulnerable to stress
-Monitor pt carefully as activity level increases
(6 weeks considered healed)
-Ventricular remodeling (normal myocardium will hypertrophy and dilate to compensate)
Complication of MI
-Dysrthmias (80% in MI pt, can be caused by ischemia, electrolyte imbalances, or SNS stimulation) *life threatening dysrhymias seen most often with anterior MI, heart failure or shot
-Heart Failure
-Ventricular problems
Acute MI diagnostic test
-EKG
-Blood test
*Enzyme CK-MB rises during acute MI (3-9 hrs elevation, 12-18 hours peak)
*Serum troponin rises in 3 hours and last 7 days
*Serum myoglobin - can indicate myocardial cell death (1 hr elevation, 4-6 hours peak)
*LDH - rises in 8-24 hrs
What does stress test show?
Significance of blockage related to pt functioning
Acute MI nursing managment
Pt/family teaching
-Dx test and treatment procedures
-Risk factors(lifestyle) modifications
-Medications (NTG)
-Increasing activity and exercise
-Resuming sexual activity
-S&S of CAD and complications
Why is anticoagulant and thrombolytics used for acute MI
Anticoagulant: IV heparin prevents clot formation at site of plaque rupture: inhibits thrombin
Thrombolytics: standard of care within 6 hours of AMI onset if PCI not available; lysis of occluding clot
(Within 6 hours: benefit outweighs the risk, after 6 hours: risks outweigh the benefit-risk of bleed) only works for 24 hours
Nursing care for Acute MI
-Frequent vital sign assessment
-Telemetry
-I&O, daily weights (need to know if kidney is being professed)
-Assess for restlessness, dyspnea or chest pain (indicates that tissues damage is worsening)
-Assess for S&S of CHF (risk for developing heart failure, congestive means fluid problems in lungs)
-Assess skin color
72 hours post acute MI
-Priority-REST - injured heart must have time to start repairing itself
-Bedside commode for BM, preferred over bedpan, stool softeners
-Assist with isometric exercise (provide muscle exercise w/out causing exhaustion)
-SCDs to prevent DVT
-No valsalva maneuver (result in sinus bradycardia and syncope)
-Place all necessary items within pt reach. Call light available, prevent stretching or straining.
-Perform physical care-provides rest and comfort
-Assistance with ADL
Acute MI diet
-NPO while evaluated for acute chest pain to prevent blood from being redirected to GI tract
-Prevents vomitting
-Small easy to digest foods
-Low fat low cholesterol
-Saturated fat less than 10% Kcals
Acute MI activity treatment
-Bedrest to decrease O2 demand
-Activity gradually increase
-Pt assessed for activity tolerance based on orthostatic changes in BP, dysrthymias (can indicate possible ischemia)
-Post infarct pt have stress test to determine safe exercise level
-Cardiac rehab for activity progression
Post MI goals
-BP lower than 140/90
-Waist circumference: Women <35 inches. Men <40 inches
-BMI between 18.5 and 24.9
-Blood cholesterol under 180
-Blood glucose under 100 during normal fasting
Acute MI complications
-Heart failure
-Dysrhythmias (most common)
-Percariditis
-Dressler's syndrome
-Ischemic cardiomyopathy
-Cardiogenic shock
-Ventricular septal defect
-Free wall rupture
-Ventricular aneurysm
Infective endocarditis
Infection of the inner layer of heart, including the cardiac valves
-Improve prognosis with antibiotic therapy (takes weeks to get rid of it)
(Occurs when blood turbulence w/in heart allows causative organism to infect previously damaged valves or other endothelial surfaces)
Causative organisms for infective endocarditis
-Bacterial most common (Streptococcus viridian's and staphylococcus aureus)
-Virus
-Fungi
Risk factors for infective endocarditis
-Cardiac, non cardiac procedural
-Principle risk factors (Age, IV drug abuse, prosthetic valves, use of intravascular device, renal dialysis)
Clinical manifestations of Infective endocarditis
-Nonspecific
-Low grade fever (90% of pt)
-Chills
-Weakness
-Malaise
-Fatigue
-Anorexia
-Murmur in most pt
-Heart failure
-Manifestations secondary to embolism (Spleen, kidneys, limbs, brain, lungs)
Vascular manifestations of infective endocarditis
-Splinter hemorrhage in nail bed
-Petechaie
-Osler's nodes on fingers or toes
-Janeway's lesions on palm or soles
-Roth's spots
Heart failure
Condition in which the heart is unable to adequately pump blood throughout the body and/or unable to prevent blood from backing up into the lungs
Heart failure risk factors
Primary risk factors
-Coronary artery disease
-Advancing age
Contributing risk factors
-Hypertension
-Diabetes
-Obesity
-High serum cholesterol
-African american descent
-Valvular heart disease
-Hypervolemia
Heart failure diagnostics
-CXR: congestion as white dense area, may show enlarged heart, liver congestion
-Lab results: HF alters many lab values: Serum BNP
-ECG: can be normal or ischemia, infarction, tach, hypertrophy, tamponade
-Echocardiogram: tells about L & R vent function, abnormal contractions, valve problems
-Cardiac cath: pt with CAD
-MRI or CT
What are the results from BNP from left ventricular failure show?
<100 - unlikely from CHF
100-500 - may be CHF
>500 - most consistent with CHF
Clinical manifestations of Chronic heart failure
(Dependent on age, underlying type and extent of heart disease and which ventricle is affected)
FACES
F-fatigue
A - limitation of activities
C-Chest congestion/cough
E-Edema
S-SOB
Left sided heart failure
-Dyspnea and orthopnea develop as a result of pulmonary congestion
-Complications: Acute pulmonary edema
-Physical assessment findings - tachypnea, use of accessory muscles of respiration, wheezing or rales (bubbling crackles), HTN, tachycardia, S3 gallop
Left sided failure clinical manifestations
-Paroxysmal nocturnal dyspnea
-Elevated pulmonary capillary wedge pressure
-Pulmonary congestion (Cough, crackles, wheezes, blood-tinged sputum, tachypnea)
-Restlessness
-Confusion
-Orthopnea
-Tachycardia
-Exertional dyspnea
-Fatigue
-Cyanosis
Right sided heart failure
-Edema, congestive hepatomegaly and systemic venous distention are more prominent
-Complications-Peripheral edema, venous congestions of organs, hepatomegaly, ABN pain, anorexia, Nausea, bloating secondary to venous congestion
-Early manifestations - dependent edema
-Anasarca develop at late HF (generalized edema - everywhere even genital area eyes, pillsbury dough boy)
*Right sided heart failure is most commonly the result of left ventricular failure
Right side heart failure clinical manifestations
-Fatigue
-Increase peripheral pressure
-Ascites
-Enlarged liver and spleen
-Cor pulmonale
-May be secondary to chronic pulmonary problems
-Distended jugular veins
-Anorexia, complaints of GI distress
-Weight gain
-Dependent edema
Heart failure goal
Improve cardiac performance without increasing cardiac workload; must manipulate preload, contractility, after load (medications are mainstay of management)

*Hemodialysis/ultrafiltration-reduce volume
*Intraaortic ballon pump-decrease after load
*Ventricular assist device - ventricles can rest
Current treatments for Heart failure
-Reduce preload (high fowler's to reduce pulmonary congestion, controlling sodium and water retention, restrict sodium intake, avoid NSAID, take diuretics)
-Reduce after load (Vasodilators)
-Increase ventricular contractility (inotropes)
Heart failure: ACE inhibitor
-Vasodilation
-Decrease in BP
-Reduction of after load
-Slows heart remodeling (prevents from getting weaker)
-Can use ARBS if cough is a problem
AE: angioedema, hypotension, hyperkalemia, renal insufficiency, cough, rash
Heart failure: Beta blocker
-Slows HR (used to manage mild to moderate left ventricular systolic dysfunction)
-Allows the left ventricle to fill completely
-Improves % of blood pumped from left ventricle
-Reduce the need for hospital stays
-Slow progression of HF
-Reduce risk of death
AE: bronchospasm, bradycardia/heart block, hypotension
Heart failure: Diuretics
-Given to decrease preload, after load and increase contraction (given with clinical S&S of overload)
-Proper dosing is important, not taking enough can reduce ACE inhibitor effectiveness and increase beta block side effects
-Enhances renal excretion of sodium and water
AE: hypokalemia, hypotension, renal insufficiency, electrolyte imbalance
*Used for symptom relief (Does not change mortality)
Heart failure: Aldosterone antagonist
(Spironolactone and eplerenone)
-30% reduction in mortality and hospitalization with class 3-4 HF and serum creatinine 2.5 (Spirolactone)
-15% reduction in risk of death and hospitalization in pt with LVEF lower than 40% after MI (eplerenone)
AE: monitor serum K, gynecomastia with spiro, watch creatinine (renal insufficiency) hyperkalemia
Heart failure: Inotropes
(Digitalis) (level: 0.6-2.0) Sodium faced out of cell in exchange for calcium-increase force of contraction and increase CO, Slows conduction/HT
-Take HR for 1 min, hold if below 60, keep in same container, report toxicity
Toxicity side effects:
Early signs: anorexia, N&V, malaise, lethargic, fatigue, generalized weakness/dizziness, insomnia
Neurovisual symptoms: Confusion, apathy, agitation, hallucination, delusions, depression, disorientations, psychic complaints, abnormal dreams, blurred vision, xanthopsia (seeing yellow-green halos around lights)
What is pink frothy sputum from?
Pulmonary edema
Acute pulmonary edema care
(Life threatening emergency)
-Supplemental O2 (intubation if necessary)
-Cardiac monitoring and pulse oximetry
-IV
-Elevate HOB to reduce venous return
-Medications: nitrates and diuretics, morphine, ACE inhibitors, beta blocker
Heart failure management
Activity: Acute HF pt on bedrest to minimize O2 demands, but increase immediately after BP, HR O2 stabilize
-Referrals - work with many providers to improve quality of life
Heart failures: medications to avoid
-Pain: tylenolol (4g/day)
-Avoid all OTC pills as they can cause you to gain fluid (NSAIDS, ASA)
-No herbals
-No ASA unless prescribed by doctor
Heart failure: Daily weights
(Sudden weight gain is sign you are retaining fluid)
-Same time every day, first thing in morning. Without clothes or in lightweight clothes
-After you urinate, before you eat breakfast
-Write down weight everyday
2 lbs in 1 day
3-5 lbs in 2 days
5 lbs in 7 days, call doctor
Chronic arterial occlusive disease
Progressive narrowing, degeneration & obstruction of arteries of extremities, usually lower involved
Chronic occlusive disease presentation
-Paresthesias - loss of position sense
-Polar or coldness
-Paralysis
-Pallor - empty superficial vessels (can progress to mottled, cyanotic and cadaverous cold leg)
-Pulselessness
-Intermittent claudication - calf pain alleviated with rest, muscle forced to contract w/out adequate supply
-Rest pain - pain at rest when limited blood flow cannot meet very low tissue requirement, numbness, coldness tingling
-Trophic changes in skin and nails: dryness, scanning, and thinning of skin, decreased or absent hair, brittle and thickened nails and gangrenous changes marking death and decay of tissues
Chronic occlusive disease: physical manifestations
-Shiny thin, tight,fragile skin is dry and scaly
-Cool to touch
-Diminished or absent pulses
-Pale appearance with elevated extremities
-Reddish color with extremities dependent
-Decreased motor function
-Ulcer formation with advanced disease
Medications for chronic occlusive disease
Pentoxifylline (Trental) and Cilostazol (Pleta) - tx for claudication

ASA or plavix - prevent formation of thromboemboli

Statin - reduce cholesterol and atherosclerosis
Nursing care for chronic occlusive disease
-Place pt's legs in dependent position in relation to heart to improve peripheral blood flow
-Avoid raising client's feet above heart unless prescribe by doctor
-Keep client in neutral flat supine position, if in doubt about the nature of his peripheral vascular problems
-Promote vasodilation (gloves, socks, warm room, warm drink/baths)
-Teach pt about vasoconstrictive effects (Nicotine, caffeine, emotional stress, chilling)
-No constrictive clothes
-Promote activity and mobility
Acute arterial occlusive disease presentation
-Severe constant pain not relieved by rest
-Pallor or mottled appearance
-Pulselessness or diminished over affected area
-Paresthesia - numbness, tingling, burning
-Poikilothermia - cool or cold to touch
-Paralysis - mobility is limited; indicates ischemic death of nerves
Acute occlusive disease medications
-Heparin - prevent further clots
-Urokinase - dissolves clot over 24-48 hrs
-Spasmolytic agents - relieve arterial spasms
-Calcium channel blocker - spasm
-Coumadin - prevent future episodes
Raynaud's Phenomenon
Episodic vasospastic disorder of the cutaneous arteries most often involving fingers and toes
-Fingers - white (lack of blood flow)
-Blue - blood vessels dilate to keep blood in the tissue
-Finger may turn red as the blood begins to return
First line therapy for acute arterial occlusive disease
Calcium channel blocker - relaxing smooth muscles of the arterioles by blocking the influx of calcium into the cells
PVD: Arterial manifestation
-Diminished or absent pulses
-Smooth shiny dry skin, no hair
-no edema
-Round regularly shaped painful ulcers on distal foot, toes or webs of toes
-dependent rubor
-pallor and pain when legs elevated
-intermittent claudication
PVD: Venous manifestation
-Normal pulses
-Brown patches of discoloration on lower legs
-Dependent edema
-Irregular shaped usually painless ulcers on lower legs and ankles
-Dependent cyanosis and pain
-Pain relief when legs elevated
Virchow's Triad
-Stasis (Decreased blood flow)
-Endothelial injury (Damage to the inside of blood vessel)
-Hypercoagulability (Blood clots are likely)
Travel to R heart and then into pulmonary artery - pulmonary embolism
DVT (deep vein thrombosis)
-More common in women and elderly
-Thrombi develop in area of slow or turbulent blood flow
-Spasm and change in pressure dislodge thrombi and move them towards heart
DVT presentation
-50% asymptomatic
-local pain or tenderness
-edema or swelling
-local warmth, redness, mild fever
-tender palpable venous cord
-<20% DVT pt have pos Homans sign
Medication for DVT
*Prophylaxis: Low dose heparin or lovenox SC
*Treatment: heparin, lovenox, coumadin, other thrombolytic therpy to dissolve existing thrombi
DVT nursing management
-Avoid prolonged standing & sitting
-Avoid crossing the legs at knee or ankle
-Do not massage legs
Pulmonary embolism manifestations
-Dyspnea
-Chest pain (pleuritic more common than non-pleuritic)
-Apprehension
-Cough
-Hemoptysis
-Sweating/diaphoresis
-Palpitations
-Wheezing
-Leg pain
-Leg swelling
What diseases are under COPD?
Bronchitis, emphysema, asthma
Chronic bronchitis
Mucus production and persistent cough
Emphysema
Over distention of air space and alveolar walls destroyed
Blue Bloater
(Chronic Bronchitis)
-Color dusky to cyanotic
-Recurrent cough and sputum production
-Hypoxia
-Hypercapnia
-Acidosis
-Edematous
-Increase rest rate
-Exertional dyspnea
-Increase in heavy cigarette smokers
-Cor pulmonale
-Cardiac enlargement
-Use of accessory muscles to breathe
Pink Puffer
(Pulmonary emphysema)
-Increase CO2 retention
-No cyanosis
-Purse lip breathing
-Dyspnea
-Ineffective cough
-Hyperreasonance on chest percussion
-Orthopenic
-Barrel chest
-Exertional dyspnea
-Prolonged exportation time
-Speaks in short jerky sentences
-Anxious
-Use of accessory muscles to breathe
-Thin appearance
-Leads to right sided failure
Asthma
Altered immune response causes breathing through narrowed airway in spasm (Bronchoconstriction of smooth muscles, increase vascular permeability and increase mucous gland secretion)
*resp acidosis
Wheezing
Early warning signs of asthma
-frequent cough, especially at night
-losing your breath easily or SOB
-Feeing very tired or weak when exercising
-Wheezing or coughing after exercise
-Feeling tired, easily upset, grouchy or moody
-Decreases or changes in lung function as measured on a peak flow meter
-Signs of a cold or allergies (sneezing, running nose, cough, nasal congestion, sore throat, HA)
-Trouble sleeping
Breathe sounds for asthma
Wheezing on expiration
Progress: wheezing on inspiration and expiration
Impending doom - diminished breath sound
Breathe sound for bronchitis
Maybe crackles or wheezes on expiration
Pneumonia manifestations
-Fever, shaking, chills, pleuritic chest pain, productive cough
-Dyspnea, tachypnea, tachycardia
-Green or blood tinged sputum
-Older adults - Change in mental status, refuse to eat or drink, general chest area pain, weakness, not feeling well
-Crackles, dullness to percussion
-Pleural pain
-Malaise
Breathe sound for asthma
Crackles on expiration and late inspiration
-Bronchial sound over area of consolidation
What kind of precaution is TB?
Droplet isolation, 3 feet, Negative air-flow room/HEPA filters
S&S of TB
-Cough for several weeks
-Fever for more than a week
-Night sweats
-Weight loss
-Weakness
-Chest pai/pleurisy
-Coughing up blood (10%)
-Induration of >5-15 mm is positive (PPD)
Pleural effusion
-dyspnea with activity/rest
-tachycardia, dysrhythmias, s3 heart sounds, hypo or hypertension
-fear, anxiety
-Pain aggravated by inspiration,
-Tachypnea, use of accessory muscles, decreased remits
-skin, pale, cyanosis, sweating
Lung surgery positions
Pneumonectomy - should not be turned on unoperative side
Lobectomy - should not be turned on operative side
Pulmonary embolus breathe sound
Rales
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