Coronary Artery Disease (CAD)

A disorder that impedes the blood flow in the arteries serving the myocardium of the heart.

Arteriosclerosis

the loss of elasticity or hardening of the arteries.

Occurs as we age

Atherosclerosis

the lumen of the artery fills with a buildup of fatty deposits (plaque). 

Coronary Artery Disease (CAD) Risk Factors

GenderMen > women before menopause, After menopause women’s incidence rises

Age 70, men = women in terms of risk, Women are twice as likely to die (esp > 65 y/o) r/t: Less likely to seek help from ERLess likely to receive aggressive state of art tx. R/t s/s atypical & taken lightly, Procedures more technically difficult

CORONARY ARTERY DISEASE

Modifiable risk factors

Smoking – major. Serum lipid levels. Chemical injury to intima. Transport fats to blood.  Physical inactivity. Body shape. High fat diet ® ­ serum lipid levels Type. “A” personality. Stress. Concurrent conditions

Concurrent conditions

R/T

CORONARY ARTERY DISEASE 

Diabetes mellitus ® alters metabolism of fats, CHO, & protein:

Causes early, aggressive atherosclerosis of all vessels involved including microvessels

            HTN ® damages vessels & overworks

Renal failure 

Obesity 

Body mass index (BMI) > 30

Coronary Artery Disease (CAD)

Clinical manifestations Occurs when............

 vessel narrowed by 70%

Coronary Artery Disease (CAD)

Clinical manifestations 

Fatigue, Poor exercise tolerance,­ Resting HR ©, Irregular hr with exercise, Pt. Often has risk factors i.e. obesity, smoking, HTN & DM

Eventually as disease progresses pt. Will start to have chest pain

Angina

CORONARY ARTERY DISEASE

Factors which ¯ O2 supply

Esp. Important in elderly pt. having surgery

§  Anemia

§  Low blood pressure

§  Hypoxemia

Thrombus in coronary artery

CORONARY ARTERY DISEASE

Factors which ­ O2 demand

Exercise

Strong emotion

Hyperthyroidism

­ ↑DBP  ® ­ ↑© work load 

Stable angina

occures when there is......

 ³ 70% narrowing of coronary arteries r/t atherosclerosis 

Stable angina

Four E’s of increased O2 demand:

1.     Exertion

2.     Eating

3.     Excitement

4.     Exposure to cold

Stable angina

Pain r/t increased O2 demand   

Stable angina

response to tx is predictable, 

response to tx. Usu. Same  

Treatment for stable angina – priority = pain relief

Rest

NTG gr. 1/150 (0.04 mg) SL x3 q3-5 min.

Pt. Can prevent pain by premedicating before activities which usu. produce pain (i.e. exercise & sex)

UNSTABLE ANGINA 

New literature calls it acute coronary syndrome (ACS)

Coronary artery narrowing is >90% 

UNSTABLE  ANGINA 

Pain occurs even at rest without precipitating factors, any time

Pain has­frequency, intensity, duration & is relieved poorly or not at all by rest or NTG

UNSTABLE  ANGINA 

Relief of pain is the highest priority

IV Nitroglycerin

Sedation: Morphine

Oxygen

Antihypertensives

Anticoagulant or Antiplatlet Therapy

PRINZMETALS (VARIANT) ANGINA

Coronary arteries are usu. wnl. (no plaque

Pt. needs to go to cath lab for dx.

Meds i.e. ergotrates are given to precipitate spasm for dx

PRINZMETALS (VARIANT) ANGINA

Pain r/t coronary artery spasm

Pain usu. Occurs at rest at night between 2400-0800

ANGINA CLINICAL MANIFESTATIONS

Hallmark is chest pain-Mild to severe

Pt. May describe it as: Crushing, Heavy – “an elephant sitting on my chest” is typical, Squeezing – “a tight band around my chest”, Pressing, Burning, Choking, Aching

Chest pain may appear suddenly or gradually

Usu. it is midsternum

Most pt.  have the levine sign when asked where the pain is

The pain may radiate, typically   to theL. Shoulder & arm, neck, or jaw, Can go through to the back

Pt. May describe weakness or numbness in the arms or back

ANGINA

Associated s/s

Dysrhythmias, ST T wave changes on EKG

Bp up or down, Anxiety, Physical exam & EKG normal between episodes 

ANGINA

DIAGNOSTIC TESTS

EKG

Stress test/thallium scan

Lipid profile 

Cardiac markers 

Liver & kidney function tests 

Angiogram  

ZONES OF MI

Zone of necrosis

Zone of injury

Zone of ischemia

Varying degrees of cellular injury can occur

Injured & stunned cells can heal if O2 supply restored

If O2 supply not restored promptly cells die & MI results

DETERMINANTS OF DAMAGING EFFECTS OF MI

Size of damaged area

Location of infarct

Collateral circulation

Increased collateral circulation leads to decreased area of damage

Can have 100% occlusion and no mi if a lot of collateral flow

CLINICAL MANIFESTATIONS

   Of MI

Chest pain not relieved by rest or NTG , 

Associated s/s: Denial “It’s just something I ate”

Weak peripheral pulses, Disorientation 

Pt. Usu. appears anxious & has a feeling of impending doom

Levine sign Muffled heart sounds, S4 S3 & crackles 

JVD if has RV failure

Mildly elevated temp (<101)

DIAGNOSIS of MI

LAB TESTS for MI

EKG -- 12 lead, CK-MB & troponin, Echocardiogram, PT/PTT, CBC

Chemistries, Angiogram

Later when pt. has recovered from mi:

o   Thallium scan/thallium stress test

EKG -- 12 lead 

Usu. Ordered initially & Q8H x3 & PRN chest pain

Changes remain even when pain is gone  

CK-MB & troponin

§  Increase in MI but not in angina

§  Usu. Ordered initially & Q8H x3

Dysrhythmias, Structural damage, Ventricular aneurysm

Pericarditis: inflammation of pericardial sac

CHF/cardiogenic shock: immediate or late complication

MANAGEMENT

Prevent increase of infarct size & minimize cell death by Early restoration of coronary blood flow to improve the balance between O2 supply & demand

DRUGS  for MI

“Mona greets all Patients”

Morphine – 2-4 mg IV Q5 min: To decrease pain, Decrease o2 demand

Oxygen – 2-4 LPM/NC 

Nitroglycerin (NTG) – give SL gr. 1/150 or by nasal spray x3  

Nitroglycerin (NTG) IV GTT

Decrease o2 demand

Increase the o2 supply

Decreases coronary artery spasm

ASA – one adult (325 mg) or one baby (81 mg)  

Other drugs possible

Thrombolytics / fibrinolytics (clot busters)

“Door to drug 30 min.”

INTERVENTIONS MI

highest priority

INTERVENTIONS (After 24 Hrs) for MI

Ø Small meals, no caffeine

Ø Cardiac rehab

Ø Planned rest

Ø Avoid straining/valsalva

Ø Monitor pt. C/O fatigue & discomfort

Ø Observe for complications 

Ø Stress reduction

Ø Encourage independence

Ø Continue cardiac rehab after D/C as out pt.

S/s to report after MI

Congestive Heart Failure
(CHF)

LEFT VENTRICULAR FAILURE:

caused by

Systemic HTN

Valvular heart disease

Cardiomyopathy

Endocarditis: inflammation/infection in the heart

Myocardial Infarct

FORWARD EFFECTS

LV unable to pump ® < CO ® < tissue perfusion ® tissue hypoxia

FORWARD EFFECTS

LEFT VENTRICULAR FAILURE

Clinical manifestations R/T low O2

o   Low BP, tachycardia, dysrhytmias

o   Fatigue, weakness

o   Oliguria, pallor

o   Angina

o   Confusion/memory lapses (esp. elderly)

o   Restlessness, dizziness

o   Weak peripheral pulses

o   Cool extremities

BACKWARD EFFECTS

LEFT VENTRICULAR FAILURE

Blood coming into the IV cannot be pumped forward

§  Blood backs up into the lungs

§  Pulmonary pressures increase

§  Fluid forced from capillaries into alveoli

§  Gas exchange impaired

o   Weakness, fatigue

o   Dyspnea on exertion (DOE)

o   Orthopnea or paroxysmal nocturnal dyspnea (PND)

o   Irregularity of the pulse, S3 and or S4 heart sounds

o   Alteration in B/P

o   Moist Crackles (Rales)

o   Hacking cough, Frothy- pink sputum

o   Oliguria in the day, nocturia at night

Restlessness, confusion, anxiety, irritability, impaired memory

Especially in elderly 

RIGHT SIDED HEART FAILURE:  ETIOLOGY

Left sided heart failure (most common)

Right ventricular infarct

Pulmonary Hypertension (Cor Pulmonale)

RIGHT SIDED HEART FAILURE

FORWARD EFFECTS

LV has inadequate volume to pump so O2 falls

§  S/S same as LV forward effects

RIGHT SIDED HEART FAILURE

BACKWARD EFFECTS

Right Ventricle is unable to empty blood so blood backs up into the venous system

Venous Pressure Increases

Fluid moves from the capillaries into the cells and interstitium (into the tissues and organs)

RIGHT SIDED HEART FAILURE

CLINICAL MANIFESTATIONS 

Weight Gain

Edema (pitting or dependent)

May disappear or decrease at night- is redistributed to sacral area.

Hepatomegaly and Spleenomegaly

Abdominal Pain

Ascieties

Distended Jugular veins (JVD)

Dyspnea caused by enlarged abdominal organs

Nausea, anorexia, flatulence

RIGHT SIDED HEART FAILURE

DIAGNOSTIC TESTS AND FINDINGS

Ø X-ray shows Right Ventricular enlargement

Ø Lung Scan and Pulmonary Arteriography can confirm Cor Pulmonale

Ø Liver Enzymes elevated if liver impaired

Ø Elevated B-natriuretic peptide

Pericarditis

Is the inflammation (or infiltration) of the pericardium associated with a wide variety of causes

Idiopathic- post viral

Infectious- viral, bacterial fungal

Acute MITrauma

After Mediastinal radiation

Neoplasm

Rheumatic fever

Inflammation ®  > pericardial permeability ® fluid leaks into space between pericardial membranes ® pericardial effusion

Pericarditis CLINICAL MANIFESTATIONS

Chest pain

Fever & malaise 

Dyspnea

Pericardial friction rub

most common presenting symptom

§  Need to differentiate from MI, PE

§  Can radiate

§  Usu. sharp, substernal & persistent

§  Worse with inspiration, movement, & coughing

§  Better with high fowlers & leaning forward  

DIAGNOSTIC TESTS

        EKG – changes

­ Sed rate & ­ WBC r/t inflammation, increased leukocytes

Cardiac markers normal

Echocardiogram shows effusion

Chest x-ray - looks enlarged if effusion

Pericarditis-Medications for Tx

NSAIDs (indocin)

Steroids for severe (lupus)

Analgesics

Antipyretics

Antianxiety drugs

Antibiotics if r/t infection

Pericarditis- COMPLICATIONS

Pericardial effusion may cause cardiac tamponade

(compression of the heart that occurs when blood or fluid builds up in the space between the myocardium and the pericardium )

Pulsus paradoxus > 10 mmHg (hallmark sign)

¯ BP & ¯ pulse pressure

JVD, ­ CVP

Muffled heart sounds

Tachycardia

S/S ¯ O2

Chest pressure (heaviness) & pain

Dyspnea

Friction rub

Anxiety & restlessness

DEFINITIVE TREATMENT FOR PERICARDIAL EFFUSION 

PERICARDIAL WINDOW

PERICARDIOCENTESIS

To Differentiate between pericardial & pleural 

Friction rub.........

Have pt. Hold breath – will go away if pleural rub

INFECTIOUS ENDOCARDITIS

Definition

Infection of the endocardial layer of the heart

Most commonly involves valve leaflets, chordae tendonae, & papillary muscles  

May also invade the lining of the heart chambers & large vessels

Mitral valve is most common valve affected

RISK FACTORS for

INFECTIOUS ENDOCARDITIS

Rheumatic fever, Valve disease/damage, Prosthetic valve surgery, Heart surgery, Heart cath/pacemaker insertion, Previous endocarditis, Cardiomyopathy, Congenital heart disease, IV drug abuse, Dental work*** , IV therapy – esp. If IV sites not changed q72h, Central lines, GU/bowel procedures & Foleys, Endotracheal tubes R/T resp. Infection, Elderly R/T more procedures

COMPLICATIONS

  INFECTIOUS ENDOCARDITIS

Vegetations can break off and travel as emboli

§  R   ® lungs

§  L  ® head, spleen & arteries

INFECTIOUS ENDOCARDITIS

Insidious onset

Fever, headache, malaise, weakness, fatigue, anorexia, wt. Loss, night sweats, new or changed murmur

INFECTIOUS ENDOCARDITIS

Acute onset

¯BP, ­ HR, T > 103°F, shaking chills, new or changed murmur

ENDOCARDITIS

CLINICAL MANIFESTATIONS

Splinter hemorrhages-Fingernails, toenails, Longitudinal dark line usu. On distal 1/3 of nail

Petechiae: in mouth, on chest-Conjunctiva, mucous membranes, wrists, ankles, neck, shoulders, clavicles,Flat red lesions usu. In groups, Fade in a few days

Splenomegaly – usu. After 6 weeks

Elderly – atypical presentation-Confusion, renal failure, neuro changes, pulmonary edema

Hypertension

Defined as a sustained BP >140/90 on 2 separate occasions

Diabetic Pt. >135/85 on 2 separate occasions

·        Normal <120 and <80

·        Prehypertension 120-139 and 80-89

·        Stage 1 140-159 and 90-99

·        Stage 2 >160 and >100

Essential Hypertension

without known cause- 95% of cases

(Theories: Hypernatremia, Hypokalemia, Increased renin, Increased aldosterone, Heightened stress = increased catecholamines)

Risk Factors for Essential HTN

Increasing age

Genetic tendency, gender (men>women)

Afro- American ethnicity

Obesity, inactivity, increased stress

Smoking, excessive alcohol use

Family History

Increase nacl and caffeine intake

Low k, ca, and mg intake

Hyperlipemia

5% . Caused by some other disease or drugs

Any disease/Drug which causes fluid volume excess or vasoconstriction

Kidney disease, pheochromocytoma, cushings disease, brain tumors, pregnancy,

Oral contraceptives, cocaine and other stimulants, caffeine

Assessment Findings

Can be a “silent killer”- person can be asymptomatic for years

H/A, dizziness, fatigue, insomnia, nosebleeds, blurred vision

Dyspnea or angina, Bounding Pulses, Flushed face, Peripheral edema, Nocturia, S/S of Target Organ Damage

Crisis= BP > 240/120

Drug management of HTN

Diuretics such as lasix or hydrochlorthiazide (HCTZ)- Monitor serum K+, supplement as needed

Beta-blockers such as inderal or Lopressor- Watch blood sugars in diabetics, Warn not to abruptly d/c, Report fluid retention, dyspnea, cough, rash, Monitor pulse for bradycardia & BP for hypotension (lying or standing)

Add As Needed

Alpha-adrenergic blockers ex. Minipres- May cause drowsiness

Alpha-beta blockers ex. Normodyne- Can cause dizziness, dyspnea, cough,impotence or decreased libido

ACE inhibitors ex. Captopril- Give 1 hr. Before or 2 hrs. After meals

Can cause tachycardia, rash, cough, dyspnea, gastric upset

Angiotension II- Receptor antagonists (Cozaar)-  Ex. Watch serum K+ levels, Can cause hypersensity reactions in certain people

Calcium Channel blockers ex. Procardia- Withhold if hypotensive; check pulse too, Monitor for CHF, fluid overload

Nursing Management for HTN

baseline cardiac assessment

§  Peripheral pulses

§  Carotid & ABD Bruit

Monitor weight and I&O

Stressors and Risk Factors

Stress need for compliance and long term consequences

Report adverse drug side effects

50% pt. Quit meds in 1 yr, encourage them to see doc again instead of stopping

Dietary instructions for HTN

Low sodium, lower calories, proper carbs, reduce cholesterol/ fats

Avoid alcohol, caffeine, tobacco

Peripheral Vascular Disease
(PVD)

Occlusive disorders of the peripheral blood vessels causing decreased blood supply through peripheral vessels to tissues.

Ø May be Arterial or Venous

Ø May be R/t Inflammation or occlusion

Ø May be Acute or Chronic

Risk factors for (PVD)

Atherosclerosis (same as mi)

Recent mi with a-fib or ventricular aneurysm

Medical emergency – can be life threatening

Without successful treatment

§  Tissues die ®amputation

§  Massive amount muscle dies ® myoglobinemia ® renal failure 

Nursing assessment- in association with PAD

Severe pain distal to occlusion, Absent pulses distal to occlusion, Blackened areas on toes

Six p’s

§  Pain – severe even at rest

§  Pallor r/t no blood flow

§  Poikelothermia (coolness)

§   Pulseless

§  Parasthesias

§  Paralysis

Management

- associated with PAD

Heparin Gtt,

Arteriography- identifies the point of obstruction

Embolectomy, Thrombolytics , Platelet inhibitors (aggrastat)

Surgery: Endarterectomy, Bypass graft, Ay graft, Axillofemoral (ax-fem), Femoral popliteal (fem-pop)

What to do if you find Decreased or absent pulses

Compare bilaterally

Move up leg until pulse found

Use doppler

Segmental systolic BP readings of thigh, calf, & ankle

R/T PAD

§  Normal

§  Thigh & calf > arms

§  Ankle ³ arms

§  Pad

§  Arms > thigh & calf

PAD  Interventions

Nonsurgical

Exercise-Walking

Increases collateral circulation

Positioning – controversial

Elevate to decrease edema but not above heart

Hang down when sleeping or sleep in chair

Never cross legs

Promote vasodilatation- Warm environment, Socks, No cold exposure, Stress reduction, No tobacco, No constrictive clothing

people at risk = stasis of bloodflow, injury to vessel wall, ­ blood coagulability

Risk for clots!!!!!

Thrombophlebitis (deep vein thrombosis – DVT)

Inflammation of a deep vein with clot formation

Can affect superficial or deep veins

Deep vein most concerning R/T can cause PE

Complications of DVT

Pulmonary embolus (PE), Chronic venous insufficiency

Chronic venous insufficiency

Clot occludes vein ® venous stasis/congestion ® ­venous  pressure ® ­vessel permeability ® edema & stretching of vein ® vessel wall & valves damaged ®inflammation ® more clot &  ¯waste removal ® chemical injury to vessel wall ® clot & inflammation

Clinical manifestations of DVT

May be none

Calf or groin tenderness/pain affected leg

Positive homan’s sign in < 30%

Sudden onset unilateral- Heat, redness, edema, Usu. Along vein but can be whole leg if severe, Cording along vein

Fever, malaise, fatigue, anorexia 

Clinical exam if S/S definitive

Doppler flow studies

Impedence plethysmography (IPG)

Venography

PT/PTT/INR to monitor anticoagulants

CBC (HCT, WBC) 

Interventions for DVT

Assess pulses, pain, color, temp & cap refill Q 4 hrs.

Arterial: keep extremities in a dependent position and warm

Venous: elevate extremities

Avoid leg crossing, change positions often,avoid prolonged standing

Provide good foot care; use a foot cradle; keep feet flat on floor when sitting

Pain control

Monitor skin condition

§  Treat skin lesions as appropriate

§  Monitor for infections

THROMBOANGIITAS OBLITERANS (BUERGAR’S DISEASE)

Is an inflammatory disease affecting the small arteries and veins (usually legs)

 Affected arteries prone to spasms- lead to constriction and occlude blood flow.

 Emboli can also be present and obstruct blood flow.

Cause- Unknown, Found Men > Women; Age: < 50

Biggest Risk Factor- Heavy Smokers !!!, or use tobacco in any form

Clinical Manifestations of BUERGAR’S DISEASE

Intermittent claudication, Cyanosis and redness of the affected extremity, Skin is ruborous (mottled purplish-red) color, shiny, sparse hair growth. Shallow, dry leg ulcers. Black gangrenous areas on toes and heels.

Pulses- Present when resting, Absent or diminished with exercise

Prolonged CRT

May also have s/s of thrombophlebitis

Diagnostic Exams for

Doppler Ultrasound

Angiogram of legs

Impedence Plethysmography

Raynaud’s

Digital arteries respond excessively to vasospastic stimuli.

§  Disease of young women (15-45)

§  Becomes progressively worse

§  Triggers:exposure to cold; emotional (stress)

§  Usually found in hands

          “white- blue red” changes

§  Idiopathic

§  Secondary to connective tissue disease:  scleraderma, systemic lupus, rheumatoid arthritis

Raynaud’s Theory

Anatomy of vessels is normal.  Vasospasms may be caused by impaired release of prostaglandins.

Raynaud’s

Clinical manifestations

Attacks intermittent and vary in frequency- common after exposure to cold.

Pain, numbness and tingling

Poor fine motor responses

Color changes:

Early stages- hands normal between attacks

Disease may improve spontaneously

If disease progresses- hands can remain cyanotic between attacks

Ulcers and gangrene may develop at fingertips- poor healing

No specific diagnostic studies

May perform tests to confirm connective tissue disorder

Raynaud’s

Management-medical/surgical

Avoid factors that precipitate attacks.

Vasodilators- Vasodilan, Nifedipine

Sympathectomy( poor results)

Amputation of gangrenous area

Acute Bronchitis

Patho

Inflammation of mucous membranes that line major bronchi & their branches

Acute Bronchitis

Clinical Manifestations

Fever, malaise

Cough – paroxysmal

–        Initially dry, nonproductive

–        Later mucopurulent

Wheezing

Crackles

Acute Bronchitis

         Complications

Laryngitis

Sinusitis

Bronchial asthma

Secondary bacterial infection

Acute Bronchitis

Antipyretics, antitussives, expectorants,

Antibiotics (if bacterial)

Pneumonia

Classification By Cause

Inflammatory process affecting   bronchioles & alveoli

Infection: Viral – most common -- Type A

                 Bacterial – less common – more serious

                 Fungi

Radiation (breast or lung CA)

Chemical (gas, kerosene)

Aspiration

Pneumonia

            Classification By Presentation

Typical organisms

Strep pneumoniae (pneumococcal)

Klebsiella pneumoniae

Pseudomonas aeruginosa

Staphylococcus aureus

Haemophilus influenzae (H-flu)

Pneumonia

     Classification By Location

Lobar – confined to ³ 1   lobe

Bronchopneumonia -- patchy, diffuse scattered throughout both lungs

Hypostatic- Prolonged hypoventilation in immobile client

Part of lung used -Accumulation of secretions

Pneumonia

     Classification By Where Acquired

Community-acquired pneumonia (CAP)

–        Illness contracted in a community setting or within 48 hrs. of admission

Hospital-acquired pneumonia (HAP)

–        Nosocomial

–        Contracted 48 hrs. after admission

Pneumonia in the immunosuppressed host

Pneumonia

Mechanism

Pathogens reach alveoli by

–        Inhaled droplets **

–        Aspiration from GI or upper airway **

–        Seeding from bloodstream

Pneumonia

Patho  Atypical

Exudate infiltrates interstitium rather than alveoli

Pneumonia more scattered

Pneumonia

Complications

Lung necrosis, Empyema, Pleurisy, Septicemia, Atelectasis,  Bronchitis, tracheitis, Heart failure, Endocarditis, pericarditis, Purulent arthritis, Otitis media, sinusitis

Pneumonia

Clinical Manifestations Bacterial

Sudden onset

Fever, chills, malaise

Increased pulse & resp.

Productive cough with rusty sputum

Chest wall muscle pain r/t coughing ® pain with breathing ® splinting ® hypoventilation

Pneumonia

     Clinical Manifestations Viral

Usu. no chills, Fever

Pulse & resp rate not as high Less severe but may last longer

Blood & sputum cultures neg for bacteria

Copious sputum 

Secondary bacterial pneumonia possible

Pneumonia

     Clinical Manifestations Bacterial & Viral

Wheezing

Crackles

Decreased breath sounds

Cyanosis of lips, oral mucosa, nailbeds

Pneumonia

Diagnostic Tests

Sputum C&S

Gram stain

CXR shows infiltrates & consolidation

WBC increased

Blood C&S may be positive

Cyranose 320

–        Electronic nose or “E-nose” 

Pneumonia

Medical Management

Prompt antibx. (before C&S results)

Bronchodilators

Analgesics

Antipyretics

Expectorants/cough suppressants

Hydration

O2

Rest

Chest PT

Ventilator & ICU if needed

Pneumonia

     Nursing care prevention

ID population at risk

–        Elderly, chronically ill, immunosuppressed

–        Teach

Pneumococcal vaccine for client. > 50 & high risk client

Smoking cessation

Tuberculosis

Etiology

Infection caused by mycobacterium tuberculosis

–        Gram positive, rod shaped, acid-fast, aerobic bacteria

–        Resistant strains have emerged

–        Can live in particles of dried sputum for months

Killed by direct sunlight, heat, UV light, pasteurization

Resistant to ordinary disinfectants

Tuberculosis

Patho

Spread by droplet nuclei produced by coughing, sneezing, spitting

Usu. don’t get sick from brief contact

Most healthy people don’t get sick

Tuberculosis

At Risk Population

People with poor health care

Malnourished people

Alcoholics  & IV drug users

Homeless

Elderly

Immunosuppressed (HIV, chemo, steroids)

Close contacts of TB client

Chronically ill (heart, lung, DM)

Immigrants from countries with TB

Institutionalized

Health care workers

Tuberculosis

  Stages of Infection

Infection

Bacilli inhaled into bronchioles or alveoli & implant there

Phagocytes engulf bacteria

Bacilli continue to multiply

Bacilli spread to lymph nodes, blood, & distant organs

Immune response limits multiplication & spreading

Tuberculosis

Stages of Infection

Immune system activation – within 2 weeks

–      Granuloma formation (Ghon tubercle)

–      Formation of cavity àlesion necrosis

Tuberculosis

Stages of Infection

Healing of primary lesion

Ghon complex forms as scar tissue forms around tubercle

Visible on CXR

Tuberculosis

Stages of Infection

        Latent period

Can persist for many years without s/s

Inadequate immune response can cause s/s (esp. in at risk client )

Tuberculosis

Secondary TB

Usu. reactivation of initial infection

Exacerbations & remissions: More lung tissue destroyed

Spread throughout lungs & to other organs

Tuberculosis

Clinical Manifestations

l   Early vary & are vague

l   Usu. no s/s until advanced disease

–        Fatigue

–        Anorexia, wt. loss

–        Slight, nonproductive cough

Tuberculosis

Clinical Manifestations

As TB progresses

Low grade fever esp. late afternoon

Night sweats

Cough with mucopurulent, blood tinged sputum

Tuberculosis

Clinical Manifestations Late

Marked weakness, wasting

Hemoptysis

Dyspnea

Chest pain r/t spread to pleura

Tuberculosis

Diagnostic Tests

Skin test (PPD) positive

QuantiFERON®-TB Gold test (QFT-G)

CXR, CT scan, MRI show scars & cavitations

Sputum & body fluid C&S and acid fast test positive

–        Sputum analysis (most effective test) – obtained by

–        1^st am sample x 3

–        Bronchoscopy

–        Gastric lavage

Tuberculosis

Retard growth & multiplication of bacilli so body can overcome

Combination rx. Is most effective

l  isoniazid (INH)

l  rifampin (RIF)

l  pyrazinamide (PZA)

l  ethambutol (EMB) or streptomycin (SM)

Tuberculosis

Prophylactic

INH x 6-12 months

Pyridoxine (vitamin B6) to decrease side effects

Pleuritis

Patho

Acute inflammation of pleurae

–        Pleurae thick & edematous

–        Exudate 

–        Pleurae rigid

–        Pleurae rub à sharp severe pain

Pleuritis 

         Complications

Pleural effusion

Atelectasis

Hypoxemia

Hypercapnea

Pleuritis 

Clinical Manifestations

Chest pain- Sharp, severe, increases with inspiration

Shallow resp. r/t pain ® atelectasis

Pleural friction rub- Pleural effusion r/t inflammation  decreased pain 

Dry cough, sob, easy fatigue

Usu. Hx. pneumonia or other lung infection- Inflammation spreads from lung to pleura

Maybe Hx. TB, lung CA, heart & renal disease, PE, systemic infection

Pleuritis 

Diagnostic Tests

CXR may show effusion

Sputum may or may not be positive

Thoracentesis – send specimen to lab

Pleuritis

Medical Management

Analgesics

Antipyretics

NSAIDs (esp. Indocin)

Pleuritis 

Nursing Care

Pleural Effusion

Collection of fluid between pleurae in pleural space

–        Usu. follows pneumonia, lung CA, TB, PE, CHF, pleuritis

–        Fluid (1-3L) compresses lungs, heart, & vessels

Pleural Effusion

              Clinical Manifestations

Fever

Pain

Dyspnea

Dullness to percussion 

Decreased or absent breath sounds 

? Friction rub if pleura still rubbing together

Pleural Effusion

   Medical management

ID & rx. cause

Antibx. if r/t infection

Analgesics

Cardiac meds if r/t CHF

Thoracentesis or chest tubes

Surgery if r/t CA

Pleural Effusion

Nursing Care

Assist with thoracentesis

Monitor chest tubes if inserted

Chronic Bronchitis

Inflammation of the bronchi chronic cough with excessive mucous

–        3 months/yr. X 2 consecutive yrs.

Chronic Bronchitis

Patho 

Inspired irritants ® mucociliary system  overwhelmed ®­ size & number mucus glands & goblet cells & damaged cilia ®­ mucus secretion, narrowed airway lumen & nonfunctional cilia ®bronchial walls inflamed & edematous ® further narrowing of airway & thickened smooth muscle ® bronchospasm ® obstruction ® air trapping ® V/Q mismatch & hypoventilation & hypoxemia

Chronic Bronchitis

Disease Course

Initially affects large airways then eventually affects all airways

Secretions are thick & tenacious ® booger balls ®­ air trapping (ball-valve effect)

Chronic Bronchitis

Clinical Manifestations Early

l   Cough with thick white mucus

–        Esp. in A.M./P.M.

l   Bronchospasm during coughing episodes

l   Freq. resp. infections in winter

Chronic Bronchitis

Clinical Manifestations

Disease Progression

Blue bloater- S/S R.        failure (cor pulmonale)

Orthopneic/tripod

Sputum becomes: Purulent yellow, Copious, Blood streaked after severe coughing

Cyanosis/clubbing/accessory muscles

­ PCO2 &  PO2  HA, confusion, photophobia

Course crackles/rhonchi/wheezing

DOE ® dyspnea with minimal activity, dyspnea at rest

Speaks in short choppy sentences

Depression r/t disability & social isolation

¯ Mobility r/t SOB

Chronic Bronchitis

Management Goals

Prevent irritation & infection of bronchial mucosa

Maintain resp. function

Remove secretions

Emphysema

Abnormal, permanent enlargement of the air spaces distal to the terminal bronchioles accompanied by destruction of alveolar walls  

Emphysema

Patho

Imbalance in proteolytic enzyme & protease ® alveoli ¯ elasticity  air trapped  over inflation  destruction of alveolar walls  one great big alveoli (blebs & bullae)

–        Have  surface area   gas exchange

–        Can rupture  pneumothorax

Capillary bed damage  fibrotic & scarred   gas exchange

Etiology

Onset

Emphysema

l   Insidious

–        S/S often attributed to aging until severe

–        Middle age if r/t smoking

–        Onset between 30-40 y/o if AAT

Emphysema

Clinical Manifestations

DOE – usu. 1^st s/s, Dyspnea at rest 

Chronic productive cough, Mucopurulent

Increased A-P diameter (barrel shaped chest) r/t hyper

inflation & air trapping

Chest rigid ® inspiratory difficult

Accessory muscle 

Breath sounds â /wheezes/crackles

Expiration: Prolonged/difficult/wheezing

Distended neck veins

Appearance – pink puffers: Drawn, anxious, pale, Short, jerky sentences

Tripod, orthopneic

Marked SOB/pursed lip breathing

Thin, cachectic

Emphysema

Clinical Manifestations

         Advanced disease

Memory loss

Impaired judgment

Drowsy, confused

Increased PCO2

Muffled  sounds

Emphysema

¯ overall lung function

­ ↑Total lung capacity & residual volume

¯ Vital capacity & forced exp. volume

Emphysema

ABG’s

¯ PO2

­ ↑PCO2

­ ↑HCO3

­ ↑pH (chronic) – ↓during acute exacerbation

Emphysema

Physical Exam

­↑ AP diameter

Like to sit leaning forward

Hypertrophy of accessory muscles of upper chest & neck

Possible cyanosis (esp. if cor    pulmonale)

¯ Breath sounds, crackles, wheezes

¯ Heart sounds, ↑Expiration time (> 4 sec.)

Emphysema

l   Meds

l   Low flow O2

l   CPT & PD

l   Change occupation if r/t chemical exposure

l   Surgery

Emphysema

Borg Category-ratio Scale

Ask client. “Using this scale from  0 - 10, how much SOB do you have right now?”

l   0    Nothing at all l   0.5 Very, very slight                            l   1    Very slight l   2    Slight l   3    Moderate              l   4    Somewhat severe l   5    Severe l   7    Very severe      l   10  Very, very severe (almost maximal)

Emphysema

Implementation

l   Teach to get flu & pneumonia shots!

l   Avoid crowds & sick people

l   Don’t turn up O2 without MD ok

l   No smoking or air pollution

l   Assist with smoking cessation

l   Push PO fluids to thin secretions

l   Humidifier/air filters at home

l   Help client ID & remove irritants

l   Refer for occupation retraining

l   Space activities to allow rest between

l   Positions for breathing

Emphysema

Implementation

             Nutrition

May be cachexic r/t : Anorexia, Not enough energy to eat 

Use high protein milkshake & nutritional supplements (ensure, boost)

Use ¯ CHO diet 

l  Extra calories can be from lipids

Emphysema

Breathing Exercises

   Teach

Pursed lip & diaphragmatic breathing

Client exhales through pursed lips while contracting abd muscles 

Practice by blowing out candle or blowing an object along a table top

Bend forward while exhaling

Emphysema

Dyspnea & Fear & Anxiety

l   Need relaxation technique 

l   Important to inform client & family of status & of improvements 

Emphysema

Continuity Of Care

Improve quality of life – home O2 ®­ activity tolerance ADL’s

If on oral steroids will need: Osteoporosis precautions

l  Wt. bearing exercises, fall precautions

PUD precautions

l  Give with food, H2 blocker, guaiac stools, call for melena or abd discomfort

Take advantage of social programs : Meals on wheels, senior clubs

Asthma Types

–        Allergic, Idiopathic, Mixed asthma 

Asthma

 Allergic

(extrinsic)

Response to allergens

Dust, pollen, spores, dander

Asthma

 Idiopathic

(intrinsic)

Associated with URI, emotional upset, exercise

Asthma

Mixed asthma 

Features of both

Most common

Asthma

Patho

Bronchospasms, bronchoconstriction, inflammation & edema ® airway obstruction

–        Thick mucus  plugged airway

–        Release of histamine & mast cell products

Alveoli unable to expel air  air trapping  hyperinflation

­ Resp. rate  PCO2

Wheezing (usu. exp.) 

Any age 

Asthma

Triggers

Common  irritants ® inflammation

–        Cold air, dry air, fine airborne particles (pollution, smoke, fumes, car exhaust), microorganisms, ASA

Common causes of bronchial constriction

–        Exercise, stress, URI, idiopathic

Asthma

Clinical Manifestations

Paroxysms of SOB, wheezing, thick tenacious sputum

Work of breathing

Feeling of suffocation

Sit forward with arms at shoulder ht. 

Fear & anxiety

Marked prolongation of expiration

Cough: Early – no sputum, Late – thick, stringy sputum

 ↑Resp. rate

Pale -- ? cyanosis 

Diaphoretic

Dyspnea, HA, anxiety, panic, tingling lips/fingers

Asthma

                 Diagnostic Findings

PFT’s

–        ¯ Forced expiratory volume & forced vital capacity

–      ↑  ­ Total lung capacity & functional residual volume

ABGs (during attack)

–        ¯PO2

–        ¯PCO2 (r/t  resp. rate) – early

–    ↑    ­PCO2 -- late

Asthma

Medical Management  Goal 

–        Rx. & Prevent attacks

–        ID cause of attacks

Asthma

Medical Management

Symptomatic during attack

Bronchodilators – SVN

Terbutaline SQ

Aminophyline IV gtt.

Asthma

Medications

Maintenance – MDI/PO

Steroids (prefer inhaler)

Mast cell inhibitors  :Cromyln inhaler

Leukotriene inhibitors:   Singulair, Accolate

Asthma

Client Teaching

Peak flow meter

Correct use of meds & MDI

Help ID & avoid triggers

Relaxation techniques

Breathing exercises

Sinusitits Cause

Bacterial spread from nose  : Strep, H. Influenzae

Blocked sinus drainage

l  Allergies

l  Deviated septum

Sinusitis

Clinical Manifestations

Headache

Fever

Pain : Over affected sinus, Worsens when head dependent, Pain & pressure around eyes

Malaise

Nasal congestion/discharge: Purulent or bloody

Sinusitis

                Medical

                        Management

Saline/antibx irrigation of affected sinus

Antibiotics (amoxicillin)

Analgesics/antipyretics

Decongestants (neo-synephrine) 

Sinusitis

           Surgical

       Management

Provide drainage & remove infected tissue

l  Endoscopic

l  Caldwell-Luc

l  Sphenoethmoidectomy

Epistaxis

Nasal bleeding r/t rupture of capillaries in the nasal mucous membranes

Anterior septum most common