ANATOMY AND PHYSIOLOGY OF REPIRATORY SYSTEM RESPIRATION REGULATION

OXYGENATION- dynamic interaction of gases to give adeq O2 for cellular survival. I. NEUROCHEMICAL CONTROL
MEDULLA OBLONGATA- resp center; initiate each breath by sending message to primary
I. UPPER AIRWAYS resp muscles over phrenic nerve
1. NOSE 2. PHARYNX (Nasopharynx, Oropharynx, Laryngopharynx)
PONS- w/2 resp centers working w/inspiration center to make normal breathing rate
3. LARYNX- connect upper & lower airways
 Apneustic center – prolongs inhalation
Fx: Warm, humidify, and filter inhaled air
 Pneumotaxic center – limit air volume inspired; produce abn inhalation.
Help make sound and send air to lower airways
-> Epiglottis – valve flap; covers opening to larynx during swallowing CHEMORECEPTORS- responds to changes in PH (↑PACO2 = ↑ RR)
 Central (Medulla)
 Peripheral (Carotid & Aortic bodies) – monitor blood levels of CO2, O2, pH

II. NEURAL CONTROL

DORSAL RESPIRATORY GROUP (INSPIRATORY CENTER) (DRG)
- @medulla; sends stimulatory signals to diaphragm thru phrenic nerve
VENTRAL RESPIRATORY GROUP
• VRG Expiratory Center (Apneustic)- stimulates expiratory muscles
• VRG Inspiratory Center (Pneumotaxic) – stimulates inspiratory muscles other than diaphragm
PERIPHERAL CHEMORECEPTORS
- carotid + aortic bodies send signals to DRG via glossopharyngeal nerve
- ↑CO2, ↓O2 (↑O2 = inhibit respiration)
STRETCH RECEPTORS
 Inflation reflex – ↑lung volume stimulates apneustic center thru vagus nerve
 Deflation reflex – ↓ “ “ “ pneumotaxic center thru vagus nerve
LUNG RECEPTORS
• Stretch R.= Hering-Breurer reflexes (baroreceptors in lung tissue detect stretching & send
impulses to medulla to depress inspiration center)
• Irritant R= Sighing & yawning
• Juxtacapillary/J receptors= Lung congestion

III. VOLUNTARY CONTROL

HYPOTHALAMUS – Modifies output from medulla (Anger = ↑RR; Fright = gasp)
CEREBRAL CORTEX –voluntarily change breathing rate/rhythm (Talking, singing)

H-B Reflex (LUNG VOLUMES)

• TIDAL VOLUME (TV)- air volume inhaled & exhaled w/each breath (500 ml)
• RESIDUAL VOLUME (RV)- After exhalation, 1200 ml of air remains in lungs
• INSPIRATION RESERVE VOLUME (IRV)- air # that can be inhaled forcibly over TV (3000
ml)
• EXPIRATORY “ “ (ERV)- air # that can be forcibly exhaled (1200 ml)

LUNG CAPACITY
II. LOWER AIRWAYS
1. TRACHEA • VITAL CAPACITY (TV+IRV+ERV = 4,600 ml)
- between larynx & primary bronchi; 10-13 cm (4.5 in) long; 2.5cm wide - Maximum air volume exhaled from point of maximum inspiration
- supported by 16-20 c-shaped cartilage rings • INSPIRATORY C. (TV+IRV = 3,500 ml)
- Carina (where trachea divides into 2 primary bronchi) - Maximum air volume inhaled after normal expiration
2. BRONCHI • FUNCTIONAL RESIDUAL C. (ERV+RV = 2,300 ml)
- RIGHT MAINSTEM BRONCHI (larger + straighter; divides to 3 lobar branch) - air volume remaining in lungs after normal expiration
- LEFT “ “ (smaller + curvier; divides to upper & lower “ “ ) • TOTAL LUNG C. (5,800 ml)
primary -> secondary (lobar) - > tertiary (segmental) - air volume in the lungs after maximum inspiration
3. LUNGS VENTILATION PERFUSION RATIO
- main resp organs; base (broad, rest on diaphragm) apex (narrow superior part @clavicle
• NORMAL RATIO = 1:1 VP ratio
- mediastinum (thorax midline)
• LOW VENTILATION-PERFUSION RATIO= Shunt (P exceeds V)
Membranes: Visceral (covers lungs) Parietal (covers thorax)
- blood will bypass alveoli w/o gas exchange (common in pneumonia, atelectasis)
Pleural Fluid (lubricate lungs + thorax for smooth motion during breathing
(5-15 ml) • HIGH VP RATIO= Dead Space (V exceeds P)
4. ALVEOLI- 300 mil arranged in clusters of 15-20 - alveoli don’t have adeq blood supply for gas exchange to occur (common in pulmonary embolism)
Alveolar cells: Type I= epithelial cells forming walls; for structure to alveoli squamous • SILENT UNIT
Type II= metabolically active; form surfactant (prevent alveolar collapse) - Absence of V & P /decrease in both V&P; common in pneumothorax.
Type III= macrophage; destroy foreign materials/bacteria

OXYHEMOGLOBIN DISSOCIATION CURVE

Three levels: NORMAL = PaO2 >70 mm HG RELATIVELY SAFE= PaO2 45-70 mm Hg
DANGEROUS= PaO2 < 40 mm Hg
• The normal (middle) curve (N) = 75% saturation occurs at PaO2 40 mm Hg
Resp Muscle: DIAPHRAGM + EXTERNAL INTERCOSTAL MUSCLE (primary) • curve shifts to right (R) = 75% sat occurs at higher PaO2 57mm Hg.
• curve shifts to left (L)= 75% saturation occurs at PaO2 25 mm Hg
GAS EXHANGE
1. VENTILATION- in & out of lungs (inspiration + expiration)
2. DIFFUSION- O2 & CO2 exchanged air-blood interface
3. RESPIRATION- external (bw alveoli & pulmonary capillaries)
internal (bw blood & systemic capillaries + tissue)
4. PERFUSION- Systemic Circulation (blood flow to oxygenate body) (heart + body)
Pulmonary Circulation (heart + lungs)

COMPLIANCE- expand d/t pulling action of pleural memb; aided by surfactant

ELASTICITY/RECOIL- return to original/resting volume
 • Peripheral– d/t ↓ blood flow to a certain area of body
- Vasoconstriction of nailbeds/earlobes from cold exposure
III. PHYSICAL ASSESSMENT (I, P, P, A)
ASSESSMENT OF RESPIRATORY STATUS 1. INSPECTION
I. COMPLETE HISTORY = External nose – lesions, asymmetry, or inflammation
A. Family history = Mucosa – for color, swelling, exudate, or bleeding
B. Past medical history Steps:
- Childhood/ infectious diseases - Respiratory immunization  Start w/nose (symmetry, swelling, others)
- Major illnesses/ hospitalizations - Medications - Allergies  Observe for dyspnea, use of accessory muscles during breathing
 Watch for chest wall symmetry, note any paradoxical chest wall movement
C. Psychosocial history
 Count RR for a full minute (longer if with abnormalities)
- Family relationship - Employment status
 Inspect the tongue, mouth, fingers and nail beds
D. Present health history
- Biographic data - Nutrition - Lifestyle (LOWER RESPIRATORY STRUCTURES)
- Chief complaint presenting problem (Dyspnea, Cough)  “WHAT’S UP” & “COLDSPAA” TRACHEA = (N) middle deviated by masses in neck/mediastinum.
(Abn) Displace d/t Pleural or pulmonary disorders (pneumothorax)
(WHAT’S UP?)
• Where is it? (Not applicable) THORAX= inspect: Color & turgor, loss of subcutaneous tissue, asymmetry
• How does it feel? Does breathing feel tight, gasping, suffocating? CHEST CONFIGURATION= (N) ratio of anteroposterior diameter : lateral diameter = 1:2
• Aggravating and alleviating factors? • Barrel chest – lung Overinflation  ↑thorax anteroposterior diameter
How much activity cause SOB? = EMPHYSEMA
Does anything else aggravate it? What do you do to lessen SOB?
• Timing? When did you first experience SOB?
Does it happen more at any particular time of the day or year?
• Severity? Rate SOB 0 to 10 (0=easy breathing, 10= worst SOB you can imagine)
• Useful other data? Do you have any other symptoms that occur along with SOB?
•Patient’s perception? What do you think is causing your shortness of breath?

2. Funnel Chest (Pectus Excavatum)

- depression in lower portion of sternum; Compress heart & great vessels
= RICKETS / MARFAN’S SYNDROME
SMOKING – single most important contributor to lung disease 3. Pigeon Chest (Pectus Carinatum)- sternum Displacement = ↑anteroposterior diameter
smoking history formula: Years of smoking x packs/day = PACK YEARS = RICKETS / MARFAN’S SYNDROME /SEVERE KYPHOSCOLIOSIS
(15 years of smoking x 2 packs/day = 30 packs years)
4. Kyphoscoliosis – scapula Elevation into S-shaped spine; limits lung expansion in thorax
= OSTEOPOROSIS
II. PRIMARY INDICATORS OF RESPIRATORY DISORDERS
1. DYSPNEA – difficult or labored breathing, SOB
Types: a. Exertional
b. Orthopnea
c. Paroxysmal nocturnal dyspnea

RESPIRATORY RATE/BREATHING/RESP PATTERN

- inspect rate, rhythm, depth
• EUPNEA – normal rate + rhythm • TACHYPNEA – increased respiratory rate
2. COUGH – d/t irritation of mucous membranes anywhere in the respiratory tract
Character: Dry – URTI Severe changing – carcinoma
Time: AM– bronchitis PM – asthma • BRADYPNEA – slow but regular respirations • APNEA – absent breathing (may be periodic)
3. SPUTUM PRODUCTION – lung reax to any constantly recurring irritant
- associated w/ nasal discharge
• HYPERVENTILATION – deeper respirations; normal rate
 Bacterial infection – thick yellow/rust-colored sputum
 Viral bronchitis – thin, mucoid sputum frequent
 Chronic bronchitis – a gradual ↑sputum
 Lung Tumor= Pink-tinged mucoid sputum
 Pulmonary edema – profuse, frothy, pink material • CHEYNE-STROKES –gradually become faster & deeper than normal, then slower;
 Lung abscess – foul-smelling sputum & bad breath - alternates w/periods of apnea

4. CHEST PAIN
• r/t pulmonary conditions = sharp, stabbing, intermittent/ dull, aching, persistent.
• may occur w/ pneumonia, pulmonary embolism w/lung infarction, pleurisy. • BIOT’S – faster & deeper resp than normal, w/abrupt pauses between; breaths have equal depth

5. WHEEZING- major finding in Bronchoconstriction/ airway narrowing.

6. CLUBBING OF THE FINGERS- sign of lung dse w/ chronic hypoxic conditions
• KUSSMAUL’S – faster & deeper respirations w/o pauses

2. PALPATION
7. HEMOPTYSIS- Expectoration of blood from resp tract = Palpate sinuses using thumbs
- Blood from lung is usually bright red, frothy, mixed w/sputum = Use palms to palpate chest crepitus, tenderness, alignment, bulging, retractions
d/t: Pulmonary infection, lung Carcinoma Palpate: tactile fremitus, crepitus Assess: chest wall symmetry & expansion
• Thoracic Palpation- tenderness, masses, lesions, crepitus
8. CYANOSIS - bluish coloring of skin (very late indicator of hypoxia)
- appears if unoxygenated Hbg = 5 g/dL • Respiratory Excursion (Tactile Fremitus)
- diaphragm movement during breathing
• Central– tongue & lips ↓ oxygen tension in blood.
- Place both hands posteriorly at level of T9/ T10. Slide hands medially to pinch a small
amount of skin between your thumbs. Observe for symmetry.
ABNORMAL / ADVENTITIOUS BREATH SOUNDS

3. THORACIC PERCUSSION
– tapping on anterior & posterior chest
- tip of other hand strikes quick taps over middle finger of 1 hand placed firmly against skin
Sound Where Characteristic Significance
I: loud L: long
RESONANCE Over lungs NORMAL lung tissue
P: Low Q: hollow
(N) children, very thin adults
HYPER- I: Very loud L: long (Abn)
Areas of ↑ air
RESONANCE P: low Q: Booming hyperinflated lungs, COPD,
asthma, pneumothorax

Over stomach (N) stomach (gastric bubbles)

I: Loud L: Moderate
TYMPANY (but not normal (Abn) excess air in chest,
P: High Q: Drum-like
chest sound) pneumothorax

Fluid-filled/solid tissue replace

Dense areas
I: Medium L: Moderate air-filled lung tissue
DULLNESS (liver, heart, FINE CRACKLES COARSE CRACKLES
P: Medium Q: Thud-like (pneumonia, tumor, pleural
diaphragm) Occur when stops inhaling Occurs when starts to inhale
effusion)
Solid areas Heard at lung bases Heard throughout lungs
FLATNESS/ I: Soft L: Short
(bone, muscle, Sound like: hair rubbed between fingers Sound like: bubbling or gurgling
STONY DULL P: High Q: Flat
sternum, thigh) Unaffected by coughing Usually clear/diminish after coughing

WHEEZES
• Sibilant rhonchi – High-pitched, squeaking sound
• Sonorous rhonchi – Low-pitched, musical snoring, moaning sound
 MORE ON BACK PART !!!
Vocal Resonance
EGOPHONY- distorted voice sound
 Say prolonged “e”
 Auscultated as “a” indicating consolidation
BRONCHOPHONY – more intense & clearer than normal
 Say “ninety-nine”
 Consolidation results in words are heard clearly
• Diaphragmatic Excursion
- thoracic diaphragm movement during breathing WHISPERED PECTORILOQUY
- vertical distance from baseline to highest point of inspiration (how far diaphragm move)  Whisper “1,2,3”
 (N) auscultated as muffled 1,2,3 = must be non-distinct
 (consolidation) = If words are distinct
4. THORACIC AUSCULTATION
- assess airflow thru bronchial tree to eval presence of fluid/ solid obstruction in lung structures.

NORMAL BREATH SOUND

TRACHEAL BRONCHIAL BRONCHOVESICULAR VESICULAR
INTENSITY Very loud Loud Moderate Soft
Low
Very high,
PITCH High Moderate
high-pitched
DESCRIPTIO Gentle rustling
Harsh Tubular Rustling, tubular
N
Extra- Over mainstem bronchi Most of
Manubrium in large peripheral lung
LOCATION thoracic (1st & 2nd intercostal
tracheal airway (lung bases)
trachea space of anterior chest
 DIAGNOSTIC TESTS Normal:
7.35 – 7.45 = pH
I. MANTOUX TEST 35 – 45 mmHg = PaCO2 (Partial Pressure of CO2 in arterial blood)
- read after 48-72 hrs 22-26 mEq/mL = HCO3 (Bicarbonate)
- Induration ≥10mm = (+); 5mm = (+) Immunocompromised/HIV 80 -100 mmHg = PaO2 (Partial Pressure of O2 dissolved in plasma)
II. CXR / RADIOGRAPH 95-100% = O2 Sat (Degree which Hgb is saturated w/O2)
Pre-procedure: - Remove all jewelry and other metal objects from the chest area. Prior: perform ALLEN’S TEST before drawing radial artery specimen
- Assess ability to inhale and hold his or her breath. -> assess collateral circ in hand; ensure circ if radial artery thrombosis occur
- Question women regarding possibility of pregnancy. 1. Obliterate radial & ulnar pulses simultaneously by pressing both blood vessels @wrist
Post-procedure: Help the client get dressed. 2. Ask to clench & unclench his first until blanching of skin occurs
3. Release pressure on ulnar artery (while still compressing radial artery).
III. BRONCHOSCOPY 4. Watch for return of skin color within 15 seconds
- direct visual exam of larynx, trachea, bronchi w/fiberoptic bronchoscope
Purpose: (Diagnostic)- examine tissue - location/extent of pathologic process Before ABG: Rest 30 min before collection to ensure accurate measurement of body oxygenation.
- collect specimen - diagnose bleeding sites Avoid suctioning before drawing ABG sample.
(Therapeutic) – remove foreign body - remove secretions DON’T turn off O2 unless ABG sample is ordered to be drawn w/breathing room air
- destroy & excise lesion After ABG: Place the specimen on ice.
Before: Permit, consent NPO 6-8 hours prior to procedure Note O2 & type of ventilation px is receiving on laboratory form.
VS Assess results of coagulation studies Pressure over site for >5- 10 min if w/anticoagulant therapy/bleeding disorder
IV) access as necessary; give sedatives as prescribed. Transport specimen to the laboratory within 15 mins.
After: - Monitor VS - Provide emesis basin Interpretation
- NPO for 2 hours post-procedure - Test gag reflex (WRITE THIS SHT)
- Offer ice ships or clear liquids
- complications (bronchospasm, bronchial perforation, hemorrhage, pneumothorax)

IV. LUNG SCAN

- after radioisotopes, take scan w/scintillation cam (measure blood perfusion thru lungs)
Before: Obtain informed consent - Assess allergies to dye, iodine, seafood.
Remove jewelry around chest area. - Establish an intravenous access.
During: instruct to remain still
After: monitor for radionuclide reaction
Instruct that radionuclide clears from body in 8 hrs

V. SPUTUM SPECIMEN (Culture & Sensitivity; AFB Gross Appearance)

Before: Obtain an early morning sterile specimen (15ml sputum)
rinse the mouth w/water before collection.
take several deep breaths & then cough deeply to obtain sputum. RESPIRATORY CARE MODALITIES
Always collect specimen as client begins antibiotic therapy.
O2 THERAPY
After: transport specimen to lab STAT - administer O2 at conc greater than env atmosphere; O2 (drug), FiO2 (doses = fraction of inspired O2)
Assist w/mouth care
Goal: - adeq O2 transport in blood while ↓breathing work & ↓myocardial stress
VI. VENTILLATION-PERFUSION LUNG SCAN Indication: Arterial hypoxemia, COPD, ARDS, Tissue & Cellular hypoxia
- PERFUSION scan evaluate bloodflow to lungs  NO SMOKING WHERE O2 IS USED
- VENTILATION scan determine pulmonary airway patency & detect ventilation abnormality
1. Radioactive agent injected into peripheral vein & obtain chest scan 2 types of O2 Delivery Sys
 detect/measure pulmonary vessel integrity relative to bloodflow & eval bloodflow abn 1. LOW FLOW SYS- contribute partially to inspired gas; breathes variable O2 percentage is delivered
like in pulmonary emboli)
• NASAL CANNULA- most common; deliver low-flow O2 thru 2 prongs inserted 1cm into nostril
2. Followed by ventilation scan: px takes deep breath of O2+radioactive gas which diffuses - 1-6L/min; 24-40% FiO2
around lungs  taken w/ventilation scan to detect ventilation abn)
Nsg care: breathe thru nose remove cannula & clean nares q8h
Use gauze pads behind ears to reduce irritation assess arterial PO2 freq
VII. PULMONARY FUNCTION TEST - bc nasal cannula is low-flow (TV supplies part of inspired gas), O2 conc varies depending on RR & TV
- measure lung fx (lung volume, ventilatory fx, breathing, diffusion, gas exchange)
- pre-op eval of pulmonary fx; eval response to bronchodilator rx, diagnose pulmonary dse O2 conc: 1L (24-25%) 3L (30-33%) 5L (36-41%)
• SPIROMETER- 2L (27-29%) 4L (33-37%) 6L (39-45%)
• PEAK EXPIRATORY FLOW METER -> flow rates >6L/min don’t significantly inc oxygenation bc anatomical reserve/dead space (oral &
• NITRIC OXIDE nasal cavity) is full
Task: px must be alert, cooperative, not sedated Interv: assess skin integrity (O2 tubing irritate skin)
Not smoked, no bronchodilators 6 hrs prior to test “ nasal mucosa (drying, mucosal irritation)
Remove cannula & clean nares q8h
VIII. PULMONARY ANGIOGRAPHY Check & change water level of humidifier as needed
- visualize pulmonary vasculature; invasive fluoroscopic procedure
- catheter inserted thru antecubital/femoral vein into pulmonary artery/its branches • FACE MASK
- inject iodine/radiopaque contrast  Simple- 6-12 L/min; 40-65% FiO2
Before: Obtain informed consent Assess allergies to iodine, seafood, radiopaque dyes. - covers nose & mouth; give additional area for O2 collection
NPO for 8 hours prior Monitor vital signs. O2 conc: 5 L/min (40%) 6 L/min (45-50%) 8 L/min (55-65%)
Establish IV access. Instruct to lie still during the procedure. Nsg care: breathe thru nose remove & clean mask every 2-3 hrs
May feel urge to cough, flushing, nausea, salty taste after dye injection Ensure mask fits securely over nose + mouth (poor fit = ↓FiO2 delivered)
After: Monitor Vital signs Avoid BP taking for 24 hrs in extremity w/ injection. skin care to area covered by mask (pressure & moisture under mask = skin breakdown)
insertion site for bleeding. Monitor for delayed reaction to the dye. monitor closely for aspiration (mask limits ability to clear mouth esp if vomiting)

IX. PULSE OXIMETRY  Partial Rebreather- 50-70% FiO2; inflatable bag stores 100% O2
- Noninvasive test; register O2 sat of hemoglobin (SaO2) - (inspiration) px inhale from mask & bag
96-100% = NORMAL <85% = COMPROMISED body tissue oxygenation - (expiration) bag refills w/O2 & expired gas exit thru holes on both sides, some enters bag
<91% = IMMEDIATE RX <70% = LIFE-THREATENING Nsg care: reservoir must remain INFLATED during inspiration & expiration
Reservoir must NOT twist, kink, deflate (deflation= d/t ↓O2 delivered & rebreathe exhaled air)
X. THORACENTESIS
- aspirate fluid/air from pleural space
 Nonrebreather- 80-100% FiO2; inflatable bag stores 100% O2
Before: Permit, consent Initial Vital Signs - 1-way valve on 1/both exhalation ports bw bag & mask so exhaled air don’t reenter bag
Upright Leaning on overbed table/straddling back of a chair
Nsg care: reservoir must NOT COMPLETELY COLLAPSE on inspiration
Instruct Patient to remain still & AVOID COUGHING
Valve & flaps must be intact & functional on each breath
May feel pressure during needle insertion
After: place on unaffected side CBR
Check VS until stable check for hemoptysis

XI. ARTERIAL BLOOD GAS (ABG)

- measure dissolved O2 & CO2 in arterial blood to indicate acid-base state & how well O2 is
carried to body
- taken from RADIAL (common), BRACHIAL, FEMORAL artery
- use 10ml pre-heparinized syringe w/ICE (prevent hemolysis)

2. HIGH FLOW SYS- receive entire inspired gas from apparatus
- flow rate exceed air volume required for px minute ventilation
• Venturi Mask- common; 24-50% O2 conc
Nsg care: give supplemental O2 by cannula during meals & other activities where mask interferes
Remove & clean mask every 2-3 hrs
(A) air flow diagram w/partial rebreathing mask
(B) “ “ w/nonrebreathing mask
Interv
- keep air entrapment port for adapter OPEN & UNCOVERED for adeq O2 delivery
- mask fit snugly & tubing is not kinked (kink/poor fit = alters FiO2)
CHEST TUBE / CHEST THORACOSTOMY TUBE
- tube in pleural space; proximal end attached to tubing connected to water-sealed container
Principles
Water Seal Drainage- 1-way valve so air & water escape pleural space into container &
prevent atmospheric air from entering pleural space
- 1/2/3 bottle system, commercial disposable device (Pleur Evac)
-> drainage results from GRAVITY & SUCTION
• 1 BOTTLE SYS- operate by gravity; bottle as collection chamber + water seal
- 2 hollow tubes inserted into bottle stopper, drainage tube collected to glass - STOP if cyanosis + exhaustion occur
rod submerged 2cm below water level (2nd glass rod allow air to escape)
• 2 BOTTLE SYS
- 1st bottle= collection; 2 short tubes (1 attached to drainage tube from px,
2 attached to 2 nd bottle’s underwater tube)
- 2nd bottle (water seal)
- air vent of water seal bottle must be open to atmospheric air
- if using suction: 2nd bottle as suction chamber
• 3 BOTTLE SYS
- drainage + water seal + suction control bottle; 3rd bottle controls pressure
- suction control bottle”: 3 tubes = 2 short, 1 long (suction control tube)
- suction control depth controls pressure # in system (determined by doctor)
• COMMERCIAL WATER SEAL UNITS (PLEUR-evac)
- lightweight, disposable, functions like 3-bottle sys; used w/w/o suction
Nsg care (w/o suction)
- check entire sys for air tightness, kinks in tubing
- note fluid level oscillation in water seal tube (fluctuation every breathing = NORMAL)
(if it stops then system is intact = NOTIFY DOC!!!)
- check drainage amount + color
- ALWAYS keep drainage sys lower than tube level falls out (must be BELOW px chest so
gravity drains fluids)
- keep Vaseline gauze at bedside all times if chest tube dislodges
- do COUGHING & DEEP BREATHING EXERCISE (remove air & drainage from pleural cavity)
Nsg care (w/suction)
- ALWAYS PRESENT!!!: CONTINUOUS bubbling = SUCTION CHAMBER
INTERMITTENT bubbling= WATER SEAL
- check air leak = w/constant bubbling in water seal (NOTIFY DOC!!!)
- NEVER CLAMP resp/chest tubes unless ordered (we can only clamp foley cath)
-> doc's order MUST BE WRITTEN ON MED ORDER!!! not verbalized by doctor
-> even if doc said "clamp it now", DONT CLAMP unless it's ACTUALLY written on med
order
-> clamping w/air in pleural space = ↑pressure build-up & cause tension pneumothorax
Nsg interv
- monitor drainage in collection chamber
- check fluid level fluctuation in water seal chamber (continuous bubbling = air leak)
- gentle bubbling (not vigorous) must be noted in suction control chamber
- keep drainage sys BELOW CHEST LEVEL & tubes w/o kinks, dependent loops, obstruction
- ensure all connections are secure
- COUGHING + DEEP BREATHING; change pos freq (for drainage + ventilation)
- DON’T MILK tubes unless ordered
- DRAINAGE CRACK/BREAK = insert chest tube into bottle of sterile water
- CHEST TUBE PULLED OUT OF CHEST = pinch skin opening together, apply occlusive
sterile dressing, & call doc
STAT
- REMOVAL: take deep breath & hold it, remove tube, tape petroleum gauze dressing in place
CHEST PHYSIOTHERAPY (CPT)
- postural drainage, percussion, vibration; for lung expansion & eliminate resp secretions
• CHEST PERCUSSION- cup hands & lightly strike chest wall in rhythmically over lung
segment to
be drained
• VIBRATION- manual compression & tremor to chest wall during exhalation
- wrists & elbow remain stiff; vibrating motion produced by shoulder muscles
• POSTURAL DRAINAGE (SEGMENTED BRONCHIAL DRAINAGE)
- allow gravity to remove secretions from smaller bronchial airway to main bronchi &
trachea
CPT Procedure:
- do in morning 1 hr AC / 2-3 hrs PC - give prescribed bronchodilator 15 min prior
- pos for postural drainage acc to assessment - percuss area for 1-2 min
- vibrate same area while exhaling 4-5 deep breaths - monitor resp tolerance to
procedure
- maintain pos for 5-20 min after procedure
- repeat all necessary pos until no longer expectorate mucus
- dispose sputum properly; give mouth care after

MECHANICAL VENTILATION
- deliver gas into lungs by mechanical device
- 2 main indications: INADEQUATE VENTILATION & HYPOXEMIA
2 types:
NEGATIVE-PRESSURE= Pressure Cycle Ventilator Time CV Volume CV
POSITIVE-PRESSURE= Iron Lung Body Wrap Chest Cuirass
• Incentive Spirometry- way to encourage voluntary deep breathing using spirometer
-> volume type spirometer- its TV is set acc to manufacturer
-> flow spirometer- w/movable balls pushed up by force of breath
Indication: Thoracic & abd surg
chronic lung dse (mucus retention, shallow breathing, confined to CBR)
(promote alveoli expansion & prevent/treat atelectasis)
Instruction:
- higher the ball rises = deeper the breath - assess pn level, give analgesics as prescribed
- SEMI-FOWLER’S/UPRIGHT POS - show how to use diaphragmatic breathing
- encourage 10 breaths/hr w/spirometer during waking hours
Microprocessor V
- record how px effectively perform & breath # achieved w/spirometer

INHALERS
- deliver liquid meds thru fine mist/aerosol
3 types
• METERED-DOSE (MDI)
- pressurized w/aerosolized powder med; precise med # released w/each canister
activation
- spacer (holding chamber) can be used to enhance med deposition in lungs & help px
coordinate MDI activation w/inspiration
Steps: 1. Remove lid 5. Breathe out 9. Hold breath 10
secs
2. shake well 6. Place mouthpiece in mouth 10. Breathe out
@nose
Ventilation modes:
3. tilt head back 7. Push down inhaler 11. Rinse mouth
• CONTROLLED- for px who cant initiate resp effort; ventilator blocks effort if px attempts to breathe4. Attach inhaler to spacer 8. Breathe in slowly & deeply by mouth
• ASSIST-CONTROLLED- programmed to respond to resp effort if initiates a breath
- deliver preset TV when px initiate breath
- can cause hyperventilation & resp alkalosis if ↑RR
• SYNCHRONIZED INTERMITTENT MANDATORY VENTILATION (SIMV)
- allow px to breath spontaneously at their own TV
- used as weaning mode (RR ↓gradually, slowly resume spontaneous breathing)

Ventilator Controls & Setting • DRY POWDER- not pressurized; no need to push cannister to release dose
- trigger dose by breathing in at mouthpiece
• TV- air vol received w/each breath • Rate- ventilator breaths # delivered per min
• FiO2- O2 conc delivered; determined by condition & ABG • NEBULIZER- hand-held; dispense moisturizing agent as microscopic particles into lungs
• Sighs- air volumes 1.5-2x the set TV, delivered 6-10/hr (prevent atelectasis) - air-driven or O2-driven
• Peak Airway Inspiratory Pressure- pressure needed by ventilator to deliver set TV at given
compliance
-> continuous positive airway pressure (CPAP) TRACHEOSTOMY
nd rd
- apply (+) Airway pressure throughout entire resp cycle for SPONTANEOUSLY BREATHING- artificial opening into trachea (@2 /3 tracheal ring) to establish airway; permanent/temporary
- keep alveoli open in inspiration, avoid alveolar collapse (air is ALWAYS being delivered) Tracheotomy- surg incision into trachea Tracheostomy- stoma/opening d/t
- primarily as weaning modal\ity; for sleep apnea tracheotomy

-> positive end-expiratory pressure (PEEP) Purpose

- (+) pressure on MECH VENTILATION (air delivered only at specific time = at expiration) - provide/maintain airway
- for severe gas exchange disturbance (pneumothorax) - permit long-term use of mechanical ventilation
- improve oxygenation by enhancing gas exchange & prevent atelectasis - remove tracheobronchial secretions
- ↑PEEP # (>15) = ↑risk for barotrauma & tension pneumothorax - avoid aspiration of oral/gastric secretions in unconscious/
paralyzed px
indication: acute resp failure
upper airway obstruction
edema/soft tissue swelling d/t head/neck trauma
cervical vertebrae fx w/spinal cord injury

Pressure Support- apply (+) pressure on inspiration to ease breathing workload

- combined w/PEEP as weaning method
Interv
Nsg interv - assess resp distress s/sx - COUGHING + DEEP BREATHING
- assess px first then assess ventilator - VS, lung sounds, resp status, breathing pattern - maintain SEMI-FOWLER’S/ HIGH FOWLER’S - suction secretions as needed
- skin color (lips & nailbeds) - chest for bilateral expansion - assess stoma & secretion for blood/purulent drainage
- obtain pulse oximetry result - monitor ABG result - clean tracheostomy site & inner cannula (w/half-strength hydrogen peroxide)
- assess need for suctioning (observe secretion type, color, amount)
- “ water level in humidifier & humidification sys temp
- ensure alarms are set SUCTIONING
- alarm cause unknown = ventilate manually w/resuscitation bag until problem is corrected - sterile; remove resp secretions in tracheobronchial airway when px cant expectorate secretions
- if alarm sets off = use mouth guard so px will not bite ventilator tubing - maintains patent airway
- low pressure alarm = APNEA -> place on EMERGENCY UNIT (not ward!!!) Purpose: remove excess saliva, secretion relieve resp distress obtain sputum culture
- empty ventilator tubing when moisture collects Clear airway promote adeq gas exchange
- turn px atleast q2h / get out of bed as prescribed (prevent immobility complic) Interv
- have resuscitation equipment available at bedside - suction NOT APPLIED when catheter is inserted
- apply suction when pulling catheter (circular/rotating motion; max time 10-15 secs)
Cause of alarms
- oxygenate after suctioning
HIGH PRESSURE ALARM LOW PRESSURE ALARM

Complication: - Hypotension - Infx - hypotension - pneumothorax - stress ulcer

- ventilator dependence - SQ emphysema - muscular deconditioning

WEANING- from ventilator dependence to spontaneous breathing

- Rapid Shallow Breathing Index (Tobin Index) <100 = ideal for extubation
- RR/TV; VS, Mental status
• SIMV- ↓gradually until px is breathing on own w/o ventilator
• T-piece- replace ventilator; weaning progress as px tolerate longer periods off ventilator
 4 Stages
1. CONGESTION- vascular engorgemnet, intra-alveolar fluid, less neutrophils, many
bacteria
2. RED HEPATIZATION- vascular congestion persists, extravasation of red cells into
alveolar spaces, ↑neutrophils & fibrin
3. GRAY HEPATIZATION- Red cells disintegrate, persisting neutrophils & fibrin; alveoli still
consolidated, but grossly paler color
4. RESOLUTION- exudate is digested by enzymatic activity & cleared by
macrophages/cough
- Macrophages are dominant
RESPIRATORY DISTURBANCE
I. UPPER RESP TRACT Pathophysio
RHINITIS (VIRAL RHINITIS / COMMON COLD)
- self-limited; histamine release -> vasodilation & edema -> symptoms
Viral agent: CORYZA
(Highly contagious= rhinovirus, parainfluenza v, coronavirus respiratory syncytial v
(RSV), influenza virus, adenovirus.
s/sx: Nasal congestion, rhinorrhea, sneezing, sore throat, general malaise
pathophysiology: 1. On exposure to sensitizing agent
2. Inflammatory response by releasing histamine & leukotrienes
3. Vasodilation & ↑ permeability of nasal mucosa
4. Swelling & congestion of nasal mucuos membranes
5. ↑ production of mucus (CLEAR & thin discharge)
Med mgmt. (symptomatic Rx) Sputum: - Rusty, bloody-tinged (streptococcal/pneumococcal)
- Adequate rest, ↑OFI & Vit C - Expectorants as needed Pink (staphylococcal)
- Warm salt-water gargle for sore throat green w/ odor (pseudomonas aeruginosa)
- Antihistamines (relieve sneezing, rhinorrhea, nasal congestion)
Prevention: VACCINE (PCV)
- Topical (nasal) decongestant agents
- Zinc lozenges ↓ duration of cold symptoms if taken within 1 st 24hrs of onset Assessment
- fast rising fever (38.5-40.5 C / 101- 105 F) - Pleuritic chest pn worsened by deep breathing &
Nsg cough
- Proper Hand Hygiene - Cough etiquette (on sleeve, not on hands) - severely ill w/tachypnea (25- 45 cpm) - Rhonchi & wheezing; purulent sputum
- Rest - Limit exposure to others - poor appetite - diaphoretic and tires easily
LARYNGITIS - respiratory distress (SOB, use of accessory muscles in respiration)
- inflamed vocal cords  partial/total voice loss Dx: CXR, Sputum C&S
PHARYNGITIS Med mgmt.
- sore throat d/t viral/bacterial infx CXR= show infiltrate & sputum smear demonstrate acute inflammatory cells support dx
(+) blood culture in px w/pulmonary infiltrates= pneumonia d/t org isolated from blood cultures
SINUSITIS
h
transtracheal aspirate of tracheobronchial secretions/bronchoscopy with brushings
(obtain material for smear & culture)
TONSILITIS & ADENOIDITIS
Antimicrobial therapy= varies w/infecting agent; reevaluated early in treatment
Humidified O2 therapy = for hypoxemia Mechanical ventilation = for respiratory
failure
II. LOWER RESP TRACT
high-calorie diet & adequate fluid intake & bed rest
PNEUMONIA
- inflammatory process, involve terminal airways & alveoli caused by infectious agents analgesic = relieve pleuritic chest pain
Cause: Bacteria, viruses, fungi/parasites, chemical/physical injury to the lungs, Idiopathic ABG = for hypoxemia; measure oxygenation & acid-base status
Causative agents Pulse oximetry= continuously monitor O2 sat & response to therapy
Antitussive meds = for associated cough
Antihistamines = to dec sneezing; decongestants= treat symptoms, improve sleep

7 Classific
1. COMMUNITY ACQUIRED
- in community / <48 hrs after hospital admission/px institutionalization who dont meet
criteria for health care associated pneumonia (HCAP)
- d/t Strep pnemumoniae, H. influenza, Legionella, Pseudomonas aeruginosa, gram (-)
2. HEALTH CARE ASSOCIATED
- non-hospitalized px w/extensive health care contact w/1 or more of ff:
 Hospitalization for >2 days in an acute care facility within 90 days of infection
 Residence in a nursing home/long-term care facility
 Antibiotic therapy, chemotherapy, wound care within 30 days of current infection
 Hemodialysis treatment at a hospital or clinic
 Home infusion therapy/home wound care
 Family member with infection d/t multidrug-resistant bacteria
- d/t Pseudomonas aeruginosa, Enterobacter species, E.coli, Klebsiella species,
Proteus, Methicillin-sensitive/methicillin-resistant, Staph. aureus.
Nsg Interv
- O2 as prescribed - coughing, deep breathing, incentive spirometer
- Monitor: respiratory status - SEMI-FOWLER’S (breathing & lung expansion)
- fluids 3L/day (to thin secretions) - check labored resp, cyanosis, cold & clammy
skin
- Provide VPT - nasotracheal suctioning (if unable to clear secretions)
- change position frequently, ambulate (mobilize secretions)
- Monitor pulse oximetry; sputum color, consistency, amount
- high-calorie, high-protein diet w/small frequent meals; rest + activity, ↑activity gradually
- antibiotics, antipyretics, bronchodilators, cough suppresants, mucolytic agents, expectorants
- handwashing & secretion proper disposal
- (health ed) rest, proper nutrition, adequate fluid intake, meds, inhalants
- Avoid chilling & exposure to those w/respiratory infections or viruses
- NOTIFY if chills, fever, dyspnea, hemoptysis, ↑fatigue
- PCV as recommended
(IMPROVE GAS EXHANGE)- check cyanosis, dyspnea, hypoxia, confusion
- UPRIGHT POS (lung expansion & aeration); O2 therapy
(AIRWAY CLEARANCE) )- cough, suction as necessary; ↑fluid
- chest wall percussion & postural drainage (loosen & mobilize secretion)
- mobilize (secretion clearance)

3. HOSPITAL ACQUIRED TB
- >48 hours after hospital admission that didn’t appear to be incubating @admission time Mycobacterium tubercle- slender rod-shaped; outer waxy capsule (resistant to
4. VENTILATOR ASSOCIATED destruction)
- >48 hours after endotracheal tube intubation. - acid fast bacilli (grow slowly, sensitive to heat & UV light)
5. OPPORTUNISTIC Transmission: Airborne droplet; coughing , sneezing, talking
- in px w/ very poor immune systems: malnutrition, HIV/AIDS, transplant clients Risk: - close contact w/active TB - immunocompromised - substance abuse
receiving steroids, cancer - preexisting medical condition - malnourishment - crowded places.
- d/t Pneumocytis carinii, cytomegalovirus, fungi Types
6. ASPIRATION PRIMARY TB- previously unexposed & unsensitized persons; clinically & radiologically
- from endogenous/exogenous substances entry into lower airway. silent
- in px w/↓LOC/impaired cough or gag flex (occur w/alcohol ingestion, stroke, general SECONDARY TB- reinfect from inhaled droplet nuclei/reactivate previously healed primary lesion
anesthesia, seizures) Classific
7. HYPOSTATIC 0: No TB exposure, not infected 3: clinically active
- px who hypoventilate d/t bedrest, immobility, shallow respirations 1: TB exposure, no evidence of infection 4: not clinically active; healed
- Secretions pool in dependent areas of lungs -> inflammation & infection. 2: TB infection, no disease 5: TB suspected
Pathophysio

antigenic shift/reassortment
- cause novel & highly pathogenic strains of
Human influenza

s/sx (abrupt onset)

- Nonproductive cough - Fever >101F - Chills and sweats - Fatigue and malaise
- Headache - myalgia ) - Watery , nasal discharge - Sore throat
Dx: Viral culture of throat / nasal swab Prevention: YEARLY FLU VACCINE
Med Mgmt (for SYMPTOMATIC)
- Acetaminophen (fever, headache, myalgia) - rest + fluids
S/sx - AVOID ASPIRIN (risk for Reye’s Syndrome in children)
- chronic, productive cough - night sweats - (Antiviral drugs) Amantadine (Symmetrel), Zanamivir (Relenza), Oseltamivir (Tamiflu)
- malaise, fatigue - hemoptysis (bacilli already ulcerated to lung tissue) (for high-risk px given within 48 hrs of exposure)
- low-grade fever (late afternoon) - wt loss - antibiotics (only if secondary bacterial infx)
Dx: Mantoux Test, PPD/Tuberculin Skin Test, CXR, Sputum Exam Nsg Mgmt
- hand hygiene - cough etiquette
Mgm: simultaneous 3 or more drugs (↑ therapeutic effect, ↓resistant bacteria devt)
6-12 mo treatment
Bedrest until symptoms; resp isolation until (-) sputum
Frequently outpatient basis SEVERE ACUTE RESPIRATORY SYNDROME (SARS)
- serious, life-threatening resp dse d/t SARS-CoV (SARS-associated coronavirus)
RIFAMPICIN= orange body fluids (urine), hepatotoxic
- BATS (natural reservoir)
ISONIAZID+ VIT B6= peripheral neuritis, “
PYRAZINAMIDE= hyperuricemia, “ Incubation: 2-7 days after SARS exposure (max 10 days)
ETHAMBUTOL= optic neuritis Transmission: DROPLET, contact
STREPTOMYCIN= nephrotoxic, CN 8 damage Risk: direct contact w/infected, healthcare workers, travellers
S/sx
Nsg interv
- initially flu-like (fever, myalgia, GI sx, cough, sore throat)
- take drugs in correct amounts & on schedule - balanced diet, avoid excessive
- (common) fever >38C / 100.4 F; SOB (occur later)
fatigue
- cough etiquette, HW, discard secretion in plastic SARS is suspected in px w/
- use HEPA (high efficient particulate air) respirator mask for all people in close contact - any of symptoms + fever of >38 C / 100.4 F
w/patient if (+) sputum - history of: sexual/casual contact w/SARS diagnosis within last 10 days OR
Travel to any regions identified by WHO as w/recent local SARS transmission
Dx: CXR, ELISA, PCR
INFLUENZA/FLU Med Mgmt: - quarantine + isolation- antiviral meds - steroids - PPE - hydration + O2
- common contagious; affect nose, throat, bronchial tubes, lungs d/t INFLUENZA VIRUSES.
Transmission: cough & sneeze droplets from infected individuals, direct contact
Incubation: time of exposure to onset of symptoms = 1-3 days AVIAN FLU / BIRD FLU (H5N1)
Vial Surface Antigen: - naturally occur in WILD BIRDS
Haemagglutinin (H/HA)- responsible for virus pathogenicity; main determinant of immunityd/t: H5N1 (HPAI H5N1) virus (strain of influenza)
- allow virus adhesion to endothelial cells in resp tract (H7N9 is novel avian influenza virus 1st reported to infect humans in 2013)
Neuraminidase (N/NA)- determinant of disease severity Incubation: 2-8 days (max 17 days)
- lets release of newly-formed virus in host Transmission: BIRDS TO HUMANS (birds shed virus in saliva, nasal mucus, stool)
 both are targets of antiviral drugs + antibodies H5N1
 basis for naming influenza A virus subtypes: - HA codes for hemagglutinin (glycoprotein on virus surface; bind virus to infected cell .
th st
H5N1= H5 (5 of known types of hemagglutinin); N1 (1 of many known neuraminidase) - NA codes for neuraminidase (antigenic glycosylated enzyme on viral surface; aids release of
progeny viruses from
infected cells)
- HA & NA RNA strands specify protein structure that are most medically relevant as targets for
antiviral drugs & antibodies & basis for naming virus subtypes
Med mgmt.
- acetaminophen (pn + fever) - O2 therapy - antiviral meds
- cough remedy + decongestant - hydration, rest
Precaution: hand hygiene, PPE

SWINE FLU (H1N1)

- 1st caused illness in Mexico & US (March & April 2009)
- d/t novel virus created from reassortment of 4 viruses in pigs + humans + birds
Transmission: SNEEZE/COUGH DROPLETS; DIRECT CONTACT W/SECRETIONS
(infected person can spread if they’re symptomatic & up to 7 days after onset)
S/sx
- similar to regular flu (Fever, headache, myalgia, sore throat, cough, runny nose, N/V, diarrhea)
- thermal imaging (detect high body temp)
Mgmt
- isolation+ quarantine - hydration, rest
- antiviral med - hand hygiene, cough etiquette, PPE
 S/sx
- progressive dyspnea - progressive cough & ↑sputum production
- Anorexia, weight loss - respiratory acidosis
- barrel chest - pursed -lip breathing
- hyperresonant chest - ↓ tactile fremitus
- digital clubbing - bronchi collapse on expiration
- SOB, speaks in short jerky sentence
- use of accessory muscles when breathing
- leads to RIGHT SIDED HEART FAILURE
Dx: Pulmonary Fx Test, Radiologic Exam, ABG, Vetilation-Perfusion Lung Scan
Serum Alpha-trypsin Level
Mgmt
- stop smoking - anticholinergics - O2 therapy - breathing exercise
- bronchodilators - O2 therapy - antimicrobials - bleb resection
OBSTRUCTIVE LUNG DSE  CHRONIC BRONCHITIS (BLUE BLOATERS)
1. COPD- group of chronic lung dse w/persistent/recurrent airflow obstruction - airway scarring + excess mucus production  SMOKER’S COUGH (chronic cough)
- d/t CIGARETTE SMOKING

 PULMONARY EMPHYSEMA (PINK PUFFERS)

- abn permanent enlargement of gas exchange airway w/alveolar destruction
- loss of elastic recoil (major mechanism of airflow limitation)
• PANACINAR- dilation + destruction of entire acinus
• CENTRIACINAR- central part of acinus

Bullae- alveoli inflation at lung parenchyma

Bleb- near pleural membrane S/sx
- persistent cough 3 months/year in 2 consecutive years
- sputum production (mucoid; copious, thick tenacious)
- cyanotic/dusky skin color, bloated appearance (edematous)S
- hypercapnia, acidosis
- COR PULMONALE (Right sided heart failure)
Dx: Pulse oximetry, ABG, CXR
Mgmt
- bronchodilator - chest percussion - hi-cal, hi-CHON, low CHO
- postural drainage - hydration - small frequent easily swallowed feeding
 Mgmt
- prevent recurrent exacerbation & chronic symptom
- maintain near-normal pulmonary fx & activity level
2. BRONCHIECTASIS - optimal pharmacotherapy w/minimal/no adverse effects
- chronic irreversible bronchi/bronchiole dilation & destruction of cartilage containing airway
d/t: cystic fibrosis, chronic acquired immunodeficiency, lung infx, toxic gas
 CYLINDRICAL/TUBULAR- dilated airways alone
 VARICOSE- focal constrictive areas between dilated airways
. SACCULAR/CYSTIC- progressive airway dilation, forming grape-like clusters

s/sx Nsg care

- chronic cough - layering out-frothy, clear layer, dense particulate - stay calm & stay w/px during acute attacks
- purulent sputum - hemoptysis - finger clubbing - position on MOD-HIGH BACK REST (MHBR)/px preference
Dx: CT scan, bronchoscopy, PFT, ABG - relaxation technique, pursed lip breathing, deep breathing
Mgmt- postural drainage - bronchoscopy - chest physiotherapy - monitor for RESPIRATORY ARREST (can’t talk, absent breath sounds)
- stop smoking - antimicrobial - bronchodilator

3. BRONCHIAL ASTHMA RESTRICTIVE LUNG DISEASE

- widespread bronchial airway narrowing d/t allergen, exertion, emotion, air pollution
 EXTRINSIC/IgE MEDIATED/ALLERGIC- children; d/t external agents of specific allergen
 INTRINCI/ NON-ALLERGIC- d/t URTI, emotional stress, colds (nonspecific factors)
 STATUS ASTHMATICUS
- if bronchospasm isn’t reversed by ususal measures
- (danger signs) UNABLE TO TALK ABSENT BREATH SOUND
INEFFECTIVE COUGH despite being repetitive & hacking
- limit lung expansion & restrict chest wall movement
 cause ↓Lung volume, ↓Pulmonary Compliance/Recoil , ↑Breathing work
CHEST TRAUMA
- injury to chest wall/lung interfere w/respiration => hypoxemia, hypovolemia, cardiac failure
• NON-PENETRATING- structure dmg within chest cavity w/o disrupting chest wall integrity
• PENETRATING- w/wall disruption = altered intrathoracic pressure (stab wounds, gunshot)

FRACTURED RIBS
- most commonly @RIBS 4-8 (collision, vehicular accident, pressure on waist, CPR)
Assess: pain (inspiration), tenderness/bruising @injury site; splinting w/shallow rapid resp
Dx: CXR (area & degree of fx)
Med mgmt: narcotics (d/t severe pn) surgery (for emergency)
chest binder Titanium plates (stabilize broken ribs; can last 20 yrs)
Nsg:
- Semi/High Fowlers (expand lungs on inhalation)
- Complic (hypoxemia, hemorrhage, cyanosis; hemoptysis, hematemesis = lung penetration)
(hemothorax, pneumothorax)

FLAIL CHEST
- fracture several ribs + chest wall instability (underlying tissue move paradoxically = see saw motion)
- chest wall cant provide bony structure needed for adeq ventilation

Assessment
- paradoxical respi
- severe pn
- tachypnea, shallow breathing
- cyanosis, tachycardia, hypotension

s/sx
- cough w/w/o sputum - intercostal retraction
- SOB aggravated by exercise - wheezing
- breathing needs increased work
Med mgmt.
d/x: Pulmonary Fx Test, Peak Flow Measurement, CXR, Allergy Test (Skin/Serum), ABG
(SUPPORTIVE)- ventilatory - clear lung secretions - control pn
Peak Flow Meter- measure highest airflow during forced expiration
- for mod to severe asthma; measure severity & degree of asthma (SMALL CHEST SEGMENT)- coughing, deep breathing (clear airway thru positioning)
control - suction (lung expansion)
- intercostal nerve blocks, high thoracic epidural block, IV opioids (pain)
(MILD-MOD)-fluid replacement - closely monitor resp compromise
(SEVERE)- ET intubation & mech ventilation - surgery (internal/external fixture)
Nsg: open airway, suction secretions; monitor ventilation Turning, deep breathing, coughing
Signs of shock

PNEUMOTHORAX
- air/gas in pleural space d/t rupture in visceral/parietal pleura
d/t: rupture bleb (COPD) thoracentesis trauma secondary infx
• SPONTANEOUS- air enters thru breach of parietal/visceral pleura
 - d/t bleb rupture, TB, bronchogenic CA, emphysema - basilar (1 section) & segmental
 Primary- d/t air accumulation in pleural space
Dx: CXR, CT Scan, Bronchoscopy
 Secondary- d/t underlying chronic lung dse
Mgmt (to improve ventilation & remove secretions)
• TRAUMATIC- air enters pleural space thru chest wall opening/lung laceration - give surfactant, antimicrobials, bronchodilator - chest tube insert
- d/t fx/dislocated rib/stab wound, transthoracic needle aspiration, intubation/mech
- O2 admin - remove foreign body/tumor
ventilation, CPR complic
Prevention: ambulation + body positioning (lung expansion)
 Open- large wound in chest wall cause air to pass freely in & out thoracic cavity every inspiration Deep breathing, coughing, incentive spirometry, CPT
 Closed- d/t air leaking into pleural space from a hole within lung (e.g. pierced visceral pleura)
 Iatrogenic- d/t invasive proc/surgery
• TENSION- air drawn into pleural space d/t small hole in chest wall
- entering air in inhalation is trapped & cant be expelled in expiration
- 1-way valve mechanism

PULMONARY VASCULAR DISEASE

PULMONARY EMBOLISM
- embolus blocks pulmonary artery, disrupting bloodflow to lung lobules
- d/t DVT in lower extremities
Factors:
- venous stasis - oral contraceptive - prolonged bed rest - MI, CHF
- venous endothelial injury - pregnant/childbirth - surgery
- hypercoagulability state - hormone replacement - hip & femur fx
Assessment:
- chest/pleuritic pain (sudden onset) (sharp, stabbing, burning during respiration)
- dyspnea, tachypnea - Low-grade fever
- productive blood-streaked cough - massive shock
Dx: Pulmonary Angiography (embolism location + extent)
Lung Scan (adequacy of pulmonary circ)
Meds:
- anticoagulant/antiplatelet (heparin, warfarin) - thrombolytic (dissolve clot)
- DEXTRAN 70 (expand blood volum - narcotics (pleuritic pain)
- vasopressors (for shock)
Surgery: EMBOLECTOMY
Nsg
- cough, Deep breathing exercise, turning
- elevate bedhead
- O2, meds as ordered, hydration
- support + reassurance

HEMOTHORAX- blood in pleural cavity compress lungs -> blood loss -> shock

COR PULMONALE / RIGHT-SIDED HEART FAILURE

- enlarged R ventricle d/t high blood pressure in lungs from chronic lung dse
d/t: COPD (most frequent cause), Pulmonary Embolism, Pulmonary Vascular Dse
s/sx (d/t underlying lung disease (COPD)
(w/R ventricular failure): - edema of feet & legs - distended neck veins - hepatomegaly
Mgmt.: - ascites - heart murmur
- CHEST TUBE PLACEMENT (initial rx of choice = insert large bore needle in 2nd intercostal - Headache, confusion, somnolence d/t ↑ CO2 (hypercapnia)
space midclavicular line to relieve ↑SOB, wheezing, cough, fatigue
pressure) dx: Radiologic exam (enlarged pulmonary trunk + hilar vessels)
- O2 THERAPY - PN MGMT. (epidural catheter) - bed rest, monitor resp Echocardiography (enlarged R ventricle)
Cardiac Catheterization (pulmonary vascular pressures)
Nsg Mgmt
- respiratory status & breath sounds - chest physiotherapy (remove mucus) Med Mgmt
- slow pursed - lip breathing - Suction as needed; care of client w/chest tube - treat underlying lung dse - ABG
-- I.V. fluids & mucolytics (reduce sputum viscosity) - long term low-flow O2 - restrict Na intake if w/edema
- chest expansion & secretion clearance (incentive spirometer, nebulization, bedhead - pulmonary vasodilator (Nitroprusside, Hydralazine) - electrolyte level
elevated 30o , turn frequently) Nsg Mgmt
Nsg dx: impaired gas exchange, ineffective airway clearance - resp status, adeq ventilation - HIGH/SEMI-FOWLERS - assess breath sounds
- O2 admin` - monitor ABG - physical + emotional rest

ATELECTASIS
- lung collapse at any structural level
d/t: carcinoma / mechanical destruction (airway obstruction, lung tissue compression)
types
• PRIMARY- d/t ↓surfactant • SECONDARY- d/t airway obstruction & lung
compression
Classific
• NON-OBSTRUCTIVE- d/t external pressure (pneumothorax, pleural effusion, large mass)
• OBSTRUCTIVE / ABSORPTION- blocked airflow into alveolus cause air currently inside to
eventually diffuse out & cause alveolar collapse
- d/t mucous plugging; foreign object; anesthesia, pn, narcotics, immobility
• POST-OP
- by general anesthesia & surgery d/t diaphragmatic dysfunction & dec surfactant activity
 Automaticity= initiate electrical impulse
Conductivity= transmit electrical impulse from 1 cell to another
Excitability= respond to electrical stimuli

Cardiac Cycle

CARDIAC OUTPUT- blood # pumped by each ventricle per minute (HEART RATE X STROKE VOL)
HEART ANAPHY STROKE VOLUME- blood vol pumped by ventricle w/each contraction (60-70 cc)
Location: - Mediastinum Factors affecting stroke vol)
- apex = over diaphragm pointing to left Preload- degree of stretch of heart muscle at diastole end; blood # heart must pump w/ each beat
- base= just below 2nd rib; 2/3 of mass is to left of body midline, 1/3 to right Afterload- pressure ventricular myocardium must overcome to eject blood during contraction
“ heart must generate to move blood into the aorta
Contractility- force generated by ability of muscle cells to contract after receiving stimulus
STARLING’S LAW  greater myocardial cells are stretched = more forceful contraction

Coverings
FIBROUS PERICARDIUM- tough, loose-fitting, inextensible sac CV Regulation
SEROUS “ - parietal layer lies inside fibrous p. & epicardium (visceral layer) adheres
SNS- norepi & epinephrine by adrenal medulla= vasoconstriction ↑HR (cardio accelerating center)
to outside of heart (pericardial space w/pericardial fluid separates 2 layers)
PNS- acetylcholine = ↓cardiac contractility = ↓HR (cardio inhibiting center)
 protect against friction
Chemoreceptors- ↑CO2 & ↓O2 = ↑HR
Walls of Heart: EPIcardium- outer Baroreceptors- influences blood pressure changes
MYOcardium- thick, contractile middle; compress cavities & blood within
them; w/great force Assessment
ENDOcardium- delicate inner layer of endothelial tissue - LOC, palpitation, fatigue, paresthesia, paralysis, dyspnea
1. INSPECTION= distended neck vein, central/peripheral cyanosis, nail bed clubbing
2. PALPATION= Pulse (bounding, thready, irregular, pulsus alternans, thrill)
= Edema
3. PERCUSSION= abn cardiac borders
4. AUSCULTATION

Chambers: ATRIA- 2 superior RECEIVING; myocardial wall not very thick

VENTRICLE- 2 lower PUMPING; great force to pump far (L thicker than R)
 divided into 4 cavities by septum
Physiologic/Normal Splitting of S2  DURING INSPIRATION (d/t delayed pulmonary valve closure)
Valves: - S2 pulmonic + aortic components can be heard
(ATRIOVENTRICULAR) Tricuspid= 3 flaps; attached to papillary muscle by chordae tendineae - inspiration cause (-) pressure in thoracic cavity, pulling blood from periphery into R heart side
Bicuspid/Mitral= 2 flaps - d/t transient augmentation in venous return, R ventricular vol ↑ & emptying is delayed, delaying
(SEMILUNAR) Pulmonary= pulmonary artery entrance pulmonic valve closure
Aortic= aorta entrance - “SPLIT SECOND HEART SOUND” = best heard over pulmonic area

Circulation: Pulmonary= low pressure syst (MAP = 12 mmHg)

Systemic = high “ “ (MAP = 90-100 mmHg)

Blood Supply ALTERATIONS IN CARDIAC PERFORMANCE

Coronary Artery- myocardial cells receive blood from R & L coronary arteries
I. VALVULAR HEART DISEASE
STENOSIS (narrowing)
- valve leaflets thicken w/scar tissue -> can’t open fully -> impede blood
- Stenotic Valvular Defect (can’t empty itself thru narrow orifice -> dilate & hypertrophy)
REGURGITATION
- leaflet/valve scarring & retract -> blood backflow thru valve when it should be closed
- ↑work demands on chamber ejecting to maintain adeq output
Disorders

CONDUCTION SYS= electrical cells make & coordinate electrical impulse to myocardial cell
Properties: Rhythmicity= impulse transmission regularity
 MAJOR manifestation
JOINTS (Polyarthritis)- painful, migratory, in larger joints
CARDITIS- heart murmurs, cardiomegaly, congestive heart failure
NODES (Subcutaneous Nodule)- hard, painless; knees, wrist, elbows
ERYTHEMA MARGINATUM- map-like, macular lesions on trunk
SYDENHAM/CHOREA/ST.VITUS DANCE- CNS disorder, irregular, aimless, involuntary
MINOR manifestations
↑WBC ↑ESR & CRP Previous history of RF
Cause
↑Temp (Fever) Prolonged PR interval Arthralgia
- inflamm (Rheumatic endocarditis = common) - trauma
- congenital defect+ snow - ischemic heart dse Dx
Dx: Auscultation (murmur) Transesophageal Echocardiography (internal heart) - (+) throat culture - ASO titer (>250 todd = adults; >333 todd = children)
Cardiac Catheterization - ↑streptococcal antibody titer - ↑WBC, ESR, CRP
- 2D-ECHO - Jones Criteria
Assessment
- Murmurs - Fatigue, weakness - Dyspnea, cough, orthopnea, nocturnal dyspnea Mgmt
- Palpitations, chest pain, dizziness - Jugular vein distention - ↓demand from weakened heart (CBR, modify lifestyle post-discharge)
- Corrigan's pulse (forceful & suddenly collapses; px w/ aortic regurgitation) - prevent further cardiac dmg (Penicillin IM once a month x 3-5 yrs; steroids)
(d/t large stroke volume & rapid run off of blood back into L ventricle) - chorea safety prec; joint pn mgmt.

Pathophysio III. CORONARY ARTERY DSE (CAD)

- blood supply to heart muscles is completely/partially blocked => ischemia
- artery narrowing -> ↓myocardial perfusion -> ischemia + anaerobic metabolism
d/t: ↓blood supply (atherosclerosis, vasospasm, thrombus, embolus)
↑blood demand (hyperthyroidism, hyperthermia, stress)
↓blood O2 (anemia, carbon monoxide)
Nonmodifiable risk factors: age, male, race, genetics
Modifiable risk: hypertension, hyperlipidemia, DM, smoking
↑Homocysteine, stress, sedentary, obesity
Pathophysio: 1. Etiological factors 4. Thrombus formation
2. Lipid accumulation 5. Blood flow obstruction
3. Lumen narrowing & ↓bloodflow 6. CAD
Mgmt
- Prophylactic antibiotic therapy -Digitalis -Diuretics - Antidysrhythmics Mgmt
- Vasodilators - Anticoagulant - Low-Na diet (EARLY)- IV access + blood for markers - 12-lead ECG
Percutaneous Balloon Valvuloplast Aim: analgesia; antithrombotic, anti-anginal, reperfusion therapy
- balloon-tipped catheter inserted -> cracking of calcified commissure & valve orifice - anginal ischemia (pain) = IMMEDIATE ACTION! - stop all activities & sit/rest in SEMI-FOWLERS
enlargement - VS, resp distress
Valvuloplasty (Closed/Open Commissurotomy) – separate fused leafletys - give NITROGLYCERIN (sublingual); give O2 therapy if ↑RR
Annuloplasty- repair valve annulus (for valve regurgitation)
2 techniques: annuloplasty ring
Tack valve leaflets to atrium w/sutures to tighten annulus IV. ANGINA PECTORIS
d/t: exertion/physical stress, emotional stress, eating, temp extremes, sex activity
Chordoplasty- repair chordae tendineae
Valve Replacement
-> Mechanical Prosthetics- durable; thromboembolism, anticoagulant therapy
-> Tissue/Biologic Valve- xeno/homo/autograft; long-term anticoagulant not indicated

II. INFECTIOUS DISORDERS OF THE HEART

RHEUMATIC FEVER
- inflamm autoimmune dse in heart connective tissue, joint, sq tissue, CNS blood vessels
- Group A beta-hemolytic streptococcus (from frequent sore throat)
- Rheumatoid Heart Dse (complication)

S/sx: chest pn relieved by rest/nitroglycerin <20 min episode

Pn spreads to left arm, neck, back, throat, jaw (left arm pain = poss HEART ATTACK)
SOB, diaphoresis, light-headedness, N/V

Med mgmt.
(reduce O2 demand of myocardium; ↑O2 supply)
- O2 therapy
- NITROGLYCERIN, beta-adrenergic blocking agent,
calcium channel blocker, antiplatelet

V. MYOCARDIAL INFARCTION
Fibrinous pericarditis- rough appearance w/adhesions
Aschoff Bodies- tiny round nodules w/localized fibrin deposits w/necrosis in myocardium Classific • TRANSMURAL- endocardium to epicardium
• SUBENDOCARDIAL- myocardium & endocardium
• INTRAMURAL- patchy area of myocardium w/longstanding angina pectoris
Classific (ACUTE MI)
KILLIP CLASS I- no clinical signs of heart failure
“ II- w/rales/crackles in lungs, S3 sound, jugular vein distention
“ III- acute pulmonary edema
“ IV- cardiogenic shock/hypotension, peripheral vasoconstriction
s/sx (D-A-N-C-E-P-A-D-S)
Dyspnea Elevated Temp Shock
Anxiety Pain/Pallor
N/V Arrhythmia & Acute Pulmonary Edema
Chest Pain Diaphoresis
JONES Criteria 3 Areas of Damage after MI
- presence of 2 major signs - presence of 1 major + 2 minor - evidence of GABHS infx
Area of INFARCTION= O2 deprived, damage irreversible, cause “Q” wave (EKG)
Area of INJURY= tissue is viable next to infarct as long as w/adeq circulation
= ↑O2 can save this area from necrosis; S-T segment elevation (EKG)
“ “ ISCHEMIA= viability not dmged if MI don’t extend & collateral circ can compensate
= Depressed S-T segment (EKG)

Dx: ECG

4 Specific Classifications
I. INCREASED PULMONARY BLOODFLOW
- bloodflow from L heart (greater pressure) to R heart (less pressure) thru abn opening /
connection bw 2 systems/great arteries
1. ATRIAL SEPTAL DEFECT
- bw R & L atria (“priming pumps”); O2-poor & -rich blood mix in R atrium
s/sx:
- ASYMPTO (rarely symptomatic - freq resp tract infx - dyspnea on mild exertion
- (+)murmur (upper left sternal border) - tachypnea - feeding difficulty
- (long-term, @20 y/o)
Mgmt- cardiac catheterization - small ASD (close by themselves)
- Open heart surgery (2-4 y/o) - large ASD (device closure, sew a patch)
Cardiac Enzymes: AST- elevated = tissue necrosis (elevated 4-6 hrs after)
2. VENTRICULAR SEPTAL DEFECT
Lactic Dehydrogenase (LDH)- ↑ = tissue dmg
- bw R & L ventricles (“power pumps”) (cause L  R shunt)
Med mgmt. (I-N-F-A-R-C-T-I-O-N-S)
- O2-poor & -rich blood mix in R ventricle  pulmonary hypertension
IV access
Narcotic Analgesic (MORPHINE) s/sx: ↑resp effort (+) murmur (lower left sternal border) (1 y/o)
Fowlers-SEMI freq resp infection congestion
Aspirin/Anticoagulant (HEPARIN, WARFARIN) small VSD (asympto)
Rest/Relieve Anxiety (DIAZEPAM) large VSD (SOB, wt gain failure, sweating while feeding, freq resp infections)
Converting enzyme inhibitor (ACE Inhibitor = CAPTOPRIL) (hypertrophy/failure ventricle)
alcium Channel Blocker (NIFEDIPINE, VERAPAMIL) Mgmt: cardiac catheterization
IV Beta blocker (PROPRANOLOL, METOPROLOL, ATENOLOL) Open repair (VSD Transcatheter)- threads umbrella-shaped tube
O2
Nitrates (NITROGLYCERIN)
Stool Softeners
Surgery
Percutaneous Transluminal Coronary Angioplasty (PTCA)
- mechanical coronary vessel wall dilation by compressing atheromatous plaque
Intravascular Stenting
- for good luminal geometry after balloon deflation & withdrawal
- prevent restenosis after PTCA; risk for thrombus

Atherectomy
- remove atheroma/plaque from coronary artery
Transmyocardial Laser Revascularization
- special CO2 shoot pinholes/channel thru heart muscle to improve O2 flow
Coronary Artery Bypass Graft (CABG
- myocardial revascularization; (grafts used) Saphenous Vein, Internal Mammary Artery 3. ATRIOVENTRICULAR CANAL/SEPTAL DEFECT
- incomplete fusion of endocardial cushions (most common in DOWN SYNDROME)
Cardiac Rehab
- affect center of heart; ASD + VSD
- live full vital life; remain within limits of heart ability to respond to activity & stress
- common AV valve (bw upper & lower chambers) leaks back into upper chambers
Complication: (A-A-C-C-C-D-E) s/sx
Arrythmia Cardiogenic shock Dressler’s Syndrome - murmur - mild-mod CHF w/cyanosis increasing w/crying - ↓cardiac output
Aneurysm Cardiac Tamponade Embolism mgmt.
Pulmonary Artery Banding (for infants w/severe sx; palliative) (1st 2-3 months of life)
Health Teaching
- ↓ excess pulmonary bloodflow & protect pulm vasculature from hypertrophy
- don’t smoke - stress mgmt
- reduce weight, diet, exercise - resume sex after 4-6 wks

CONGENITAL HEART DEFECTS

- d/t failure of heart structure to progress beyond early stage of embryonic devt
(MATERNAL RUBELLA & FAMILIAL)

4. PATENT DUCTUS ARTERIOSUS

- fetal ductus arteriosus (connects aorta & pulmonary artery; must close shortly after birth-2 y/o)
don’t close within 1st weeks of life
- ↑pressure & bloodflow to pulmonary arteries; usually in premature infant
- risk: mothers exposed to rubella during pregnancy
- complication: heart/lung problems
s/sx:
- (+) murmur (machinery type @middle to upper left sternal border)
- CHF & ↓cardiac output - poor feeding • VENTRICULAR SEPTAL DEFECT
- dyspnea - asympto • OVERRIDING AORTA- (normal) aorta is attached to L ventricle which pumps o2-rich blood
- tiring easily - freq resp infx - aorta moved forward directly over hole in VSD
 o2-poor blood from R ventricle flow to aorta
mgmt.: • RIGHT VENTRICULAR HYPERTROPHY- d/t R ventricle work harder thru stenotic pulm valve
INDOMETHACIN (Indocin)- stimulate muscles in PDA to to constrict) s/sx:
LIGATION (closes tube) - cyanosis in 1st years of life (demands surgical repair)
PDA OCCLUSION (remove excess bloodflow to lungs from PDA - 1st presentation (poor feeding, fussy, tachypnea, agitation)
(catheter insertion - SQUATTING POS (coping; ↑bloodflow to lungs & sys vasc resistance, ↓R-L shunt d/t VSD)
- dyspnea in exertion; scoliosis (common) cyanosis & clubbing (variable)
- low birth wt; retarded growth; delayed devt & puberty
- R ventricular predominance on palpation; - retinal engorgement; hemoptyisis
- bulging left hemothorax
- single S2 (pulmonic valve closure not heard)
- LOUD MURMUR (@ L upper sternal border d/t pulmonary stenosis)
(@ L mid-sternal border d/t VSD)
- hypoxic “TET” SPELLS (cyanosis during crying & feeding d/t sudden blood O2 drop)
 potentially lethal, unpredictable epi in noncyanotic px w/TOF
 can be aborted w/simple procedures)
Dx: cardiac catheterization, 2D ECHO

II. OBSTRUCTION TO BLOODFLOW OUT OF HEART

- blood exerting a portion of heart meets stenotic area  blood flow obstruction
1. AORTIC STENOSIS
- aortic valve stricture  blood flow resistance in L ventricle, ↓cardiac output,
L VENTRICULAR HYPERTROPHY, pulmonary vascular congestion
- most common type; d/t malformed cusps
s/sx
- murmur (crescendo-decrescendo/”diamond-shaped”)
(@ R upper sternal border radiating to neck & carotid arteries )
- SOB, fainting, angina w/activity - rapid, fluttering heartbeat (palpitation)
Mgmt.
- KNEE-CHEST POS (calm effect, reduce systemic venous return)
- O2 therapy; hydration, prevent infx,
- DON’T allow to cry for long period of time; MORPHINE SULPHATE (↓sys venous return)
- Surgery: Blalock-Taussig (palliative)
Brock Procedure (corrective)- incise R ventricle & cut stenosed pulm valve/remove
obstructing tissue in outflow tract of R ventricle

Mgmt.:
Cardiac Catheterization- dilate narrowed valve
Aortic Valvotomy/Balloon Aortic Valvoplasty
- palliative; balloon catheter inside to open stenotic aortic valve
Valve Replacement

2. COARCTATION OF AORTA
- localized aorta narrowing; blood shunts to head & arms (impede bloodflow to lower body)
- vessels before coarctation has higher BP than those after; ↑BP above constriction
- ↑BP in L ventricle  heart pumps harder thru stricture  L VENTRICULAR HYPERTROPHY
s/sx
- ABSENT FEMORAL PULSE (pathognomonic sign)
2. TRICUSPID ATRESIA- absent tricuspid valve = no communic bw R atrium & R ventricle
- severe coarctation (1st few wks of life); less severe (undiscovered for years) - hypoplastic R ventricle + ASD/VSD  COMPLETE INTERCARDIAC MIXING
- BP (↑ upper extremities = headache, epistaxis, rapid & bounding pulse) s/sx:
(↓ lower “ = leg pn, cold feet muscle spasm; weak, delayed/absent pulse) - chronic hypoxemia, clubbing, SOB - poor feeding
- ↓bloodflow to abdomen & legs - ↑BP difference in arms & legs (20-40 mmHg)- murmur (@ upper L sternal border) - associated w/pulm stenosis & transposition of great arteries
- ↑ pulse pressure in carotid & radial pulse - warm upper body Pathophysio
Mgmt.: (depends on degree of narrowing) 1. No communic between RA & RV 5. Enter LV
Balloon Angiolasty- repair narrowed vessel 2. RV underdeveloped, systemic venous blood received by RA 6. Enter RV thru VSD
Resection- coarcted portion resection w/end-end aorta anastomosis (reconnect 2 ends) 3. Enter LA thru PFO/ASF 7. Blood enter pulmonary trunk
4. mixing of systemic + pulmonary blood
3. PULMONARY STENOSIS Mgmt.
- narrowed pulmonary valve doesn’t open completely  less blood to lungs Continuous PROSTAGLANDIN E1 INFUSION until surgery (maintain blood circ to lungs)
- ↑BP in R ventricle  heart pumps harder thru stenosis  R VENTRICULAR HYPERTROPHY  allow ductus arteriosus to remain open
s/sx:  for neonates whose pulmonary bloodflow on ductus arteriosus patency
- murmur (crescendo-decrescendo/”diamond-shaped”) ATRIAL SEPTOSTOMY- small hole bw R & L atria
(@L upper sternal border, radiate less to neck & carotid arteries ) FONTAN PROCEDURE- superior vena cava disconnected from heart & attached to pulmonary artery
- hypoxemia + cyanosis  all de-O2 blood from body goes to lungs w/o passing thru heart)
- RSHF sx (exertional dyspnea, hepatojugular reflux, hepatic congest, lower extremity edema)
Mgmt.:
Cardiac catheterization (dilate narrowed valve)
Closed Valvotomy (infants), Pulmonary Valvotomy w/Cardiopulmonary Bypass (children)

III. DECREASED PULMONARY BLOODFLOW

- pressure on R side increase, exceeding L side pressure  desaturated blood shunts right
to left  ↓pulmonary bloodflow
- ASD & VSD bw R & L sides are PRESENT

1. TETRALOGY OF FALLOT- cause cyanotic skin & mucous memb d/t lack O2
• PULMONARY STENOSIS
IV. MIXED BLOODFLOW (O2 & DE-O2 BLOOD MIXING)
- fully saturated systemic bloodflow mix w/BLABLABLA
Mgmt
1. HYPOPLASTIC LEFT HEART SYNDROME Surgery (early infancy)
- underdeveloped L heart  hypoplastic L ventricle, aortic atresia, mitral atresia, ASD - pulmonary vein anastomosed to L atrium, ASD is closed, anomalous pulmonary venous
- fatal in 1st months of life w/o interv connection is ligated
S/sx
- progressive deterioration w/cyanosis 4. TRUNCUS ARTERIOSUS
- ↓cardiac output - embryonic bulbar trunk coming out of heart fails to divide into pulmonary artery & aorta
- poor feeding; lethargy (sleepy/unresponsive)  SINGLE VESSEL (TRUNCUS) (sits over VSD)
- d/t single artery, there’s no specific path to lungs for O2 before going to heart to deliver O2
Mgmt (necessary) - blood from both ventricles mix w/common great artery  desaturation + hypoxemia
Transplantation (necessary for newborn)
s/sx:
(pre-op) Mech Ventilation
- murmur (@ mid-L sternal border) - mod-severe CHF
Continuous PROSTAGLANDIN E1 INFUSION
- cyanosis - poor growth, activity intolerance
mgmt.:
SURGERY- close hole between 2 ventricles (VSD) w/patch to separate sys + pulmonic blood
Rastelli Repair- pulmonary arteries disconnected from truncus
- conduit/tunnel placed from R ventricle to pulmonary arteries

2. COMPLETE TRANSPOSITION OF GREAT VESSELS SUMMARY

- switching of Pulmonary Artery & Aorta + ASD
- blood flow cycle:
O2-rich blood = L side heart- lungs – L side heart (w/o delivering O2 to body)
O2-poor blood = body – R atrium – R ventricle – body (w/o being oxygenated in lungs)
s/sx
- cyanosis - tachypnea - poor feeding - SOB
- peripheral hypoxemia - finger/toe clubbing - severe progressive pulm hypertension
- Complication (arrhythmia, heart failure) - no murmur
Mgmt
Intra-atrial Baffle (Mustard/Senning Procedure)
- tunnel/baffle bw atria (atrial switch) redirect O2-rich blood to R ventricle & aorta
- O2-poor blood to L ventricle & pulmonary artery
Arterial Switch- switched back to normal positions
Balloon Atrial Septostomy
- for O2-rich blood to reach rest of body by creating/enlarging ASD, allowing O2-rich & O2-
poor blood to mix

3. TOTAL ANOMALOUS PULMONARY VENOUS CONNECTION (TAPVC)

- failure of pulmonary veins to join L atrium
pathophysio
1. O2-rich blood from lungs in pulmonary veins mix w/ O2-poor blood from body
2. mixed blood return to R atrium thru ASD into L atrium
3. Enter into L ventricle, into aorta, then out to body
S/sx
- cyanosis - weak pulse - poor feeding - extreme sleepiness
- murmur not usually present
 N= 11-16 secs - time for clotting to occur after
(Int’l Normalized Ratio) thromboplastin & Ca are added to decalcified
• PT plasma
- for COUMADIN (WARFARIN) EFFICACY
N = 60-70 secs - time for clotting to occur after partial thromboplastin
reagent is added to plasma
• PTT - for COAGULATION DISORDERS
- for HEPARIN EFFICACY
• Activated PTT N = 30-45 secs - most specific test for HEPARIN EFFICACY

3. BUN- ↓cadiac output  ↓renal perfusion & ↓GFR = ↑BUN

- 10-20 mg/dl
4. BLOOD LIPID / LIPID PROFILE- for RISK OF CAD DEVT
• Serum Cholesterol N= 150-250 mg/dl

• Triglycerides N = 40-150 mg/dl - fasting 10-12 hrs prior test

HDL= <130 mg/dl
• Lipoprotein LDL= 35-65 mg/dl (men)
= 35-85 mg/dl (female)

5. SERUM ELECTROLYTES TEST- ↑K, ↑Ca, ↓N= ↑CARDIAC CONTRACTILITY

(NORMAL) • Na = 135-145 • K+ = 3.5-5 mEq • Ca= 4.5-5.5

6. INFLAMMATION MARKERS- predict FUTURE CORONARY EVENTS in healthy person

• CRP- CHON synthesized by liver; not normally present in blood except w/TISSUE TRAUMA
CARDIAC DIAGNOSTIC TESTS • Homocysteine- AA from meat; linked to ATHEROSCLEROSIS
- associated w/genetics & diet low in folic acid, vit B6, vit B12
INVASIVE
1. CARDIAC CATHETERIZATION- insert catheter into heart & vessels aided by fluoroscopy • Brain (B-Type) Natriuretic Peptide (BNP)
- check structure & performance of chambers, valve, coronary circ - neurohormones, from ventricles in response to ↑preload; for identifying & treating CHF
R-sided- sterile radiopaque catheter into antecubital/femoral vein HEMODYNAMIC MONITORING
L-side- via brachial/femoral artery 1. CENTRAL VENOUS PRESSURE (CVP)
Interv: - pressure in VENA CAVA, R ATRIUM, VENOUS RETURN
(BEFORE) psychosocial support, obtain IC allergy to seafood/iodine - catheter threaded into large central vein (subclavian, int/ext jugular, median basilic, femoral)
NPO 6-8 hrs; baseline VS shave & clean insertion site w/antiseptic - catheter placement confirmed thru CXR
th
Wt & ht, void, mark distal pulse give sedatives/local anesthesia as ordered - O level of manometer, Phlebostatic axis = @ R midaxillary line, 4 ICS (R atrium in supine pos)
(DURING) Cardiac monitoring feel warm/flushing, pn as contrast is injected Values
Fluttering/palpitations as catheter enters heart chambers 3-8 mmHg (5-12 cm H2O) = NORMAL
↑Blood vol (fluid retention, PA stenosis, heart failure) = ↑CVP
(AFTER) strict bed rest 6-12 hrs (turn px side to side) VS, ECG, peripheral pulse
O ↓Blood vol (venodilation, hypovolemic shock, (-) breathing) =↓CVP
DON’T ELEVATE BED HEAD >15 report chest pn, hematoma @site
Extremities color, temp, tingling inc OFI
Measuring CVP
Extend extremity 4-6 hrs (keep leg straight to avoid arterial occlusion)
- 0 point on transducer = R atrium level
If antecubital vessel is used, immobilize arm w/armboard
- supine, bed head 45o
- must be relaxed; coughing/straining = false increase in readings
2. ANGIOGRAPHY
- complication: air embolism, infection
- IV contrast into heart during catheterization to detect coronary obstruction
- x-rays taken immediately (fluoroscopy) after injection to show pathway of contrast
- catheter inserted into arm/groin artery & threaded into heart Nsg interv: inspect site daily for infx
Strict asepsis (cleanse catheter insertion site & change sterile dressings daily)
Interv (SAME W/CATHETERIZATION)
Monitor BP (d/t contrast medium diuretic effect)
2. PULMONARY ARTERY PRESSURE (PAP)
3. TRANSESOPHAGEAL ECG- higher qual pic than regular ECG - ventricular fx, diagnose shock, eval med response
- throat anesthetized & esophageal scope is inserted - Swan Ganz Catheter (balloon-tipped flow-directed, 4-lumen) inserted via antecubital vein to R heart
side & floated into pulmonary artery
Interv: NPO 8 hrs prior check gag reflex b4 resuming oral fluid intake
1st lumen- ends in R atrium; measures CVP, fluid infusion, venous access for blood samples
2nd lumen - “ Pulmonary Artery; measures PA systolic pressure, diastolic pressure, mean pressure
3rd lumen-for inflation & deflation of balloon (1-1.5 cc)
LABORATORY TESTS 4th lumen-thermistor port, measure cardiac output
1. CARDIAC ENZYME ANALYSIS
(MI) - catalyst for energy production; in brain,
3-6 hrs (ONSET) myocardium, skeletal muscle
• Creatine Kinase 12-18 hrs (PEAK) CK-MB- accurate, most specific for ACUTE MI
(CK) 3-4 days (NORMALIZE) CK-BB (brain)
CK-MM (skeletal muscle)

(MI) - elevated = TISSUE NECROSIS

• Aspartate
4-6 hrs (ONSET)
Aminotransferase
4-36 hrs (PEAK)
(AST)-
4-7 days (NORMALIZE)
(MI) - for MYOCARDIAL NECROSIS
• Lactic 24 hrs post MI (ONSET) - “flipped pattern”
Dehydrogenase 48-72 hrs (PEAK) (N= LDH1 < LDH2 ; after MI: LDH1 > LDH2) Normal: 20-30 mmHg = PAP
(LDH)
8-13 mmHg = PCWP
Troponin I >25 PCWP = impending pulmonary edema
= contractile CHON found only in cardiac Nsg interv
muscles; most specific for MI INJURY - inflate balloon ONLY for PCWP readings (deflate bw reading)
Troponin C= binds Ca - assess insertion site & culture site q48h
• Troponin (I, C, T): Troponin T
- complication: infx, pulmonary artery rupture, pulm embolism, dysrhythmia
= binds I & C
= elevated = as sensitive as CK-MB for MI
= for dx after 4-6 hrs & 4-7 days post MI
NONINVASIVE
I. ELECTROCARDIOGRAPHY (ECG/EKG)
MI) - for SILENT MI (remains elevated for long
• Hydroxybutyrate - electrical activities using rhythm strip; for cardiac dysrhythmia, MI location & extent; med efficacy
10-12 hrs (ONSET) period even after other enzymes normalize)
Dehydrogenase Interv
48-72 hrs (PEAK)
(HBD) (BEFORE)- px will not experience electrocution/shock remove all metal objects
12-13 days (NORMALIZE)
- O2-binding CHON in cardiac & skeletal muscles Wash skin to reduce skin oil lie still, breathe normally, don’t talk
• Myoglobin Waveforms Component
- for MI EARLY DETECTION

2. COAGULATION TESTS

1. P-WAVE
- ATRIAL DEPOLARIZATION (precedes QRS complex); rounded & upright
- must not exceed 2-2.5 mm in ht; 0.06-0.11 secs
2. PR INTERVAL
- time for impulse to travel from atria thru AV node, bundle of his, bundle branches, to purkinje
- P wave beginning to QRS beginning; 0.12-0.20 secs
3. QRS COMPLEX
- VENTRICULAR DEPOLARIZATION; differs in each 12 leads; 3 waveforms = Q, R, S)
- 0.06-0.12 secs
4. ST SEGMENT
- VENTRICULAR DEPOLARIZATION END, V. REPOLARIZATION BEGINNING
- S wave end to T-wave beginning; duration not measured
5. T-WAVE
- VENTRICULAR REPOLARIZATION; rounded, smooth, upright
- follows QRS complex & ST srgment; <5mm in standard leads
6. QT INTERVAL
- time for V. depolarization & repolarization takes place
- QRS complex beginning to T-wave end
- duration varies w/age, sex, HR (avg 0.36-0.44 secs)
6. J POINT
- where QRS complex meets ST segment; benign variation, hypothermia, vagal stimulation
- ER pattern = EARLY REPOLARIZATION
7. U WAVES
- Papillary muscle /Purkinje fibers REPOLARIZATION
-> Prominent U- hypokalemia, hypercalcemia, thyrotoxicosis
-> Inverted U- myocardial ischemia, L ventricular vol overload; normal (younger, athletic)
Obtaining ECG
- place electrodes in standard pos on chest wall & extremities
- attached to cable wire connected to ECG machine
- 12-lead ECG (standard, most common to diagnose DYSRHYTHMIA)
SINUS RHYTHM (SR)
- Normal P, QRS, T-waves; HR = 56-99 bpm; P:QRS ratio = 1:1; regular rhythm
1. Identify Rhythm (R-R interval)
Paper & Pencil Method (straight edge of paper along strip; identify peak of 2 consecutive
R-wave & make a dot on paper. Compare)
2. Determine Rate
Times Ten (6-sec Method)- count P-waves # (atrial rate) or R-waves (ventricular rate)
within 6-second strip then multiply by 10 = RATE
II. CONTINUOUS ELECTROCARDIOGRAPHIC MONITORING
- standard for w/risk of dysrhythmia
• Hardware Monitor- 3-5 electrodes, lead cable, bedside monitor
• Telemetry- battery-operated transmitter; transmit radiowaves to monitors
Interv: clean skin w/soap & water change electrodes q24-48h skin irritation
III. HOLTER
fibers MONITORING
- portable (small tape recorder); to continuously monitor CV sys for atleast 24 hrs
Interv: assess precipitating factors, time of day keep diary of activities
IV. CARDIAC STRESS TESTING- eval CV response to external stress in controlled env
• Exercise ST- px walks on treadmill/stationary bicycle @1.5 mph 10% incline for 6-12 min)
HEd: avoid tea, coffee, smoke, alcohol on day of test
Fast 4 hours prior; Report chest pn, SOB, dizziness
Loose-fitting clothes & low-heeled rubber shoes
• Pharmacologic ST- physically disabled/deconditioned px
-> Dipyridamole (Persantine) & Adenosine (Adenocard) mimic exercise effects by
maximally dilating coronary arteries
-> Dobutamine (Dobutrex)- sympathomimetic; ↑HR, contractility, BP
HEd: NPO q4h prior NO caffeine Flushing/Nausea (common SE)
• Emotional/Mental ST
V. CXR- overall size & configuration of heart & chambers
HEd: remove brassiere, practice holding breath, lead shield for pregnant
VI. MRI- magnetic field + radiowaves; define difference bw healthy & diseased tissues
HEd: consent, claustrophobia, remain still, loud knocking noise
VII. CT SCAN- cross-sectional image of chest, heart, great vessels
- px on top of table while scanner rotates around him
HEd: lie still; IV line inserted w/contrast medium; assess for pregnancy & claustrophobia
NPO if w/contrast; sedate if unable to stay still
VIII. MYOCARDIAL SCINTIGRAPHY /PERFUSION IMAGING
- (most common) Thalium Imaging, Multigated Blood Pool Imaging (MUGA)
- myocardium absorb radioisotopes via catheter, emitting photons
- external gamma cam produce image of myocardial fx, motion, perfusion
IX. MUGA/MULTIPLE-GATED ACQUISITION
- study L ventricular fx & wall motion; use ECG, gamma cam, computer
- technetium-99m injected in red cells to form image of blood pool in heart (LIE STILL!!)
X. 2D ECHOCARDIOGRAPHY
- US; assess cardiac structure & mobility; painless, 30-60 min; no special preparation
HEd: Lie still; supine; slightly turn to L side w/bed head elevated 15-20o
OTHERS (VASCULAR DX)
• LIMB BLOOD PRESSURE- Acute & chronic arterial occlusion produce regional hypotension
• DOPPLER US- probe that emits high frequency sound waves moved over a skin surface
Interv: Supine w/ head of bed elevated 20-30o
legs are externally rotated to permit adequate access to medical malleolus
• DUPLEX TRANSONOGRAPHY- Localizes site of obstruction & eval degree of narrowing
• PLETHYSMOGRAPHY- Measures venous blood volume changes in extremities & compares each
lower & upper extremity systolic BP of to R/O disease blocking arteries in
extremities
Interv: Pressure cuff is applied to extremities Cuffs attached to a pulse volume recorder
Lasts 30-60 minutes supine pos
involved extremity elevated above heart level
• VENOGRAPHY- inject contrast into veins via catheter, followed by radiographic studies
• VASCULAR ENDOSCOPY- imaging of intra-arterial disease in color & 3D thru fiber-optic endoscope
• ANGIOGRAPHY- inject contrast into artery via catheter followed by radiographic study
- measure changes in volume in different parts of the body.
- NOT FOR: pregnancy, allergy to contrast medium, w/ impaired renal fx
(before) NPO 2-6 hrs seafood/iodine allergy Mild sedative is administered
Local anesthesia @injection site brief flushing feeling as contrast is injected
(after) VS, LOC, peripheral pulse Bed rest 6-8 hrs, extend punctured extremity
hematoma, bleeding @puncture site pressure dressing & small ice pack @puncture site
IVG 6-8 hrs (to excrete contrast)
• PULSE GRADING = 0 – absent +1 weak; difficult to palpate, faint +2 normal +3 full bounding
• CAPILLARY REFILL TIME- for peripheral circ adequacy; pressure on nail bed until white (N= <2 secs)
• TRENDELENBERG TEST- for vein valvular competency
1. elevate lower extremities for 5 min 3. Px stand for 2-3 min
2. apply tourniquet to lower leg 4. Note blood filling to veins
 Rapid filling = abn  slow filling = N
• D-DIMER- product of fibrinolysis (elevated = VENOUS THROMBOEMBOLISM)
 Risk: hypertension, DM, smoking, hyperlipidemia
S/sx (6 Ps)
Pain Paralysis gangrene & ulcer
Paresthesia Pulselessness sexual dysfx
Poikilothermia (coolness) Pallor hair loss on extremity

Dx: Doppler USD, treadmill testing, serum triglycerides (elevated)

Mgmt: (V-A-P-A-A)
Vasodilators (PAPAVERINE, ISOXUPRINE HCL (vasodilan)
Antihyperlipidemics (SIMVASTATINE)
Pain relievers
Anticoagulants
Antiplatelets (PENTOXYFYLLINE (trental) (O2 supply by ↓blood viscosity & RBC flexibility)
CILOSTAZOL (pletal) – inhibit platelet aggregation
Surg: VASCULAR GRAFTING (pass grafts to reroute blood around stenosis)
ENDARTERECTOMY (incise artery & atheromatous obstruction is removed)
Amputation
Mgmt
ALTERATIONS IN VASCULAR INTEGRITY Risk modification daily walking program avoid chill/cold exposure
ARTERIAL DISORDERS Skin & foot care tissue perfusion Comfy shoes
Low Fat, Low chol maintain warm env temp
HYPERTENSION (CONSTRICTIVE) avoid pressure on extremity, padding for support
Essential/Idiopathic/Primary- >40 y/o, male; (risk) race, genetics, obesity, stress, excess
Na, alcohol, smoking THROMBOANGITIS OBLITERANS (OBSTRUCTIVE & INFLAMMATORY)
Secondary- d/t comorbidities Labile- intermittently elevated -acute, inflamm; medium/smaller arteries/veins of lower extremity; idiopathic
Resistant- unresponsive to meds White Coat- on clinic visits (d/t anxiety); self-limiting - SMOKERS, male 25-40
Hypertensive Crisis- need immediate bp lowering s/sx
Htn Emergency- must be lowered STAT (not necessarily <140/90) to avoid organ dmg -intermittent claudication
- Acute, life-threatening in ICU (cold sensitivity, absent peripheral pulse, ulcer/gangrene)
- MI, aortic aneurysm, intracranial hemorrhage (Muscular, crampy pain in extremities consistently reproduced w/same degree of exercise/activity
- FAST -ACTING IV VASODILATORS & relieved by rest; d/t peripheral arterial insufficiency = inadeq bloodflow to tissues during
Htn Urgency- must be lowered within few hours to avoid organ dmg ↑nutrient demand during exercise)
- PO ANTIHYPERTENSIVES Dx: Same w/ASO, no ↑triglycerides

Dx: Renal fx study, lipid profile, 2D ECHO

Mgmt: (Same w/ASO)
SMOKING CESSATION (only effective rx)
Nsg
-prepare for surgery
-drug regimen
-avoid trauma to affected extremity, stop smoking
-maintain warmth

ANEURYSM (DEGENERATIVE)
- localized, irreversible dilation of artery secondary to altered wall integrity
- d/t ATHEROSCLEROSIS, CONGENITAL WEAKNESS
Risk: genetics, smoking, hypertension, men 4x than women, Caucasian, elderly
Types: Fusiform- outpouching on both sides of artery (sausage-like)
Saccular- one side (berry-like)
Dissecting- separation/tear in tunica intima & media; weak medial layer cause blood to enter

• ABDOMINAL AORTIC ANEURYSM (most common type)

-pulsatile mass w/systolic bruit over abd aorta esp when lying down
S/sx: - Asympto - Flank/lower back/lower abd pain - Hypertension
- (Complication) RUPTURED ANEURYSM
Dx: Abd US, CT Scan, Arteriography (determine size & location)

Surgery:
Open Surgical Repair
(resect vessel & sew bypass graft in place)
Endovascular grafting
(transluminal placement & attach sutureless aortic graft
Mgmt: (L-I-F-E-S-T-Y-L-E) prosthetics across aneurysm)
Limit salt & alcohol Exercise regularly Your meds must be taken daily
Include daily K, Ca, Mg Stress mgmt. Lose wt Nsg
Fight fat & cholesterol Try to quit smoke End-stage complic must be avoided -NO ABD PALPATION -NO BENDING, STRAINING
-monitor BP; antihypertensives

ATHEROSCLEROSIS OBLITERANS (OBSTRUCTIVE & INFLAMMATORY)

-chronic occlusive arterial dse; affect aorta & lower extremities; male 50-60 RAYNAUDS DSE (FUNCTIONAL)
- d/t ATHEROSCLEROSIS -intermittent/episodic arterial SPASMS; most freq involve FINGERS; idiopathic
-women 15-40; worsened by emotional stress, smoking, cold sensitivity  Tunica externa - collagen fibers
S/sx: Pallor (vasoconstriction) Cyanosis (pooling of de-O2 blood during vasospasm) Veins/venules- thin, less; muscle vein walls
Rubor (↑ blood flow) Numbness, tingling, swell, bilateral coldness of affected parts
Dx: Allens Test

Mgmt
CA CHANNEL BLOCKERS (relieve vasospasm)
NSAIDS
AMPUTATION (Surgery)
Nsg
-avoid cold exposure, stop smoking
-gloves when handling cold/frozen object
-avoid emotional stress

VENOUS DISORDERS
DVT/THROMBOPHLEBITIS
Risk; endothelial dmg, traums, surgery, central venous catheter, venous statis, immobility, obesity,
varicose, spinal cord injury, cancer, pregnancy, polycythemia
• Superficial Thrombophlebitis- d/t venous thrombosis & inflamed superficial vein
-common in greater of lesser saphenous veins of lower extremity
-risk: SMOKING
S/sx: Pain, Tenderness, Redness, Warmth Dx: Doppler US / VENOGRAPHY (gold standard!!!)
Mgmt: Bed rest, avoid prolonged sitting/standing
Warm moist packs, elastic compression stocking, walking, elevation
Maintain ideal body wt, measure thigh & calves OD

• Deep Vein Thrombosis

- (VIRCHOW’S TRIAD) ALTERATION IN OXYGEN
BLOOD
Venous stasis/Impaired Bloodflow, Vessel Wall/Endothelial injury, blood hypercoagulability
S/sx: Calf pain, (+) Homans, warmth, tenderness, edema - 5L (humans); cellular + acellular; PLASMA (55%), RBC (5-6 mil/ml), WBC (5000/ml), PLT
Fx: deliver nutrients (O2, vitamin, food) remove waste (CO2, nitrogenous, cellular toxin)
Med/Surg/Nsg Mgmt: Repair conduit protect from microorg
(same w/superficial thrombophlebitis) PLASMA- liquid; transports soluble food mol, waste product, hormone, antibody
RBC- transport O2, CO2; 45% of blood vol; 120 days lifespan; flexible memb,
- biconcave shape (↑surface area = more O2); NO NUCLEUS (extra space)
- mainly Hbg (250mil/cell) = carry 4 O2 mol; w/Fe, gives red color
Erythropoiesis: ↓O2  erythropoietin release by kidney  stimulate BM to produce RBC
= reqs: Erythropoietin Vit B12 (cyanocobalamin) Folic Acid (folate) Fe
Ascorbic acid (Vit C) Pyridoxine (B6) Amino acids

VARICOSE VEINS
-prominent, abnormally dilated, dark & torturous veins of lower extremity; women 30-50
D/t:- Congenital absence of valve veins - Prolonged sitting/standing
- Constrictive clothing - Hereditary weakness of vein valves
- Obesity, pregnancy, thrombophlebitis, disease conditions
S/sx: - Dilated purplish tortuous veins - Leg pain (dull, aching), edema, heaviness

Dx: Duplex Scan (valvular reflux severity)
Plethysmography, Venography, Trendelenburg Test
Mgmt
Vein Ligation
Vein Stripping- post vein ligation, incise ankle then plastic metal wire passes thru full vein
length to point of ligation, wire is removed (pulling vein as it’s removed
Sclerotherapy- inject sclerosis agent (Na Murrhate)
- irritates & damage vein, force it to close & redirect blood to healthy veins)
Incision & Drainage- drain trapped blood in sclerosed vein 2-3 wks post sclerotherapy
Nsg
- (Post vein ligation & stripping): bed rest 24 hrs. then walking q2h for 5- 10 mins.
-( Post sclerotherapy): burning sensation normal for 1-2 days
: elastic compression stocking for 5 days (removed by physician)
: walking exercises to dilute the sclerosing agent
- Elastic compression stockings
- Assist in exercises; Elevate foot of the bed; Avoid prolonged sitting and standing
- Monitor peripheral pulses
ANATOMY OF BLOOD VESSELS
VASCULAR SYS- blood flow, capillary filtration & reabsorption, hemodynamic resistance,
peripheral vascular regulating mechanism
Artery/Arteriole- thick-walled; carry blood from heart to tissue
Capillary- thin-walled; rapid, efficient; Transports nutrients to cell, remove metabolic waste
 Tunica intima - inner endothelial cell layer
 Tunica media - smooth muscle & elastic fibers, make up the vessel walls
● RBC are normally phagocytized by macrophages of splenic & hepatic sinusoids at 120 days of age.
● Hgb is degraded into GLOBIN (CHON component), IRON (for later use), HEME as RBC disintegrate
● porphyrin ring of heme is oxidized by microsomal heme oxygenase -> biliverdin -> Fe is released
● Fe is salvaged, transported to BM by transferrins, & used again in eryhtopoiesis
● remaining Hgb forms the basis of bilirubin (free, unconjugated).
● bilirubin is then transported from plasma to the liver for conjugation.
● Bilirubin is conjugated within hepatocyte to glucuronic acid by uridine-diphosphoglucuronic
glucuronosyltransferase (UDPGT).
 glucuronidation- crucial detoxification mechanisms of human body.)
● bilirubin is excreted as part of bile into intestine. (why feces & urine is yellow = bilirubin)
● globin is broken down into amino acids (sent back to BM to for eryhtopoiesis)
HEMATOPOIESIS- exclusively in BM; all cellular elements derived from pluripotent stem cells (PPSC)
- PPSC retains ability to both replicate itself & differentiate (determined by cytokine)
Blood Cell Devt (HUMAN EMBRYO)
- (3rd wk) Clusters of blood cells called blood islands appear in the yolk sac
- (3rd mo) - cells migrate to liver (chief site of blood cell formation)
- (4th mo) - hematopoiesis starts in the В.М.
- (At birth)- marrow is active; sole source of bld cells
- (Up to puberty)- all the marrow is active
- (18 y/o)- only vertebrae, ribs, sternum, skull, pelvis, & proximal femur & humerus are active
- Remaining marrow becomes yellow, fatty & inactive
ASSESSMENT
I. HEALTH HX: weakness, fatigue, generalized malaise, dyspnea, pallor, ulcer, mouth sore, anxiety
: infx risk
II. MANIFESTATION: Tissue Hypoxia  angina, night cramps, fatigue, weakness & & dyspnea
Brain hypoxia  headache, faintness & dim vision
Blood Redistribution from cutaneous tissues
Low Hbg  pallor of skin/ mucous membranes, conjuctiva & nail beds
Compensation w/ Cardiac Output  tachycardia & palpitations
Changes in blood viscosity  flow-type systolic murmur
 pre-existing heart disease  ventricular hypertrophy, high- output heart failure  prevent DNA formation = impaired RBC production
Diffuse bone pain & sternal tenderness  d/t accelerated erythropoiesis  folate NOT stored in body
hemolytic anemia  jaundice
macrocytic cells= enough Hgb but are not concave & less in number
aplastic anemia  petechiae & bleeding d/t reduced platelet function.
= more easily damaged, causing anemia
Hemorrhagic Tnedencies: PETECHIAE, ECCHYMOSIS, CONJUNCTIVA BLEEDING
VIT B12/Extrinsic Factor- combine w/intrinsic factor made by stomach parietal gland
III. IPPA - receptor binding & distal ileum cell phagocytosis
 INSPECTION: Mucous Memb = pallor, cyanosis (↓O2), redness (polycythemia), jaundice, - Extrinsic+intrinsic absorbed in terminal ileum (7-12 yr supply)
petechiae, eccyhmosis, glossitis
a. MEGALOBLASTIC ANEMIA / FOLIC ACID DEFICIENCY
 PALPATION: spleno- & hepatomegaly, lymphadenopathy
• Pernicious/B12 Deficiency Anemia- d/t autoimmune dse destroying stomach parietal cell
- achlorhydria (absent HCl in gastric fluid)  halitosis
DIAGNOSTIC EXAM
CBC- RBC count, Hemoglobin, hematocrit, RBC indices, WBC w/w/o differential count, platelet count
Causes of VIT B12 DEFICIENCY
• RBC INDICES- anemia dx Malabsorption
-> MCV (Mean Corpuscular Vol) / Avg blood cell size = 80-100 femtoliter (N) -> inadeq intrinsic factor prod = pernicious anemia, gastrectomy (partial/total), gastric
-> MCH (Mean Corpuscular Hbg)/ Hbg # per RBC = 27-31 picograms/cell (N) mucosa & gland atrophy
-> MCHC ( “ “ Hbg Conc)/ Hbg # r/t cell size = 32-36 g/dL -> inadeq B12 release from food = partial gastrectomy, impaired stomach fx,
chronic pancreatic insufficiency
-> terminal ileum dse = sprue, ileal resection, Crohn’s
-> Intestinal B12 competition = bacteria overgrowth, jejunal diverticula
Inadequate intake (vegetarians meat products & dairy= best B12 source)
“ utilization (drugs = PAS, Neomycin, Colchicin, Nitrous oxide)

PERIPHERAL BLOOD SMEAR- RBC, WBC, Plt abnormalities Causes of FOLIC ACID DEFICIENCY
- Normocyte (normal size), Normochromic (normal color) Inadeq Folate Intake = alcoholic, teenager, infants; lacking fresh, slightly cooked food
Malabsorption= d/t barbiturates, phenytoin, oral contraceptive
RETICULOCYTE COUNT- for anemics; young RBC still has small RNA #
= small bowel dse (sprue, celiac dse), alcoholism
- takes 1 day to mature; 1/120th of RBC (N)
Impaired metabolism= d/t methotrexate, enzyme deficiency
COAGULATION SCREENING TEST ↑Requirements= pregnancy + lactation, infancy, chronic hemolysis, hemodialysis
• Plt # • PT (11-16 sec) • PTT (60-70 sec) • Bleeding Time (1-9 min) Defective utilization = folate antagonists (methotrexate, trimethoprim, triamteren),
BONE MARROW ASPIRATION & BIOPSY purine analogs (azathioprine)
- blood dyscrasias (aplasti anemia, leukemia); from posterior iliac crest (alt = sternum) primidine analogs (zidovudine)
(before): pain during procedure Secure & verify informed consent Sedation as ordered RNA reductase inhibitor (hydroxyurea), (phenytoin, N2)
(after): apply pressure dressing & sandbags check bleeding @site mild analgesics s/sx (MEGALOBLASTIC)
- angular cheilitis (mouth sores) - smooth tender tongue - malaise - numbness - pallor
s/sx (PERNICIOUS)
I. ANEMIA - swollen, beefy tongue (glossitis) - dizziness - pallor/pale yellow skin
- ↓RBC; Hypoproliferative Anemia (1st), Maturation Disorder (2nd), Hemolytic (3rd) - paresthesia - arm & leg weakness - ataxic gait
d/t: blood loss ↓RBC production (BM failure) Dx:
↑hemolysis reticulocyte # (↑hemolysis, ↓production) SCHILLING TEST (N = ↑B12 in urine) ( + Pernicious Anemia = ↓B12 excretion in urine)
s/sx: fatigue, dyspnea, arrhythmia (palpitation), cold clammy skin, get tired easily = measure oral radioactive B12 absorption after intrinsic factor parenteral injection
= oral radioactive B12 given + IM nonradioactive B12 (push radioactive B12 into urine)
Approach: Anemia  check MCV  Microcytic Anemia (MCV <80)
= collect 24-48 hr urine specimen!!!!
 Normocytic “ (MCV 80-100)
 Macrocytic “ (MCV >100) Rx
- VIT B12 (must be ingested, not synthesized in body)
HYPOPROLIFERATIVE ANEMIA -> meat, eggs, dairy products -> multivitamins -> cyanocobalamin injection
- FOLIC ACID THERAPY
II. MICROCYTIC (Fe deficiency, thalassemia, sideroblastic, anemia of chronic dse) -> green veg, nuts, cereal, fruit, yeast, liver (only from certain farm source)
a. IRON DEFICIENCY ANEMIA- most common cause; LEAD TOXICITY (pica = fave infant food) -> multivitamins; folic acid 5mg tablet
• Microcytic hypochromic anemia-↓Fe, ↑transferrin, ↓ferritin); lacking stainable Fe Nsg: bed rest (if w/severe anemia) Mouth care ac & pc
- small ragged RBC precursor NO highly seasoned, coarse, very hot food (if w/mouth sores)
d/t: menstruation GI bleeding (most common pathologic cause) tissue loss
iatrogenic ID in males (must be worked up)
Poor Intake/Absorption
III. NORMOCYTIC
- Milk baby - Early childhood - Achlorhydria - Inflammatory bowel dse
- postnatal infant - after menarche - adolescents - pregnancy
Increased Need
- early childhood + adolescence growth spurt - lactation
- pregnancy (extra 2.8 mg/day over baseline)

Rx:
Heme Fe (well-absorbed, in muscle myoglobin)
Nonheme Fe (not absorbed well; forms bulk of dietary Fe) (DON’T drink coffee & tea) a. PURE RED CELL APLASIA- very rare cause; immune-mediated RBC destruction in BM
DON’T EAT BLOODY MEAT (cause severe food poisoning) - low reticulocyte # & RBC #; Rx: IMMUNE SUPPRESSION
Ferrous sulphate, F. gluconate, F. fumarate (iron absorbed well only in ferrous form) - WBC & platelet # remain normal (unlike aplastic anemia = pancytopenia)
(ferric form only 10% absorbed)
b. APLASTIC ANEMIA- d/t hypocellular BM (blood cell destruction in BM)
Fe Therapy (PO) (nausea, GI discomfort, constipation, diarrhea); start on small dose, inc gradually
• acquired (drugs, toxins, hepa, genetics, immune dse, pregnancy, idiopathic, virus
Nsg mgmt. s/sx: PANCYTOPENIA: anemia (↓Hbg, HCT) = fatigue, lassitude/lethargy, dyspnea, pallor
-bleeding - adeq rest thrombocytopenia = bruise, petechiae, bleeding, epistaxis, gums, GI tract bleed
- Fe PO (take w/empty stomach; give meals after to avoid GI upset) neutropenia = recurrent infections
- dilute Fe liquid preparation, use STRAW, give w/Orange juice as vit C Rx: (past) transfusion, antibiotics
-> antacids = ↓Fe absorption -> ascorbic acid = enhance Fe absorption (present) stem cell transplant transfusion
immunosuppression (Antithymocyte globulin + cyclosporine A)
Nsg: infx s/sx (minimize risk) bleeding high CHON & VIT diet (reduce infx)
II. MACROCYTIC (Megaloblastic anemia, reticulocytosis) reverse isolation (d/t severe immunocompromised)
- d/t ↓FOLIC ACID / VIT B12  folic interacts w/B12= normal blood & nerve fx
c. HEMOLYTIC ANEMIA- d/t HEREDITARY SPHEROCYTOSIS
Hereditary Spherocytosis Hgb- w/alpha & beta CHON; dec synthesis of one leads to RBC destruction
- most common inherited red cell memb disorder; autosomal dominant - (N) HgbA = 98% HgbF= 1% HgbA2= <3.5%
- d/t gene mutation that encode RBC memb cytoskeleton protein
- spectrin & ankyrin deficiency (memb proteins)  tight sphere (instead of biconcave shape)• α-thalassemia- ↓alpha chain synthesis w/↑beta-chain
- mem loss = SA loss = deformability loss (cant squeeze thru spleen slits) = ↑splenic clearance - silent carrier, minima, minor, intermedia, major
Spherocyte- almost spherical RBC, no central pallor (unlike RBC) Normal (α α/ α α ) Minor (- α/- α or --/ α α) Barts hydrops fetalis (--/--)
- macrospherocyte = HEMOLYTIC ANEMIA; microspherocyte = SEVERE BURNS Silent Carrier (- α/ α α) Hgb H dse (--/- α)

Rx: splenectomy, most don’t need Rx; inheritance education

s/sx (HEMOLYTIC ANEMIA)
- splenomegaly
- jaundice/hyperbilirubinemia (d/t hemolysis)
- hemoglobinuria (red urine)
- leg ulcers
- scleral icterus (yellow sclera)

• G6PD (Glucose-6-Phosphate Dehydrogenase) Deficiency Anemia -> Hemoglobin Bart’s- most severe form; high O2 affinity, cant release O2 in tissues
- most common congenital hemolytic anemia type; acute hemolysis - infants die stillborn unless w/intrauterine BT
Rx: NO KNOWN; possibly genetic therapy
s/sx: jaundice, splenomegaly, SOB, tachypnea, tachycardia, extreme fatigue, cola-colored urine
Dx: bite cells, Heinz bodies, G6PD levels • β-thalassemia- ↓beta chain synthesis (↓/absent HgbA, ↑HgbF, ↑HgbA2)
Rx: hydration, screening b4 blood donation (hazardous), avoid precipitants -> β-thalassemia trait/minor – asympto; mild microcytic anemia (heterozygous/trait)
-> β-thalassemia major/Cooley’s Anemia (homozygous)
- NO beta-chain produced (no HgbA); severe microcytic anemia gradually in 1st year
- marrow expansion; Fe overload; growth failure & death
- Rx: transfusion, iron chelation, stem cell transplant
HEMOGLOBINOPATHIES (abn hbg structure) Iron Chelators:
SICKLE CELL ANEMIA (Normocytic hemolytic) • Deferoxamine (Desferal)= 3y/0+ or serum ferritin > 1000ng/ml
- most common inherited; autosomal recessive (inherit 2 abn genes causing RBC shape change) = Male: 22-322 ng/mL; female: 10-291 ng/mL
- valine (AA) substitutes glutamic acid  sickling  hemolysis, vascular obstruction, vaso-occlusion = SC 40—50 mkd once a week
- when O2 is released, RBC shape turn crescent, rigid, inflexible = ototoxicity, retinal changes, bone dysplasia
- local hypoxia & continue sickling  vessel plugging • Deferiprone (L-1)= oral ; neutropenia, arthritis, hepatic fibrosis

POLYCYTHEMIA (polys = many, kyots = cells, haima = cells)

- abnormally ↑total RBC mass w/HCT >55%
- primary: myeloproliferative syndrome (in BM)
- secondary: reax to chronically low O2 levels/malignancy
• Relative Polycythemia- d/t reduced blood plasma (fluid loss, burns, dehydration)
• Absolute “ : Primary= d/t BM abnormality (myeloproliferative dse)
Secondary= d/t natural/artificial ↑erythropoietin prod
= physiologic (high altitude), infx, malignancy
S/sx: - Headache, weakness, dizziness, diaphoresis - Flushed Pruritus (After warm bath)
- Thrombosis - Nonspecific Gl upset
- Erythromelalgia (Burning hands or feet) (Erythema, pallor, cyanosis w/normal pulses)
(+) Disease = px homozygous for sickle cell gene (>80% of hgb is NORMAL) - bleeding, bruise, high BP delayed clotting (extra blood cells thicken blood & slow circu)
(+) Trait = px heterozygous for sickle cell gene (predominant Hgb A, 50% Hgb S (abn Hgb)
Physical Exam: Facial plethora (puffiness) Hepatomegaly, Splenomegaly,
Factors r/t sickling: cold, stress, exertion, infx, hypoxia, acidosis, dehydration Excoriations Injection of conjunctival vessels
s/sx: Engorgement of optic fundus veins Gouty arthritis
hemolysis ↑reticulocyte # Dx: • CBC – Hgb = Adult: (males): 13.5 - 17 g/dl (Females): 12 - 15 g/dl
BV occlusion= bone (“painful crisis”) lung (“acute chest syndrome”) Pregnancy: 11 - 12 g/dl
Spleen (“acute splenic sequestration”) Brain, heart • hematocrit
hand (dactylitis/hand foot syndrome/sausage fingers = soft tissue swell w/o • Erythropoietin level
obvious trauma)
splenomegaly = weak bones/spinal defects d/t marrow hyperplasia & osteoporosis Rx: Phlebotomy Aspirin (bleeding) Antihistamine, avoid warm bath (pruritus)
= H.influenza freq infx; leg ulcers (adolescents) Atleast 3L fluid/day (prevent thrombus)
delayed growth & development CVA infarct in CNS
Pain (d/t vaso-occlusive crisis) Jaundice (d/t hemolysis)
Renal failure (cant concentrate urine) Heart failure (d/t hemosiderosis/Fe overload)
Priapism (prolonged penis erection; result in impotence 6-12%)
Sickle Cell Trait = heterozygous state for HbAS; no serious consequence & asympto
= NOT a dse; person inherited sickle cell gene from parents
= sudden death during intensive training; hematuria ( chronic renal failure)
SICKLE CELL CRISIS (episodes of EXTREME PAIN/PAIN CRISIS = MAJOR symptom)
Vaso-occlusive/Thrombocytic Crisis- most common; crescent RBC clump  small BV blockage
Splenic Sequestration (toddler/preschooler)
- sickle cells block outflow tract  sudden massive collection in spleen  hypovolemia
Prevent: normal hydration Rx: O2, hydrate, pn mgmt., bed rest
Dx: CBC (anemia) Sickle Cell Test (deoxygenation of blood drop on slide w/cover slip)
Sickledex (blood drop from fingerstick mix w/solu)  (+) HgbS = cloudy mixture
Hgb electrophoresis- for dse & trait; accurate & fast
Prenatal (fetus DNA via amniocentesis)
Prognosis: sickled RBCs live for 6-20 days (cause hemolytic anemia)
(6 mos or less) negative symptoms d/t fetal hgb levels
Death in early adulthood (d/t occlusion/infx)
Med mgmt.: Penicillin (prophylaxis @ 3mos- 5 yrs) routine vaccination BT
Hydroxyurea (↑HgbF synthesis) Stem cell transplant
Nsg: hydration NO tight clothing (impair circ) wounds dry & clean
Maintain warm arms & legs ↓emotional stress skincare, CBR
test siblings for sickle cell trait

THALASSEMIA (Microcytic)
- d/t ↓globin chain production & ↑hemolysis in spleen (↓HEMOGLOBIN)
- reduced production of selected globin chain (basic defect); heme part unaffected
- Globin (CHON w/4 globin polypeptide chain)
 Infection Lack physical activity
Delivery (pregnancy) Unhealthy lifestyle

Functional Classific

Compensatory Response
(attempt to ↑cardiac output but eventually
cause ↑myocardial O2 consumption & damage)

Frank-Starling Mechanism
- normal relationship bw
Myocardium length & tension
- greater preload =
stronger ventricular contraction

INFECTIVE/BACTERIAL ENDOCARDITIS LSHF- most severe (end-stage) manifestation of heart dse; d/t MYOCARDIAL INFARCTION
- bacteria enters bloodstream & settle in heart lining, valve, BV - d/t systolic dysfx (LV can’t empty well), diastolic dysfx (LV can’t relax/fill well)
Etiology (viral & fungal) ↓Cardiac output -> backflow to lungs -> pulmonary congestion -> forward failure (↓cardiac output)
- staphylo aureus - streptococcus -> backward “ (congestion)
- HACEK (gram (-): Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, Kingella Backward effect
 most notable, treated only w/CEFTRIAXONE - LV grow weaker & thinner -> bloodflow backwards to organs -> lung fluid buildup/pulmonary edema
Forward Effect
Risk: - doesn’t pump enough to satisfy body cell needs  ↓cardiac output  fluid retention & edema
- preexisting heart condition (valvular, RF)
- contaminated IV needles
- recent invasive proc
(minor surg, dental proc involving urinary tract)
2 factors:
- damaged endothelial surface
- organism portal of entry

S/sx
Osler Nodes
- reddish tender/painful lesions (finger pads, hands, toes)
Janeway Lesions
- nontender hemorrhagic lesions (finger, toes, nose, earlobe)
Splinter hemorrhage (capillaries under fingernail burst)
Roth’s spots
- hemorrhages w/pale centers in eye fundi
- (white-centered retinal hemorrhage)
petechiae, murmur, night sweats, anorexia, fever

DUKE’S CRITERIA

RSHF- d/t LHSF; inc fluid pressure from LV failure is transferred back to lungs, damaging right side
-↓R pumping power ->backflow in vein->peripheral & visceral edema (extremity, stomach, liver)
- COR PULMONALE (not r/t LHSF)

Nsg Goal: normal/baseline cardiac fx

ADL performance w/Do fatigue
Knowledge of therapeutic regimen

CONGESTIVE HEART FAILURE

- heart doesn’t pump blood as well as it should
- blood backflow -> fluid buildup in lungs (pulmonary edema + pulm hypertension)
-> body tissue congestion
Risk factors (R-A-P-I-D F-A-I-L-U-R-E)
Renal Dse Forgot to take meds R
Anemia Arrhythmia E
Pulmonary Embolism Ischemia/infarction