Summary NURS 172 Unit 2 Study Guide

Unit 2 exam study guide – circulation and perfusion
*friends note: some things not included b/c I already understand the concept. Everything on here is
things I need reminding of or have no idea wtf it is.

Week 5-
Wilkinson p.490-99:
Pulmonary circulation: O2 depleted blood goes from heart to lungs, becomes oxygenated by
alveoli then goes back to heart.
Systemic circulation: L ventricle pumps blood via arterial system
* Coronary circulation: circulates blood through heart (part of systemic circulation)
Capillaries: Arteries that are subdivided into tissues and organs. How O2 goes into tissues.
Venous system: collects O2 depleted blood and returns it to R atrium to begin circulation again
Diastole: relaxation (filling) DUB systole: contraction (emptying) LUB
Pulmonary arteries O2 depleted blood from R ventricle to lungs
Systemic arteries O2 enriched blood from L ventricle to body periphery
Pulmonary veins O2 enriched blood from lungs to L atrium
Systemic veins O2 depleted blood from periphery to R atrium


JVD- R side of heart is congested due to inadequate pump function (see more detail later)
Wilkinson p.955-89
R (lung) lobe=3 L (lung) lobe=2
Pathway of airflow: nosenasal cavity
pharynxlarynxtracheabronchusbronchiolesalveoliblood (back to alveoli, then
bronchioles, etc.*process reverses)
Ventilation: physical breathing respiration: gas exchange (O2+CO2)
External respiration Internal respiration
O2- diffuses across alveolar capillary membrane into O2- diffuses from blood through capillary cellular
blood of pulmonary capillaries membrane into tissue cells (used for metabolism)

CO2- diffuses out of blood into alveoli to be exhaled CO2- waste product, transported to lungs and exhaled.
(Capillary membrane blood  lungs  out)


TABLE 36-1 (Wilkinson p. 964)  respiratory medications to be reviewed
Kussmaul’s respirations: regular, but increased in rate and abnormally deep respirations (think of
as a form of hyperventilation)

,Biots respirations: irregular respirations of variable depth (usually shallow), alternating with
periods of apnea
Cheyne- Stroke: gradual increase in depth, then decrease in depth, then apnea.
Orthopnea: difficulty breathing laying down.
Stridor: high pitched, harsh, crowing- PARTIAL OBSTRUCTION of larynx/trachea. Hear w/o
stethoscope. (MORE SOUNDS FOUND HOFFMAN P.450)
ABG-P.977 wilkinson (to be reviewed later) – see hoffman notes below
Hoffman 439-56
Perfusion: oxygenated blood moving into tissues.
Acid base balance: exchange of CO2 for O2 in lungs + renal secretion of HCO3 (bicarb)
maintain body ph between 7.35-7.45
Surfactant: substance secreted by alveoli that prevent collapse (atelectasis)
Visceral pleura: thin membrane covering lungs Parietal pleura: membrane covering chest cavity
Pleural space: space between two membranes (V & P) has fluid that acts as a lubricant that
allows lungs to move freely as ventilation occurs.
Phrenic nerve- responsible for movement/contraction of diaphragm
Shunt: blood that returns to L heart without being oxygenated. can occur as result of atelectasis
or collapsed alveoli. 2 types:
Anatomical: blood moving from R to L heart w/o traveling through lungs.
physiological: alveoli are not functioning (returns to L heart w/o being oxygenated)
Crepitus: palpation finding. Air trapped under the skin – “Crackling feeling”. Can be caused by
pneumothorax or chest trauma.
Respiratory alkalosis Respiratory acidosis
Ph: >7.45 Ph: <7.35
PaCO2: <35mmHg PaCO2: >45mmHg
Associations: Associations:
Hyperventilation, Anxiety, +/- early asthma or COPD, Pneumonia, Respiratory failure
pneumonia
>7.45 alkalosis <7.35 acidosis PaCO2: 35-45 mmhg PaO2: 80-95 mmhg HCO3: 22-26meq/l
Diagnostic studies (ABG above):
Pulse ox: utilizes wave lengths to measure saturation of hemoglobin with O2
Pulse OX: 91-94%: mild hypoxemia, 86-90%: moderate hypoxemia, <85%: severe hypoxemia
Capnography: monitors the PaCO2 in airway during inhalation and exhalation- provides written
tracing.

, Capnometry: measures amount of CO2 exhaled w/o continuous tracing.
Sputum analysis: check for microorganisms +/- abnormal cell growth.
Pulmonary function test: evaluate lung volume to determine lung function.
Bronchoscopy: direct visualization of the respiratory tract down to secondary bronchi.
*needs to be NPO 8 hours prior for sedation. May get tissue specimens.
Asses for bleeding/hypoxia after procedure.
Thoracentesis: diagnostic/treatment (depending). Needle inserted into pleural space to remove
excess fluid/air.
*tell pt to deep breathe, cough. Nurse monitor vitals, SPO2, lung sounds. Pt report
elevated HR, palpitations, SOB/Dyspnea, angina, hemoptysis to MD STAT.
Lung biopsy: small piece of lung tissue to be removed & analyzed under microscope
*same nursing implications as bronchoscopy and thoracentesis!!


Week 6-
Hoffman p.460-75
LOWER AIRWAY DISORDERS
Alveolar macrophages: eat the bad things in the alveoli via phagocytosis
Mucociliary elevator: sneeze/cough to get bad debris out of respiratory tract.
Colonization: small number of bacteria not causing infection of resident bacteria and some
viruses *ex. staphylococcus, streptococcus
Bactericidal effect: surface epithelium secrete proteins to kill bacteria.
Influenza A, B, C: highly contagious, droplet, rapidly spreads, fomite transfer (objects)
Incubation period: 18-72 hours. Shedding: 2-5 days. INFECTIOUS for 7-10 days.
Severity of symptoms are dependent on number of viruses shed during replication phase.
Diagnostic: gold standard= sample respiratory secretions for viral culture (can take up to 10 days
for results). Common test= rapid flu test (RIDTs), swab test, results less then 30 min – not
always accurate
Tx/prevention: flu vaccine, medications use symptomatically. Severe cases: antivirals (does not
cure, only reduces symptoms)
*Primary influenza viral pneumonia= least common severest complication. Affects
mostly >65yrs. Progressive SOB, persistent fever, and cardiovascular compromise.
p. 464 hoffman for interventions/teaching