Thoracic Surgeries Flashcards
- Understand structure and function of the upper and lower respiratory tract, and the chest wall.
- Understand the oxygen supply and demand framework and how to utilize it in nursing practice
- Understand the significance of arterial blood gas values and the oxygen-hemoglobin dissociation curve in relation to respiratory function.
- Identify signs and symptoms of inadequate oxygenation and the implications of these findings.
- Learn nursing management of the patient who requires a tracheostomy.
- Identify the mechanisms involved and the clinical manifestations of pneumothorax, fractured ribs and flail chest.
- Describe the purpose, methods and nursing responsibilities related to chest tubes.
- Explain the types of chest surgery and appropriate preoperative and postoperative care.
- Understand structure and function of the upper and lower respiratory tract, and the chest wall.
upper resp tract:
Rt bronchiole is less curved/straighter, sits higher = aspirates NG/suction catheter/food into RT lung > Lt lung
Nose to bronchioles is only a conducting pathway = “anatomical deadspace” = has air in it all the time but no O2 diffusion or ventilation happening. Normal tidal volume = 500 ml and 150 ml is anatomic deadspace
lower resp tract:
is below the carina bifurcation
-surfactant= lipid protein that is on the surface of alveoli = lowers surface tension and decreases pressure needed to inflate the alveoli. When surfactant is insufficient = alveoli collapse = atelectasis
-pulm circ: pulm arteries carry deoxygenated blood. Viens bring O2 blood back to heart
ventilation
thoracic cage, pleura, and resp muscles
Lungs are lined with 2 membranes. Pleura join and forms a closed sac and has afferent pain fibers so each breath causes pain.
Space between pleural layers = interpleural space. Filled with 25 ml fluid = lubrication and increase coeision
Diaphram creates negative pressure. Controlled by the phrenic nerve. So paralysis/injury at or above C3 will lead to problems with ventilation dt paralysis of the diaphragm
Fluid is drained by lymphatic circulation so >25-30ml fluid means an issue with drainage mechanism. Fluid accumulation decreases lung expansion.
Reasons: -malignant cells block lymphatic drainage -imbalance between intravascular and oncotic fluid pressures in HF -pleural effusion = third spacing, ascites
ventilation problems
empyema____: the Presence of purulent fluid with bacterial infection (like an abcsess in the plureal space)
pneumothorax_______: air in the pleural space
hemothorax________: blood in the pleural space
Each of these conditions can lead to partial or complete collapse of the lung.
ventilation
inspiration and expiration, changes in pressure
inspiration: contraction of the diaphragm and thoracic muscles, rib cage expands, negative pressure
exhalation: diaphragm relaxes, rig cage contracts
O2 and CO2 move across the alveolar-capillary membrane by diffusion.
Compliance: a measure of the elasticity of the lungs and the thorax.
compliance decreases = lung inhalation difficult
1 Conditions that increase fluid in lungs ex.
edema,
2.Conditions that make lung tissue less elastic ex.
pulm fibrosis,
3. Conditions that restrict lung movement -
pleural effusion
curve
Normal PaO2: 80-100 mmHg
SaO2= % of o2 bound to hemoglobin
PaO2 = amount of O2 dissolved in blood
O2 delivered to the tissues depends on the amount of O2 transported to the tissues and the ease with which hemo gives up the O2
Upper flat:
large changes in Pa cause small changes in hemoglobin saturation. 100 can drop down to 60 mmHg without seeing big changes in Sats. Drops 7%, so from 97% to 90%. Pt is adequately oxygenated when paO2 is at at least 60 mmHg
Lower portion:
as hemoglobin is desaturating, larger amounts of O2 is released for tissue use. Important for adequate O2 supply to peripheral tissues to protect tissue oxygenation.
shift RIGHT: hemo gives O2 to tissues
conditions: low pH, high temp, high CO2
shift LEFT: affinity for O2.
conditions: low temp, low CO2, high pH
O2 = end organ perfusion = life
urine output, lab. BUN creatinine UP, eGFR, DOWN
Poor cap refill, tachycardia, chest pain/angiana, SOB, ECG changes,
GUT: nausea, pain
oxygen supply vs oxygen demand balance
Compensatory VS pathologic things that happen to increase O2 supply= changes treatment. Ex. Tachypnea could be a useful way to increase O2 into lungs OR a symptom of a condition
Oxygen supply
relies on:
1) Arterial oxygen content: “Amount of oxygen that is present in the arterial blood when it leaves the lungs” (PaO2)
2) HEMOGLOBIN: “Capacity of the blood to transport oxygen to the cells” (Hgb)
3) HEART FUNCTION: “Effectiveness of the pump that circulates the blood throughout the body” (Cardiac output)(Gillespie & Shakell, 2008)
Oxygen demand
depends on:
1) Temperature
2) Activity level
3) Stress (emotional and physiological)
Factors affecting oxygen supply
Ventilation:
-PaCO2
-RR
-Tidal volume, vital capacity, functional residual capacity
-Work of breathing (WOB)
-Respiratory muscle function
-Lung compliance
-Airway resistance
Tidal Volume: amount of air moving in and out of lungs with each resp cycle
Impact on tidal volume: Pain while breathing ex. abd sx
Vital capacity: greatest volume that can be expelled by lugs after taking the deepest possible breath
-less vital capacity will have less capacity to compensate
Functional residual capacity: volume remaining in lungs after a normal exhale. Normal passive normal: 3L
WOB: To meet O2 supply needs
-Resp muscle func: MS, neuromuscular problems, spinal cord injury, pts who don’t have accessory muscle function to expel mucous
Lung compliance: lungs ability to stretch and expand Ex COPD (things that cause scarring of lungs) fibroids
Alveolar gas exchange
-PaO2
-V/Q mismatch
-Alveoli ventilated?
-Alveoli perfused?
-ventilation: perfusion sould be 1:1.
-Mismatch= either the lung is receiving o2 but no
blood flow
OR
receiving blood flow but no O2.
-mismatch causes: PE (no blood flow = no diffusion),
pulm edema, pain (no ventilation)
-Cardiac Output (CO)
-HR x Stroke volume
-stroke volume is influenced by:
Contractility
Preload
Afterload
Contractility: muscle effectiveness to eject full volume of blood (effectiveness of the pump)
preload: amount of blood in V’s before contraction
Afterload: amount of resistance/pressure to pump against, includes systemic vascular resistance
-Diffusion
-CO2 diffuses 20x more rapidly than O2
-CO2 levels are significantly affected by
ventilation
-Driving pressure of CO2
*CO2 is more valuable to monitor than PaO2
Oxygen transport and delivery impacted by:
- Hemoglobin levels
- O2-hemoglobin affinity
pH, Co2, temp
ACIDOCIC CONDITIONS (SEPSIS): High CO2, low pH= reduced affinity= tissues get more O2
Sepsis – high metabolic needs – hgb trying to let go of O2 to meet needs
ALKALOTIC CONDITIONS: Low CO2 = high pH = O2 does not want to leave hgb
Cool temp= minimize workload on heart = minimize metabolic demands = tissues don’t need as much O2
HR and BP
Map: 70-100 mmHg
Essentially reflects the diameter and elasticity of the blood vessels
-How does HR compensate for changes in BP?
drop in BP = HR increases to perfuse
-What is Mean Arterial Pressure (MAP)?
MAP: during one heart cycle – influenced by
vascular resistance. More accurate than BP.
Tells us tissues are getting perfused.
Low MAP = end organ perfusion not good
