Unit 3: Alterations In Diffusion

Front 1

This determines the amount of light absorbed by the vascular bed and calculates the saturation:

Back 1

-Oximeter (Well-oxygenated blood absorbs light differently than deoxygenated blood does)

Front 2

An abnormal accumulation of fluid in the alveoli and interstitial spaces of the lungs; considered a medical emergency and may be life threatening

Back 2

-Pulmonary edema

-If the hydrostatic pressure increases or the colloidal oncotic pressure decreases, the net effect will be fluid leaving the pulmonary capillaries and entering the interstitial space

Front 3

What is the most common cause of pulmonary edema?

Back 3

-Left-sided HF

Front 4

True or False:
O2 is considered a drug (clinically speaking)?

Back 4

-True

Front 5

What are the goals of O2 therapy?

Back 5

-Reduce WOB
-Maintain PaO2
-Reduce the workload of the heart
-Keep SaO2 >90% during rest, sleep, and exertion or PaO2 >60 mm Hg

Front 6

-Most common form of HF
-Results from left ventricular dysfunction, which prevents normal blood flow and causes blood to back up into the left atrium and into the pulmonary veins:

Back 6

-Left-sided HF

Front 7

-Causes a backup of blood into the right atrium and venous circulation
-Results in jugular venous distention and peripheral edema

Back 7

-Right-sided HF

Front 8

What is the primary cause of right-sided HF?

Back 8

-Left-sided HF

Front 9

Describe clinical manifestations of chronic HF:

Back 9

-Fatigue: one of the earliest symptoms, and caused by decreased CO, impaired perfusion to vital organs, decreased oxygenation of the tissues, and anemia
-Dyspnea: common and caused by increased pulmonary pressures secondary to interstitial and alveolar edema (may have dry, persistent cough, unrelieved by position change or suppressants)
-Tachycardia: early sign and the body's way to compensate for a failing ventricle
-Edema: common and may occur in the liver, abdomen, peripherally, and lungs
-Nocturia: impaired renal perfusion and decreased output during the day; when laying down, pulls fluid from the interstitial spaces back into the circulatory system is enhanced
-Skin Changes: dusky, swollen, diaphoretic
-Behavioral Changes: restlessness, confusion, decreased attention span or memory
-Chest Pain: increased myocardial work
-Weight Changes: from fluid retention

Front 10

Shortness of breath that occurs when the patient is in the recumbent position.

Back 10

-Orthopnea (Paroxysmal nocturnal dyspnea)

***Pay attention how many pillows a patient is using to sleep

Front 11

What drug classification would you use to decrease intravascular volume by reducing venous return?

Back 11

-Loop Diuretics

-By decreasing venous return to the LV and thereby reducing preload, the overfilled LV may contract more efficiently and improve CO which also increases LV function, decreases pulmonary vascular pressure, and improves gas exchange

Front 12

The resistance against which the LV must pump; that is, it is the amount of work the LV has to produce to eject blood into the systemic circulation:

Back 12

-Afterload

Front 13

This is the determinant of afterload, as is LV filling:

Back 13

-Systemic Vascular Resistance

Front 14

What medications would you choose to decrease afterload?

Back 14

-Sodium Nitroprusside
-Morphone Sulfate

Front 15

If you were wanting to reduce your patient's anxiety, which medications would you choose?

Back 15

-Morphine sulfate
-Benzodiazepines

Front 16

Name positive iontropes that help to improve cardiac function by increase contractility and also increasing myocardial O2 consumption:

Back 16

-Digitalis
-dopamine
-dobutamine
-epinephrine
-norepinephrine

Front 17

Name the 3 phases at which changes in ARDS are divided:

Back 17

1.) Injury or Exudative Phase
2.) Reparative or Proliferative Phase
3.) Fibrotic Phase

Front 18

During this phase of ARDS: usually occurs approx 1-7 days after the initial direct injury or host insult; engorgement of the interstitial space produces interstitial edema which then crosses over the alveolar epithelium and enters the alveolar space; Intrapulmonary shut develops because the alveoli fill with fluid, and blood passing through them cannot be oxygenated; Alveolar cells that produce surfactant (type I & II) are damaged and the decreased synthesis of surfactant causes atelectasis; Hyaline membranes develop and contribute to the development of fibrosis and atelectasis, leading to a decrease in gas exchange capability and lung compliance; Severe V/Q mismatch and shunting occur and lead to refractory hypoxemia; Eventually compensation mechanisms fail and hypoventilation, decreased CO, and decreased O2 perfusion eventually occur:

Back 18

-Injury or Exudative Phase

Front 19

Hypoxemia unresponsive to increasing concentrations of O2:

Back 19

-Refractory hypoxemia

Front 20

During this phase of ARDS: usually begins 1-2 weeks after the initial lung injury; There is an influx of neutrophils, monocytes, and lymphocytes and fibroblast proliferation as part of the inflammatory response; This phase is complete when the diseased lung becomes characterized by dense, fibrous tissue; Increased pulmonary vascular resistance and pulmonary HTN may occur in this stage because fibroblasts and inflammatory cells destroy the pulmonary vasculature; Lung compliance continues to decrease; Hypoxemia worsens; if this phase persists, widespread fibrosis results, but if this phase is arrested, the lesions resolve:

Back 20

-Reparative or Proliferative Phase

Front 21

During this stage of ARDS: usually occurs about 2-3 weeks after the initial injury; Called the chronic or last phase of ARDS; The lung is completely remodeled by sparsely collagenous and fibrous tissues; Diffuse scarring and fibrosis resulting in decreased lung compliance; Surface area for gas exchange is significantly reduced because the interstitium is fibrotic, and therefore hypoxemia continues; Pulmonary HTN results from pulmonary vascular destruction and fibrosis:

Back 21

-Fibrotic Phase