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107 Cards in this Set
- Front
- Back
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Pneumothorax |
air in pleural cavity *Lungs cannot expand and may collapse |
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hemothorax |
blood in pleural cavity *Lungs cannot expand and may collapse |
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Cause of pneumothorax or hemothorax |
-external trauma -internal trauma |
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Dx Pneumothorax or hemothorax |
-chest x-ray |
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Thoracentesis (same as pleurocentesis) |
-Aspiration (removal) of fluid, blood, pus, or air from pleural space using a hollow needle -there is a risk of causing pneumothorax -too much fluid taken out at one time could possibly lead to a fluid shift in the body |
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Tx Pneumothorax or hemothorax |
-thoracentesis -chest tube (hemo-tube is placed low to drain fluid, pneumo-tube is placed high because air rises) *Analgesics*
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S/S Pneumothorax or hemothorax |
*Chest Pain* (pleuritic) -shallow, rapid resps -fever -changes in LOO/LOC secondary to hypoxemia -dyspnea -decreased SaO2 -hypoxemia (decrease O2 in blood) which leads to hypoxia (decrease O2 to tissues & organs |
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Tension Pneumothorax Patho |
-increased intrapleural pressure
-mediastinal shift -tracheal shifting -compressed vena cava - HR rises |
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Tension Pneumothorax S/S |
-tracheal deviation (away from side of pneumo) -decreased ventilation -increased resp distress -decreased BP -Increased HR |
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Exudate pleural effusion |
d/t inflammatory process, there is increased vessel permeability and increased exudate which leads to increased pleural edema and pulmonary edema. -Tx: Antibiotics & diuretics |
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empyema |
the collection of pus in a cavity in the body, especially in the pleural cavity |
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Pleural vs. Pulmonary effusion |
Pleural Effusion - decreased lung sounds, SOB, Pain, decreased O2SAT; chest tube and pleuroscentesis Pulmonary Effusion - crackles, decrease O2SAT; diuretics and chest physio |
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How does a V/Q scan work? (also called a ventilation/Perfusion scan)
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-pt breaths in radioactive gas, chest scan shows the exchange of arterial perfusion of lungs and reveals degree of gas distribution in the lungs.
(no fasting required, unless sedation is to be used)
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How does a D-Dimer work? |
-blood test to check clot degradation product in the blood -if positive, this test tells us that there is clots somewhere in the body - further testing required for location and extent -if negative, effectively rules out DVT and PE. |
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SARS management |
-corticosteriods (prednisone) to decrease inflammation -manage symtoms (fever, cough, SOB, dypnea, chills, headache, muscle ache, sore throat, diarrhea) -isolation (for 10days) |
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How does Heparin help with PE? |
it stops the growth and allows the body to break down clot. |
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ARDS (acute respiratory distress syndrome) causes |
-anything that causes a sever inflammatory response in the lung tissue (sepsis, trauma, aspiration, infection)
-pulmonary tissues are damaged and fibroic tissue takes it's place - leading to "lung stiffness" **these people will most likely be in ICU, d/t being on mechanical ventilator** |
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Early S/S of ARDS |
increased HR, BP, RR (trying to compensate to get more O2, and rid the body of excess CO2 -these people can't ventilate properly d/t pain! -restlessness, early dyspnea, X-Ray clear -on an ABG: they will also be presenting with mild decrease in O2 & mild decrease in CO2 |
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Later S/S of ARDS |
higher HR, BP, RR d/t anxiety and confusion -diaphoresis, anxiety, changes in LOO/LOC, cyanosis/pallor, increased crackles and wheezes -On an ABG: a decrease in O2 & an increase in CO2 |
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crepitus |
-is a medical term to describe the grating, crackling or popping sounds and sensations experienced under the skin and joints or a crackling sensation due to the presence of air in the subcutaneous tissue |
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Systolic |
when the heart contracts |
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Diastolic |
when the heart is a rest. |
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How is pulse pressure calculated? |
is the difference between the systolic and diastolic BP -Normal is between 30-40. (PP = systolic BP [SBP] - diastolic BP [DBP]) |
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Difference between angina and MI |
Angina = not enough O2 getting to tissues of heart MI = tissue DEATH which occurs d/t NO O2 to the heart tissue |
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unique features of unstable angina |
-new onset (not predictable) -occurs at rest -unresponsive to Nitro (sometimes) -worsening pattern |
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What test is the most reliable blood test for diagnosing an MI? |
Triponin - because it's related to cardiac muscle ONLY (specific test) myoglobin - unhelpful because it only tells that there has been muscle damage somewhere in the body (non-specific test) CK - useful only if correct band is ordered |
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What does the "lub" sound indicate? |
it marks the end of ventricular diastole (rest) |
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What does the "dub" sound indicate? |
it marks the end of ventricular systole (contraction) |
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What may cause Pulse Pressure (PP) to increase in range? |
-exercise (according to P&P, healthy adults can have a PP of 100 while exercising) -atherosclerosis (narrowing arteries yields an increased SBP) -anything that increases vascular resistance |
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What may cause Pulse Pressure (PP) to decrease in range? |
-trauma or blood loss -decreased preload -decreased cardiac output (cardiac failure) -decreased SBP |
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What are some risk factors for developing coronary artery disease (CAD)? |
-elevated serum lipids from diet (LDL deposit; cholesterol in artery walls) -Gender -Genetics: 1) (hypercholesterolemia: an excess of cholesterol in the bloodstream); 2) defects in artery walls -Type II DM (d/t neuropathy, leading to silent ischemia) -chronic renal failure -corticosteroids -hormone replacement therapy -high alcohol intake -refined sugar -sedentary lifestyle -smoking -obesity -having a high BP |
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What is silent ischemia? |
-have ischemia (restricted or reduced blood flow, and thus O2) without pain -they may have a heart attack with no prior warning -people with angina also may have undiagnosed episodes of silent ischemia -people who have had previous heart attacks or those with diabetes are especially at risk for developing silent ischemia |
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Arteriosclerosis |
-stiffening of blood vessel walls (loss of flexibility) in the large & medium sized arteries |
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Atherosclerosis |
-process of deposits of fat on the artery walls, causing blockages in the large and medium arteries, and also causing fibrous, calcified tissue underneath those deposits, thus causing stiffening of that portion of the wall of the artery. -this leads to arteriosclerosis! |
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stable angina |
-thoracic pain caused most often by myocardial anoxia as a result of atherosclerosis or spasm of the coronary arteries -pain usually radiates along neck, jaw, shoulder, and down the aspect of the left arm -often accompanied by impending death and feeling of suffocation, crushing pressure or pain in the chest -typically starts with physical or emotional exertion and subsides with rest -nursing interventions: prompt administration of nitrates, O2, narcotic analgesics as needed; provide comfort and supportive calm reassurance to reduce anxiety. |
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unstable angina |
-thoracic pain that may mark the onset of acute myocardial infarction -typically occurs at rest and has a sudden onset, sudden worsening, and stuttering reoccurence over days and weeks -it carries a more severe short-term prognosis than stable chronic angina |
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ectopic foci |
-an area in the heart that initiates abnormal beats -may occur in both healthy and diseased hearts and are usually associated with irritation of a small area of the myocardial tissue -they are produced in association with myocardial ischemia, drug effects (catecholamine), including pacemaker catheters. |
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What does preload mean?
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-what the chambers of the heart need to push out to the rest of the body
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What does afterload mean? |
-what the heart has to push against; anything outside of the heart!
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electrocardiogram (ECG) |
-a device for recording electrical activity of the myocardium to detect transmission of cardiac impulses through the conductive tissues of the muscle -leads are affixed to certain points of pt's chest which are hooked up to a monitor |
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troponin's test |
-assists in evaluating pt's with suspected acute coronary ischemic syndrome -useful in differentiating cardiac from non-cardiac chest pain, estimating MI size. - Levels of troponin can become elevated in the blood within 3 or 4 hours after heart injury and may remain elevated for 10 to 14 days. |
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dysrhythmia
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abnormality in a physiological rhythm, especially in the activity of the brain or heart |
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myoglobin test
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- used to detect muscle damage (non-specific) - myoglobin in the blood starts to rise within 2-3 hours of a heart attack or other muscle injury, reaches its highest levels within 8-12 hours, and generally falls back to normal within 24hrs - is excreted in the urine - NOT A GREAT TEST FOR SUSPECTED MI
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angiography |
-an X-Ray of the internal anatomy of the heart and blood vessels after the intravascular introduction of radiopaque contrast medium via a catheter that is placed through the femoral artery into the heart -used as a diagnostic aid in MI, vascular occlusion, CVA, portal hypertension, PE, and other heart/lung related events |
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angioplasty |
-cardiac catheter is placed through femoral artery and a stent in placed to expand artery where the blockage was -artery lumen is expanded and blood flow is restored! |
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coronary artery bypass graft surgery (CABG) |
-a type of surgery that improves blood flow to the heart -a healthy artery or vein from the body is connected, or grafted, to the blocked coronary artery -The grafted artery or vein bypasses (that is, goes around) the blocked portion of the coronary artery. This creates a new path for oxygen-rich blood to flow to the heart muscle. |
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pericardium |
-sack around the heart -can become inflamed/fluid filled, leading to pericarditis (antibiotics are needed and also may be drained of fluid with needle (pericardiocentesis) |
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myocardium |
-muscle of the heart -can have an infection of the muscle (usually caused from autoimmune disorders, bacteria/virus, radiation) -diagnostic tests would include an ECG, being on the cardiac ward, and having regular blood work taken |
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endocardium |
-inner lining of the heart (valves, inner most lining) -may have inflammation/infection, and blood may flow back into atria (called regurgitation) -decreased cardiac output, increased risk of stroke d/t pooling of blood in the atria -would need antibiotics to treat, also can have valve replacement surgery |
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MONA |
M-morphine O-oxygen N-nitro A-aspirin **Not specifically in this order!!** |
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atrial fibrillation (Afib) |
-is an irregular and often very fast heart rate -this may cause symptoms like heart palpitations, fatigue, and shortness of breath -we may see a BP of 180 bpm, but remember, the atrial rate could be as high as 350-600bpm, d/t irregular beating! |
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endocarditis |
an infection of the inner lining of your heart |
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pericarditis |
-Inflammation of the lining around the heart (the pericardium) that causes chest pain and accumulation of fluid around the heart -S/S: sharp chest pain on inspiration and when lying down; pericardial friction rub (from friction between roughened pericardium and epicardial surface); cough, dyspnea, tachycardia; confusion, restlessness -Treatment: antibiotics (infection), corticosteriods (inflammation), NSAIDs (inflammation/pain), pericardiocentesis (drain fluid) |
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myocarditis |
-an inflammation of the myocardium, the middle layer of the heart wall -can affect both the heart's muscle cells and the heart's electrical system, leading to reduction in the heart's pumping function and to irregular heart rhythms -is usually caused by a viral infection |
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How does Nitro increase cardiac output ? |
vasodilation occurs leading to decreased preload, decreased afterload, & decreased workload overall leads to increased cardiac output! **Always check BP first, before administering nitro!** |
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How does Morphine decrease cardiac workload? |
decreased pain leads to decreased RR, BP, & HR...therefore, decreased preload & afterload lead to decreased cardiac workload! **Always check BP first before administering Morphine!** |
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What are the beneficial effects of aspirin? |
lowers platelet aggrigation, which helps maintain arteries during acute inflammation and vaso-spasms; this leads to maintained blood flow to cardiac tissue. |
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What are some nursing considerations for a pt who has just undergone an angioplasty and/or angiography? |
**patient will probably be NPO before these procedures!** -monitor the site for bleeding -maintain pressure dressing -pt should be in supine position -monitor V/S -Check facility policy for specific's! |
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What is fibrinolytic therapy? |
-given to pt who has had an MI within 6 hrs. -given IV to dissolve the thrombus to restore circulation -pt will need to be closely monitored for further cardiac issues and will also be put on IV heparin to prevent new clots from forming ** The challenge is getting the person to hospital within the time frame needed.** **These people may also be on regular blood thinners, so increased risk of bleeding being on this kind of therapy.** |
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pathway of electrical conduction of the heart |
SA node (pacemaker) to atria, to AV node to the bundle of His (a collection of heart muscle cells specialized for electrical conduction) to the respective Purkinje fibers for each side of the heart |
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explanation of the P, QRS, & T waves of an ECG |
P - depolarization & contraction of atria (systoli) QRS - impulse through atria, bundles of His fibers and Purkinji fibers (depolarization of ventricles) T - ventricles repolarize |
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S/S of uncontrolled Afib |
-dizziness (decreased perfusion) -fatigue -S/S of stroke -increased RR -SOBOE (decreased CO, decreased O2) -crackles (pulmonary edema d/t inefficient L ventricle contractions, blood is backing up in the lungs) -irregular & elevated pulse (chaotic electrical firing) -increased BP (esp. if underlying HTN isn't controlled) -edema in lower extremities (inefficient R side, blood is backing up in lower extremities) |
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action of digitalis glycosides (Digoxin) |
slows heart rate down, strengthens contraction **check HR prior to administration: needs to be above 60bpm) |
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action of calcium channel blockers |
affect smooth muscles, slows HR **check HR prior to administration: needs to be above 50bpm) |
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action of beta blockers |
slows HR; causes vasodilation, dropping BP **check HR/BP prior to administration: needs to be above 50bpm) |
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other diagnostic tests |
ESR: non-specific test for inflammation C reactive protein: non-specific test for inflammation echocardiogram: sounds waves create picture of the heart, usually looking at valve function |
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subcutaneous emphysema |
-bubbles of air become trapped under the skin -can occur after surgery or traumatic accidents and can also develop locally in cases of gas gangrene One of the frequent causes is rupture of the lung tissue -air released from the alveoli during trauma seeks an escape route from the lungs; one of the pathways it can take is through the lung tissue to the region between the lungs (mediastinum), then rises to the neck, where it becomes trapped under the skin |
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mediastinum |
contains the heart and its vessels, the esophagus, trachea, phrenic and cardiac nerves, the thoracic duct, thymus and lymph nodes of the central chest |
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tracheostomy |
-a surgical procedure to create an opening through the neck into the trachea -indications for getting one: A large object blocking the airway, an inability to breathe on your own, Cancer of the neck, Paralysis, Severe neck or mouth injuries |
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atelectasis |
partial or complete collapse of the lung |
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leukopenia |
a reduction in the number of white cells in the blood, typical of various diseases |
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neutropenia |
-the presence of abnormally few neutrophils in the blood, leading to increased susceptibility to infection which can lead to sepsis. -indicated with <1-1.5 x 10/9/L (Normal count range: 1.5-8x10/9/L) -It is an undesirable side effect of some cancer treatments -HUGE INFECTION RISK - CHECK TEMP FREQUENTLY. Normal S/S of infection will not show as there is an extremely low WBC count - hardly any "fighters" coming to fight the infection. -reverse isolation (+pressure room), +++hygiene, change linens daily, no shared washroom, monitor for low-grade fever, as this is the only sign that will tell you an infection is present, monitor neutrophil count |
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pancytopenia |
deficiency of all three cellular components of the blood (red cells, white cells, and platelets) |
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petechiae |
-small red or purple spots caused by bleeding into the skin. |
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polycythemia |
-this increased viscosity & blood volume, thus increasing workload of heart, increasing afterload, and increasing coagulation events (increased clots!) -an abnormally increased concentration of hemoglobin in the blood, through either reduction of plasma volume or increase in red cell numbers -may be a primary disease of unknown cause, or a secondary condition linked to respiratory or circulatory disorder or cancer |
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thrombocytosis |
is a disorder in which your body produces too many platelets (thrombocytes), which play an important role in blood clotting |
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hemochromatosis |
a hereditary disorder in which iron salts are deposited in the tissues, leading to liver damage, DM, and bronze discoloration of the skin |
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myeloma |
a malignant tumor of the bone marrow |
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thalassemia |
-any of a group of hereditary hemolytic diseases caused by faulty hemoglobin synthesis, widespread in Mediterranean, African, and Asian countries -treatments: blood transfusion, spleenectomy (rare), bone marrow transplant, IV fluids to flush kidneys |
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disseminated intravascular coagulation |
- is a pathological process characterized by the widespread activation of the clotting cascade that results in the formation of blood clots in the small blood vessels throughout the body - can ultimately lead to multiple organ damage |
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What are the components of blood? |
RBCs, WBCs & Platelets (make up about 45%) Plasma (proteins, H2O, other solutes - makes up about 55%) |
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What % of blood is water? |
about 91% |
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Anemia |
a lack of red blood cells or hemoglobin in the blood |
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What causes anemia? |
-blood loss -lack of RBC production -a diet lacking in iron, folic acid, vitamin B12 -pregnancy -certain diseases -increased rate of RBC destruction (sickle cell, hemolytic anemia, thalassmais) |
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What is aplastic anemia? |
-it is a deficiency of all types of blood cells caused by failure of bone marrow development |
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complications of acute aplastic anemia |
1) arrythmias 2) heart failure 3) infections |
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how is aplastic anemia managed? |
-Neupogen (drug to treat neutropenia) given to stimulate WBC growth -erythropoietin to stimulate RBC growth -blood transfusion -bone marrow transplant -immunosuppresants |
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What is hemolytic anemia? |
it is any breakdown of RBCs which jams up the kidneys with all the cell breakdown debris |
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S/S of hypovolemicanemia d/t massive blood loss |
Pallor Tachycardia,weak pulse Hypotension Cool, damp skin Thirst Decreased u/o Restlessness Decreasing LOC Low hgb, hctand RBC count |
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Whatwill be the overall medical goals of treating someone with a gunshot would and hypovolemic anemia? |
1) Stop thebleeding & restore fluid and lytes (Surgery toclean and close the wound) 2) Preventinfection of his wound (A bloodtransfusion) |
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What are the S/S ofIron Deficiency anemia or B12 deficiency? |
Pallor irritability reduced energy coldness fatigue dyspnea Decreased serumiron, Hgb, hct, CBC |
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What things would you recommend someone with Iron Deficiency anemia if they have a poor diet? |
-Dietarychanges-meats, beans, leafy green veges etc -Ironsupplements-expect black/tarry stool, possible constipation -Vitamin Cassists in absorption of iron…encourage orange juice -Also, Fish& egg (B12) |
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Whatis the common Tx for pernicious anemia? |
Increase PO B12(diet / tablets) – IM injections for people with malabsorption problems or lackof intrinsic factor – this must be continued for life |
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A pt presents with fatique, abdominal pain, chest pain, andshortness of breath. He is running a slight fever and has tachycardia. His labresults show low Hct, and a rising Cr and BUN. Whattype of anemia would you diagnose him with? |
Sickle cell anemia |
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What is the major complication for sickle cell anemia? |
thickening of the blood (d/t the bunching up of RBCs), causing occlusions in the vessels. |
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What are two of the primarygoals associated with the treatment of polycythemia? |
decrease the blood volume and decrease the bone marrow activity |
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Which system is most often implicated ascausative in the different types of thrombocytopenia? |
the immune system |
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Why do patients get an RBC transfusion? |
low Hgb, low RBCs, hemorrhage or part of disease process |
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Why do patients get a plasma transfusion? |
clotting factors low - cancers, liver disease, to preventhemorrhage (ie if platelets low) |
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Why do patients get an albumin transfusion? |
To increase albumin levels – to create oncoticpressure to draw fluid back into circulation – ie ascites associated with liverdisease |
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Why do patients get a platelet transfusion? |
-to replace platelets toprevent bleeding – diseases that lower platelet count and / or low coagulationfactors |
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When is a hemolytic reaction most likely to happen? |
Within 15mins of transfusion (the first 25cc of blood) -Stay with your patient for the first 15mins of EACH unit infused! |
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What are the typical S/S of a hemolytic reaction to a blood transfusion? |
chills, flank pain, hives, itchiness, pulmonary edema,decrease BP, increase HR, ***cardinal sign: increase of >= 1 degree C |
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George has just started his second unit of packedRBCs. He is complaining of slight itchiness and has a rash on his chest. Whatdo you do? |
Stop or slowdown transfusion and contact physician immediately for direction – this is notyet a major reaction and the MD may order you to stop the infusion, but likelywill order you to continue at a slower rate and monitor – chart that MD orderand continue at a slower rate with close monitoring. |
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Andy is half way through his platelet transfusion.His baseline vitals before the transfusion were 120/87, HR 76, RR20, Sao2 98%on RA and temp 36.2C. You check his vital signs now and they are 130/95, HR 81,Sao2 94% on RA, temp 37.3C. Hesays he is feeling fine. Do you need to do anything? |
YES, the classic sign of atransfusion reaction is a rise in temp >= 1C. Even though he is feelingfine, his body may be reacting. Stop the blood infusion, start the NS line andcontact the physician immediately. Follow the agency protocol for transfusionreactions. |
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treatments for sickle cell anemia |
-bone marrow transplant -increase in IV fluids (flush kidneys & increase perfusion to organs) -IV marcotics (to treat pain) -RBC transfusion, erythropoeitin - to treat cause -hydroxurea (anti-sickling agent) |
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S/S of polycythemia |
-headache, dizziness -stroke (d/t increased viscosity & clotting) -hemorrhagic pneumonia (vessel rupture from increased pressure) -increased BP, Heart Failure -itchiness -GI bleeds & rupture -Claudication, thrombophelbitis -Gout (d/t increased urea) |
