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which labs would indicate someone is in respiratory distress/failure?
an ABG (arterial blood gas) is the primary lab used to diagnose and measure respiratory distress and failure by checking oxygen, carbon dioxide, and blood pH levels
low PaO2 (Hypoxemia) during an ABG means?
a partial pressure of oxygen in arterial blood below 60 mmHg shows the lungs fail to oxygenate blood
high PaCO2 (Hypercapnia) during an ABG means?
a carbon dioxide level above 45 mmHg means the lungs cannot remove waste gas properly
low pH (Acidosis) during an ABG means?
a blood pH level below 7.35 indicates acid buildup caused by trapped carbon dioxide
low PaO2/FiO2 ratio during an ABG means?
a ratio of 300 or less helps define Acute Respiratory Distress Syndrome (ARDS)
What is tension pneumothorax?
life-threatening medical emergency where air continuously leaks into the space between the chest wall and the lung (the pleural space) and cannot escape
What are signs and symptoms of tension pneumothorax?
early signs are sudden severe shortness of breath, sharp one-sided chest pain, a racing heart rate, and absent breath sounds on the injured side.
As the condition worsens, it causes severe low blood pressure, bulging neck veins, and a shifted windpipe away from the affected side
what is flail chest?
a serious medical emergency that happens when three or more adjacent ribs are broken in at least two places, causing a section of the chest wall to become completely detached from the rest of the rib cage
what are the signs and symptoms of flail chest?
paradoxical breathing, extreme pain and tenderness, rapid, shallow breathing (tachypnea), shortness of breath, and a low blood oxygen level (hypoxia)
what is paradoxical breathing?
a broken segment of the chest wall moves inward when you inhale and bulges outward when you exhale, doing the exact opposite of the rest of the chest
simple: segment moves in on inspiration, out on expiration
What is the pathophysiology of asthma?
airways that are very sensitive/easily triggered. when triggered, they constrict (bronchoconstriction) and tighten the airway, making it harder to breathe. the airways also produce too much mucus
triggered → bronchoconstriction → airways swell → mucus produced → difficulty moving air, especially out
wheezing, shortness of breathe, cough
What is the pathophysiology of emphysema?
Alveolar wall destruction → loss of elastic recoil, air trapping, "pink puffer," barrel chest, pursed-lip breathing
What is the pathophysiology of chronic bronchitis?
Mucus gland hypertrophy, productive cough ≥3 months for 2 consecutive years, "blue bloater," cyanosis, edema
what are the common causes of pulmonary embolism?
Deep vein thrombosis (most common), immobility, surgery, long travel, estrogen, clotting disorders, fat embolus after long-bone fracture
what are the signs/symptoms of pulmonary embolism?
sudden dyspnea, pleuritic chest pain, tachycardia, tachypnea, hypoxia, cough/hemoptysis, anxiety
What interventions help prevent pulmonary embolism?
early ambulation, compression stockings/SCDs, leg exercises, hydration, prophylactic anticoagulants.
what is atelectasis?
the partial or complete collapse of a lung or a specific section (lobe) of the lung that happens when the tiny air sacs (alveoli) deflate or lose their volume
What interventions help prevent atelectasis?
incentive spirometry, deep breathing/coughing, early ambulation, repositioning, pain control
Orthopnea
dyspnea (shortness of breath) lying flat
Empyema
pus in pleural space
Pleurisy
inflamed pleura, sharp pain on breathing
Chyle
lymph fluid with fat (milky) in the pleural space
Pneumothorax
air in pleural space
What is a normal blood pressure for an adult?
120/80 mmhg
Thromboembolus
A clot that has broken off and traveled
Embolus
Any traveling mass (clot, air, fat)
Ischemia
Reduced blood supply, reversible
Infarction
Tissue death from prolonged ischemia
Atherosclerosis
Plaque (lipid) buildup in artery walls
Arteriosclerosis
Hardening/thickening of arteries
Angina
Chest pain from myocardial ischemia
Sepsis
Life-threatening dysregulated response to infection
What are the risk factors for the development of atherosclerosis?
HTN (hypertension), high LDL, smoking, diabetes, obesity, sedentary lifestyle, age, family history, male sex, stress
What is the pathophysiology of coronary artery disease?
endothelial Injury: Chronic irritation from high blood pressure, smoking, or high cholesterol damages the inner lining of the coronary artery
fatty Streak: Cholesterol (LDL) enters the damaged lining and gets eaten by immune cells, creating trapped, fatty "foam cells."
plaque Growth: Smooth muscle cells form a hard, fibrous cap over this fatty core, creating a mature plaque that narrows the artery and limits oxygen to the heart.
rupture & Clotting: If the plaque's cap cracks or ruptures, it triggers an immediate blood clot that can completely block the artery and cause a heart attack.
What causes coronary artery disease?
mainly atherosclerosis (also spasm, clot).
stable angina causes
Fixed plaque narrowing
what makes stable anginas worse?
Exertion, stress, cold
what makes stable anginas better?
rest, nitroglycerin
unstable angina causes
Plaque rupture/clot, unpredictable
what makes unstable anginas worse?
when a growing blood clot or a ruptured plaque further cuts off blood and oxygen to the heart muscle, rapidly causes HA
uniquely dangerous because it worsens unpredictably, often occurring with minimal physical effort or even while a person is completely resting.
what makes unstable anginas better?
does not get better with simple rest or standard home medicines, it requires emergency medical treatment in a hospital.
variant (Prinzmetal) angina causes
Coronary vasospasm
what makes variant (Prinzmetal) angina worse?
Smoking
Cocaine/vasoconstricting drugs
Cold exposure
Stress/emotional upset
Certain medications that cause vasoconstriction
Key idea: It’s caused by coronary artery spasm, often occurring at rest, especially at night/early morning.
what makes variant (Prinzmetal) angina better?
Nitroglycerin
đź’Š Calcium channel blockers
🛌 Rest (often resolves on its own)
Key idea: Treat the coronary artery spasm → blood flow improves → pain goes away.
Hypertrophic cardiomyopathy
thickened septum/ventricle wall, small chamber, diastolic filling impaired; genetic; risk of sudden death in athletes.
Dilated cardiomyopathy
enlarged, thin-walled, weak ventricle → systolic failure; causes: alcohol, viral infection, ischemia, genetic
Dilated cardiomyopathy causes
alcohol, viral infection, ischemia, genetic
Hypertrophic cardiomyopathy causes
genetic
left-sided heart failure
Blood backs up into lungs: dyspnea, orthopnea, crackles, cough, pink frothy sputum, fatigue
right-sided heart failure
Blood backs up into systemic veins: JVD, peripheral edema, hepatomegaly, ascites, weight gain
Systolic HF (HFrEF)
ventricle can't contract/eject (low EF)
Diastolic HF (HFpEF)
ventricle can't relax/fill (stiff, normal EF)
Iron deficiency anemia causes
Blood loss, poor intake
Iron deficiency anemia symptoms
Fatigue, weakness, pallor, SOB, tachycardia, pica
Iron deficiency anemia blood smear
Microcytic, hypochromic cells
B12 (pernicious) anemia causes
Vitamin B12 deficiency from lack of intrinsic factor
B12 (pernicious) anemia symptoms
Fatigue, pallor, neurologic symptoms (numbness/tingling), sore tongue
B12 (pernicious) anemia blood smear
Macrocytic, megaloblastic cells
Sickle cell anemia causes
inherited abnormal hemoglobin (HbS)
Sickle cell anemia symptoms
Pain crises, anemia, fatigue, jaundice
Sickle cell anemia blood smear
Sickle-shaped RBCs
Define shock
inadequate blood flow (perfusion) to the body's tissues → cells don't get enough oxygen.
What are the signs and symptoms of someone in septic shock?
early warm, flushed, fever, tachycardia, bounding pulse; late cold, clammy, hypotension unresponsive to fluids, altered mental status, oliguria, ↑ lactate.
What is MODS?
Multiple Organ Dysfunction Syndrome, When 2 or more organ systems become dysfunctional because of severe illness, often due to sepsis/shock.
What is the most common cause of MODS?
sepsis
What is DIC?
Disseminated Intravascular Coagulation, the body forms lots of tiny blood clots all over the body → uses up platelets & clotting factors → causes serious bleeding.
1st stage of DICs
First Stage (Clotting): Small blood clots form in tiny blood vessels across the body, which blocks blood flow to major organs like the kidneys, brain, or liver
2nd stage of DICs
Second Stage (Bleeding): The body uses up all its available platelets and clotting factors to make these unnecessary clots, leaving no resources left to stop normal bleeding. This leads to severe, uncontrollable bleeding internally and externally. [1, 2, 3]
What is the most common cause of DICs?
sepsis (also trauma, obstetric complications, malignancy); simultaneous clotting and bleeding.