EXAM 3 CARDIAC AND RESPIRATORY
ARDS - ANS -an acute injury to the alveolocapillary membrane producing massive pulmonary
inflammation
-increased capillary permeability
-severe pulmonary edema causing further impaired diffusion of oxygen through the alveolocapillary
membrane.
ARDS - First phase - ANS · >> Dyspnea and hypoxemia with poor response to oxygen
supplementation
ARDS - Second phase - ANS · >> Hyperventilation and respiratory alkalosis
ARDS-·THIRD PHASE - ANS >> Decreased tissue perfusion, metabolic acidosis, and organ dysfunction
ARDS-· FOURTH PHASE - ANS >> Increased work of breathing, decreased tidal volume, and
hypoventilation
ARDS-FIFTH PHASE - ANS >> Hypercapnia, respiratory acidosis, and worsening hypoxemia
Acute respiratory failure is caused by - ANS inadequate gas exchange or ventilation (PaO2, ≤50
mmHg or PaCO2 ≥50 mmHg and pH ≥7.25).
What is the difference in pathophysiology between a female and male who may be diagnosed with
an NSTEMI? - ANS Women have smaller and less stable vessels
Prinzmetal angina (also known as variant angina) cause - ANS occurs due to vasospasm—a sudden
narrowing of the coronary arteries caused by contraction of the heart's smooth muscle tissue within
the vessel walls.
Prinzmetal angina (also known as variant angina) timing - ANS It typically happens at rest, often
during the night or early morning.
,Prinzmetal Angina (Variant Angina): symptoms - ANS Chest pain or discomfort that may radiate to
the arm, head, or shoulder.
Prinzmetal Angina (Variant Angina): testing - ANS Coronary artery disease may not always be evident
on diagnostic tests.
Prinzmetal Angina (Variant Angina): treatment - ANS Medications are commonly used for Prinzmetal
angina
Stable Angina (Classic Angina): Cause - ANS Stable angina results from permanent vessel occlusion
due to atherosclerosis (buildup of fatty plaque) in the coronary arteries.
Stable Angina (Classic Angina):Timing: - ANS It occurs predictably during exertion or exercise
Stable Angina (Classic Angina):Symptoms: - ANS Chest pain or discomfort related to physical activity.
Stable Angina (Classic Angina): Testing: - ANS Coronary artery disease is usually detectable on
diagnostic tests.
Stable Angina (Classic Angina): Treatment: - ANS Lifestyle modifications, medications, and
sometimes invasive procedures are used for stable angina
A prolonged QT interval indicates that the heart: - ANS is experiencing an extended refractory
period, making the ventricles more vulnerable to dysrhythmias.
Long QT Syndrome (LQTS):
Arrhythmias
Torsades de Pointes (TdP):
Long QT Syndrome (LQTS) - ANS A heart rhythm disorder that can potentially cause fast, chaotic
heartbeats.
,LQTS is a heart rhythm disorder characterized by an abnormally lengthy QT interval.
It increases the risk of irregular heartbeats, which can cause fainting, seizures, or sudden death.
Episodes may be triggered by exercise or stress
A prolonged QT interval-Arrhythmias: - ANS Prolonged QTc (corrected QT interval) can cause
premature action potentials during late phases of depolarization.
This increases the risk of developing ventricular arrhythmias, including ventricular fibrillation (a life-
threatening arrhythmia)
A prolonged QT interval-Torsades de Pointes (TdP): - ANS TdP is a specific type of ventricular
tachycardia associated with prolonged QT intervals.
It can lead to fainting, drowning, or sudden cardiac death
A patient has a transudative pleural effusion but has minimal symptoms. What blood test should be
performed for the evaluation of this condition? - ANS Serum Albumin Concentration Gradient:
Measure the albumin concentration gradient between serum and pleural fluid. In almost all patients
with transudative effusion, this gradient exceeds 1.2 mg/dL1.
Pleural Fluid Cholesterol Level: Check the concentration of cholesterol in the pleural fluid. If it's >60
mg/dL, it suggests a transudative effusion.
Additional Tests: Serum LDH (lactate dehydrogenase) and total protein levels can also be helpful
What is the most appropriate measurement of the severity of an acute asthma exacerbation? - ANS
Forced FEVI
A patient with a prior history of diabetes, and an injury that has severely limited his ability to walk
now presents with acute onset of dyspnea and severe hypoxemia. Upon arrival in the ED, his BP
drops as well. What tests would you order? What do you think you would find during the work up? -
ANS Pulmonary embolism
, Asthma: Pathophysiology: - ANS is primarily an inflammatory disorder of the airways that leads to
bronchial hyperresponsiveness and reversible airway obstruction.
It is characterized by episodes of wheezing, breathlessness, chest tightness, and coughing,
particularly at night or in the early morning.
Asthma: Triggers: - ANS Asthma attacks are often triggered by allergens, cold air, exercise, or
respiratory infections.
Asthma: Reversibility: - ANS Airflow limitation in asthma is usually reversible either spontaneously or
with treatment.
COPD pathophysiology - ANS persistent airflow limitation that is usually progressive and associated
with an enhanced chronic inflammatory response in the airways and the lung to noxious particles or
gases.
COPD Causes: - ANS is long-term exposure to irritants that damage the lungs and airways, typically
cigarette smoke. Other pollutants and occupational dusts can also contribute.
COPD Inflammation - ANS involves neutrophils, macrophages, and lymphocytes, and is characterized
by structural changes in the lung tissue, including destruction of the alveoli (emphysema) and
thickening of the airway walls (chronic bronchitis).
COPD Irreversibility - ANS Unlike asthma, the airflow limitation in COPD is not fully reversible, even
with medication.
Early asthmatic response (Phase1): Asthma - ANS o a maximum in the first 30 minutes and resolves
within one to three hours
§ Inhaled antigen (1) binds to mast cells covered with preformed immunoglobulin E (IgE). Mast cells
degranulate.
§ Mast cells release inflammatory mediators such as histamine, bradykinins, leukotrienes,
prostaglandins, platelet-activating factor, and interleukins.
ARDS - ANS -an acute injury to the alveolocapillary membrane producing massive pulmonary
inflammation
-increased capillary permeability
-severe pulmonary edema causing further impaired diffusion of oxygen through the alveolocapillary
membrane.
ARDS - First phase - ANS · >> Dyspnea and hypoxemia with poor response to oxygen
supplementation
ARDS - Second phase - ANS · >> Hyperventilation and respiratory alkalosis
ARDS-·THIRD PHASE - ANS >> Decreased tissue perfusion, metabolic acidosis, and organ dysfunction
ARDS-· FOURTH PHASE - ANS >> Increased work of breathing, decreased tidal volume, and
hypoventilation
ARDS-FIFTH PHASE - ANS >> Hypercapnia, respiratory acidosis, and worsening hypoxemia
Acute respiratory failure is caused by - ANS inadequate gas exchange or ventilation (PaO2, ≤50
mmHg or PaCO2 ≥50 mmHg and pH ≥7.25).
What is the difference in pathophysiology between a female and male who may be diagnosed with
an NSTEMI? - ANS Women have smaller and less stable vessels
Prinzmetal angina (also known as variant angina) cause - ANS occurs due to vasospasm—a sudden
narrowing of the coronary arteries caused by contraction of the heart's smooth muscle tissue within
the vessel walls.
Prinzmetal angina (also known as variant angina) timing - ANS It typically happens at rest, often
during the night or early morning.
,Prinzmetal Angina (Variant Angina): symptoms - ANS Chest pain or discomfort that may radiate to
the arm, head, or shoulder.
Prinzmetal Angina (Variant Angina): testing - ANS Coronary artery disease may not always be evident
on diagnostic tests.
Prinzmetal Angina (Variant Angina): treatment - ANS Medications are commonly used for Prinzmetal
angina
Stable Angina (Classic Angina): Cause - ANS Stable angina results from permanent vessel occlusion
due to atherosclerosis (buildup of fatty plaque) in the coronary arteries.
Stable Angina (Classic Angina):Timing: - ANS It occurs predictably during exertion or exercise
Stable Angina (Classic Angina):Symptoms: - ANS Chest pain or discomfort related to physical activity.
Stable Angina (Classic Angina): Testing: - ANS Coronary artery disease is usually detectable on
diagnostic tests.
Stable Angina (Classic Angina): Treatment: - ANS Lifestyle modifications, medications, and
sometimes invasive procedures are used for stable angina
A prolonged QT interval indicates that the heart: - ANS is experiencing an extended refractory
period, making the ventricles more vulnerable to dysrhythmias.
Long QT Syndrome (LQTS):
Arrhythmias
Torsades de Pointes (TdP):
Long QT Syndrome (LQTS) - ANS A heart rhythm disorder that can potentially cause fast, chaotic
heartbeats.
,LQTS is a heart rhythm disorder characterized by an abnormally lengthy QT interval.
It increases the risk of irregular heartbeats, which can cause fainting, seizures, or sudden death.
Episodes may be triggered by exercise or stress
A prolonged QT interval-Arrhythmias: - ANS Prolonged QTc (corrected QT interval) can cause
premature action potentials during late phases of depolarization.
This increases the risk of developing ventricular arrhythmias, including ventricular fibrillation (a life-
threatening arrhythmia)
A prolonged QT interval-Torsades de Pointes (TdP): - ANS TdP is a specific type of ventricular
tachycardia associated with prolonged QT intervals.
It can lead to fainting, drowning, or sudden cardiac death
A patient has a transudative pleural effusion but has minimal symptoms. What blood test should be
performed for the evaluation of this condition? - ANS Serum Albumin Concentration Gradient:
Measure the albumin concentration gradient between serum and pleural fluid. In almost all patients
with transudative effusion, this gradient exceeds 1.2 mg/dL1.
Pleural Fluid Cholesterol Level: Check the concentration of cholesterol in the pleural fluid. If it's >60
mg/dL, it suggests a transudative effusion.
Additional Tests: Serum LDH (lactate dehydrogenase) and total protein levels can also be helpful
What is the most appropriate measurement of the severity of an acute asthma exacerbation? - ANS
Forced FEVI
A patient with a prior history of diabetes, and an injury that has severely limited his ability to walk
now presents with acute onset of dyspnea and severe hypoxemia. Upon arrival in the ED, his BP
drops as well. What tests would you order? What do you think you would find during the work up? -
ANS Pulmonary embolism
, Asthma: Pathophysiology: - ANS is primarily an inflammatory disorder of the airways that leads to
bronchial hyperresponsiveness and reversible airway obstruction.
It is characterized by episodes of wheezing, breathlessness, chest tightness, and coughing,
particularly at night or in the early morning.
Asthma: Triggers: - ANS Asthma attacks are often triggered by allergens, cold air, exercise, or
respiratory infections.
Asthma: Reversibility: - ANS Airflow limitation in asthma is usually reversible either spontaneously or
with treatment.
COPD pathophysiology - ANS persistent airflow limitation that is usually progressive and associated
with an enhanced chronic inflammatory response in the airways and the lung to noxious particles or
gases.
COPD Causes: - ANS is long-term exposure to irritants that damage the lungs and airways, typically
cigarette smoke. Other pollutants and occupational dusts can also contribute.
COPD Inflammation - ANS involves neutrophils, macrophages, and lymphocytes, and is characterized
by structural changes in the lung tissue, including destruction of the alveoli (emphysema) and
thickening of the airway walls (chronic bronchitis).
COPD Irreversibility - ANS Unlike asthma, the airflow limitation in COPD is not fully reversible, even
with medication.
Early asthmatic response (Phase1): Asthma - ANS o a maximum in the first 30 minutes and resolves
within one to three hours
§ Inhaled antigen (1) binds to mast cells covered with preformed immunoglobulin E (IgE). Mast cells
degranulate.
§ Mast cells release inflammatory mediators such as histamine, bradykinins, leukotrienes,
prostaglandins, platelet-activating factor, and interleukins.
