20181219-20190109 Flashcards
A 65-yr-old woman presents to the ER with shortness of breath. She has a history of diabetes and myocardial infarction 2 years ago. Cardiac exam reveals a displaced point of maximal impulse. Pulmonary auscultation reveals bilateral crackles and decreased breath sounds. Examination of her neck reveals normal JVP. Which of the following physical exam findings is most likely associated with this patient’s condition?
a. S3
b. Ascites
c. Pedal edema
d. Spleen and liver enlargement
A 65-yr-old woman presents to the ER with shortness of breath. She has a history of diabetes and myocardial infarction 2 years ago. Cardiac exam reveals a displaced point of maximal impulse. Pulmonary auscultation reveals bilateral crackles and decreased breath sounds. Examination of her neck reveals normal JVP. Which of the following physical exam findings is most likely associated with this patient’s condition?
a. S3
b. Ascites
c. Pedal edema
d. Spleen and liver enlargement
Explanation: Left heart failure. C, and D are all right heart failure.
Learning objectives:
137a Define the heart failure syndrome from a physiologic perspective
Atherosclerosis is associated with numerous well-known risk factors, such as age, smoking, diabetes, hyperlipidemia, and a family history of atherosclerosis. LDL-C is believed to be a key factor in the pathway through which hyperlipidemia causes atherosclerosis. What is the most likely first step in the pathogenesis of atherosclerosis caused by hyperlipidemia?
A. Endothelial dysfunction
B. Foam cell formation
C. LDL cholesterol oxidation
D. Monocyte activation
E. Plaque formation
Atherosclerosis is associated with numerous well-known risk factors, such as age, smoking, diabetes, hyperlipidemia, and a family history of atherosclerosis. LDL-C is believed to be a key factor in the pathway through which hyperlipidemia causes atherosclerosis. What is the most likely first step in the pathogenesis of atherosclerosis caused by hyperlipidemia?
A. Endothelial dysfunction
B. Foam cell formation
C. LDL cholesterol oxidation
D. Monocyte activation
E. Plaque formation
Explanation: Hyperlipidemia is a recognized risk factor for atherosclerosis. Current concepts describing the pathogenesis of this process suggest that
endothelial damage permits the movement of LDL-C into the subendothelial space. This LDL may then be modified (e.g. oxidized to oxLDL), which then may be taken up by macrophages, leading to the formation of foam cells, smooth muscle proliferation, and subsequent arterial plaques. The oxidation of LDL cholesterol increased monocytes/macrophage receptor affinity for the molecules and traps the lipid in the endothelial space. Macrophages that phagocytose these molecules become foam cells, which ten lead to other downstream effects of atherosclerosis such as calcification of occlusion of the vessel lumen. This in turn can lead to ischemia of various tissues, most notably the heart.
Learning objectives:
153a Explain the natural history and pathophysiology of peripheral arterial disease
129a Describe the natural history of atherosclerosis and understand how it manifests itself as MI, stroke, peripheral vascular disease, etc.
129a Describe the cellular and molecular etiology of atherosclerosis, and summarize how these cellular and molecular changes leads to the histopathologic changes seen.
132a Describe the role of endothelial dysfunction in leading to plaque rupture and erosion
Nitrates are often given as part of the management of angina. What is the primary mechanism by which nitrates work in the treatment of this condition?
A. Decrease in atrioventricular node conduction velocity
B. Decrease in heart rate and contractility
C. Increase in oxygen delivery to myocytes
D. Stimulate dilation of coronary arterioles
E. Stimulate venodilation
Nitrates are often given as part of the management of angina. What is the primary mechanism by which nitrates work in the treatment of this condition?
A. Decrease in atrioventricular node conduction velocity
B. Decrease in heart rate and contractility
C. Increase in oxygen delivery to myocytes
D. Stimulate dilation of coronary arterioles
E. Stimulate venodilation
Explanation: Nitrates are first line treatment in the management of angina. They act by stimulating the release of NO in smooth muscle, causing an increase in cGMP levels and subsequent smooth muscle relaxation, primarily in the venous system. Such venodilation causes a decrease in preload, which reduces left venticular wall stress and in turn minimizes myocardial oxygen consumption.
A. Mechanism of CCBs and adenosine
B. Beta blocker mechanism (also used to treat angina)
C. Nitrates act by stimulating venodilation to decrease preload and thereby reduce myocardial oxygen consumption. They do not act by increasing the oxygen supply to the myocardium. In the case of angina, cardiac vessels have depleted the dilation reserve.
D. Angina is caused by atherosclerotic stenosis within coronary arteries that limit blood flow through those vessels. Coronary arterioles in patients with flow limiting coronary stenosis are already dilated to maintain resting blood flow. Therefore, any vasodilating effects nitrates have on coronary arteries are negligible in the setting of already maximally dilated coronary arteries. Thus, stimulating the vasodilation of coronary arterioles is not the primary mechanism of nitrates in the treatment of angina.
Learning objective
131a Explain the role of medical therapy to reduce symptoms and improve quality of life
134a Predict the effects of anti-ischemic drugs on heart rate, blood pressure, myocardial inotropy, and coronary blood flow
Which of the following is not true regarding the coronary circulation?
A. During an event of angina, endocardium is the first part of the heart that is damaged.
B. Increased narrowing of coronary artery rapidly depletes the reserve vasodilation because of decreased coronary pressure after the stenotic area.
C. Most of the coronary resistance is controlled by the microvascular resistance, which in turn is controlled by metabolic factors and flow.
D. Atenolol would increase coronary circulation flow.
Which of the following is not true regarding the coronary circulation?
A. During an event of angina, endocardium is the first part of the heart that is damaged.
B. Increased narrowing of coronary artery rapidly depletes the reserve vasodilation because of decreased coronary pressure after the stenotic area.
C. Most of the coronary resistance is controlled by the microvascular resistance, which in turn is controlled by metabolic factors and flow.
D. Atenolol would increase coronary circulation flow.
Explanation: A. Because of higher compressive resistance, the vessel perfusing deeper myocardium are often at greater level of dilation and have lower dilatory reserve. This results in vulnerability when there is an increased demand of perfusion. B. Coronary artery stenosis would result in increased coronary pressure to maintain flow after the stenotic area. The majority of increased pressure is dissipated at the blockage (think about narrowing a hose to increase the water flow speed). C. In the myocardium, microvascular resistance plays a big role in determining the coronary resistance. This factor can be influenced by metabolism (the levels of adenosine) as well as the flow rate (which determines the production of vasodilator NO). D. Atenolol is a selective beta-1 antagonist would would have no effect on coronary circulation. The microvasculature of coronary vessel is mainly controlled by alpha and beta-2 adrenergic receptor. The blockade of former would lead to vasodilation and the blockade of latter would result in constriction. This is why selective beta-1 antagonist such as atenolol would be preferred.
Learning objective:
133a Explain coronary flow reserve and factors affecting its magnitude
133a Explain coronary atherosclerosis and factors determining the severity of a coronary artery stenosis
133a Explain the major factors governing coronary vascular resistance and coronary blood flow
133a Describe the normal balance between myocardial oxygen demand and coronary blood flow
134a Predict the effects of anti-ischemic drugs on heart rate, blood pressure, myocardial inotropy, and coronary blood flow
You are running a stress test. The patient has resting blood pressure 130/80 and heart rate of 75. The exercise goal is blood pressure 160/120 and heart rate of 150. Using the following diagram, at least what percentage of blockage would you expect if the patient experience angina at the goal of exercise?
- 50%
- 70%
- 80%
- 85%
- 90%
You are running a stress test. The patient has resting blood pressure 130/80 and heart rate of 75. The exercise goal is blood pressure 160/120 and heart rate of 150. Using the following diagram, at least what percentage of blockage would you expect if the patient experience angina at the goal of exercise?
- 50%
- 70%
- 80%
- 85%
- 90%
Explanation: Using the double product, we can determine the goal exercise would result in 2.46X in coronary flow (160*150/130/75). If the patient is symptomatic at the exercise goal, the maximal dilation would be below 2.46X. Therefore, the patient would have a 80% blockage based on the figure.
Learning objective:
133a Describe functional testing of stenosis severity
Elevations in cardiac enzymes are used to diagnose a myocardial infarction. Which cardiac enzyme becomes elevated approximately four hours after an MI and remains elevated 7-10 days afterward?
A. Aspartate aminotransferase
B. Brain natriuretic peptide
C. C-reactive protein
D. Creatine kinase-MB fraction
E. Lactate dehydrogenase
F. Myoglobin
G. Troponin
Elevations in cardiac enzymes are used to diagnose a myocardial infarction. Which cardiac enzyme becomes elevated approximately four hours after an MI and remains elevated 7-10 days afterward?
A. Aspartate aminotransferase
B. Brain natriuretic peptide
C. C-reactive protein
D. Creatine kinase-MB fraction
E. Lactate dehydrogenase
F. Myoglobin
G. Troponin
Explanation:
Cardiac troponin I levels (line A) become elevated in the first four hours after an MI and remain elevated for 7-10 days. It is the most specific protein marker for MI. However CK-MB is the enzyme of choice for detection of re-infarction within the first week. If re-infarction occurs, CKMB levels would again increase, whereas troponin levels remain elevated from the previous event.
A. Third enzyme to be elevated; nonspecific.
B. BNP is elevated in CHF when atria are stretched chronically. Not acutely elevated in MI.
C. CRP is a marker of inflammation. Not used to diagnose MI.
D. CK-MB peak in the first 24 hours and then decrease (line B)
E. LDH (line D) is the last cardiac enzyme to become elevated, on ~day 2 post MI
F. Myoglobin rises and falls within 6 hours post MI. Nonspecific for MI. Not used in the diagnosis of MI.
Learning objective:
130a Define the laboratory tests to confirm the diagnosis of MI.
132a Explain the various diagnostic tools to detect and quantify myocardial injury and necrosi
A 56-year-old man was admitted for a diagnostic evaluation of recent onset of chest pain. Three days before admission, he had woken up in the middle of the night with a tight precordial pain of strong intensity, lasting for 20 minutes, radiating to the upper left limb and accompanied by dyspnea, which led him to seek medical attention. The myocardial injury markers were not increased, and the ECG was not considered suggestive of acute myocardial ischemia. After receiving a prescription of atenolol and aspirin, the patient was instructed to seek the Cardiology Department for outpatient care. In the days following the initial clinical presentation, he had two new episodes with lower intensity and sought medical assistance at this Hospital. How would you classify the chest pain?
A. Stable angina.
B. Unstable angina
C. Atypical angina
A 56-year-old man was admitted for a diagnostic evaluation of recent onset of chest pain. Three days before admission, he had woken up in the middle of the night with a tight precordial pain of strong intensity, lasting for 20 minutes, radiating to the upper left limb and accompanied by dyspnea, which led him to seek medical attention. The myocardial injury markers were not increased, and the ECG was not considered suggestive of acute myocardial ischemia. After receiving a prescription of atenolol and aspirin, the patient was instructed to seek the Cardiology Department for outpatient care. In the days following the initial clinical presentation, he had two new episodes with lower intensity and sought medical assistance at this Hospital. How would you classify the chest pain?
A. Stable angina.
B. Unstable angina
C. Atypical angina
Explanation: Stable vs unstable refer to whether there is fixed pattern, trigger event and changes in quality. For this patient, the fact that there is no obvious trigger is worrisome for unstable angina. It should be noted that unstable angina often cannot be relieved with rest. Atypical angina refers to difference in the location patient experience the pain.
Learning objective:
131a State the definition, characteristics, and epidemiology of angina
At which of the following stage does platelet play a role in contributing to coronary artery disease?
A. Endothelial dysfunction
B. Foam cell formation
C. Monocyte activation
D. Plaque formation
E. Plaque rupture
At which of the following stage does platelet play a role in contributing to coronary artery disease?
A. Endothelial dysfunction
B. Foam cell formation
C. Monocyte activation
D. Plaque formation
E. Plaque rupture
Explanation: The atherosclerotic plaque formation starts from endothelial dysfunction and release of chemoattractants. Endothelial damage permits the movement of LDL-C into the subendothelial space. This LDL may then be modified (e.g. oxidized to oxLDL), which then may be taken up by macrophages, leading to the formation of foam cells, smooth muscle proliferation, and subsequent arterial plaques. The plaque may cause narrowing of the vasculature, and contribute to stable angina symptom. However, clot is not formed until the plaque is ruptured and the inside content activates tissue factor.
Learning objective:
131a Explain the interactions between platelets, clotting factors, and atherosclerotic plaques
A 64-year-old woman is evaluated in the ED 6 hours after the onset of severe crushing chest pain associated with diaphoresis, nausea, vomiting. Her medical history is significant only for hyperlipidemia; her medications are atorvastatin and aspirin. On physical exam, her BP is 140/88, and HR is 77bpm. The lungs are clear, and no cardiac murmurs are heard. Examination of the abdomen and extremities is normal. ECG shows a 3-mV ST elevation in leads II, III and aVF, with occasional premature ventricular contractions. The patient is given fibrinolytic therapy due to the inability to access a cath lab. The pain resolves, but she has two episodes of 6- to 10-beat ventricular tachycardia and stable hemodynamics parameters. ECG now shows <0.5mV ST elevation.
In addition to heparin and ASA, which of the following drug is the most appropriate next step to manage the patient?
A. Amiodarone
B. beta-blocker
C. Verapamil
D. Lidocaine
A 64-year-old woman is evaluated in the ED 6 hours after the onset of severe crushing chest pain associated with diaphoresis, nausea, vomiting. Her medical history is significant only for hyperlipidemia; her medications are atorvastatin and aspirin. On physical exam, her BP is 140/88, and HR is 77bpm. The lungs are clear, and no cardiac murmurs are heard. Examination of the abdomen and extremities is normal. ECG shows a 3-mV ST elevation in leads II, III and aVF, with occasional premature ventricular contractions. The patient is given fibrinolytic therapy due to the inability to access a cath lab. The pain resolves, but she has two episodes of 6- to 10-beat ventricular tachycardia and stable hemodynamics parameters. ECG now shows <0.5mV ST elevation.
In addition to heparin and ASA, which of the following drug is the most appropriate next step to manage the patient?
A. Amiodarone
B. beta-blocker
C. Verapamil
D. Lidocaine
Explanation: The arrhythmia patient is experiencing is most likely associated with reperfusion injury. Think about the accessory pathway, scarred tissue naturally conduct the electricity at a different rate. Usually these would not require additional medical therapy, but beta-blocker has been shown to reduce infarct size. Other drugs to consider are satin, and ACEI, especially if the patient have additional risk factors.
Learning objective:
131a Explain the role of medical therapy to reduce symptoms and improve quality of life
A 49-yr-old man is evaluated in the ED for chest discomfort accompanied by nausea and dyspnea that began 2 hr ago. On physical exam, BP is 109/78 and HR is 88bpm. There is no JVD and no carotid bruits. The lungs are clear. Cardiac exam shows normal S1 and S2, no gallops, rubs, or murmurs. Toponin is 6ng/mL (nl <0.5ng/mL). ECG shows ST elevation in lead II, III, and AVF.
He is treated with enoxaparin, ASA, metoprolol, and glycoprotein receptor blocker and is taken to the cath lab. A stent is placed into RCA. Follow-up echo shows normal wall motion, valvular function, and normal EF. By day 4, he has no complication and is ready to be discharged.
In addition to ASA, clopidogrel, and metoprolol, which of the following medication should be given at discharge?
A. Atorvastatin
B. Gemfibrozil
C. Nicacin
D. Wafarin
A 49-yr-old man is evaluated in the ED for chest discomfort accompanied by nausea and dyspnea that began 2 hr ago. On physical exam, BP is 109/78 and HR is 88bpm. There is no JVD and no carotid bruits. The lungs are clear. Cardiac exam shows normal S1 and S2, no gallops, rubs, or murmurs. Toponin is 6ng/mL (nl <0.5ng/mL). ECG shows ST elevation in lead II, III, and AVF.
He is treated with enoxaparin, ASA, metoprolol, and glycoprotein receptor blocker and is taken to the cath lab. A stent is placed into RCA. Follow-up echo shows normal wall motion, valvular function, and normal EF. By day 4, he has no complication and is ready to be discharged.
In addition to ASA, clopidogrel, and metoprolol, which of the following medication should be given at discharge?
A. Atorvastatin
B. Gemfibrozil
C. Nicacin
D. Wafarin
Explanation: For patients with previous MI histroy, statin should be maintained. He does not have additional risk factor of clotting, so there is no need to put him on anticoagulant (warfarin). If he has hyperlipidemia, fibrate should be added to reduce the risk of future cardiac event.
Learning objective:
128a Explain the pharmacologic properties of the various lipid drug classes
131a Explain the role of medical therapy to reduce symptoms and improve quality of life
134a
Inhibitors of the renin-angiotensin system are effective for blood pressure control and have beneficial effects upon endothelial dysfunction that can slow the progression of coronary artery disease and prevent atherothrombotic events such as stroke and heart attack.
A 50-year-old Caucasian male notices substernal chest pain while walking his dog uphill in Central Park on a sunny Saturday morning. The pain disappears after 5 minutes of rest, and he continues to enjoy his weekend. As he smokes a cigarette later in the day, he wonders: which of the following pathologies were most likely responsible for his chest pain that morning?
A. A fixed atherosclerotic plaque obstructing 80% of one of his coronary arteries
B. An ulcerated fibrous plaque in one of his coronary arteries
C. A pulmonary embolism
D. A ruptured atherosclerotic plaque in one of his coronary arteries
E. Weakening of aortic wall.
A 50-year-old Caucasian male notices substernal chest pain while walking his dog uphill in Central Park on a sunny Saturday morning. The pain disappears after 5 minutes of rest, and he continues to enjoy his weekend. As he smokes a cigarette later in the day, he wonders: which of the following pathologies were most likely responsible for his chest pain that morning?
A. A fixed atherosclerotic plaque obstructing 80% of one of his coronary arteries
B. An ulcerated fibrous plaque in one of his coronary arteries
C. A pulmonary embolism
D. A ruptured atherosclerotic plaque in one of his coronary arteries
E. Weakening of aortic wall.
Explanation: The patient has stable angina, which is most likely due to narrowing of coronary vessel. Ulcerated fibrous plaques are associated with unstable angina. Ruptured plaques with a fully obstructive thrombus are associated with a transmural MI.
Learning objective:
131a Explain the determinants of myocardial blood flow and how an imbalance between supply and demand can cause ischemia.
132a Describe the role of endothelial dysfunction in leading to plaque rupture and erosion
132a Explain how thrombosis requires the interaction of platelets and clotting factors
A 64-year-old male with a past medical history of obesity, diabetes, hypertension, and hyperlipidemia presents with an acute onset of nausea, vomiting, diaphoresis, and crushing substernal chest pain. Vital signs are temperature 37° C, HR 110, BP 149/87, and RR of 22 with an oxygen saturation of 99% on room air. Physical exam reveals a fourth heart sound (S4), and labs are remarkable for an elevated troponin. EKG is shown below. The pathogenesis of the condition resulting in this patient’s presentation involves:
A. Genetic inheritance of a mutation in ß-myosin or troponin expressed in cardiac myocytes
B. A fully obstructive thrombus at the site of a ruptured, ulcerated atherosclerotic plaque
C. A partially occlusive thrombus at the site of a ruptured, ulcerated atherosclerotic plaque
D. Destruction of the vasa vasorum caused by vasculitic phenomena
E. A stable atheromatous lesion without overlying thrombus
A 64-year-old male with a past medical history of obesity, diabetes, hypertension, and hyperlipidemia presents with an acute onset of nausea, vomiting, diaphoresis, and crushing substernal chest pain. Vital signs are temperature 37° C, HR 110, BP 149/87, and RR of 22 with an oxygen saturation of 99% on room air. Physical exam reveals a fourth heart sound (S4), and labs are remarkable for an elevated troponin. EKG is shown below. The pathogenesis of the condition resulting in this patient’s presentation involves:
A. Genetic inheritance of a mutation in ß-myosin or troponin expressed in cardiac myocytes
B. A fully obstructive thrombus at the site of a ruptured, ulcerated atherosclerotic plaque
C. A partially occlusive thrombus at the site of a ruptured, ulcerated atherosclerotic plaque
D. Destruction of the vasa vasorum caused by vasculitic phenomena
E. A stable atheromatous lesion without overlying thrombus
Explanation: The patient is having a STEMI (see V1-V3). This is due to complete occlusion of coronary artery either due to a thrombus or a ruptured plaque. A partially occlusive thrombus causes unstable angina, and usually do not cause ST segment change. (Note: the distinction b/w unstable angina and non-STEMI depends on the cardiac enzyme in the blood). Destruction of the vasa vasorum is associated with syphilis. A stable atheromatous lesion without overlying thrombus is usually associated with stable angina.
Learning objective:
132a Explain the various diagnostic tools to detect and quantify myocardial injury and necrosis
131a Compare the multiple techniques to diagnose ischemia
A 66-year-old gentleman presents to a new primary care physician to establish care after a recent relocation. His past medical history is significant for gout, erectile dysfunction, osteoarthritis of bilateral knees, mitral stenosis, and diabetic peripheral neuropathy. He denies any past surgeries along with the use of any tobacco, alcohol, or illicit drugs. He has no known drug allergies and cannot remember the names of the medications he is taking for his medical problems. He states that he has recently been experiencing chest pain with strenuous activities. What part of the patient’s medical history must be further probed before starting him on a nitrate for chest pain?
A .Gout
B. Erectile dysfunction
C. Arthritis
D. Mitral stenosis
E. Diabetic peripheral neuropathy
A 66-year-old gentleman presents to a new primary care physician to establish care after a recent relocation. His past medical history is significant for gout, erectile dysfunction, osteoarthritis of bilateral knees, mitral stenosis, and diabetic peripheral neuropathy. He denies any past surgeries along with the use of any tobacco, alcohol, or illicit drugs. He has no known drug allergies and cannot remember the names of the medications he is taking for his medical problems. He states that he has recently been experiencing chest pain with strenuous activities. What part of the patient’s medical history must be further probed before starting him on a nitrate for chest pain?
A .Gout
B. Erectile dysfunction
C. Arthritis
D. Mitral stenosis
E. Diabetic peripheral neuropathy
Explanation: Nitrate is contraindicated if the patient is simultaneously taking phosphodiesterase inhibitors (eg. Viagra).
Learning objective:
134a Predict the effects of anti-ischemic drugs on heart rate, blood pressure, myocardial inotropy, and coronary blood flow
A 55-year-old male is started on nitrate therapy for treatment of stable angina. He experiences significant and immediate relief of his symptoms within minutes of starting therapy. Approximately 48 hours after initiating this new medication, he notes return of chest pain and pressure with exertion that no longer responds to continued nitrate use. Which of the following regimen could explain the patient’s symptom?
A. Transdermal nitroglycerin patch placed at 7am then replaced with another at 7pm
B. Transdermal nitroglycerin patch placed at bedtime and removed at 7am
C. Transdermal nitroglycerin patch placed at 7am and removed at night
D. PO extended release isosorbide-5-mononitrate once daily at 8am
A 55-year-old male is started on nitrate therapy for treatment of stable angina. He experiences significant and immediate relief of his symptoms within minutes of starting therapy. Approximately 48 hours after initiating this new medication, he notes return of chest pain and pressure with exertion that no longer responds to continued nitrate use. Which of the following regimen could explain the patient’s symptom?
A. Transdermal nitroglycerin patch placed at 7am then replaced with another at 7pm
B. Transdermal nitroglycerin patch placed at bedtime and removed at 7am
C. Transdermal nitroglycerin patch placed at 7am and removed at night
D. PO extended release isosorbide-5-mononitrate once daily at 8am
Explanation: The patient likely is experience tolerance to nitrate becsauase he does not have sufficient nitrate free period (at least 8hr is needed). The regimen in B is good for night-time angina and C is good for angina associated with activities.
Learning objective:
134a Predict the effects of anti-ischemic drugs on heart rate, blood pressure, myocardial inotropy, and coronary blood flow
29-year-old woman is evaluated in the ED at 30 weeks gestation for increasing DOE. On physical exam, BP is 110/80 and HR is 98bpm regular. Bilateral crackles are heard. Cardiac exam shows a normal S1, a fixed split S2, a grade 2/6 early systolic murmur at the base, and grade 2/6 holo systolic murmur a the apex radiating to the axila. Echo shows global LV hypokinesis, 30% EF and moderate mitral regurgitation. Peripartum cardiomyopathy and HF are diagnosed. Which of the following HF medication is contraindicated:
A. Atenolol
B. Furosemide
C. Isosorbide dinitrate
D. Lisinopril
29-year-old woman is evaluated in the ED at 30 weeks gestation for increasing DOE. On physical exam, BP is 110/80 and HR is 98bpm regular. Bilateral crackles are heard. Cardiac exam shows a normal S1, a fixed split S2, a grade 2/6 early systolic murmur at the base, and grade 2/6 holo systolic murmur a the apex radiating to the axila. Echo shows global LV hypokinesis, 30% EF and moderate mitral regurgitation. Peripartum cardiomyopathy and HF are diagnosed. Which of the following HF medication is contraindicated:
A. Atenolol
B. Furosemide
C. Isosorbide dinitrate
D. Lisinopril
Explanation: ARB and ACE-inhibitor are associated with fetal renal agenesis and should be avoided in pregnancy. Exposure in second and third trimester exposure are related to impaired fetal/neonatal renal function, which results in oligohydramnios during pregnancy (amniotic fluid is largely derived from the fetal kidneys), and anuria and renal failure after delivery.
Learning objective:
Pharmacology of Anti-Hypertensives
Describe the different physiologic mechanisms that contribute to blood pressure
Describe the different options for treating hypertension
