the lecture on the conventional drugs used to treat chest pain-- otherwise known as angina. there are three types of angina, stable, unstable, and prinzmetal / atypical. stable is brought on by exertion, relieved by rest, and palliated with vasodilators. unstable is pain that is increasing in frequency and severity, brought on by diminishing levels of exertion and not aided by vasodilators. prinzmetal is a type related to vasospasm of the coronary artery. out of these three types, stable angina is the most treatable by anti-angina drugs, which come in three classes: nitrates, calcium channel blockers, and beta blockers.
nitrates work by way of nitric oxide, a natural vasodilator that stimulates the guanyl cyclase enzyme which activates the cGMP pathway, producing smooth muscle relaxation and vasodilation. there are two classes of nitrates; nitroglycerins and isosorbide dinitrates. both are used in acute MI's as well as prophylaxis before exertional activity. nitroglycerins can be administered in a number of different ways; sublingually and IV for quick onset (1-2 minutes), topically and transdermally for longer duration (12-24 hours). side effects might include headache and hypotension, which is especially a danger for patients taking viagra simultaneously. isosorbide dinitrates are similar to nitroglycerins in their mechanism and indications but are longer lasting and slightly less potent.
beta blockers are agents that inhibit the beta adrenergic receptors in the heart, leading to less stimulation by catecholamines. this has several effects: decreased cardiac contractility and rate decreases oxygen demand, thereby reducing the risk for ischemia in a post-MI. propranolol is an example of a non-selective beta blocker, meaning it acts upon both the beta-1 receptors in the heart as well as the beta-2 receptors in the bronchi, causing potential for bronchoconstriction as a side effect. atenolol / tenormin is a beta blocker that is more selective for beta-1 receptors, allowing for less potential for bronchoconstriction. both have the danger of rebound hypertension if stopped abruptly.
another class of anti-angina drugs are calcium channel blockers, which inhibit the influx of calcium into myocardial cells. this has the effect dilating the cardiac and peripheral arteries, as well as lowering rate of contraction. amlodopine / norvasc is an example, which is indicated especially in variant angina due to vasospasm. NB: calcium channels should not be combined with beta blockers for danger of hypotension / bradycardia due to synergistic effects.
morphine disulfate is the number one drug of choice in pain relief in cases of unstable angina or an MI. it is administered intravenously and titrated until symptoms are lessened. it is an opiate receptor agonist which also causes peripheral vasodilation. thus it has the potential for hypotension, but its effects can be reversed through naloxone.
questions
nitrates...
1. what are the three classes of drugs used to treat angina?
2. mechanism of nitrate action?
3. two main classes of nitrate drugs?
4. two indications for nitroglycerin?
5. effect on preload?
6. which methods of administration have the quickest onset?
7. which methods of administration have the longest duration?
8. two main side effects of nitroglycerins?
9. which other drug is contraindicated for simultaneous use and why?
10. how does the potency of isosorbide dinitrate compare with nitroglycerin?
propranolol / inderal...
11. mechanism of action of beta blockers?
12. indications for beta blockers?
13. indications for propranolol?
14. potential effect on another organ system?
15. abrupt continuation may cause...
16. difference between propranolol and atenolol.
amlodopine / norvasc...
17. class / mechanism?
18. indication?
19. onset of action?
20. calcium channel blockers should not be combined with...
morphine sulfate...
21. mnemonic of protocol for patient with unstable angina?
22. morphine's effects are reversible via...
23. mechanism of action?
24. potential for what adverse effect?
answers
1. nitrates, beta blockers, calcium channel blockers. [NBC]
2. conversion of drug to nitrate ion, formation of nitric oxide, activation of guanyl cyclase, increased cGMP levels, smooth muscle relaxation, vasodilation. [nitrate, nitric, guanyl, cGMP, relaxation]
3. nitroglycerin / nitrostat
isosorbide dinitrate / isordil
4. acute MI relief or prophylaxis before exertion.
5. preload reduced due to relaxed peripheral venous tone.
6. sublingual and IV both have 1-2 minute onsets.
7. topical and transdermal.
8. headache and hypotension.
9. viagra because of the danger of severe hypotension.
10. lower potency.
11. beta blockers block the beta-1 cardiac receptors, leading to a decrease in cardiac contractility and rate, leading to a decrease in oxygen requirement.
12. acute MI to reduce infarct size as well as post MI.
13. post MI
hypertension
panic attacks
migraine headaches
14. potential blockage of beta-2 receptors in the bronchi, leading to bronchoconstriction.
15. rebound hypertension and tachycardia.
16. atenolol is a selective beta blocker whereas propranolol is not-- less chance for bronchoconstriction.
17. blocks influx of calcium into myocardial cells, thus dilating cardiac and peripheral arteries, as well as decreasing contractility and rate.
18. angina, especially variant / vasospastic. hypertension.
19. 3-6 hours.
20. beta blockers.
21. MONA
morphine if pain not relieved by nitrates
supplemental oxygen
sublingual nitroglycerin
aspirin.
22. naloxone.
23. opiate receptor agonist.
24. hypotension.
Showing posts with label angina. Show all posts
Showing posts with label angina. Show all posts
Tuesday, November 30, 2010
Tuesday, January 19, 2010
pathology III: cardiovascular pathologies
this was the first lecture of the cardiac pathology series by dr. marcus miller, MD ND. we talked about the pathogenesis of coronary artery disease, atherosclerosis, and the ischemic heart diseases that can result from occlusion of the coronary artery. the first topic was atherosclerosis and the development and disruption of atherosclerotic plaques. in short, plaques are formed in the walls of blood vessels by high LDL levels which then penetrate into the intima of vessels and are oxidized, stimulating monocyte recruitment which leads to fatty streaks (clusters of macrophages that have ingested high levels of LDL). smooth muscle migration, extracellular matrix deposition, and formation of a fibrous cap around a core made largely of lipids and necrotic cellular debris eventually forms, protruding into the lumen of arteries.
if the fibrous cap of atherosclerotic plaques are disrupted by various factors such as sheer forces or simply a weakened area of the cap attracting inflammatory cells, the highly thrombogenic subendothelium and lipid core is exposed and thrombosis occurs, which generally leads to complete occlusion of the artery. if this occurs in the coronary artery, several conditions can result, such as angina pectoris refers to retrosternal chest pain that radiates to the left side that can be caused by ischemia or thrombosis.
the most severe condition results from ischemia that progresses to complete infarction of the myocardium, leading to an acute MI. infarction of the myocardium causes a switchover to anaerobic metabolism that decreases ATP levels in the myocardial cells-- this causes increased cellular permeability and decreased cellular function and eventual cell death. ATP levels can decrease as soon as 1-2 minutes and drop down to 50% of original levels in 10 minutes after the infarction. morphological changes of heart tissue include blue darkening and interstitial edema (4-12 hours), appearance of darker purple spots (12-24 hours), followed by tannish yellow areas of infarction (1-3 days), hyperemia, coagulation necrosis, decreased cell wall thickness (3-7 days). scar formation begins in 2-8 weeks and is completed in 2-3 months.
questions...
atherosclerosis...
1. where are atherosclerotic lesions usually located?
2. describe the role of smooth muscle in the development of atherosclerotic lesions.
3. what is the most commonly accepted theory of etiology for atherosclerosis?
4. what are some factors that contribute to endothelial damage?
coronary artery disease...
5. what is the most common cause of CAD?
6. describe a typical atherosclerotic plaque which might result in sudden thrombosis of the coronary artery.
7. describe the progression of the rupture of an atherosclerotic plaque in the coronary artery.
ischemic heart disease...
8. what are the four major results of ischemia of blood flow to the heart?
9. what is angina pectoris?
10. what is stable angina caused by? what are some unique symptoms?
11. An unstable angina is most likely the prodrome to what?
12. what is variant / Prinzmetal angina?
myocardial infarctions...
13. what is the most common pathogenesis of acute MI's?
14. what are some other possible etiologies of AMI's?
15. describe the reduction of ATP production with the amount of ischemia that leads to an MI.
16. describe the sequence of cellular injury that occurs with decreased ATP production in an MI.
17. when does irreversible cell death of myocardium occur?
18. what is the number 1 sequelae to an MI?
gross morphological changes in an MI during...
19. less than 4 hours...
20. 4-12 hours...
21. 12-24 hours...
22. 1-3 days...
23. 3 to 7 days...
24. 2 to 8 weeks...
25. 2 to 3 months...
answers
1. vessel bifurcations, large/mid sized arteries.
2. smooth muscle migrates from the media to the intima of atherosclerotic regions and builds up extracellular matrix around the plaque.
3. the "response to injury" theory in which endothelial damage causes inflammation which recruits monocytes, which then extravasate into the vessels and make fatty streaks, and then atherosclerotic plaques.
4. obesity, high LDL levels, diabetes mellitus, hyperglycemia, hypertension, turbulent blood flow, cigarette smoke.
5. fixed atherosclerotic narrowing or thrombus of disrupted atherosclerotic plaque of coronary artery.
6. the typical plaque that causes CAD is an unstable plaque that only causes mild or moderate stenosis and blocks less than 50% of the lumen prior to rupture and thrombosis.
7. a weakened fibrous cap attracts inflammatory cells which increases likelihood of rupture, which then exposes the thrombogenic subendothelium and lipid core, resulting in thrombosis.
8. myocardial infarction, angina pectoris, chronic heart failure, sudden cardiac death.
9. retrosternal chest pain that radiates to the left side and comes in paroxysmal and recurrent attacks, caused by ischemia that falls short of necrosis.
10. ischemia due to a fixed lesion; symptoms might include claudication and mesenteric angina.
11. generally a prodrome to an MI, transient ischemic attack or stroke.
12. angina caused by coronary artery vasospasm; pain at rest.
13. coronary artery plaque rupture and thrombosis.
14. coronary artery emboli from high cholesterol or infection, coronary artery vasospasm, hypoxia from underlying pulmonary disease or CO poisoning, arteritis.
15. ATP decreases starting 1-2 mins and can be reduced to 50% by 10 mins.
16. decreased ATP production inhibits action of Na/K ATPase pump which increases cell permeability. cell function further disrupted by degradative enzymes that are released from myocytes upon influx of calcium into cardiac muscle cells.
17. 15-20 minutes from onset of injury.
18. pericarditis.
19. often no change notable.
20. pale, blue, edematous.
21. darker spots of blue and purple.
22. tannish yellow areas of infarction.
23. hyperemia around infarcted areas, decreased wall thickness, coagulation necrosis.
24. greyish white scar formation.
25. scar formation complete.
if the fibrous cap of atherosclerotic plaques are disrupted by various factors such as sheer forces or simply a weakened area of the cap attracting inflammatory cells, the highly thrombogenic subendothelium and lipid core is exposed and thrombosis occurs, which generally leads to complete occlusion of the artery. if this occurs in the coronary artery, several conditions can result, such as angina pectoris refers to retrosternal chest pain that radiates to the left side that can be caused by ischemia or thrombosis.
the most severe condition results from ischemia that progresses to complete infarction of the myocardium, leading to an acute MI. infarction of the myocardium causes a switchover to anaerobic metabolism that decreases ATP levels in the myocardial cells-- this causes increased cellular permeability and decreased cellular function and eventual cell death. ATP levels can decrease as soon as 1-2 minutes and drop down to 50% of original levels in 10 minutes after the infarction. morphological changes of heart tissue include blue darkening and interstitial edema (4-12 hours), appearance of darker purple spots (12-24 hours), followed by tannish yellow areas of infarction (1-3 days), hyperemia, coagulation necrosis, decreased cell wall thickness (3-7 days). scar formation begins in 2-8 weeks and is completed in 2-3 months.
questions...
atherosclerosis...
1. where are atherosclerotic lesions usually located?
2. describe the role of smooth muscle in the development of atherosclerotic lesions.
3. what is the most commonly accepted theory of etiology for atherosclerosis?
4. what are some factors that contribute to endothelial damage?
coronary artery disease...
5. what is the most common cause of CAD?
6. describe a typical atherosclerotic plaque which might result in sudden thrombosis of the coronary artery.
7. describe the progression of the rupture of an atherosclerotic plaque in the coronary artery.
ischemic heart disease...
8. what are the four major results of ischemia of blood flow to the heart?
9. what is angina pectoris?
10. what is stable angina caused by? what are some unique symptoms?
11. An unstable angina is most likely the prodrome to what?
12. what is variant / Prinzmetal angina?
myocardial infarctions...
13. what is the most common pathogenesis of acute MI's?
14. what are some other possible etiologies of AMI's?
15. describe the reduction of ATP production with the amount of ischemia that leads to an MI.
16. describe the sequence of cellular injury that occurs with decreased ATP production in an MI.
17. when does irreversible cell death of myocardium occur?
18. what is the number 1 sequelae to an MI?
gross morphological changes in an MI during...
19. less than 4 hours...
20. 4-12 hours...
21. 12-24 hours...
22. 1-3 days...
23. 3 to 7 days...
24. 2 to 8 weeks...
25. 2 to 3 months...
answers
1. vessel bifurcations, large/mid sized arteries.
2. smooth muscle migrates from the media to the intima of atherosclerotic regions and builds up extracellular matrix around the plaque.
3. the "response to injury" theory in which endothelial damage causes inflammation which recruits monocytes, which then extravasate into the vessels and make fatty streaks, and then atherosclerotic plaques.
4. obesity, high LDL levels, diabetes mellitus, hyperglycemia, hypertension, turbulent blood flow, cigarette smoke.
5. fixed atherosclerotic narrowing or thrombus of disrupted atherosclerotic plaque of coronary artery.
6. the typical plaque that causes CAD is an unstable plaque that only causes mild or moderate stenosis and blocks less than 50% of the lumen prior to rupture and thrombosis.
7. a weakened fibrous cap attracts inflammatory cells which increases likelihood of rupture, which then exposes the thrombogenic subendothelium and lipid core, resulting in thrombosis.
8. myocardial infarction, angina pectoris, chronic heart failure, sudden cardiac death.
9. retrosternal chest pain that radiates to the left side and comes in paroxysmal and recurrent attacks, caused by ischemia that falls short of necrosis.
10. ischemia due to a fixed lesion; symptoms might include claudication and mesenteric angina.
11. generally a prodrome to an MI, transient ischemic attack or stroke.
12. angina caused by coronary artery vasospasm; pain at rest.
13. coronary artery plaque rupture and thrombosis.
14. coronary artery emboli from high cholesterol or infection, coronary artery vasospasm, hypoxia from underlying pulmonary disease or CO poisoning, arteritis.
15. ATP decreases starting 1-2 mins and can be reduced to 50% by 10 mins.
16. decreased ATP production inhibits action of Na/K ATPase pump which increases cell permeability. cell function further disrupted by degradative enzymes that are released from myocytes upon influx of calcium into cardiac muscle cells.
17. 15-20 minutes from onset of injury.
18. pericarditis.
19. often no change notable.
20. pale, blue, edematous.
21. darker spots of blue and purple.
22. tannish yellow areas of infarction.
23. hyperemia around infarcted areas, decreased wall thickness, coagulation necrosis.
24. greyish white scar formation.
25. scar formation complete.
Sunday, January 10, 2010
CPD II: cardiovascular pathologies
in the second lecture of the cardiac pathologies series we began with the different cardiac tests used to diagnose heart conditions, then went into specific cardiac pathologies. there are several different tests for diagnosing cardiac pathologies, each with their own advantages and disadvantages. the ECG is a measure of the electrical activity of the heart and is best in discerning arrhythmias, ischemia, enlarged chambers. the electrical impulse of the beating heart are manifested on a realtime graph, which can be dissected into several components: PQRST, where the P wave represents atrial depolarization, QRS represents ventricular depolarization, and T represents ventricular repolarization. deviations of shape/rhythm in the ECG wave can indicate various cardiac pathologies (for example, pericarditis induces an elevated ST wave). the echocardiogram is an ultrasound of the heart that is best for determining valvular dysfunction, chamber hypertrophy, cardiomyopathies. EBCT is electron bean computed tomography, useful in determining coronary artery dysfunction. the PET test measures myocardial perfusion by means of radionuclides such as thallium and technitium. finally, stress testing is a ECG measured concurrently with exercise or chemical stimulation of the heart; the best way to measure coronary artery dysfunction.
there are countless pathologies available to the heart and circulatory system. arterial hypertension is high blood pressure either from a multitude of factors (primary) or from a single underlying disease (secondary). atherosclerosis results from high LDL levels which causes plaque formation in arteries and is exacerbated by diabetes mellitus. angina pectoris is chest pain generally caused by ischemia caused by coronary artery dysfunction and can be stable (worse upon exertion, better with rest) or unstable (happens at rest). acute coronary syndromes result from more severe coronary artery ischemia leading to infarction and necrosis, and include unstable angina, NSTEMI, STEMI. congestive heart failure is the dysfunction of the right or left ventricle and have symptom pictures that appear as fluid overload (right) or respiratory problems (left). cor pulmonale is right ventricular hypertrophy that is secondary to a lung disorder such as COPD. finally, cardiomyopathies are dysfunctions of myocardium that are diagnosed when other main etiologies such as valvular, HTN, pulmonary are ruled out. there are three types: dilated, restrictive, hypertrophic.
questions
cardiac testing...
1. what are ECG's used to assess?
2. what do the different components of the PQRST wave represent in the ECG?
3. which test is better to assess valvular dysfunction, the ECG or echocardiography?
4. what is the echocardiogram useful for assessing?
5. describe the difference between the TTE and TEE.
6. what does the EBCT test stand for and what does it measure?
7. what are MRI/MRA tests useful in determining?
8. PET measures...
9. examples of myocardial perfusion nuclides...
10. stress testing is a good way to assess....
arterial hypertension...
11. describe the demographic / racial trends for arterial hypertension.
12. what is the most common cause of arterial hypertension in children?
13. what are some risk factors for arterial hypertension?
14. what is the difference between primary and secondary hypertension?
15. what are some possible etiologies for primary arterial hypertension?
16. what are some examples of diseases that can cause secondary hypertension?
17. arterial hypertension patients are usually...
18. describe the symptom picture of patients with arterial hypertension.
19. what is an early sign of arterial hypertension?
20. what are some signs in a patient with arterial hypertension that might indicate an emergency situation?
21. what would you ask in a medical history of a patient with arterial hypertension?
22. what are some important aspects of the physical examination of a patient with arterial hypertension?
23. how might the specific lab tests differ for a patient who was newly diagnosed with HTN vs. a patient who has left ventricular hypertrophy or ST depression?
24. what are some blood tests that one might perform to aid in the diagnosis of arterial hypertension?
atherosclerosis...
25. describe the role of LDL in the pathogenesis of atherosclerosis.
26. what are the risk factors for developing atherosclerosis?
27. relationship of diabetes and pathophysiology of atherosclerosis.
28. describe the symptom picture/timeline for a patient with atherosclerosis.
29. what are some tests to screen for atherosclerosis?
angina...
30. angina is the result of...
31. describe the general location and sensation of the symptoms in angina pectoris.
32. unique aspects of symptom picture of angina pectoris?
33. what heart sound might be heard in a patient with angina pectoris?
34. how does the way that women experience angina pectoris differ from that of men?
35. what is variant / prinzmetal angina?
36. what is microvascular angina?
37. what is a silent ischemia?
38. what are some clues from the physical exam of a patient with chest pain that indicate coronary artery disease?
39. point tenderness over the chest wall indicates...
40. angina EKG characteristics.
41. possible differential diagnoses for angina pectoris.
acute coronary syndromes...
42. what are the hallmarks of unstable angina?
43. define NSTEMI.
44. define STEMI.
45. in general what is the etiology of acute coronary syndromes?
46. describe the symptom picture of a patient with NSTEMI or STEMI.
47. what are the tests that are diagnostic of these conditions?
48. what are some sounds one might hear upon auscultation of heart in a NSTEMI or STEMI patient?
49. blood tests.
50. ECG characteristics.
51. prognosis of the three types of acute coronary syndromes.
52. complications of MI?
53. what is the "post MI syndrome"?
left congestive heart failure...
54. what is congestive heart failure?
55. what are some possible etiologies for congestive heart failure?
56. LCHF causes...
57. what is the relationship between renal failure and CHF?
58. what is the relative difference in overall presentation of LCHF and RCHF?
59. general/systemic S/SX of LCHF.
60. respiratory S/SX of LCHF.
61. cardiac S/SX of LCHF.
62. etiologies of LCHF?
63. what are some complications of LCHF?
64. what are the differential diagnoses for LCHF?
right congestive heart failure...
65. general S/SX of RCHF.
66. cardiac S/SX of RCHF.
67. what are some possible etiologies of RCHF?
68. what are some possible differential diagnoses of RCHF?
69. what are the classes of CHF as defined by the New York Heart Association?
70. what would the chest xray of a CHF patient show?
71. what is a blood test that might aid in the diagnosis of CHF?
72. what is the best test for diagnosis of CHF and what might the test show?
73. ∂escribe the utility of a stress test in congestive heart failure.
74. what are some blood markers that might be abnormal in CHF?
75. why must water intake/output be monitered in CHF patients?
cor pulmonale...
76. what is cor pulmonale?
77. what is the etiology of cor pulmonale?
78. S/SX of cor pulmonale.
79. a chest xray of a patient with cor pulmonale might show...
80. tests that aid in the diagnosis of cor pulmonale are...
cardiomyopathies...
81. when are cardiomyopathies suspected?
82. what are the three types of cardiomyopathies?
83. describe the symptom picture dilated cardiomyopathy?
84. prognosis for dilated cardiomyopathy?
85. what is hypertrophic cardiomyopathy?
86. etiology of hypertrophic cardiomyopathy?
87. describe the typical patient and symptom picture of hypertrophic cardiomyopathy.
88. hypertrophic cardiomyopathy might result in...
89. what is a typical heart sound of hypertrophic cardiomyopathy?
90. which tests aid in the diagnosis of hypertrophic cardiomyopathy?
91. what is the least prevalent form among the types of cardiomyopathies and what is it characterized by?
92. what does restrictive cardiomyopathy result in?
93. what are common symptoms of a patient with restrictive cardiomyopathy?
94. what are the cardiac symptoms of a patient with restrictive cardiomyopathy?
answers
1. arrhythmias, myocardial ischemia, enlarged chambers.
2. P=atrial depolarization, QRS=ventricular depolarization, T=ventricular repolarization
3. echocardiography-- ECG cannot assess valvular dysfunction.
4. valvular disorders, chamber hypertrophy or dilation, blood flow, cardiomyopathies, heart failure, pericarditis.
5. TTE is more common and less invasive. TEE is used for more posterior structures of the heart, pacemaker implantation, prosthetic valves.
6. electron beam computed tomography, useful for assessing coronary artery disease.
7. mediastinal evaluation, dysfunction of aorta, muscles, non-coronary vessels.
8. myocardial perfusion via radionuclides.
9. thallium and technitium.
10. coronary artery disease.
11. more prevalence in african americans (32%) than european or mexican americans.
12. kidney disease.
13. genetic predisposition, poor lifestyle, diet (high salt intake in particular), stress, obesity.
14. primary is due to multiple factors whereas secondary is caused by a single underlying disease.
15. alcohol, OCP's, corticosteroids, cocaine, licorice (extreme, ridiculous amounts).
16. renal disease, pheochromocytoma, cushing's, primary aldosteronism, hyperthyroidism, myxedema, aortic coarctation.
17. asymptomatic.
18. associated with very high blood pressure: dizziness, flushing, headache, fatigue, epistaxis,
19. the 4th heart sound (S4).
20. diastolic BP above 120mmHg, JVD, CNS disorders, lung crackles (might indicate the pulmonary edema associated with heart failure), severe retinopathy.
21. history of heart disease, any lifestyle risk factors, DM, hyper/dyslipidemia, salt intake, stimulant use (especially cocaine), known duration of HTN.
22. besides vitals: fundoscopic exam to assess for retinopathy, ausculation of neck and abdominal bruits, CVP and neuro exam.
23. new dx- urinalysis and resting ECG. left ventricular hypertrophy: echocardiogram.
24. creatinine, BUN, K, Na, Mg, Calcium, glucose, lipids, TSH, homocysteine, CRP-hs, fibrinogen, fractionated lipids.
25. oxidized LDL uptake into subendothelial layers of blood vessels causes inflammation and atheroma formation, increasing risk for ischemia or stenosis.
26. obesity, atherogenic dyslipidemia, HTN, insulin resistance, prothrombic states, pro-inflammatory states, smoking, hyperhomocysteinemia.
27. diabetes can increase "advanced glycation end products" which damage endothelial cells and increase inflammation.
28. might be asymptomatic for years or decades, then symptoms of ischemia (angina, TIA, IC), then progress to acute symptoms such as unstable angina, stroke, limb pain, sudden death.
29. besides history and risk factor screening: blood tests (lipid profile, blood sugar, homocysteine, CRP-hs, fibrinogen, CBC), stress testing, imaging tests (fast CT, carotid ultrasound, catheterization) can be helpful.
30. myocardial ischemia.
31. a "substernal heaviness or pressure" that may radiate to jaw, neck, left shoulder/arm.
32. pain lasts 15-30 seconds, worse in cold weather, after a meal, or contact with cold air.
33. S4 gallop.
34. various differences: for women, angina pectoris occurs more often with diabetes, is accompanied by more muscular discomfort, nausea, shortness of breath, fatigue, and is more often mistaken for indigestion.
35. angina that is due to coronary artery spasm as opposed to arteriosclerosis.
36. angina that develops from small vessel dysfunction- which results in a normal arteriogram.
37. coronary artery dysfunction that has no symptoms, most often occuring in diabetics.
38. decreased peripheral pulses, bruits in femoral/carotid arteries, xanthomas.
39. indicates that angina probably not due to CAD.
40. usually normal between attacks. during attacks: visible Q waves, T wave inversion, maybe ST depression. possible: smaller R wave, bundle branch disturbances.
41. cervicothoracic spine abnormalities, costochondral separation, Gi disease, pulmonary disease, pericarditis, mitral valve prolapse.
42. prolonged chest pain at rest, increasing/worsening symptoms, transient ECG changes.
43. Non ST Elevation MI: "myocardial necrosis without ST elevation of Q waves"
44. myocardial necrosis with ST elevation (and possible Q waves)
45. acute obstruction of an artery, usually a coronary artery thrombus.
46. deep, intense substernal pain that is not relieved by anything. restlessness, apprehension, dyspnea, diaphoresis, nausea, vomiting.
47. ECG within 10 minutes of MI and cardiac marker tests are diagnostic.
48. murmurs, S4 gallop, split S2, soft heart sounds, tachy/bradycardia, ventricular arrhythmias.
49. cardiac markers: troponin I/T, CK-MB, myoglobin, CBC, ESR.
50. inverted T wave, ST elevation, Q waves greater than 1mm wide or 1/3 QRS height.
51. unstable angina: 30% have MI in 3 months. STEMI/NSTEMI: mortality is ~30%.
52. heart failure, myocardial disorders and rupture, arrhythmias, aneuryism, cardiogenic shock, pericarditis.
53. pericarditis, pleural effusion, pneumonitis, fever. [pppf]
54. ventricular dysfunction which leads to reduced pumping action of the heart, ventricular hypertrophy and catecholamine elevation.
55. cardiomyopathies, valvular disease, MI, ischemia, CAD, HTN, PDA, VSD, arrhythmias.
56. RCHF, renal insufficiency, liver disease.
57. renal failure causes volume overload which contributes to HTN which contributes to CHF.
58. RCHF looks more like fluid buildup, whereas LCHF looks like respiratory problem.
59. dyspnea/fatigue upon exertion, intolerance to cold, cyanosis.
60. due to pulmonary edema: dyspnea, mb bronchospasm/wheezing, cough, right sided pleural effusions with basilar rales.
61. displaced apical impulse due to hypertrophy, S3 and S4.
62. CAD, ischemia, MI, HTN, aortic stenosis, cardiomyopathy, PDA, VSD, valvular dysfunction.
63. acute p. edema and associated symptoms, abnormal serum proteins (sudden onset cases).
64. p. edema, ARDS, COPD, IPF, cancer, chronic bronchitis.
65. fatigue, peripheral cyanosis, pitting edema, JVD, hepatomegaly, nocturia, light headedness. [i'm tired because my pee is swollen swollen swollen and blue]
66. tricuspid murmur, systemic HTN, low cardiac output. [tri murmuring "COHTN"]
67. LCHF, cor pulmonale, multiple p.edema, infarction, primary pulmonary HTN, stenosis of mitral valve, pulmonary valve, pulmonary artery. [look left, right: many die; one blocked]
68. edema: peripheral, idiopathic, myedema, angioneurotic, lymphedema. nephrotic syndrome, liver cirrhosis, hemiplegia, pericarditis. [edema, kidney/liver, stroke, heart protector]
69. class I: no physical activity limitation, no dyspnea/fatigue/palpitations. class II: slight limitation, dyspnea upon normal physical activity. class III: moderate limitation, dyspnea upon "less than ordinary" activities. class IV: severe limitation, dyspnea at rest.
70. enlarged cardiac silhouette, kerly-b lines, pleural effusion.
71. B natriuretic peptide, which is released in the body during excessive fluid release in general.
72. echocardiography, will show that ejection fraction less than 50%.
73. never do one of those things.
74. high BUN, creatinine, proteinuria, abnormal liver enzymes, electrolytes.
75. because excess water intake will exacerbate edema and contribute to volume overload.
76. right ventricular hypertrophy due to lung disease.
77. COPD, lung tissue loss, p. emboli, scleroderma, obesity.
78. that of underlying lung disorder, right ventricular hypertrophy or failure. in chronic cases: slight dyspnea at rest, syncope, chest pain, S3.
79. right heart and proximal pulmonary artery enlargement.
80. echocardiogram (most helpful), CXR, ECG.
81. when valve disease, HTN, lung disease are ruled out as etiologies.
82. dilated, hypertrophic, restrictive.
83. related to ventricular dilation/systolic dysfunction: dyspnea/fatigue/edema, mb atypical chest pain, tachyarrythmias.
84. poor without transplant.
85. ventricular hypertrophy with diastolic dysfunction.
86. mostly inherited.
87. aged 20-40, =pain/dyspnea/palpitation/syncope upon exertion.
88. sudden death.
89. systolic ejection murmur that is increased with Valsalva.
90. ECG/echocardiogram/chest xray. chest xray might not show hypertrophy.
91. restrictive cardiomyopathies, characterized by low ventricular compliance.
92. pulmonary hypertension.
93. exertional dyspnea, orthopnea, p. edema, JVD.
94. S4, S3, mitral/TC regurgitation murmur, quiet heart sounds, rapid carotid pulse, arrhythmias.
there are countless pathologies available to the heart and circulatory system. arterial hypertension is high blood pressure either from a multitude of factors (primary) or from a single underlying disease (secondary). atherosclerosis results from high LDL levels which causes plaque formation in arteries and is exacerbated by diabetes mellitus. angina pectoris is chest pain generally caused by ischemia caused by coronary artery dysfunction and can be stable (worse upon exertion, better with rest) or unstable (happens at rest). acute coronary syndromes result from more severe coronary artery ischemia leading to infarction and necrosis, and include unstable angina, NSTEMI, STEMI. congestive heart failure is the dysfunction of the right or left ventricle and have symptom pictures that appear as fluid overload (right) or respiratory problems (left). cor pulmonale is right ventricular hypertrophy that is secondary to a lung disorder such as COPD. finally, cardiomyopathies are dysfunctions of myocardium that are diagnosed when other main etiologies such as valvular, HTN, pulmonary are ruled out. there are three types: dilated, restrictive, hypertrophic.
questions
cardiac testing...
1. what are ECG's used to assess?
2. what do the different components of the PQRST wave represent in the ECG?
3. which test is better to assess valvular dysfunction, the ECG or echocardiography?
4. what is the echocardiogram useful for assessing?
5. describe the difference between the TTE and TEE.
6. what does the EBCT test stand for and what does it measure?
7. what are MRI/MRA tests useful in determining?
8. PET measures...
9. examples of myocardial perfusion nuclides...
10. stress testing is a good way to assess....
arterial hypertension...
11. describe the demographic / racial trends for arterial hypertension.
12. what is the most common cause of arterial hypertension in children?
13. what are some risk factors for arterial hypertension?
14. what is the difference between primary and secondary hypertension?
15. what are some possible etiologies for primary arterial hypertension?
16. what are some examples of diseases that can cause secondary hypertension?
17. arterial hypertension patients are usually...
18. describe the symptom picture of patients with arterial hypertension.
19. what is an early sign of arterial hypertension?
20. what are some signs in a patient with arterial hypertension that might indicate an emergency situation?
21. what would you ask in a medical history of a patient with arterial hypertension?
22. what are some important aspects of the physical examination of a patient with arterial hypertension?
23. how might the specific lab tests differ for a patient who was newly diagnosed with HTN vs. a patient who has left ventricular hypertrophy or ST depression?
24. what are some blood tests that one might perform to aid in the diagnosis of arterial hypertension?
atherosclerosis...
25. describe the role of LDL in the pathogenesis of atherosclerosis.
26. what are the risk factors for developing atherosclerosis?
27. relationship of diabetes and pathophysiology of atherosclerosis.
28. describe the symptom picture/timeline for a patient with atherosclerosis.
29. what are some tests to screen for atherosclerosis?
angina...
30. angina is the result of...
31. describe the general location and sensation of the symptoms in angina pectoris.
32. unique aspects of symptom picture of angina pectoris?
33. what heart sound might be heard in a patient with angina pectoris?
34. how does the way that women experience angina pectoris differ from that of men?
35. what is variant / prinzmetal angina?
36. what is microvascular angina?
37. what is a silent ischemia?
38. what are some clues from the physical exam of a patient with chest pain that indicate coronary artery disease?
39. point tenderness over the chest wall indicates...
40. angina EKG characteristics.
41. possible differential diagnoses for angina pectoris.
acute coronary syndromes...
42. what are the hallmarks of unstable angina?
43. define NSTEMI.
44. define STEMI.
45. in general what is the etiology of acute coronary syndromes?
46. describe the symptom picture of a patient with NSTEMI or STEMI.
47. what are the tests that are diagnostic of these conditions?
48. what are some sounds one might hear upon auscultation of heart in a NSTEMI or STEMI patient?
49. blood tests.
50. ECG characteristics.
51. prognosis of the three types of acute coronary syndromes.
52. complications of MI?
53. what is the "post MI syndrome"?
left congestive heart failure...
54. what is congestive heart failure?
55. what are some possible etiologies for congestive heart failure?
56. LCHF causes...
57. what is the relationship between renal failure and CHF?
58. what is the relative difference in overall presentation of LCHF and RCHF?
59. general/systemic S/SX of LCHF.
60. respiratory S/SX of LCHF.
61. cardiac S/SX of LCHF.
62. etiologies of LCHF?
63. what are some complications of LCHF?
64. what are the differential diagnoses for LCHF?
right congestive heart failure...
65. general S/SX of RCHF.
66. cardiac S/SX of RCHF.
67. what are some possible etiologies of RCHF?
68. what are some possible differential diagnoses of RCHF?
69. what are the classes of CHF as defined by the New York Heart Association?
70. what would the chest xray of a CHF patient show?
71. what is a blood test that might aid in the diagnosis of CHF?
72. what is the best test for diagnosis of CHF and what might the test show?
73. ∂escribe the utility of a stress test in congestive heart failure.
74. what are some blood markers that might be abnormal in CHF?
75. why must water intake/output be monitered in CHF patients?
cor pulmonale...
76. what is cor pulmonale?
77. what is the etiology of cor pulmonale?
78. S/SX of cor pulmonale.
79. a chest xray of a patient with cor pulmonale might show...
80. tests that aid in the diagnosis of cor pulmonale are...
cardiomyopathies...
81. when are cardiomyopathies suspected?
82. what are the three types of cardiomyopathies?
83. describe the symptom picture dilated cardiomyopathy?
84. prognosis for dilated cardiomyopathy?
85. what is hypertrophic cardiomyopathy?
86. etiology of hypertrophic cardiomyopathy?
87. describe the typical patient and symptom picture of hypertrophic cardiomyopathy.
88. hypertrophic cardiomyopathy might result in...
89. what is a typical heart sound of hypertrophic cardiomyopathy?
90. which tests aid in the diagnosis of hypertrophic cardiomyopathy?
91. what is the least prevalent form among the types of cardiomyopathies and what is it characterized by?
92. what does restrictive cardiomyopathy result in?
93. what are common symptoms of a patient with restrictive cardiomyopathy?
94. what are the cardiac symptoms of a patient with restrictive cardiomyopathy?
answers
1. arrhythmias, myocardial ischemia, enlarged chambers.
2. P=atrial depolarization, QRS=ventricular depolarization, T=ventricular repolarization
3. echocardiography-- ECG cannot assess valvular dysfunction.
4. valvular disorders, chamber hypertrophy or dilation, blood flow, cardiomyopathies, heart failure, pericarditis.
5. TTE is more common and less invasive. TEE is used for more posterior structures of the heart, pacemaker implantation, prosthetic valves.
6. electron beam computed tomography, useful for assessing coronary artery disease.
7. mediastinal evaluation, dysfunction of aorta, muscles, non-coronary vessels.
8. myocardial perfusion via radionuclides.
9. thallium and technitium.
10. coronary artery disease.
11. more prevalence in african americans (32%) than european or mexican americans.
12. kidney disease.
13. genetic predisposition, poor lifestyle, diet (high salt intake in particular), stress, obesity.
14. primary is due to multiple factors whereas secondary is caused by a single underlying disease.
15. alcohol, OCP's, corticosteroids, cocaine, licorice (extreme, ridiculous amounts).
16. renal disease, pheochromocytoma, cushing's, primary aldosteronism, hyperthyroidism, myxedema, aortic coarctation.
17. asymptomatic.
18. associated with very high blood pressure: dizziness, flushing, headache, fatigue, epistaxis,
19. the 4th heart sound (S4).
20. diastolic BP above 120mmHg, JVD, CNS disorders, lung crackles (might indicate the pulmonary edema associated with heart failure), severe retinopathy.
21. history of heart disease, any lifestyle risk factors, DM, hyper/dyslipidemia, salt intake, stimulant use (especially cocaine), known duration of HTN.
22. besides vitals: fundoscopic exam to assess for retinopathy, ausculation of neck and abdominal bruits, CVP and neuro exam.
23. new dx- urinalysis and resting ECG. left ventricular hypertrophy: echocardiogram.
24. creatinine, BUN, K, Na, Mg, Calcium, glucose, lipids, TSH, homocysteine, CRP-hs, fibrinogen, fractionated lipids.
25. oxidized LDL uptake into subendothelial layers of blood vessels causes inflammation and atheroma formation, increasing risk for ischemia or stenosis.
26. obesity, atherogenic dyslipidemia, HTN, insulin resistance, prothrombic states, pro-inflammatory states, smoking, hyperhomocysteinemia.
27. diabetes can increase "advanced glycation end products" which damage endothelial cells and increase inflammation.
28. might be asymptomatic for years or decades, then symptoms of ischemia (angina, TIA, IC), then progress to acute symptoms such as unstable angina, stroke, limb pain, sudden death.
29. besides history and risk factor screening: blood tests (lipid profile, blood sugar, homocysteine, CRP-hs, fibrinogen, CBC), stress testing, imaging tests (fast CT, carotid ultrasound, catheterization) can be helpful.
30. myocardial ischemia.
31. a "substernal heaviness or pressure" that may radiate to jaw, neck, left shoulder/arm.
32. pain lasts 15-30 seconds, worse in cold weather, after a meal, or contact with cold air.
33. S4 gallop.
34. various differences: for women, angina pectoris occurs more often with diabetes, is accompanied by more muscular discomfort, nausea, shortness of breath, fatigue, and is more often mistaken for indigestion.
35. angina that is due to coronary artery spasm as opposed to arteriosclerosis.
36. angina that develops from small vessel dysfunction- which results in a normal arteriogram.
37. coronary artery dysfunction that has no symptoms, most often occuring in diabetics.
38. decreased peripheral pulses, bruits in femoral/carotid arteries, xanthomas.
39. indicates that angina probably not due to CAD.
40. usually normal between attacks. during attacks: visible Q waves, T wave inversion, maybe ST depression. possible: smaller R wave, bundle branch disturbances.
41. cervicothoracic spine abnormalities, costochondral separation, Gi disease, pulmonary disease, pericarditis, mitral valve prolapse.
42. prolonged chest pain at rest, increasing/worsening symptoms, transient ECG changes.
43. Non ST Elevation MI: "myocardial necrosis without ST elevation of Q waves"
44. myocardial necrosis with ST elevation (and possible Q waves)
45. acute obstruction of an artery, usually a coronary artery thrombus.
46. deep, intense substernal pain that is not relieved by anything. restlessness, apprehension, dyspnea, diaphoresis, nausea, vomiting.
47. ECG within 10 minutes of MI and cardiac marker tests are diagnostic.
48. murmurs, S4 gallop, split S2, soft heart sounds, tachy/bradycardia, ventricular arrhythmias.
49. cardiac markers: troponin I/T, CK-MB, myoglobin, CBC, ESR.
50. inverted T wave, ST elevation, Q waves greater than 1mm wide or 1/3 QRS height.
51. unstable angina: 30% have MI in 3 months. STEMI/NSTEMI: mortality is ~30%.
52. heart failure, myocardial disorders and rupture, arrhythmias, aneuryism, cardiogenic shock, pericarditis.
53. pericarditis, pleural effusion, pneumonitis, fever. [pppf]
54. ventricular dysfunction which leads to reduced pumping action of the heart, ventricular hypertrophy and catecholamine elevation.
55. cardiomyopathies, valvular disease, MI, ischemia, CAD, HTN, PDA, VSD, arrhythmias.
56. RCHF, renal insufficiency, liver disease.
57. renal failure causes volume overload which contributes to HTN which contributes to CHF.
58. RCHF looks more like fluid buildup, whereas LCHF looks like respiratory problem.
59. dyspnea/fatigue upon exertion, intolerance to cold, cyanosis.
60. due to pulmonary edema: dyspnea, mb bronchospasm/wheezing, cough, right sided pleural effusions with basilar rales.
61. displaced apical impulse due to hypertrophy, S3 and S4.
62. CAD, ischemia, MI, HTN, aortic stenosis, cardiomyopathy, PDA, VSD, valvular dysfunction.
63. acute p. edema and associated symptoms, abnormal serum proteins (sudden onset cases).
64. p. edema, ARDS, COPD, IPF, cancer, chronic bronchitis.
65. fatigue, peripheral cyanosis, pitting edema, JVD, hepatomegaly, nocturia, light headedness. [i'm tired because my pee is swollen swollen swollen and blue]
66. tricuspid murmur, systemic HTN, low cardiac output. [tri murmuring "COHTN"]
67. LCHF, cor pulmonale, multiple p.edema, infarction, primary pulmonary HTN, stenosis of mitral valve, pulmonary valve, pulmonary artery. [look left, right: many die; one blocked]
68. edema: peripheral, idiopathic, myedema, angioneurotic, lymphedema. nephrotic syndrome, liver cirrhosis, hemiplegia, pericarditis. [edema, kidney/liver, stroke, heart protector]
69. class I: no physical activity limitation, no dyspnea/fatigue/palpitations. class II: slight limitation, dyspnea upon normal physical activity. class III: moderate limitation, dyspnea upon "less than ordinary" activities. class IV: severe limitation, dyspnea at rest.
70. enlarged cardiac silhouette, kerly-b lines, pleural effusion.
71. B natriuretic peptide, which is released in the body during excessive fluid release in general.
72. echocardiography, will show that ejection fraction less than 50%.
73. never do one of those things.
74. high BUN, creatinine, proteinuria, abnormal liver enzymes, electrolytes.
75. because excess water intake will exacerbate edema and contribute to volume overload.
76. right ventricular hypertrophy due to lung disease.
77. COPD, lung tissue loss, p. emboli, scleroderma, obesity.
78. that of underlying lung disorder, right ventricular hypertrophy or failure. in chronic cases: slight dyspnea at rest, syncope, chest pain, S3.
79. right heart and proximal pulmonary artery enlargement.
80. echocardiogram (most helpful), CXR, ECG.
81. when valve disease, HTN, lung disease are ruled out as etiologies.
82. dilated, hypertrophic, restrictive.
83. related to ventricular dilation/systolic dysfunction: dyspnea/fatigue/edema, mb atypical chest pain, tachyarrythmias.
84. poor without transplant.
85. ventricular hypertrophy with diastolic dysfunction.
86. mostly inherited.
87. aged 20-40, =pain/dyspnea/palpitation/syncope upon exertion.
88. sudden death.
89. systolic ejection murmur that is increased with Valsalva.
90. ECG/echocardiogram/chest xray. chest xray might not show hypertrophy.
91. restrictive cardiomyopathies, characterized by low ventricular compliance.
92. pulmonary hypertension.
93. exertional dyspnea, orthopnea, p. edema, JVD.
94. S4, S3, mitral/TC regurgitation murmur, quiet heart sounds, rapid carotid pulse, arrhythmias.
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