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Cardiology Flashcards

1
Q

How is systolic heart failure differentiated from diastolic?

A

based on an ejection fraction of less than or greater than 40%

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2
Q

List several causes for systolic, diastolic, and high-output cardiac failure.

A
  • systolic: ischemic heart disease or infarction, hypertension leading to cardiomyopathy, valvular disease, myocarditis, alcohol abuse
  • diastolic: hypertension lead to myocardial hypertrophy, aortic or mitral stenosis, aortic regurgitation, or restrictive cardiomyopathy as in amyloidosis, sarcoidosis, or hemochromatosis
  • high-output: chronic anemia, pregnancy, hyperthyroidism, AV fistulas
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3
Q

Describe the signs and symptoms of left-sided heart failure.

A
  • dyspnea, orthopnea, paroxysmal nocturnal dyspnea, and nonproductive nocturnal cough
  • confusion and memory impairment in severe cases with inadequate brain perfusion
  • leftwardly displaced PMI
  • S3 or S4
  • crackles at the lung bases, dullness to percussion and decreased tactile remits in the lower lung fields
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4
Q

What is orthopnea?

A

difficulty breathing in the recumbent position which is relieved by elevation of the head; due to left-sided heart failure exacerbated by increased venous return in the recumbent position

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5
Q

Describe the signs and symptoms of right-sided heart failure.

A
  • peripheral pitting edema
  • nocturia
  • JVD
  • hepatomegaly
  • ascites
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6
Q

What is an S3 heart sounds? Describe it. What is it associated with? Under what circumstances is it considered normal?

A
  • it is a sound in early diastole after S2 during rapid passive filling of the ventricles
  • it is often described as a “ken-tuck-y” sound (1 2 2)
  • it is associated with increased filling pressures and occurs with sudden cessation of filling as the ventricle reaches its elastic limit
  • may be normal in individuals under 40 or during pregnancy
  • pathologic in systolic heart failure, mitral regurgitation, and high-output states
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7
Q

What is an S4 heart sounds? Describe it. What is it associated with? Under what circumstances is it considered normal?

A
  • it is a late diastolic sound best heart at the apex just before S1
  • it is often described as a “ten-nes-see” sound (1 1 2)
  • it occurs after atrial contraction as blood is forced into a stiff ventricle
  • may be normal in healthy older adults
  • pathologic in younger adults and in those with diastolic dysfunction
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8
Q

What lifestyle modifications are recommended in the treatment of heart failure?

A
  • sodium restriction to less than 2-4 grams per day
  • fluid restriction less than 1.5-2.0 liters per day
  • weight loss
  • smoking cessation
  • restricted alcohol use
  • monitor daily weight
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9
Q

Describe the role of each of the following in the treatment of heart failure:

  • diuretics
  • aldosterone antagonist
  • ACE inhibitors
  • ARBs
  • beta-blockers
  • digitalis
  • hydralazine and isosorbide dinitrates
A
  • diuretics, specifically loop diuretics, are recommended for symptomatic relief in patients with volume overload
  • aldosterone antagonists, specifically spironolactone, reduce mortality in class III and IV heart failure only
  • ACE inhibitors reduce mortality, prolong survival, and alleviate symptoms for all classes of heart failure and are the first line of treatment
  • ARBs should replace ACE inhibitors only for those unable to tolerate the side effects of ACE inhibitors
  • beta-blockers decrease mortality in patients with post-MI heart failure by slowing tissue remodeling, but this is true only for metoprolol, bisoprolol, and carvedilol
  • digitalis provides short-term symptomatic relief only by increasing inotropy
  • hydralazine and isosorbide denigrates can be used in patients that cannot tolerate ACE inhibitors but have a smaller benefit on mortality
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10
Q

Name four medications that are contraindicated in patients with CHF and why.

A
  • metformin may cause a potentially lethal lactic acidosis
  • thiazolidinediones cause fluid retention
  • NSAIDs may increase the risk for CHF exacerbation
  • some antiarrhythmics have negative inotropic effects
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11
Q

What therapy is shown to have the most benefit in patients with heart failure?

A

ACE inhibitors

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12
Q

Certain beta-blockers have been shown to have a benefit on mortality in heart failure patients. What kind of heart failure patients benefit and which specific beta-blockers has this been demonstrated in?

A
  • specifically used in patients with post-MI heart failure because they slow tissue remodeling
  • only shown for metoprolol, bisoprolol, and carvedilol
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13
Q

Stable Angina:

  • definition/pathogenesis
  • risk factors
  • prognostic indicators
  • clinical presentation
  • methods for diagnosis
  • treatment options
A
  • an ischemic heart disease caused by fixed atherosclerotic lesions that narrow the major coronary arteries and limit oxygen supply
  • diabetes mellitus is the worst risk factor while hypertension is the most common risk factor
  • prognosis depends on left ventricular function and involvement of the left main coronary or more than one vessel
  • presents as chest pain: gradual onset, brought about by exertion or emotion, described as substernal heaviness or pressure, relieved with rest or nitroglycerin, does not change with breathing or body position, and without tenderness to palpation
  • stress ECG or stress echocardiography can be used for those with intermediate pretest probability of CAD, but those who have a positive result or a high pretest probability should then undergo cardiac catheterization with coronary angiography
  • standard of care is a daily aspirin and beta-blocker which improve mortality plus a nitrate for symptomatic relief
  • revascularization with PCI or CABG is considered in high-risk patients for symptomatic relief, but does not reduce mortality compared to maximal medical therapy
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14
Q

What are the prognostic indicators for stable angina?

A
  • left ventricular function: an EF less than 50% is associated with increased mortality
  • involvement of the left main coronary has a poor prognosis
  • involvement of 2 or 3 vessels has a worse prognosis
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15
Q

Compare and contrast the methods that can be used to diagnose coronary artery disease.

A
  • resting ECG is likely normal in those with stable angina
  • stress ECG will show ST-depression, indicative of subendocardial ischemia
  • stress echocardiography is more sensitive than stress ECG at detecting ischemia, which presents as wall motion abnormalities
  • holter monitoring can be used to detect clinically silent ischemia
  • cardiac cauterization is the definitive test
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16
Q

How does a stress echo detect coronary artery disease and how does it compare to stress ECG?

A
  • ischemia presents as wall motion abnormalities on stress echo
  • it is preferred to stress ECG because echo is more sensitive, can asses LV size and function, can diagnose valvular disease, and can be used to identify CAD in the presence of pre-existing ECG abnormalities
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17
Q

What is the gold standard for diagnosing coronary artery disease?

A

cardiac catheterization with coronary angiography

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18
Q

Describe pharmacologic stress testing.

A
  • adenosine or dipyridamole cause generalized coronary vasodilation; since disease coronary arteries are already maximally dilated, these drugs cause relatively less blood flow to ischemic areas
  • dobutamine increase myocardial oxygen demand by increasing heart rate, blood pressure, and cardiac contractility
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19
Q

How is thallium or technetium used to diagnose coronary artery disease?

A

viable myocardial cells extract the isotope form the blood, so ischemia is indicated by areas that don’t absorb radioisotope

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20
Q

What degree of coronary stenosis is required before it will produce stable angina?

A

more than 70% stenosis becomes clinically apparent

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21
Q

What does it mean that diabetes is a cardiovascular heart disease equivalent?

A

it means that the risk of a coronary event like MI is equal to that of an individual with coronary artery disease

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22
Q

What medical therapy is involved in the treatment of stable angina?

A
  • aspirin reduces the risk of MI
  • beta-blockers, specifically atenolol and metoprolol, lower myocardial oxygen consumption by reducing HR, BP, and inotropy
  • nitrates cause generalized vasodilation to relieve angina and reduce preload, but have little mortality benefit
  • calcium channel blockers cause coronary vasodilation and after load reduction but may increase heart rates and therefore increase mortality
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23
Q

What role does revascularization in the form of PCI and CABG play in the treatment of stable angina?

A
  • it is considered in high-risk patients

- however, it provides symptomatic relief but does not improve mortality when compared to maximal medical therapy alone

24
Q

What are the indications for CABG in those with stable angina?

A

three vessel disease with more than 70% stenosis in each, 50% stenosis of the left main coronary, or left ventricular dysfunction

25
Q

Unstable Angina

A
  • unstable angina is used to describe patients with chronic angina that is increasing in frequency, duration, or intensity or those with angina at rest
  • caused by stenos enlarged via thrombosis, hemorrhage, or plaque rupture
  • treat with aspirin, clopidogrel, beta-blockers, LMWH, nitrates, oxygen, and morphine on admission
  • importantly, stress testing may cause adverse events so these patients should be stabilized with medical management before stress testing; if symptoms or ECG changes persist for 48 hours, proceed directly to cardiac catherization
  • continue clopidogrel for 9-12 months, LMWH for 2 days, and aspirin, beta-blockers, and nitrates indefinitely
26
Q

How should unstable angina be evaluated? Why?

A
  • these patients are more likely to experience adverse events during stress testing
  • so they should be stabilized with initial medical management before stress testing or should undergo cardiac catheterization as the initial test of choice
27
Q

How is unstable angina treated in the acute setting?

A

treated as an MI except for fibrinolysis

  • aspirin
  • clopidogrel
  • beta-blockers
  • LMW heparin
  • nitrates
  • oxygen if hypoxic
  • morphine
28
Q

How is unstable angina managed in the chronic setting?

A

continue aspirin, beta-blockers, and nitrates

29
Q

What role does clopidogrel play in the treatment of unstable angina?

A

it has been shown to reduce the incidence of MI compared to aspirin alone and should be continued alongside aspirin for 9-12 months

30
Q

What role does LMWH play int he treatment of acute unstable angina? How long should it be continued for?

A
  • it is given to prevent progression or development of a clot
  • enoxaparin for 2 days is the preferred course
31
Q

Variant Angina

A
  • angina caused by a transient coronary vasospasm that is usually accompanied by a fixed atherosclerotic lesion
  • may be accompanied by ventricular dysrhythmias
  • occurs at rest and classically at night
  • the hallmark is ST elevation because it causes transmural ischemia
  • coronary angiography is the definitive test as vasospasm can be elicited by IV ergonovine or acetylcholine
  • treat with CCBs and nitrates
32
Q

How is variant angina diagnosed?

A

coronary angiography in the setting of IV ergonovine or acetylcholine which provoke coronary vasospasm

33
Q

List the medications shown to reduce mortality in systolic heart failure patients and which are used for symptomatic relief?

A 
improve mortality:
- ACE inhibitors and ARBs 
- B-blockers
- aldosterone antagonists
- hydralazine plus nitrate
symptomatic treatment: loop diuretics and digoxin
34
Q

Why are calcium channel blockers not used in the treatment of heart failure? Which are safe to use if needed?

A
  • they can ultimately cause a rise in heart rate and increase mortality
  • amlodipine and felodipine are safe if needed for another indication
35
Q

Name two inotropic agents used in the treatment of heart failure? What is the primary difference between the two?

A
  • digoxin and dobutamine are the typical inotropic agents
  • dobutamine takes immediate effect and can be used in the treatment of acute decompensated heart failure; whereas digoxin requires several weeks to start working
36
Q

Myocardial Infarction

A
  • a necrosis of the myocardium, most often caused by an acute coronary thrombosis
  • risk factors include a history of angina, risk factors for CAD, and a history of arrhythmias
  • presents with chest pain similar in character and distribution to angina but much more severe, longer lasting, and unresponsive to nitroglycerin
  • often accompanied by some combination of dyspnea, diaphoresis, n/v, syncope, weakness, etc.
  • atypical presentations are more common int he elderly, females, diabetics, and those in the post-op period
  • diagnosed based on ECG changes and cardiac enzymes (troponin I has more specificity and sensitivity while CK-MB is better for detecting recurrent MI)
  • treatment involves aspirin, beta-blockers, and ACE inhibitors which reduce mortality; statins, oxygen, nitrates, morphine, and heparin also have a role in management
  • PCI is preferred if it can be performed within 90 minutes of hospital arrival and thrombolysis is preferred for later presentations
37
Q

How does MI chest pain differ from that of angina?

A
  • it tends to be more severe, longer lasting, and unresponsive to nitroglycerin when compared to angina
  • it also tends to be more associated with symptoms of dyspnea, diaphoresis, n/v, syncope, weakness, etc.
38
Q

What is the most common cause of death in those with an MI?

A

sudden cardiac death, usually due to ventricular fibrillation

39
Q

What ECG changes are markers for MI?

A
  • peaked T waves are a very early sign and may be missed later in the course
  • ST segment elevation with transmural injury
  • pathologic Q waves are evidence of necrosis and are usually seen late rather than acutely
  • T-wave inversion is sensitive but not specific
40
Q

What is unique about a right ventricular infarct compared to other MIs with regards to presentation and treatment?

A
  • it presents with inferior ECG changes, hypotension, elevated jugular venous pressure, hepatomegaly, and clear lungs
  • because this is preload dependent, it is very important not to administer nitrates or diuretics as this can cause cardiovascular collapse
41
Q

Describe the timeline for troponin I changes in those with an MI. How does troponin I compare to CK-MB as a test for MI? What can cause a false positive?

A
  • troponin I increases within 3-5 hours, peaks at 24-48 hours, and returns to normal in 5-14 days
  • it has more sensitivity and specificity than CK-MB for myocardial injury
  • may be falsely elevated in patients with renal failure
42
Q

Describe the timeline for CK-MB changes in those with an MI. How does it compare to troponin I as a test for MI? What can cause a false positive?

A
  • CK-MB increases within 4-8 hours, peaks at 24 hours, and returns to normal around 48-72 hours
  • has high sensitivity and specificity if measured early enough
43
Q

Which agents have been shown to reduce mortality in those with an acute MI?

A
  • aspirin
  • B-blockers
  • ACE inhibitors
44
Q

What can cause cardiac troponins to be elevated other than an MI?

A

renal failure

45
Q

Describe the agents used to treat MI and what benefit they provide.

A
  • aspirin inhibits platelet aggregation on top of any existing thrombus to reduce mortality
  • beta-blockers reduce oxygen demand and reduce remodeling of the myocardium post-MI to reduce mortality
  • ACE inhibitors reduce mortality
  • statins reduce the risk of further coronary events if initiated as part of maintenance therapy
  • oxygen limits ischemic injury
  • nitrates dilate coronary arteries, decrease preload, and relieve chest pain
  • morphine is for symptomatic analgesia
  • enoxaparin is used to prevent the progression of any thrombus but has not been shown to provide any mortality benefit
46
Q

How does PCI differ from fibrinolysis in the treatment of myocardial infarction?

A
  • PCI provides greater benefit if it can be performed within 90 minutes of hospital arrival or if patients have contraindications to fibrinolysis
  • fibrinolysis is a better option for those with delayed presentation
47
Q

On what medical therapy should those who undergo PCI and receive a stent be placed?

A
  • dual anti platelet treatment with aspirin and clopidogrel

- for 30 days in patients with a bare metal stent and for at least 12 months with a drug-eluting stent

48
Q

How long can thrombolytic therapy be initiated after the onset of chest pain in those with an MI?

A

up to 24 hours, but outcomes are best in those who receive therapy within 6 hours

49
Q

What are absolute contraindications to thrombolytic therapy in those with an MI?

A
  • recent trauma
  • previous stroke
  • recent invasive procedure or surgery
  • dissecting aortic aneurysm
  • active bleeding or bleeding diathesis
50
Q

What complications arise from the microscopic and macroscopic changes following MI?

A
  • from 0-4 hours there is risk for arrhythmia, cariogenic shock, and heart failure
  • with coagulative necrosis in the first 4-24 hours, there is an increased risk of arrhythmia
  • in the 1-3 days post-MI there is a risk for fibrinous pericarditis if the damage was transmural as neutrophils invade the myocardium and may invade the pericardium; this would present with chest pain and a friction rub
  • 4-7 days post-injury, macrophage activity makes the wall weak and there is a risk of rupturing the wall, papillary muscle or interventricular septum
  • in the months following, as granulation tissue turns to scar tissue, there is a risk of aneurysm, mural thrombus, and Dressler syndrome
51
Q

What is Dressler syndrome?

A
  • a complication of MI that arises 6-8 weeks post-injury
  • results from auto-antibodies that form after immune cells are exposure to pericardial antigens
  • the end result is fibrinous pericarditis and it typically presents with fever, malaise, pericarditis, leukocytosis, and pleuritis
  • the most effective therapy is aspirin
52
Q

What are the possible complications of an acute MI to consider?

A
  • pump failure leading to cardiogenic shock
  • arrhythmias
  • recurrent infarction
  • free wall rupture
  • rupture of inter ventricular septum
  • papillary muscle rupture
  • ventricular pseudoaneurysm
  • ventricular aneurysm
  • acute pericarditis
  • Dressler syndrome
53
Q

What is a ventricular pseudoaneurysm?

A
  • an incomplete free wall rupture, which is contained by the pericardium after myocardium ruptures
  • a possible complication of acute MI, which often becomes a free wall rupture
54
Q

What is the difference between a ventricular pseudoaneurysm and a ventricular aneurysm in the post-MI period?

A

the major difference is that a true aneurysm rarely ruptures because it is still contained by all three layers of the heart

55
Q

What system is the most common cause of non cardiac chest pain presenting to the emergency room?

A

gastrointestinal disorders

56
Q

What are the “serious six” causes of chest pain that must be ruled out?

A
  • MI
  • unstable angina
  • aortic dissection
  • pulmonary embolism
  • tension pneumothorax
  • esophageal rupture

IM (13 decks)

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