Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CV Exam III > Ischemic Heart Disease, Angina, and Myocardial Infarction > Flashcards

Ischemic Heart Disease, Angina, and Myocardial Infarction Flashcards

1
Q

Ischemic heart disease physiology

A

–Coronary blood demand exceeds coronary blood flow
•Decreased supply vs. Increased demand
•Myocardial metabolism is aerobic!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Ischemic heart disease physiology

A

–Coronary blood demand exceeds coronary blood flow
•Decreased supply vs. Increased demand
•Myocardial metabolism is aerobic!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Ischemic heart disease etiology

A 
–Atherosclerosis
–Hyperthyroidism
–Anemia
–Emotional stress
–Variant angina
     •Prinzmetal’s -vasospasm in etiology, associated with other vasospastic phenomena
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Ischemic heart disease physical presentation

A

–Retrosternal, aching or squeezing, may radiate to neck, shoulder (usually left), back, teeth, epigastrium

msk you can pinpoint bc it is innervated heavily heart is not so they cant pinpoint

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Ischemic equivalents/Associated symptoms

A 
–Shortness of breath
–Diaphoresis
–Nausea and/or vomiting
–Dizziness
–Weakness

due to visceral overlap

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

IHD risk factors Framingham

A

after WWII

–1948
–5209 men and women ages 30-62
–Return every two years
–Second generation 1971 with 5124 patients
–Third generation 2002
–Omni cohorts in 1994 (blacks too)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

IHD risk factors

A
  • Increasing age
  • Male

•Smoking
–Dose-response relationship
–2-3 fold increase risk of dying form cardiovascular disease
–Rapid risk reduction in 2 years after quitting

  • Hypertension
  • Diabetes
  • High cholesterol/Dyslipidemia –the most powerful modifiable risk factor

•Family history
–Premature heart disease in a first-degree relative
•Male

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

IHD risk factors metabolic syndrome

A

–Clustering of risk factors with a two fold increase in CAD risk

  • Insulin Resistance
  • Hyperglycemia
  • Hypertension
  • Elevated Triglycerides
  • Low HDL cholesterol
  • Obesity

–Nearly doubles the risk of cardiovascular disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

IHD risk factors Conditional

A

lack validation and/or used to supplement clinical judgment

–Homocysteine (an intermediate amino acid in methionine metabolism)

–Lipoprotein(a)

–hsCRP -(High-sensitivity C-reactive protein)

–LDL particle size

–Antioxidant therapies (vitamins E &C and beta-carotene) (largely disproven)

–Omega-3-fatty acids intake has been shown to reduce cardiovascular risk but direct study of supplementation is not well-defined

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

–Homocysteine (an intermediate amino acid in methionine metabolism)

A

Cardiac risk not improved with folate supplementation

b12 folate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

–Lipoprotein(a)

A
  • Resembles LDL with an added glycoprotein
  • Few pharmacological agents lower Lipoprotein(a) [Niacin can reduce levels]
  • No research has demonstrated efficacy in CV risk reduction by lowering Lipoprotein(a)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

–hsCRP -(High-sensitivity C-reactive protein)

A

Useful in assessing patients with intermediate Framingham risk scores, reclassifies up to 30% into either low or high risk

association between inflammation and heart disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

–LDL particle size

A

Inconclusive and needs further study

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Cardiovascular Inflammation Reduction Trial (CIRT)

A
  • directly test the inflammatory hypothesis of atherothrombosis
  • determine whether the common anti-inflammatory drug low-dose methotrexate (LDM, target dose of 15 to 20 mg po weekly) will reduce rates of recurrent myocardial infarction, stroke, or cardiovascular death among patients with established coronary artery disease and either type 2 diabetes or metabolic syndrome
  • determine whether LDM will reduce the rate of new onset type 2 diabetesamong those with metabolic syndrome at study entry
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

IHD low risk

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

IHD intermediate risk

A

10-20% 10-year Framingham risk

–Further evaluation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Reynolds risk score

A

Sex specific tool that accounts for family history and high sensitivity C-reactive protein

most accurate one

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Reynolds risk score

A

Sex specific tool that accounts for family history and high sensitivity C-reactive protein

most accurate one

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Ischemic heart disease etiology

A 
–Atherosclerosis
–Hyperthyroidism
–Anemia
–Emotional stress
–Variant angina
     •Prinzmetal’s -vasospasm in etiology, associated with other vasospastic phenomena
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

risk factors from greatest odds to least odds

A

cholesterol

current smoking

psychosocial stressors

diabetes mellitus

htn

abdominal obesity

moderate alcohol intake

exercise

veggies and fruit daily

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Ischemic equivalents/Associated symptoms

A 
–Shortness of breath
–Diaphoresis
–Nausea and/or vomiting
–Dizziness
–Weakness

due to visceral overlap

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

IHD risk factors Framingham

A

after WWII

–1948
–5209 men and women ages 30-62
–Return every two years
–Second generation 1971 with 5124 patients
–Third generation 2002
–Omni cohorts in 1994 (blacks too)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

IHD risk factors

A
  • Increasing age
  • Male

•Smoking
–Dose-response relationship
–2-3 fold increase risk of dying form cardiovascular disease
–Rapid risk reduction in 2 years after quitting

  • Hypertension
  • Diabetes
  • High cholesterol/Dyslipidemia –the most powerful modifiable risk factor

•Family history
–Premature heart disease in a first-degree relative
•Male

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

IHD risk factors metabolic syndrome

A

–Clustering of risk factors with a two fold increase in CAD risk

  • Insulin Resistance
  • Hyperglycemia
  • Hypertension
  • Elevated Triglycerides
  • Low HDL cholesterol
  • Obesity

–Nearly doubles the risk of cardiovascular disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

IHD risk factors Conditional

A

lack validation and/or used to supplement clinical judgment

–Homocysteine (an intermediate amino acid in methionine metabolism)

–Lipoprotein(a)

–hsCRP -(High-sensitivity C-reactive protein)

–LDL particle size

–Antioxidant therapies (vitamins E &C and beta-carotene) (largely disproven)

–Omega-3-fatty acids intake has been shown to reduce cardiovascular risk but direct study of supplementation is not well-defined

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

–Homocysteine (an intermediate amino acid in methionine metabolism)

A

Cardiac risk not improved with folate supplementation

b12 folate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

–Lipoprotein(a)

A
  • Resembles LDL with an added glycoprotein
  • Few pharmacological agents lower Lipoprotein(a) [Niacin can reduce levels]
  • No research has demonstrated efficacy in CV risk reduction by lowering Lipoprotein(a)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

–hsCRP -(High-sensitivity C-reactive protein)

A

Useful in assessing patients with intermediate Framingham risk scores, reclassifies up to 30% into either low or high risk

association between inflammation and heart disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

–LDL particle size

A

Inconclusive and needs further study

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Cardiovascular Inflammation Reduction Trial (CIRT)

A
  • directly test the inflammatory hypothesis of atherothrombosis
  • determine whether the common anti-inflammatory drug low-dose methotrexate (LDM, target dose of 15 to 20 mg po weekly) will reduce rates of recurrent myocardial infarction, stroke, or cardiovascular death among patients with established coronary artery disease and either type 2 diabetes or metabolic syndrome
  • determine whether LDM will reduce the rate of new onset type 2 diabetesamong those with metabolic syndrome at study entry
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

IHD low risk

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

IHD intermediate risk

A

10-20% 10-year Framingham risk

–Further evaluation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

IHD High risk

A

> 20% 10-year Framingham risk

–Aggressive risk modification

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Reynolds risk score

A

Sex specific tool that accounts for family history and high sensitivity C-reactive protein

most accurate one

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

IHD reduction of risk factors

A 
-Aspirin
     •Risk vs. benefit
–Reduction of blood pressure
–Reduction of hyperlipidemia
–Smoking cessation
–Regular exercise
–Weight reduction and reduction of BMI (
36
Q

Acute Coronary Syndromes

•History and Physical Exam

A

–Necessary to distinguish between syndromes that mimic acute coronary syndromes or may change the disease management

  • Onset –timing of treatment
  • Risk factor evaluation
  • Recent medication use (aspirin etc)
  • Aortic dissection
  • Pericarditis
  • Pulmonary embolism
  • CHF –SOB, orthopnea
37
Q

Aortic dissection

A

–in the back, often described as a tearing sensation (Type A dissection may extend into the right coronary artery and the presentation may be that of an actual inferior wall MI with the dissection, although the left coronary artery can be involved but less often)

–Widened mediastinum on chest X-Ray

38
Q

Pericarditis

A

–recent viral illness, pleuritic chest pain, pulses paradoxus

39
Q

Pulmonary embolism

A

–inactivity, malignancy/hypercoagulable state, pleuritic chest pain

–New onset of Atrial fibrillation

40
Q

Troponin

A

can show up with just angina

41
Q

mm

A

skeletal muscle

42
Q

mb

A

heart

43
Q

bb

A

brain

44
Q

exercise stress test

A

–Bruce protocol
–HRmax= 220 − age

every 3 mintues it goes up in grade and speed until you hit max hr, if you hit it and ekg shows no changes your heart is in good shape

45
Q

Pharmacological stress test

A

–Dobutamine (b agonist)
•Increase cardiac stress and oxygen demand

–Adenosine/Dipyridamole
•Vasodilation (work with coronary steal phenomenon)

46
Q

Imaging

A

•Imaging
–Nuclear (dye that goes where its supposed to?)
–Echocardiograph (us that shows wall motion abnormalities)

•Angiography
–Lower dose radiation
–Gold standard for defining coronary occlusion

•CT/MRI
–Good to estimate coronary artery calcium scoring and anatomy, but no functional information

47
Q

IWMI is?

A

volume dependant so we treat it with volume

48
Q

Coronary Artery Calcifications

A

incidental finding?

49
Q

Acute Coronary Syndromes

A

•A spectrum of a single disease

•Unstable Angina ST-elevation MI
–Stratified based upon ECG and serum biomarkers (troponin and creatine kinase –CPK)

50
Q

Typical chest pain clinical presentation

•(Central, Visceral, Exertional)

A

1) Central substernal pain/discomfort –usually retrosternal
2) Exertional –Brought on or increased with activity/emotional stress
3) Relieved by nitrates or rest

51
Q

1) Central substernal pain/discomfort –usually retrosternal

A
  • May radiate to the shoulder, arms, jaw or back

* Visceral –usually poorly located; associated with nausea, vomiting, diaphoresis and/or shortness of breath

52
Q

2) Exertional –Brought on or increased with activity/emotional stress

A

•25% maybe silent ischemia
•25% atypical
–Woman, diabetics, elderly

53
Q

Acute Coronary Syndromes

•History and Physical Exam

A

–Necessary to distinguish between syndromes that mimic acute coronary syndromes or may change the disease management

  • Onset –timing of treatment
  • Risk factor evaluation
  • Recent medication use (aspirin etc)
  • Aortic dissection
  • Pericarditis
  • Pulmonary embolism
  • CHF –SOB, orthopnea
54
Q

Aortic dissection

A

–in the back, often described as a tearing sensation (Type A dissection may extend into the right coronary artery and the presentation may be that of an actual inferior wall MI with the dissection, although the left coronary artery can be involved but less often)

–Widened mediastinum on chest X-Ray

55
Q

Pericarditis

A

–recent viral illness, pleuritic chest pain, pulses paradoxus

56
Q

Pulmonary embolism

A

–inactivity, malignancy/hypercoagulable state, pleuritic chest pain

–New onset of Atrial fibrillation

57
Q

Acute Coronary Syndromes

ST-elevation myocardial infarction

A

–Early reperfusion indicated –time is muscle!
•Thrombolytic therapy versus rapid revascularization in the catheterization lab
–Most significant determining factor is “Door to Balloon” time (75)

tpa if cant get to cath lab

58
Q

Absolute contraindications to thrombolytic therapy

A

»Intracranial Hemorrhage
»Ischemic CVA in the last 3 months
»Facial trauma in the last 3 months
»Bleeding diathesis

59
Q

Relative contraindications to thrombolytic therapy

A

»Thrombolytic therapy does not has a clear benefit weighed against the risks beyond 12 hours
»Chronic, severe, poorly-controlled hypertension
»Severe uncontrolled hypertension on presentation
»Ischemic CVA > 3 months, known intracranial pathology
»Dementia
»Internal bleeding within the last 4 weeks
»Noncompressible vascular site
»Pregnancy
»Peptic Ulcer disease
»Current anticoagulant use

60
Q

Myocardial Infarction Complications -Early

A

Early complications –immediate or first few hours

–Thrombolytics

–IWMI

–AWMI

61
Q

Early complications

thrombolytics

A
  • Bleeding (2-3 times higher incidence of hemorrhagic CVA in women)
  • Reperfusion arrhythmias (be patient it will go back to normal)
62
Q

Early complications

IWMI

A
  • Bradycardia and AV block –AV nodal perfusion by the right coronary artery
  • Right ventricular infarction, always think about RV infarct with inferior wall MI
  • Hypotension for volume depletion
63
Q

Coronary artery calcium (CT or MRI)

A

•Highly effective in negative predictive value, also used to evaluate patients with an intermediate Framingham score

64
Q

IWMI is?

A

volume dependant so we treat it with volume

65
Q

Post ACS Mortality Risk Stratification

A

To determine level of intervention prior to hospital discharge

Angiography vs. Non-invasive testing

Angiography indications

66
Q

Angiography vs. Non-invasive testing

A
  • Used to identify high-risk patients -three vessel disease and left main disease require revascularization
  • Patients should have evaluation of ejection fraction and a provocative ischemic test, if they hav
67
Q

Angiography indications

A

•EF

68
Q

Post Acute Coronary Syndrome Mortality Intervention

Mortality reduction

A

–Beta-blockers 20%
–Aspirin 33%
–Angiotensin-Converting Enzyme Inhibitors
–HMG-CoA Reductase Inhibitors 25-30%
–Intense management of hyperglycemia, maintaining blood sugars below 180 mg/dL, during the acute hospital stay

69
Q

–Angiotensin-Converting Enzyme Inhibitors

A
  • Normal EF 17%

* Reduced EF 23%

70
Q

–HMG-CoA Reductase Inhibitors 25-30%

A
  • Proportional to the reduction in LDL levels

* LDL goal

71
Q

Post Acute Coronary Syndrome Mortality Intervention

Coronary Revascularization

A

–Percutaneous intervention (PCI)

–Coronary Artery Bypass Grafting

72
Q

–Percutaneous intervention (PCI)

A

shown not to have improvement overall in survival or recurrent acute events, except those with silent ischemia by noninvasive stress testing. It is primarily reserved for those with positive stress tests, failure of medical therapy or poor surgical risk

angiopalsty cardiac cath are all synonymous terms

73
Q

–Coronary Artery Bypass Grafting

A

in stable CAD is only indicated in patients with Left Main disease, Left Main equivalent (high grade stenosis >70% Proximal LAD and Circ), Three vessel disease, two vessels involving proximal LAD and EF

74
Q

Chronic Coronary Artery Disease Stratification

Diagnostic evaluation

A 
–Pretest probability
–Ability to exercise
–ECG findings
–Co-morbid diseases (pulmonary)
–Non-cardiac surgery risk stratification
–Assess exercise capacity
75
Q

pretest probabilty

A

•Patients with high pretest probably may be treated empirically and then stressed tested in order to evaluate therapy

76
Q

Chronic Coronary Artery Disease Stratification

Type of tests/indications

A

Exercise stress test

Chemical stress test

Coronary angiography –the gold standard

Coronary artery calcium (CT or MRI)

77
Q

Exercise stress test

A
  • Intermediate risk

* Assess treatment (stable vs. unstable)

78
Q

Chemical stress test

A
  • Dobutamine, dipyridamole, adenosine

* Inability to exercise/physical limitations due to lack of conditioning or co-morbidities

79
Q

Coronary angiography –the gold standard

A
  • Positive stress test
  • Successfully resuscitated for cardiac arrest
  • Life limiting angina despite medical therapy
  • Unclear diagnostic evaluation
  • ST segment elevation MI –interventional as well as diagnostic
80
Q

Coronary artery calcium (CT or MRI)

A

•Highly effective in negative predictive value, also used to evaluate patients with an intermediate Framingham score

81
Q

Females IHD

A

–Average age of diagnosis 10 years later than for males
•Originally thought to be an estrogen protective effect
•Results in more comorbidities and more complicated course of disease
•Due to alterations in pharmacokinetics of aging/volume of distribution, medications often dosed inappropriately

–Have more vasospastic presentation and therefore less obstructive coronary disease
•Lower specificity with higher false positive exercise ECG testing

–More non-cardiac chest pain syndromes

–More atypical presentations
•Shortness of breath, palpitations, dizziness, and syncope

–Hormone replacement
•Has not been shown to reduce CAD risk; has lead to increase venous thromboembolism and CVA

82
Q

females have less collaterization bc

A

of the increase after menopause so they get more devastating mi they also have more false positive stress tests

83
Q

estrogen is

A

not protective

84
Q

Diabetics IHD

A

–Between two and eight times more likely to suffer from and die from cardiovascular diseases

–Patients typically have more advanced and higher grade disease and less collateralization at presentation

–Risk reduction
•Glycemic control
•Blood pressure control

85
Q

Diabetics Diagnosis

A
  • Often difficult due to autonomic neuropathy
  • Fatigue, dyspnea, nausea and vomiting may predominate the presentation
  • Silent ischemia
  • Exercise stress testing has similar diagnostic value
  • Some care with angiography, but not an absolute contraindication –contrast nephropathy

contrast is nephrotoxic

86
Q

diabetics have no chest pain bc

A

diabetic neuropathy

CV Exam III (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions