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AHN 572 > Cardiovascular I > Flashcards

Cardiovascular I Flashcards

1
Q

What is Coronary heart disease?

A

Inadequate blood supply to the myocardium most commonly due to obstruction of the coronary arteries due to atherosclerosis

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2
Q

Who is most affected by CHD

A

55% male predominance

Aged >40 years

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3
Q

Pathophysiology of myocardial ischemia

A

Increased demand and decrease in oxygen supply

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4
Q

Distinguishing factors of Stable angina

A

Brief (less than 10 minutes) during exertion of emotional stress
Correlate to significant stenosis but nonocclusive

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5
Q

Unstable angina

A

Pain at rest

Correlates to a thrombi projecting into lumen but not occluded

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6
Q

NSTEMI

A

Acute MI

Severe occlusion

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7
Q

STEMI

A

Acute MI

Coronary occlusion

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8
Q

Risk factors for CAD

A 
Hereditary
ethnicity
gender
hypertension
age
family history
Inflammation
Diet
inactivity
stress
smoking/alcohol
obesity
DM
Hyperglycemia
Hyperlipidemia (LDL)
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9
Q

Primary prevention of CAD

A

Lifestyle modification (healthy diet, physical activity, weight loss, smoking cessation)
Blood pressure control
Dyslipidemia treatment
management of DM

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10
Q

Secondary prevention of CAD

A 
Aggressive lifestyle modifications
Statin therapy
BP <140/85
Antiplatelet therapy 
ACE-I
Beta Blockers
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11
Q

The most important aspect of classifying angina appropriately?

A

Differentiating Stable ischemic heart disease from Acute coronary syndrome

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12
Q

Diagnostic measures of CHD

A 
Resting EKG
Exercise EKG
myocardial stress imaging
CT/MRI
Coronary angiography
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13
Q

Resting EKG guidelines

A

Recommended in patients without an obvious noncardiac cause of chest pain
Purpose to distinguish from stable and unstable
Assess for old MI, silent ischemia, nonspecific changes, hypertrophy

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14
Q

Indications of Exercise EKG

A

Confirmation of angina
Assess severity of activity limitations
Prognostic tool
Evaluate therapeutic effectiveness

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15
Q

Interpretation of exercise EKG

A

Should include exercise capacity and clinical, hemodynamic and ECG response
ST depression of > 1 mm
Downsloping ST > 80 msec pas the J point

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16
Q

Myodcardial stress imaging indications

A

exercise EKG difficult to interpret
Confirmation of results of exercise EKG
Ischemic localization

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17
Q

Indications for coronary angiography

A

Patients with Stable angina who have survived sudden cardiac death or potentially life threatening ventricular arrhythmia
Patients with Stable angina who develop symptoms and signs of heart failure
Patients with stable angina who have depressed LV function
Unsatisfactory quality of life
Testing shows high likelihood of lesion

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18
Q

Coronary angiography is

A

The gold standard for diagnosing CAD

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19
Q

What is considered clinically significant stenosis?

A

> 50%

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20
Q

Stable angina treatment approaches

A 
Medication adherence
Modifiable risks
daily activity
self monitoring
recognizing worsening symptoms
Adherence to diet
manage stress
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21
Q

Recommended threshold for antihypertensive therapy

A

BP of 130/80 or higher

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22
Q

Goal HbA1C

A

<7% for younger patients

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23
Q

What Diabetes management should not be initiated in patients with SIHD?

A

Therapy with rosiglitazone (Actos)

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24
Q

Antiplatelet therapy guidelines for Stable HD

A

Aspirin 75-162 mg

Plavix when aspirin is contraindicated

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25
Anti-Ischemic therapy guidelines for Stable HD
Beta blockers Calcium channel blockers or long acting nitrates Sublingual nitro Ranolazine (if others not able to be used)
26
Goal of anti-anginal agents
to decrease myocardial oxygen demand and increase oxygen supply Nitro (Short term) (decrease O2 demands, Decrease venous return, decrease preload) Beta blockers (long term control 1st line) (Decrease HR, Decrease contractility, decrease blood pressure) Calcium channel blockers (long term control, 2nd line) Amlodipine, verapamil, diltiazem (decrease HR, Decrease contractility, decrease AV node conduction velocity)
27
Prinzmetal angina
``` Coronary vasoconstriction with or without spasm Common in females <50 Treatment coronary angiography medical management avoid precipitating factors ```
28
Acute coronary syndrome types
unstable angina without necrosis (negative biomarkers) NSTEMI-necrosis, nontransmural (positive biomarkers STEMI- Transmural necrosis (positive biomarkers, ST elevation, need immediate reperfusion)
29
Clinical manifestations of ACS without ST elevation
Typical presentation- Substernal chest pain, radiation, dyspnea, N/V, Diaphoresis, syncope Atypical presentation- For women, DM, and elderly
30
Clinical manifestations of ACS with ST elevation
Chest pain, pain occurring at rest, NTG has minimal effects, >30 minutes in duration Weakness, dyspnea, diaphoresis, sense of impending doom 50% of the deaths occur prior to presentation to the ED
31
Review of cardiac biomarkers
Troponin-released with myocardial necrosis occurs- highly cardiospecific, detectable within 4-6 hours, CKMB- moderately specific, detectable within 2-5 hours, elevated also during rhabdo Myoglobin- nonspecific
32
Troponin detectable, peak, how long elevated, what is normal?
Detectable 4-6 hours after necrosis, peaks at 24-48 hours, may remain elevated for 5-7 days, normal is < 0.04 Cardiospecific
33
Myoglobin detectable, baseline, specificity
Detectable within 1-3 hours, returns to baseline within 12-24 hours, very nonspecific
34
CKMB detectable, elevation length, specificity
moderately specific, detectable within 2-5 hours, returns to baseline within 2-4 days
35
Noncardiac causes of troponin elevation
``` Trauma PE toxicity (anthracyclines) CHF Renal failure Sepsis Stroke SAH Electrical shocks ```
36
EKG testing should be performed within ... of arrival
10 minutes
37
Additional diagnostic testing if ACS
CXR (heart failure, aortic dissection) ECHO Labs- CBC, CMP, Lipid panel, PT/INR & Ptt
38
Beta blockers should be started within... and continued with
24 hours | metoprolol, carvedilol, bisoprolol
39
If beta blockers are contraindicated you can use
Calcium channel blockers
40
ACE inhibitors should be started and continued indefinitely for patients with a LVEF less than
40%
41
Common ACE inhibitor side effect
Cough
42
Aldosterone blockers recommended for patients post-MI without renal dysfunction who are intolerant to...
ACE inhibitors
43
Antiplatelet agent
chew an aspirin 162-325 immediately | Long term 81-162 to be continued indefinitely
44
Goal for reperfusion of STEMI at facility with intervention
90 minutes
45
Goal of fibrinolytic of STEMI at facility with no intervention
10 minutes to bolus, infusion completed 60-90 minutes- transfer to PCI capable facility
46
Recommendations for Cardiac arrest
Primary PCI recommended in patients resuscitated and ECG with STEMI TTM indicated early
47
Recommendations for reperfusion therapy
indicated for all patients with STEMI
48
Antiplatelet and anticoagulant indicated for all patients during
primary PCI
49
Absolute contraindications to fibrinolytic therapy
``` hemorrhagic stroke ischemic stroke within the last year intracranial hemorrhage aortic dissection internal bleeding ```
50
Complications of AMI
``` Sinus Brady (inferior wall MI, DC any offending medications & administer atropine if symptomatic) SVT- sinus tach- avoid BB, check electrolytes, correct abnormalities, treat hypoxemia Afib- intact LV function- Metoprolol BB contraindicated- IV diltiazem amiodarone Ventricular arrhythmias- Normal for reperfusion ectopy ```
51
AMI complications
``` AV block Bundle branch blocks (anterior wall MI) Complete heart block (5% of IWMI) Acute LV failure Cardiogenic shock Papillary muscle rupture Myocardial rupture (2-7 days post MI) LV aneurysm (requires immediate surgical correction) Pericarditis Mural thrombus ```
52
RV infarcts are
Preload dependent
53
LV infarcts need to
Reduce volume, reduce afterload
54
Cardiogenic shock
SBP <90 with signs of hypo perfusion, non responsive to fluid
55
RV infarction complications
JVD Elevated CVP hypotension with preserved LV function
56
Clinical signs and symptoms of Papillary muscle rupture
new systolic murmur, hemodynamic compromise Occur with AWMI, IWMI High mortality
57
Treatment of Papillary muscle rupture
Surgical intervention IABP Nipride
58
What type of MI does a mural thrombus occur? | Treatment?
AWMI | Heparin initially, Warfarin for 3 months
59
All cholesterol is synthesized in the...
Liver
60
Lipoprotein classes
HDL, IDL, LDL, VLDL, Chylomicrons
61
High triglyceride treatment
Dietary modifications-decrease calories, decrease sugar, decrease alcohol medication-Niacin (usually combined with a Statin) Omega 3 fatty acids HMG-CoA reductase inhibitors (statins)
62
Who should be screened for hyperlipidemia?
Patients with known CVD Patients 40-75 years old with Diabetes Adults >20 years without CVD but with risk factors Men age 35 and older without risk factors
63
Goals for Lipid parameters
Total- <200 LDL <130 TG <150
64
Statin benefit groups
``` Clinical ASCVD LDL-C > 190 and Age > 21 years Primary prevention: Diabetes age 40-75, LDL 70-189 No diabetes >7.5% 10 year ASCVD risk, Age 40-75 years, LDL-C 70-189 ```
65
Statins benefits
Decrease CRP Increase Plaque stability Decrease thrombin production
66
Statin Adverse effects
Hepatotoxicity Myositis (muscle pain) Rhabdomyolysis
67
High intensity statin
Rosuvastatin 20 mg | Atorvastatin 40-80mg
68
Moderate intensity statin
``` Atorvastatin 10-20 Rosuvastatin 5-10 Simvastatin 20-40 Pravastatin 40-80 Lovastatin 40 Fluvastatin XL 80 Pitavastatin 2-4 ```
69
Low intensity statin
``` Simvastatin 10 Pravastatin 10-20 Lovastatin 20 Fluvastatin 20-40 Pitavastatin 1 ```
70
Management of Myositis
Unexplained severe muscle symptoms- stop the statin, check CK, Creatinine, UA for Myoglobin Mild to moderate muscle symptoms- D/C statin, evaluate the symptoms, evaluate for other syndromes
71
Nicotinic Acid (niacin) Benefits
Drug of choice for patients with pancreatitis
72
Niacin adverse effects
``` Intense flushing Pruritis Hepatotoxicity Hyperglycemia Exacerbate gout PUD symptoms Vasodilation (hypotension) ```
73
Niacin safety recommendations
baseline hepatic transaminases, fasting BG, and uric acid and every 6 months
74
Bile Acid Sequestrants
Cholestyramine, Cholesvelam, Coletipol
75
Bile acid sequestrates benefits
Decrease CV events by 20% | Reduce LDL in combo with statin
76
BAS education
Other meds must be taken at least 1 hour before or 4 hours after
77
BAS adverse effects
Constipation | Flatulence
78
BAS safety recommendations
not to be used in patients with baseline fasting triglycerides > 300
79
Fibric acid derivatives
Gemfibrozil | Fenobicrate
80
Fibric acid benefits
CV risk reduction
81
Fibric acid Lipid activity
lower LDL, increase HDL, lower TG
82
Fibric acid adverse effects
Myositis Hepatitis Cholelithiasis
83
Fibric acid safety
gemfibrozil should not be used in patients on statins
84
Ezetimibe Lipid activity
Decrease LDL
85
Ezetimibe benefits
Good alternative to statins, approved for mono therapy or combo therapy with statins
86
Ezetimibe adverse effects
Slight risk of gall stones | Caution with hepatic disease
87
Omega 3 fatty acids
decrease Triglycerides
88
Fish oil benefits
CHD risk reduction Decrease platelet aggregation Antiinflammatory Stabilize plaque
89
Fish oil safety
Be careful with patients on anticoagulants
90
PCSK9 inhibitors
Given SubQ every 2-4 weeks Alirocumab Evolocumab Very expensive
91
PCSK9 Lipid activity
Reduce LDL

AHN 572 (1 decks)

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