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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
Q

Anti-Ischemic therapy guidelines for Stable HD

A

Beta blockers
Calcium channel blockers or long acting nitrates
Sublingual nitro
Ranolazine (if others not able to be used)

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26
Q

Goal of anti-anginal agents

A

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)

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27
Q

Prinzmetal angina

A 
Coronary vasoconstriction with or without spasm
Common in females <50
Treatment
coronary angiography
medical management
avoid precipitating factors
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28
Q

Acute coronary syndrome types

A

unstable angina without necrosis (negative biomarkers)
NSTEMI-necrosis, nontransmural (positive biomarkers
STEMI- Transmural necrosis (positive biomarkers, ST elevation, need immediate reperfusion)

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29
Q

Clinical manifestations of ACS without ST elevation

A

Typical presentation- Substernal chest pain, radiation, dyspnea, N/V, Diaphoresis, syncope
Atypical presentation-
For women, DM, and elderly

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30
Q

Clinical manifestations of ACS with ST elevation

A

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

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31
Q

Review of cardiac biomarkers

A

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

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32
Q

Troponin detectable, peak, how long elevated, what is normal?

A

Detectable 4-6 hours after necrosis, peaks at 24-48 hours, may remain elevated for 5-7 days, normal is < 0.04
Cardiospecific

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33
Q

Myoglobin detectable, baseline, specificity

A

Detectable within 1-3 hours, returns to baseline within 12-24 hours, very nonspecific

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34
Q

CKMB detectable, elevation length, specificity

A

moderately specific, detectable within 2-5 hours, returns to baseline within 2-4 days

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35
Q

Noncardiac causes of troponin elevation

A 
Trauma
PE
toxicity (anthracyclines)
CHF
Renal failure
Sepsis
Stroke
SAH
Electrical shocks
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36
Q

EKG testing should be performed within … of arrival

A

10 minutes

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37
Q

Additional diagnostic testing if ACS

A

CXR (heart failure, aortic dissection)
ECHO
Labs- CBC, CMP, Lipid panel, PT/INR & Ptt

38
Q

Beta blockers should be started within… and continued with

A

24 hours

metoprolol, carvedilol, bisoprolol

39
Q

If beta blockers are contraindicated you can use

A

Calcium channel blockers

40
Q

ACE inhibitors should be started and continued indefinitely for patients with a LVEF less than

A

40%

41
Q

Common ACE inhibitor side effect

A

Cough

42
Q

Aldosterone blockers recommended for patients post-MI without renal dysfunction who are intolerant to…

A

ACE inhibitors

43
Q

Antiplatelet agent

A

chew an aspirin 162-325 immediately

Long term 81-162 to be continued indefinitely

44
Q

Goal for reperfusion of STEMI at facility with intervention

A

90 minutes

45
Q

Goal of fibrinolytic of STEMI at facility with no intervention

A

10 minutes to bolus, infusion completed 60-90 minutes- transfer to PCI capable facility

46
Q

Recommendations for Cardiac arrest

A

Primary PCI recommended in patients resuscitated and ECG with STEMI
TTM indicated early

47
Q

Recommendations for reperfusion therapy

A

indicated for all patients with STEMI

48
Q

Antiplatelet and anticoagulant indicated for all patients during

A

primary PCI

49
Q

Absolute contraindications to fibrinolytic therapy

A 
hemorrhagic stroke
ischemic stroke within the last year
intracranial hemorrhage
aortic dissection
internal bleeding
50
Q

Complications of AMI

A 
Sinus Brady (inferior wall MI, DC any offending medications &amp; 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
Q

AMI complications

A 
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
Q

RV infarcts are

A

Preload dependent

53
Q

LV infarcts need to

A

Reduce volume, reduce afterload

54
Q

Cardiogenic shock

A

SBP <90 with signs of hypo perfusion, non responsive to fluid

55
Q

RV infarction complications

A

JVD
Elevated CVP
hypotension with preserved LV function

56
Q

Clinical signs and symptoms of Papillary muscle rupture

A

new systolic murmur, hemodynamic compromise
Occur with AWMI, IWMI
High mortality

57
Q

Treatment of Papillary muscle rupture

A

Surgical intervention
IABP
Nipride

58
Q

What type of MI does a mural thrombus occur?

Treatment?

A

AWMI

Heparin initially, Warfarin for 3 months

59
Q

All cholesterol is synthesized in the…

A

Liver

60
Q

Lipoprotein classes

A

HDL, IDL, LDL, VLDL, Chylomicrons

61
Q

High triglyceride treatment

A

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
Q

Who should be screened for hyperlipidemia?

A

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
Q

Goals for Lipid parameters

A

Total- <200
LDL <130
TG <150

64
Q

Statin benefit groups

A 
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
Q

Statins benefits

A

Decrease CRP
Increase Plaque stability
Decrease thrombin production

66
Q

Statin Adverse effects

A

Hepatotoxicity
Myositis (muscle pain)
Rhabdomyolysis

67
Q

High intensity statin

A

Rosuvastatin 20 mg

Atorvastatin 40-80mg

68
Q

Moderate intensity statin

A 
Atorvastatin 10-20
Rosuvastatin 5-10
Simvastatin 20-40
Pravastatin 40-80
Lovastatin 40
Fluvastatin XL 80
Pitavastatin 2-4
69
Q

Low intensity statin

A 
Simvastatin 10
Pravastatin 10-20
Lovastatin 20
Fluvastatin 20-40
Pitavastatin 1
70
Q

Management of Myositis

A

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
Q

Nicotinic Acid (niacin) Benefits

A

Drug of choice for patients with pancreatitis

72
Q

Niacin adverse effects

A 
Intense flushing
Pruritis
Hepatotoxicity
Hyperglycemia
Exacerbate gout
PUD symptoms
Vasodilation (hypotension)
73
Q

Niacin safety recommendations

A

baseline hepatic transaminases, fasting BG, and uric acid and every 6 months

74
Q

Bile Acid Sequestrants

A

Cholestyramine, Cholesvelam, Coletipol

75
Q

Bile acid sequestrates benefits

A

Decrease CV events by 20%

Reduce LDL in combo with statin

76
Q

BAS education

A

Other meds must be taken at least 1 hour before or 4 hours after

77
Q

BAS adverse effects

A

Constipation

Flatulence

78
Q

BAS safety recommendations

A

not to be used in patients with baseline fasting triglycerides > 300

79
Q

Fibric acid derivatives

A

Gemfibrozil

Fenobicrate

80
Q

Fibric acid benefits

A

CV risk reduction

81
Q

Fibric acid Lipid activity

A

lower LDL, increase HDL, lower TG

82
Q

Fibric acid adverse effects

A

Myositis
Hepatitis
Cholelithiasis

83
Q

Fibric acid safety

A

gemfibrozil should not be used in patients on statins

84
Q

Ezetimibe Lipid activity

A

Decrease LDL

85
Q

Ezetimibe benefits

A

Good alternative to statins, approved for mono therapy or combo therapy with statins

86
Q

Ezetimibe adverse effects

A

Slight risk of gall stones

Caution with hepatic disease

87
Q

Omega 3 fatty acids

A

decrease Triglycerides

88
Q

Fish oil benefits

A

CHD risk reduction
Decrease platelet aggregation
Antiinflammatory
Stabilize plaque

89
Q

Fish oil safety

A

Be careful with patients on anticoagulants

90
Q

PCSK9 inhibitors

A

Given SubQ every 2-4 weeks
Alirocumab
Evolocumab
Very expensive

91
Q

PCSK9 Lipid activity

A

Reduce LDL

AHN 572 (1 decks)

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