Cardiovascular I Flashcards
What is Coronary heart disease?
Inadequate blood supply to the myocardium most commonly due to obstruction of the coronary arteries due to atherosclerosis
Who is most affected by CHD
55% male predominance
Aged >40 years
Pathophysiology of myocardial ischemia
Increased demand and decrease in oxygen supply
Distinguishing factors of Stable angina
Brief (less than 10 minutes) during exertion of emotional stress
Correlate to significant stenosis but nonocclusive
Unstable angina
Pain at rest
Correlates to a thrombi projecting into lumen but not occluded
NSTEMI
Acute MI
Severe occlusion
STEMI
Acute MI
Coronary occlusion
Risk factors for CAD
Hereditary ethnicity gender hypertension age family history Inflammation Diet inactivity stress smoking/alcohol obesity DM Hyperglycemia Hyperlipidemia (LDL)
Primary prevention of CAD
Lifestyle modification (healthy diet, physical activity, weight loss, smoking cessation)
Blood pressure control
Dyslipidemia treatment
management of DM
Secondary prevention of CAD
Aggressive lifestyle modifications Statin therapy BP <140/85 Antiplatelet therapy ACE-I Beta Blockers
The most important aspect of classifying angina appropriately?
Differentiating Stable ischemic heart disease from Acute coronary syndrome
Diagnostic measures of CHD
Resting EKG Exercise EKG myocardial stress imaging CT/MRI Coronary angiography
Resting EKG guidelines
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
Indications of Exercise EKG
Confirmation of angina
Assess severity of activity limitations
Prognostic tool
Evaluate therapeutic effectiveness
Interpretation of exercise EKG
Should include exercise capacity and clinical, hemodynamic and ECG response
ST depression of > 1 mm
Downsloping ST > 80 msec pas the J point
Myodcardial stress imaging indications
exercise EKG difficult to interpret
Confirmation of results of exercise EKG
Ischemic localization
Indications for coronary angiography
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
Coronary angiography is
The gold standard for diagnosing CAD
What is considered clinically significant stenosis?
> 50%
Stable angina treatment approaches
Medication adherence Modifiable risks daily activity self monitoring recognizing worsening symptoms Adherence to diet manage stress
Recommended threshold for antihypertensive therapy
BP of 130/80 or higher
Goal HbA1C
<7% for younger patients
What Diabetes management should not be initiated in patients with SIHD?
Therapy with rosiglitazone (Actos)
Antiplatelet therapy guidelines for Stable HD
Aspirin 75-162 mg
Plavix when aspirin is contraindicated
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)
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)
Prinzmetal angina
Coronary vasoconstriction with or without spasm Common in females <50 Treatment coronary angiography medical management avoid precipitating factors
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)
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
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
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
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
Myoglobin detectable, baseline, specificity
Detectable within 1-3 hours, returns to baseline within 12-24 hours, very nonspecific
CKMB detectable, elevation length, specificity
moderately specific, detectable within 2-5 hours, returns to baseline within 2-4 days
Noncardiac causes of troponin elevation
Trauma PE toxicity (anthracyclines) CHF Renal failure Sepsis Stroke SAH Electrical shocks
EKG testing should be performed within … of arrival
10 minutes
Additional diagnostic testing if ACS
CXR (heart failure, aortic dissection)
ECHO
Labs- CBC, CMP, Lipid panel, PT/INR & Ptt
Beta blockers should be started within… and continued with
24 hours
metoprolol, carvedilol, bisoprolol
If beta blockers are contraindicated you can use
Calcium channel blockers
ACE inhibitors should be started and continued indefinitely for patients with a LVEF less than
40%
Common ACE inhibitor side effect
Cough
Aldosterone blockers recommended for patients post-MI without renal dysfunction who are intolerant to…
ACE inhibitors
Antiplatelet agent
chew an aspirin 162-325 immediately
Long term 81-162 to be continued indefinitely
Goal for reperfusion of STEMI at facility with intervention
90 minutes
Goal of fibrinolytic of STEMI at facility with no intervention
10 minutes to bolus, infusion completed 60-90 minutes- transfer to PCI capable facility
Recommendations for Cardiac arrest
Primary PCI recommended in patients resuscitated and ECG with STEMI
TTM indicated early
Recommendations for reperfusion therapy
indicated for all patients with STEMI
Antiplatelet and anticoagulant indicated for all patients during
primary PCI
Absolute contraindications to fibrinolytic therapy
hemorrhagic stroke ischemic stroke within the last year intracranial hemorrhage aortic dissection internal bleeding
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
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
RV infarcts are
Preload dependent
LV infarcts need to
Reduce volume, reduce afterload
Cardiogenic shock
SBP <90 with signs of hypo perfusion, non responsive to fluid
RV infarction complications
JVD
Elevated CVP
hypotension with preserved LV function
Clinical signs and symptoms of Papillary muscle rupture
new systolic murmur, hemodynamic compromise
Occur with AWMI, IWMI
High mortality
Treatment of Papillary muscle rupture
Surgical intervention
IABP
Nipride
What type of MI does a mural thrombus occur?
Treatment?
AWMI
Heparin initially, Warfarin for 3 months
All cholesterol is synthesized in the…
Liver
Lipoprotein classes
HDL, IDL, LDL, VLDL, Chylomicrons
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)
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
Goals for Lipid parameters
Total- <200
LDL <130
TG <150
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
Statins benefits
Decrease CRP
Increase Plaque stability
Decrease thrombin production
Statin Adverse effects
Hepatotoxicity
Myositis (muscle pain)
Rhabdomyolysis
High intensity statin
Rosuvastatin 20 mg
Atorvastatin 40-80mg
Moderate intensity statin
Atorvastatin 10-20 Rosuvastatin 5-10 Simvastatin 20-40 Pravastatin 40-80 Lovastatin 40 Fluvastatin XL 80 Pitavastatin 2-4
Low intensity statin
Simvastatin 10 Pravastatin 10-20 Lovastatin 20 Fluvastatin 20-40 Pitavastatin 1
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
Nicotinic Acid (niacin) Benefits
Drug of choice for patients with pancreatitis
Niacin adverse effects
Intense flushing Pruritis Hepatotoxicity Hyperglycemia Exacerbate gout PUD symptoms Vasodilation (hypotension)
Niacin safety recommendations
baseline hepatic transaminases, fasting BG, and uric acid and every 6 months
Bile Acid Sequestrants
Cholestyramine, Cholesvelam, Coletipol
Bile acid sequestrates benefits
Decrease CV events by 20%
Reduce LDL in combo with statin
BAS education
Other meds must be taken at least 1 hour before or 4 hours after
BAS adverse effects
Constipation
Flatulence
BAS safety recommendations
not to be used in patients with baseline fasting triglycerides > 300
Fibric acid derivatives
Gemfibrozil
Fenobicrate
Fibric acid benefits
CV risk reduction
Fibric acid Lipid activity
lower LDL, increase HDL, lower TG
Fibric acid adverse effects
Myositis
Hepatitis
Cholelithiasis
Fibric acid safety
gemfibrozil should not be used in patients on statins
Ezetimibe Lipid activity
Decrease LDL
Ezetimibe benefits
Good alternative to statins, approved for mono therapy or combo therapy with statins
Ezetimibe adverse effects
Slight risk of gall stones
Caution with hepatic disease
Omega 3 fatty acids
decrease Triglycerides
Fish oil benefits
CHD risk reduction
Decrease platelet aggregation
Antiinflammatory
Stabilize plaque
Fish oil safety
Be careful with patients on anticoagulants
PCSK9 inhibitors
Given SubQ every 2-4 weeks
Alirocumab
Evolocumab
Very expensive
PCSK9 Lipid activity
Reduce LDL
