Cardiology Flashcards
Statins
- lovastatin
- pravastatin
- atorvastatin
- rosuvastatin
decreases synthesis of cholesterol in liver by inhibiting HMG-CoA reductase
best drug to lower LDL
increases HDL
side effects: muscle injury (test CK in any patient on a statin with muscle symptoms), hepatic dysfunction (check LFT before you start, and then again later if there is a clinical indication to do so)
ezetimibe
cholesterol absorption inhibitor
impairs dietary and biliary cholesterol absorption at the brush border of the intestine
- does not affect TG or fat-soluble vitamin absorption
- primarily lowers LDL
- side effects:myalgias, increased LFTs
fibrates
gemfibrozil, fenofibrate
primary effect on triglycerides and also raise HDL 5-20%
Fibrates work primarily by reducing hepatic secretion of VLDL
Side effects: myositis and LFT elevation
Bile acid sequestrants
aka bile-acid binding resins
Cholestyramine, colestipol, colesevelam
Primarily lower LDL (10-20%)
so not as strong as an effect as is seen with high intensity statins (50%)
Can serve a dual role in diabetics, as it lowers HbA1C in these patients by 0.5%
Side effects: GI side effects, LFT elevation, bad taste
Cholestyramine can bind C.Diff toxin!
Niacin
Primary effect on HDL
Side effect: flushing, but this improves with continued use, or prevent with dose at bedtime (sleep through the side effects), aspirin/NSAID use
Omega-3 fatty acids
Primary effect on TGs
Can be added on to other treatments
side effect: fishy burp
SE: facial flushing
niacin
SE: elevated LFT, myositis
statin, fibrates, ezetimibe
SE: Gi discomfort, bad taste
bile acid binding resins
Best effect on HDL
niacin
Best effect on TGs
fibrates
Best effect on LDL/cholesterol
statins
Binds C. difficile toxin
cholestyramine
2013 AHA/ACC guildelines
Who should be on statins?
- Those with clinical ASCVD
- acute coronary syndrome
- myocardial infarction
- stable or unstable angina
- revascularization procedures
- stroke or TIA
- peripheral arterial disease - Anyone with LDL>190
- Diabetics (type 1 and 2), and between age 40-75yo
- 10-year ASCVD risk of 7.5% between age 40-75 (this calculation based on diabetes, anihypertensive use, age, SBP, total cholesterol, tobacco use)
Angina
chest pain associated with myocardial ischemia
chest discomfort, pressure sensation, “like something is sitting on my chest”
- left-sided, midsternal
- radiates to back/jaw/left arm
- diaphoresis, SOB, palpitations
atypical symptoms:
- female, diabetic, older
- abdominal pain, exercise intolerance, generalized fatigue
Myocardial ischemia
myocardial oxygen demand exceed oxygen supply predisposing factors: -atherosclerosis -shock -hypoxemia -anemia -coronary artery vasospasm
increased demand:
- vigorous exertion
- tachycardia
- HTN
- ventricular hypertrophy
- increased catecholamines
stable (predicatable) angina
resolves with rest, does not occur at rest
diagnosed with exercise or pharmacologic stress test
Labs: cardiac enzymes (troponin I, CKMB)
How do we treat stable angina?
- Beta blockers decrease HR and contractility
- CCBs promote coronary and peripheral vasodilation, and decrease contractility
- Nitrates: promote peripheral venous vasodilation (decrease preload, which decreases oxygen demand on the heart)
Prinzmetal angina (variant angina)
Caused by coronary artery vasospasm (NOT atherosclerosis)
RF: smoking
More often in younger patients (
What is the major RF associated with Prinzmetal angina?
smoking (
How does Prinzmetal angina present?
Pain at rest occurring at night, lasting 5-15 minutes
often indistinguishable from classic angina
How is prinzmetal diagnosed?
Coronary arteriography shows no sign of high grade coronary artery stenosis
in the setting of recurrent CP at rest, and transient ST-segment elevation on ECG
What medication class is used first-line to treat Prinzmetal angina?
CCB (diltiazem) and nitrates promote vasodilation in the coronary arteries
Smoking cessation is also very important
Why avoid beta blockers in Prinzmetal angina?
they may exacerbate vasospasm
Causes of CP
MSK- costochondritis GERD Esophageal spasm (relieved by nitrates) Cocaine intoxication Hyperventilation Herpes zoster Aortic stenosis Trauma Pulmonary embolism Pneumonia Pericarditis Pancreatitis Angina Aortic dissection Aortic aneurysm Infarction Neuropsychiatric diseases
ST segment elevation only during brief episodes of chest pain
Prinzmetal angina (coronary vasospasm)
Patient is able to localize the pain by pointing to it, and it is tender to palpation
Costochondritis
Rapid onset sharp chest pain that radiates to the scapula
aortic dissection
Rapid onset sharp pain in a 20-year old, with associated dyspnea
spontaneous pneumothorax, which is more common in young males
occurs after heave meals and is improved by antacids
GERD, maybe esophageal spasm, but still needs to be worked up
sharp pain lasting hours-days and is somewhat relieved by sitting forward
pericarditis
pain made worse by deep breathing and/or motion
musculoskeletal pain, pleuritic chest pain (irritation of the lining of the lung)
chest pain in a dermatomal dist
zoster
MCC noncardiac chest pain
GERD
musculoskeletal pain
acute onset dyspnea, tachycardia, confusion in a hospitalized patient
PE
widened mediastinum on CXR
aortic dissection
How does nitroglycerin relieve pain?
dilates peripheral veins
decreases preload
reduces myocardial O2 demand
inhibits COX1 and COX2
aspirin
ADP receptor inhibitor
clopidogrel
ticlopidine
Glycoprotein 2b/3a inhibitor
TIrofiban, Eptifibatide
abciximab
Activates antithrombin
heparin. enoxaparin
converts plasminogen to plasmin
streptokinase
streptokinase reversal agent
aminocaproid acid
drugs that can cause type 2 heart block (Mobitz I)
beta blockers
digoxin
calcium channel blockers
Narrow QRS, rate>100
SVT
No relationship between pulses and QRS
complete heart block
3 p-wave readings, rate>100
MAT
rate
bradycardia
PR interval >0.2 second
first degree heart block
Early, wide WRS beat without p-wave
PVT
wide QRS, HR 160-240
ventricular tachycardia
PR interval becomes longer with dropped beat
second- degree type I heart block
chaotic pattern, no P wave, no QRS
ventricular fibrillation
PR normal, occasional dropped beat
2nd degree type 2 heart block
sawtooth pattern
atrial fibrillation
no p waves, narrow QRS, iregularly irregular
atrial fibrillation
sinusoidal pattern of QRS
torsades des pointes
Which heart med is associated with pulmonary fibrosis and therefore requires pre-check of PFT and diffusion capacity every 6 months?
amiodarone