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
contraindications to triptans
sulfa allergy
pregnancy
CAD
Prinzmetal angina
which drugs block transmission through the AV node?
beta blockers
nondihydropyridine CCBs
digoxin
adenosine
stones, bones, groans, and psychiatric overtones
hypercalcemia (consider hyperparathyroidism)
diastolic murmur best heard at left lower sternum that increases with inspiration
tricuspid stenosis
late diastolic murmur with opening snap (no change with inspiration)
mitral stenosis
systolic murmur best heard in the second right interspace, parasternal
aortic stenosis
late systolic murmur best heard at apex
mitral prolapse
Diastolic murmur with widened pulse pressure
aortic regurgitation
holosystolic murmur at the left lower sternum that is louder with inspiration
tricuspid regurgitation
holosystolic murmur heart at the apex, and radiates to the axilla
mitral regurgitation
systolic murmur best heard in the second left interspace, parasternal
pulmonic stenosis
things that can cause acute pericarditis
viral infection TB lupus uremia renal failure neoplasm drugs (INH, hydralazine) Post- MI inflammation (Dressler syndrome) radiation recent heart surgery
Acute pericarditis H and P
worse when supin
better when sitting up, leaning forward
dyspnea
pericardial friction rub
pulsus peridoxus (SBP drops more than 10mmHg during inspiration)
EKG changes (global ST elevation), PR depression
The pericardial effusion is usually transudative (thin, watery, low in protein)
If exudative, consider neoplasm, fibrotic disease, TB
Acute pericarditis:
Echo- pericardial effusion
CXR- enlarged globular canteen heart
Tx: treat the underlying cause
Constrictive pericarditis
diffuse thickening of pericardium
decreased diastolic filling
decreased cardiac output
most common causes are radiation and heart surgery
symptoms- consistent with heart failure, Kussmaul sign
What causes dilated cardiomyopathy?
ischemic heart disease chronic alcohol use chronic cocaine use doxodubicin CoxsackieB Beriberi Chagas hemochromatosis peripartum cardiomyopathy S3
What causes restrictive cardiomyopathy?
amyloidosis
sarcoidosis
hemochromatosis
(infiltrative causes)
What causes hypertrophic cardiomyopathy?
aotosomal dominant systolic murmur sudden death in young athlete S4 avoid diuretics, restrict exercise
indications for prophylactic antibiotics against infectious endocarditis
NOT rheumatic heart disease, and NOT GU/GI procedures
prosthetic cardiac valves
previous infective endocarditis
Some congenital heart diseases (unrepaired heart defect)
cardiac transplants with valvulopathy
unrecovered heart transplant
If indicated, give 2g amoxicillin 30-60 minutes prior to procedure
Endocarditis predisposing factors
congenital heart defects
IVDA
prosthetic heart calces
normal blood pressure
prehypertension
120-139/ 80-89
counsel these patients to stop smoking, reduce alcohol intake, reduce sodium in their diet, and lose weight
hypertension
> 140/90
3 readings on 3 separate occasions
Essential hypertension risk factors
family history high sodium diet tobacco use obesity age black> white
MCC secondary hypertension
kidney diseases, such as
chronic renal insufficiency
end stage renal disease
renal artery stenosis
How do we treat renal disease in end-stage hypertension?
ACEI to delay progression
renal artery stenosis
MCC fibromuscular dysplasia of renal artery
renal artery stenosis >50yo
MCC atherosclerosis
signs and symptoms of renal artery stenosis
renal artery bruit
What tests can be used to diagnose renal artery stenosis?
MRA of renal arteries- MOST FREQUENTLY used screening test
spiral CT scan of renal arteries with IV contrast
renal artery duplex scan- is time- consuming (2 hours) and requires well- trained operator
renal arteriogram- gold standard, but invasive
Why are ACEI contraindicated in renal artery stenosis?
They impede renal blood flow and renal GFR, thereby accelerating renal issues
Combination OCPs and HTN
obese, women, >35yo
poorly controlled HTN is a contraindication to starting OCP
-stop OCP and change to progestin-only pill if hypertensive, or use IM medroxyprogesterone
Pheochromocytoma and HTN
young patients
screen for MEN
Episodic HTN diaphoresis tachycardia palpitations headache
24-hr urine: catecholamines, VMA
serum: metanephrines, normetanephrines
CT or MRI: see the tumor?
Pheochromocytoma treatment
surgically remove the tumor
pharmacologic contrl of HTN, pre-operatively
Alpha- blocker before beta- blocker (labetalol would be a suitable plan B, since it blocks both alpha and beta blockers)
Primary hyperaldosteronism: Conn syndrome
HTN
hypokalemia
metabolic alkalosis
high PAC: PRA ratio
Treat this with surgical removal of tumor
possibly pre-treat with an aldosterone antagonist such as spironolactone or epleronone
Cushing syndrome
Cushingoid features obesity hirsutism buffalo hump glucose intolerance
Dexamethasone suppression test
Coarctation of the aorta- focal narrowing
kink in the hose associated with: 1. Congenital aortic valve pathology 2. Turner syndrome 3. Patent ductus arteriosis
high BP in arms but low BP in the legs, and weak dosalis pedis pulses
Diagnosis: LVH on EKG, echocardiogram
Treatment: surgical repair
Hyperparathyroidism
hypercalcemia
- confusion ans psychosis
- calcium kidney stones
- constipation
Hypertensive urgency
SBP>180 or higher
or DBP>120 or higher
No sumptoms, no evidence of end organ damage
If there is evidence of end organ damage then we call this hypertensive emergency
Hypertensive emergency
SBP>180 or higher
or DBP>120 or higher
with signs of end organ damage:
- renal failure
- changes in mental status
- papilledema
- retinal vascular changes
- unstable angina
- MI
- aortic dissection
- pulmonary edema
How do we treat hypertensive urgency and hypertensive emergency?
reduce DBP to 100mmHg
with something that will work quickly
-in the first 2 hours, initial decrease should not exceed 25% of presenting pressure
lowering it too much would risk ischemia
start maintenance oral antihypertensive
High BP in UE but low BP in LE
coarctation of the aorta
proteinuria
renal disease
hypokalemia
Cushing disease (primary hypoaldosteronism) or renal artery stenosis
tachycardia, diarrhea, heat intolerance
hyperthyroidism
hyperkalemia
renal failure
episodic sweating, tachycardia
pheochromocytoma
What tests do you order when you’re trying to rule out infectious endocarditis?
- rule out infection with blood/urine cultures, UA, +/- CXR
- Toxicology screen
- Rule out pancreatitis with amylase/lipase
- rule out MI with EKG and cardiac enzymes x3
Beta blockers that reduce mortality in CHF
bisoprolol
carvedilol
extended-release metoprolol
antihypertensive to use in DM
ACEI or ARB
antihypertensive to use in heart failure (multiple
ACEI, ARB, Beta- blocker, aldosterone antagonist
antihypertensive to use in BPH
alpha-1 antagonists
antihypertensive to use in left ventricular hypertrophy
ACE I or ARB, which lower afterload
antihypertensive to use in hyperthyroidism
propanolol
antihypertensive to use in osteoporosis
thiazides
antihypertensive to use in benign essential tremor
beta blociers
antihypertensive to use in postmenopausal woman
thiazides, which will help with retaining calcium and reduce risk of osteopososis
migraines
beta blockers
antihypertensive to with the side effect of first-does orthostatic hypertension
alpha blockers
antihypertensive to with the side effect of hypertrichosis
minoxidil
antihypertensive to with the side effect of dry mouth, sedation, severe rebound HTN
clonidine (wears off every six hours or so)
antihypertensive to with the side effect of bradycardia, impotence, asthma exacerbation
Nonselective beta blockers
antihypertensive to with the side effect of reflex tachycardia
vasodilators
antihypertensive to with the side effect of cough
ACE-I
antihypertensive to avoid in patients with sulfa allergy
thiazides and loop diuretics
antihypertensive to with the side effect of angioedema
ACE-I
antihypertensive to with the side effect of development of drug- induced lupus
hydralazine
antihypertensive to with the side effect of cyanide toxicity
sodium nitroprusside
consequences of longterm treatment with NE
ischemia/necrosis of fingertips and toes
mesenteric ischemia
renal failure
underlying mechanism of cardiogenic shock
failure of the pump
underlying mechanism of extracardiogenic shock
pump compression
underlying mechanism of hypovolemic shock
not enough fluid to pump
mechanism of anaphylactic shock
vasodilation, releaes of vasodilatory agents (histamine)
mechanism of neurogenic shock
vasodilation, loss of autonomic-regulated vascular tone
mechanism of septic shock
vasodilation, massive release of inflammatory mediatiors
AAA risk factors
tobacco use age>55 atherosclerosis htn family history
usually asymptomatic, pulsatile abdominal mass, abdominal bruit, hypotension, severe abdominal pain
radiology: us
CT or MRI if the US is positive
AAA screening
all men between 65-75 who have a history of smoking
1-time screening abdominal US
follow with
US every 6 months if
5.5cm in men or >5cm in women
or if diameter has increased by more than 0.5cm in a 6-month interval (should be having abdominal ultrasounds every 6 months)
or if the aneurysm is symptomatic (tenderness, pain in abdomen or back)
Aortic dissection
key difference between aortic dissection and AAA is that dissections tend to occur in the thorax, in the aortic arch.
RIsk factors: HTN, trauma, coarctation of the aorta, syphilis, Ehlers-Danlos syndrome, Marfan syndrome
Tear in the intima of the aorta
blood forces its way into the media and forms a false lumen
Stanford A- ascending aorta
B- confined to the distal aorta, below the branches
H and P: acute ripping/tearing chest pain radiating to the back
syncope or TIA, decreased peripheral pulses
EKG:
normal
+/- LVH
Radiology: CXR (widening of the mediastinum)
CT of the chest with contrast
B/L upper and lower extremity pulses, if unequal will be indicative of aortic dissection
Treatment: stabilize BP with beta blocker that will minimize the slope of rise of BP
Stanford A- emergency surg
Stanford B- beta blocker, surgery if uncontrolled
Peripheral vascular disease
atherosclerosis of peripheral arteries
HTN, DM, coronary disease
symptoms- claudication- leg pain that comes with activity and improves with rest
Skin changes- dryness, ulcers, decreased leg hair growth
erectile dysfunction
PVD- ankle-brachial index (ABI)
ratio ankle SBP: brachial SBP
ABI0.4: severe disease
What are components of conservative medical management of peripheral artery disease?
smoking cessation
glucose and BP control
daily exercise to increase collateral flow
cilostazol to improve flow to LE and decrease claudication (improves flow to LE and decreases claudication, more effective than pentoxifylline which is supposed to make RBCs more bendy)
contraindicated if any heart failure, due to increased mortality
Daily aspirin or clopidogrel to reduce cardiovascular events
Statin therapy to reduce cardiovascular events and increase pain-free walking distance
PVD surgical interventions
angioplasty
bypass grafting
amputate if there is prolonged ischemia
PVD and CAD
screen them with cardiac stress test before surgery
varicosities
dilated veins due to incompetent valves
blood pools in the veins
H and P:
enlarged veins, visible veins, palpable veins, increased skin pigmentation, edema, ulceration
How do we treat varicose veins?
weight reduction, avoid prolonged standing, leg elevation
compression stockings
sclerotherapy (injection of a substance that causes injury and thrombosis)
thermal ablation (external or internal)
surgery or ligation of the vein
AVM
abnormal communication between arteries and veins
palpable, warm, pulsating masses if superficial
pain
local ischemia
Treat: surgical removal or sclerosis if in brain or bowel where it might bleed
DVT
blood clot in large vein
usually in the lower extremity
RF: prolonged inactivity (travel or immobilization), recent surgery
Ted hose, SCDs, heart failure, hypercoag states
Cancer, pregnancy, OCPs, tobacco use, vascular trauma
DVT: hemostasos, hypercoagulability, vascular endothelial damage
H and P:
often asymptomatic
deep leg pain
calf sweeling and warmth
Homan sign (very unreliable) measure circumference of the calf
Labs:
D-dimer
compressive venous ultrasound
Ts: elevate the leg
LMWH or unfractionated heparin, warfarin (long-term)
IVC filter (Greenfield filter) if the patient can’t take warfarin
Dilates veins
nitroglycerine
dilates veins and arteries
dihydropyridine CCBs
dilates arteries
hydralazine
dilates veins and arteries
nitroprusside
