Cardiology Flashcards
Goals of primary prevention in CAD
Maintain or achieve ideal weight
Physical activity
Eat healthy diet
Fruits, vegetables, fiber, low glycemic index, unsaturated fats, omega-3 fatty acids (Mediterranean diet)
Refrain from cigarette smoking (and vaping)
Maintain blood pressure at goal
<140/90 if low risk
<130/80 if risk factors of known CAD
Maintain normal ‘bad’ cholesterol levels (LDL)
Glycemic control in diabetes
High risk patients <70 y/o without bleeding risk, should take aspirin daily (*new guidelines)
Small amount of alcohol consumption (less than 2 drinks/day)
Risk Factors for CAD
- Age >65yrs
- Gender (male > female until menopause)
- Cigarette smoking
- Dyslipidemia (abnormal cholesterol levels)
- Hypertension (HTN)
- Abdominal obesity (central obesity)
- Family history of 1st degree relative with premature MI (men age <55 women <65)
risk factor that is considered a “coronary artery disease equivalent”
Diabetes
Define Metabolic Syndrome
•Constellation of metabolic abnormalities that confer increased risk of CAD
Three or more of the following
- Abdominal obesity
- Triglycerides >150mg/dL
- HDL <40mg/dl for men and <50mg/dl for women
- Fasting glucose ≥ 110mg/dL (hyperglycemia/insulin resistance)
- Hypertension
what artery supplies blood to left ventricle and atrium
Left main coronary a.
The left anterior descending artery branches off the left coronary artery and supplies blood to the front of the left
The circumflex artery branches off the left coronary artery and encircles the heart muscle. This artery supplies blood to the outer side and back of the heart.
Which coronary artery supplies blood to the right ventricle, the right atrium, and the SA (sinoatrial) and AV (atrioventricular) nodes
Right coronary artery (RCA).
symptoms of chronic stable angina
- Chest discomfort or dyspnea with exertion lasting ~5-15 minutes, predictable & reproducible (due to flow limiting lesion)
- Relieved by rest and/or nitroglycerin
- Description of discomfort varies
- Tightness, squeezing, burning, gas, indigestion or ill characterized
- Typically located central or slightly left side of chest
- Pre-syncope (lightheadedness)
- Fatigue
exclusion criteria for ETT
- ST abnormalities
- LVH
- LBBB
- Vent-paced
- WPW
when would we include imaging stress tests
include imaging if patient has known CAD or multiple risk factors 2
Name types of imaging and nonimaging stress tests
- Non-Imaging Test
- Exercise tolerance testing (ETT) (uses treadmill & EKG)
Imaging Tests – include imaging if patient has known CAD or multiple risk factors 2.
- Echocardiography (exercise or pharmacologic)
- Radionuclide myocardial perfusion imaging (exercise or pharmacologic)
- Positron emission tomography (PET) (almost always pharmacologic)
first line stress test for most pts
ETT
describe Radionuclide myocardial perfusion imaging
Exercise or pharmacologic
Imaging before and after stress
Inject radioactive nucleotide
Poorly perfused areas of the heart do not take up color, localize lesion to coronary artery
Highly sensitive
what test would we use to look for stress induced regional wall motion abnormalities (RWMAs
stress echo
to localize lesion to particular coronary artery
Wont contract normally with the rest of the heart
**operator dependent
when would we use Nuclear Medicine PET CT stress test
Very sensitive
Very expensive
Best test for obese patients
Not readily available
classif presentation of ACS
- Early morning
- Substernal chest pressure, “like and elephant sitting on my chest.”
- Severe
- Sense of impending doom
- Radiates to L arm, both arms or jaw
- Associated shortness of breath, nausea, diaphoresis, lightheadedness
- Lasts >20min but <1 hr
- Risk factors
- Poor exercise tolerance at baseline
3 types of ACS
- Unstable Angina
- Non-ST Elevation Myocardial Infarction (NSTEMI)
- ST Elevation Myocardial Infarction (STEMI)
- **(most serious of the three)
Unstable plaque without plaque rupture is what type of ACS?
What would we see on EKG
unstable angina
Ischemic symptoms suggestive of ACS and no elevation of cardiac biomarkers (Troponin).
May or may not have ST depressions or non-specific changes (i.e. T wave inversion).
EKG can be normal
Potentially same manifestations as UA but do have elevated cardiac biomarkers (Troponin) suggestive of myocardial tissue death
sx?
NSTEMI
Unstable plaque +/- rupture (incomplete or complete occlusion)
Plaque rupture with complete occlusion
STEMI
what are the anterior leads and corresponding artery
V2, V3, V4
LAD
what are the left lateral leads
I, aVL, V5, V6
Left circumflex a
Name inferior leads and corresponding a.
II, III, aVF
Right coronary a.
name right ventricular leads and corresponding a.
aVR, V1
Right coronary a
name osterior leads and corresponding a
ST depressions in V2-V4
RCA
New LBBB in setting of acute CP is ____ until proven otherwise
MI
Recall which patients need urgent coronary artery reperfusion (catheterization and percutaneous intervention)
- Hemodynamic instability or cardiogenic shock
- Severe left ventricular dysfunction or heart failure
- Recurrent or persistent rest angina despite intensive medical therapy
- New or worsening mitral regurgitation
- Sustained ventricular arrhythmias
Immediate tx of ST elevation in MI
- cute Triage
- Responsiveness, airway, breathing, and circulation
- Evidence of systemic hypoperfusion/cardiogenic shock (hypotension, tachycardia, impaired cognition, cool/clammy)
- Congestive heart failure
- Ventricular arrhythmias
- Activate cardiac catheterization lab (cath lab)
- IV heparin bolus then continuous infusion
- MONA (morphine, oxygen (if needed), nitrates, aspirin)
- Oxygen if arterial O2 saturation ≤90% or respiratory distress
- Consider Glycoprotein IIb/IIIa inhibitors (Eptifibatide- (Integrilin))
- Percutaneous coronary intervention (PCI) – if available yields highest rates of survival if reperfusion is done within 90min (Door to balloon time). (consider transfer – ?allow 120min)
- Fibrinolytic therapy if PCI not available
- Beta-blocker
- Optimize potassium & magnesium
- * If patient is found to have severe 3 vessel disease during PCI à will need coronary artery bypass graft surgery (CABG)
All patients with known CAD should be on
•Asa, BB, and statin if no contraindications
recognize demand ischemia
Describe the pathophysiology of Prinzmetal angina
Vascular smooth muscle hyper-reactivity
- Generally caused by focal spasm of a major coronary artery
- Results in high grade obstruction
- Transient myocardial ischemia
- Occasionally myocardial infarction
Spasm occurs in the absence of oxygen supply/demand mismatch
• Can happen in normal or diseased vessels
clinical features of Prinzmetal angina
Angina symptoms at rest
Often between midnight and early morning
Associated with transient (15min) ST segment elevation
Triggered by coronary artery vasospasm
Generally in the absence of high grade coronary artery stenosis
Few if any cardiovascular risk factors
Drug use
Repeat EKG after 15min with total resolution of ST segments
EKG findings in vasospastic angina
Repeat EKG after 15min with total resolution of ST segments
tx of vasospastic angina
Sublingual nitroglycerin as needed during episodes
Smoking cessation
Long acting nitrates
CCBs
Si/sx of Hypertrophic obstructive cardiomyopathy
fatigue, dyspnea, chest pain, palpitations, presyncope or syncope
– Diastolic dysfunction
Myocardial ischemia
Mitral regurgitation
Systolic dysfunction (end-stage)
– Heart failure
Supraventricular and ventricular arrhythmias
Sudden death - most common cause in young people
Teenagers and young adults who collapse and lose consciousness during exercise
PE finding of Hypertrophic obstructive cardiomyopathy
Harsh crescendo-decrescendo systolic murmur
– Increase intensity with Valsalva maneuver
– Decrease intensity with squatting
**preload dependent
Hypertrophy of the ventricular septum – Significant left ventricular outflow tract (LVOT) obstruction
how does heart look in hypertrophic obst ructive cardiomyopathy
– Hypertrophy of the ventricular septum – Significant left ventricular outflow tract (LVOT) obstruction
Diastolic dysfunction
systolic dys (late-stage)
Takotsubo cardiomyopathy si/sx
severe psychological stress
Takotsubo cardiomyopathy PE / EKG findings
– Left ventricular apical ballooning
– ST elevation without CAD
dilated cardiomyopathy - impaired systolic function
cause of Chagas dz
– Protozoan infection (Trypanosoma cruzi)
Leading cause of DCM in Central and S. America
si/sx chagas dz
– Nonspecific EKG abnormalities
– Left ventricular apical aneurysms
•Apex of the heart dilates
– Heart failure
– Arrhythmias & heart blocks (all types)
Thromboembolism (right or left ventricular mural thrombi)
• Pulmonary Embolism
• Cerebrovascular accident (CVA) = stroke
– Chest pain
dilated vs restrictive cardiomyopathy
dilated:
Dilatation and impaired contraction of one or both ventricles –
- Impaired systolic function
- (Ejection Fraction (EF) <40%
restrictive
Non-dilated ventricles with impaired ventricular filling
Hypertrophy is typically absent (normal wall thickness)
Muscle layers are stiff and reduced stretching
Rigid ventricular walls resulting in diastolic dysfunction
Systolic function usually remains normal à cardiac output is reduced bc total volume in ventricle in diastole is reduced
•EF is preserved
Biatrial enlargement
dilated MC is a systolic / diastolic dysfunction white restrictive CM is systolic / diastolic
dilated - systoluc
restrictive - diastolic
dilated MC EF is _____ while in restrictive CM EF is ____.
dilated: EF reduced
restrictive EF preserved
common causes of dilated CM
1.Idiopathic (most common – often familial/gene mutations LMNA Gene mutations (LaminA/C)
Infections (i.e. viral myocarditis, Chagas disease)
- Toxins (drugs, meds, alcohol)
- Tachycardia induced CMP 5.
- Stress (takotsubo) – sometimes considered “unclassified”
which toxic CM is most common
alcohol
common causes of restrictive cardiomyopathy
- Idiopathic – build up of scar tissue, unknown reason *most common
- Amyloidosis – build up of abnormal proteins
- Radiation exposure
- Hemochromatosis – excess iron deposition
- Sarcoidosis
physiology of hypertrophic obstructive cardiomyopathy
Hypertrophy of the ventricular septum – Significant left ventricular outflow tract (LVOT) obstruction
When ventricles contract during normal systole they become hyperdynamic and walls collapse on themselves
More likely to develop obstruction of outflow tract
LV volume is normal or reduced, diastolic dysfunction is usually present
treatment plan for hypertrophic obstructive cardiomyopathy
Stay hydrated
Restrict intense physical exertion
Medical therapy to treat chest pain and dyspnea
Medical therapy to treat arrhythmias àat risk ventricular arrythmias
•Optimize electrolytes Mg
when would we perform alcohol septal ablation or septal myectomy)
Hypertrophic obstructive cardiomyopathy (HOCM
Invasive procedures to improve LV outflow tract
- Do not perform alcohol ablation on patients <21 y/o iscourage in patient’s <40 years à
- (scar - ↑risk of ventricular arrhythmias)
Implantable cardioverter-defibrillator is best therapy for patients w/ HOCM who have either
- survived SCD, have known ventricular arrhythmias
- or unexplained syncope
features of arrhythmogenic right ventricular cardiomyopathy (ARVC/D)
Myocardium of right ventricle is replaced by fibrous and/or fibro-fatty tissue
Genetically determined
Sudden cardiac death in young adults (can be exercise induced but not always
Right ventricular function is abnormal with regional akinesias or dyskinesis – part of the wall of the right ventricle is not contracting with the rest of the right ventricle
best imaging modality for diagnosis of ARVC/D
Cardiac MRI – gold standard à see fibrous deposits within myocardium
where would we see
Right ventricular function is abnormal with regional akinesias or dyskinesis – part of the wall of the right ventricle is not contracting with the rest of the right ventricle
Arrhythmogenic right ventricular cardiomyopathy (ARVC)
Recognize when a cardioverter-defibrillator is indicated for treatment of dilated cardiomyopathy
- Patients with dilated CMP & EF < 35% -
- Patients with dilated CMP & significant arrhythmia -
- Patients with dilated CMP & FmHx of sudden death OR known LMNA gene mutation
what is considered HTN stage
1
2
crisis
what is normal BP
•Normal Blood Pressure: 140/>90
“gold standard” for dx HTN
Ambulatory blood pressure monitoring (ABPM)
most common cause of secondary HTN
rendal disease
explain masked vs white coat HTN
masked
A blood pressure that is consistently elevated by out-of-office measurements but does not meet the criteria based on office readings.
assoc w/ increase risk of mortality and morbidity
white coat
A blood pressure that is consistently elevated by office readings but does not meet diagnostic criteria for hypertension based on out-of-office readings.
dx tx for HTN in CKD
ACEs and ARBs have been shown to delay the progress of kidney disease and protects the kidneys
tx of HTN in lederly
Treatment verse non-treatment
Benefits verse risks
Diuertics
CCBs
ACE
tx of HTN in AAs
Low plasma renin activity and increased sodium/fluid loading which can make them resistant to ACEs/ ARB
Diuertics
CCBs
tx HTN in diabetics
Due to renal protective nature of ACEs and ARBs, it is recommended that these should be used for reduction of renal nephropathy
Most often this patient population requires multiple agents (average 3-5) to control their hypertension
tx HTN in HF w/ EF <40%
Diuretics – helps with fluid maintenance and decreasing pre-load
ACE/ARB – decreases comorbidities and hospitalizations
Beta-blockers – decreases LV remodeling
tx of HTN in prior MI
Found to reduce size of infarct after an acute MI
b-blockers!!!! A MUST
labs evaluating HTN
chem 10 - electrolytes and renal function
fasting glucose hemaglobinn A1C
Lipid profile
labs evaluating HTN crisis
ADD
EKG (LVH)
CBC
TSH
what HTN drugs should we NEVER combine
ACE + ARB + potassium sparing diuretic - hyperkalemic CRISIS
HTN drugs you should never combine
- Alpha OR beta blocker + Clonidine
- Nifedepine + diuretic synergism
- Hydralazine + direct acting vasodilators OR Prazosin
- Diltiazem + Verapamil + Beta-blocker
- ACE + ARB + Potassium sparing diuretic
define resistant HTN
Blood pressure remains above goal in spite of the concurrent use of 3 antihypertensive agents of different classes
Rule out secondary causes prior to labeling someone with resistant hypertension
clasic triad of medication in reistant htn
- ACE (prils)
- ARB (sartans)
CCB (amlodipine, Diltiazem, Nifedipine, Verapamil
management of resistant HTN
Consider using different drug mechanisms and optimize the management of comorbidities
Classic triad of medication:
- ACE (prils)
- ARB (sartans)
- CCB (amlodipine, Diltiazem, Nifedipine, Verapamil)
Potassium sparing diuretics
•Potential to decrease SBP 5-20 mmHg and DBP 5-10 mmHg
Addition of beta-blockers if patient has:
- CHF
- CAD
Alpha blockers (-zosin)
Malignant Hypertensive is characterized by
encephalopathy or nephropathy with accompanying papilledema
HTN urgency is most often seen in pts who
Most often patients present who are not adherent to their blood pressure regimen
tx of HTN urgency
Blood pressure must be reduced within a few hours and is not a medical emergency.
Usually this can be treated within the office setting and does not require transfer to a higher level of care
define HTN emergency
an elevated BP (usually DBP >120 mmHg) with evidence of end-organ damage
tx of HTN emergency
Required substantial reduction in BP within 1 hour to avoid the risk of severe morbidities or mortality
IV MEDS
Goal is to reduce the pressure by no more the 25% within minutes to 1-2 hours and then towards a level of 160/100 mmHg within 2-6 hours
•Excessive reduction in BP may precipitate coronary, cerebral, or renal ischemia.
examples of meds used to tx HTN emergency
IV
- Nitroprusside (Nipride)
- Nitroglycerin
- Beta-Blockers (Labetalol or Esmolol)
- Nicardipine
- Diuretics
- Hydralazine
- Multiple other choices that are less widely used
compare good vs bad chlesterol
Low-density lipoprotein (LDL) “bad cholesterol”
•Main carrier of cholesterol, deliver to cells
High-density lipoprotein (HDL) “good cholesterol”
- Acceptor of cholesterol from various tissues
- 50% protein
LDL is removed from system in 2 ways:
Receptor- dependent
Binds to cell surface receptors → endocytosis
LDL is enzymatically degraded → chol released into cytoplasm and excreted
Non-receptor-dependent
Ingestion by phagocytic monocytes
Macrophage uptake of LDL in the arterial wall can result in accumulation of insoluble cholesterol ester → formation of foam cells →development of atherosclerosis due to large foam cell deposition next to arterial walls
define limits of dyslipidemia in regards to
HDL
LDL
TGs
- LDL >160 mg/dL
- HDL < 40 mg/dL
- Triglyceride > 150mg/dL
(all three are independent risk factors for CAD)
•Total cholesterol is not a risk factor for heart disease but rather the ratio of plasma___ to plasma ____.
LDL to HDL
how do we measure LDL
•LDL = total cholesterol – HDL – Triglycerides
Friedwald equation
primary vs secondary causes of dyslipidemia
- Primary causes
- Disorders of lipid metabolism (overproduction and/or impaired removal of lipoproteins)
- Secondary causes
- Type2 DM
- Excessive alcohol consumption
- Cholestatic liver disease
- Nephrotic syndrome
- Chronic renal failure
- Hypothyroidism
- Cigarette smoking
- Obesity
Drugs
who do we screen for dyslipidemia
- Age; men > 35yrs & women >45yrs (LDL levels increase with age)
- Men >25yrs with cardiovascular risk factors (more than one RFs, including HTN, tobacco use, or +FMHx or one RF that is severe)
- Women >35 with cardiovascular risk factors
- Patients with diabetes
- Patients with a first degree relative with premature CAD (before 55yrs for men and before 65yrs for women)
how often do we screen pts for dyslipidemia
every 5 years in patients clearly above therapy threshold.
Every 3 years in patients near threshold.
Explain familial dyslipidemia
- Autosomal dominant
- Strongly link to premature CAD
- >200 LDL receptor mutations
french canadiana and lebonese
underexpression of LDL R
clinical presentation of familial disorders of LDL R
- Xanthomas
- high LDL
- FHx
first line tx for dyslipidemia
lifestyle modifications
Unsaturated fats Decrease cholesterol by upregulating the LDL receptor - removing more LDL
name the most commonly used lipid lowering medication anf the ONLY medication to prove positive CV outcomes
Statins
•All patients with known atherosclerosis (CAD, CVD, PVD) regardless of LDL level should receive ____ therapy
statin
4 statin benefit groups
- Clinical Atherosclerotic cardiovascular disease (ASCVD)
- LDL-C ≥190 mg/dL, Age ≥21 years
- Primary prevention – Diabetes: Age 40-75 years, LDL-C 70-189 mg/dL
- Primary prevention - No Diabetes: ≥7.5% 10-year ASCVD risk, Age 40-75 years, LDL-C 70-189 mg/dL
High Intensity statin therapy lowers LDL on average by ___
about 50%
atorvastatin (40-80mg)
Rosuvstatin 20, 40 mg
moderate intensity statins lower LDL by approx ____ to ____
30-<50%
atorv 10, 20
simvas 20-40
pravas 40,80n
pts with an LDL > 190 should be started on
high intensity
pts w DM and LDL 70-189 should be started on
mod intensity
UNLESS ASCVD risk is >7.5% = start on high intesity
pts w/ clinical ASCVD should be started on
high-intensity
unless >75 moderate
pt starting statin therapy complains of severe fatigue and muscle weakness - CK is extremely high
dx
tx
Rhabdomyolysis
- Promptly discontinue the statin
- Address possibility of rhabdomyolysis with:
- CK
- Creatinine –
- acute kidney injury as myoglobin can deposit onto kidney
- Urinalysis for myoglobinuria
- (+) for blood
- (-) for red cells
what labs should we check before initiating statin therapy
fasting lipid
ALT
CK
other reasons for elevated CK
Thyroid disease
Inflammatory myopathies
Polymyalgia Rheumatica (age greater than 50)
Injury/Trauma or excessive exercise
Alcohol misuse/DT’s
Seizures/CVA
Neuropathies/motor neuron dz (GBS,ALS,post-polio syndrome
what would we see in UA of pt w Rhabdomyolysis
- myoglobinuria
- (+) for blood
- (-) for red cells
exosgenous causes of increased statin intolerance
- Erythromycin
- Cyclosporin
- HIV retroviral inhibitors
- Grapefruit juice
- Combination lipid therapy
- Fibrates
- Niacin
what could we use
- In combination with statin, reduces LDL even more
- May be good alternative to high dose statin (if pts don’t tolerate high dose statin)
Cholesterol Absorption Inhibitors
- Ezetimibe (Zetia) -
- Inhibits intestinal absorption of cholesterol
monitor LFTs
when would we tx increased TGs
>500
Severe hypertriglyceridemia (levels over 1000 mg/dL) what are we concerned for
- Risk of pancreatitis
- Fibrates & fish oils
SEE Lipemic blood sample
Tx of elevated TGs
- Weight loss in obese patients
- May reduce TG levels by 22% and increase HDL 9%
- Aerobic exercise
- Avoid concentrated sugars
- Low fat diets coupled with complex carbohydrates reduce LDL and HDL
- Diet consisting of complex carbs and mono- and polyunsaturated fats probably a good approach.
- Avoid medications that raise triglyceride levels
- Strict glycemic control in diabetics
pharmacotherapies used to tx elevated TGs
unclear if they make a differenc
- Fish Oil
- Decreases TG by 15 to 30% o 1 to 2 Grams a day
- Niacin
- 15 to 30 % increase in HDL and 20-30 % decrease in TG
- Lots of side effects, flushing (15 to 50% don’t tolerate; ?Worsens diabetes
- Titrate very slowly
- Fibrates
- 15% increase in HDL and 15-20% reduction in TG
- Fenofibrate, Gemfibrozil
- ACCORD showed no differences in primary outcomes, CVD death, all cause death with Fenofibrate
define metabolic syndrome
- Perfect “storm” of risk factors for atherogenesis
- DM, CAD, CVA, NAFLD, CA
- Pro-inflammatory state
how would we Dx metabolic syndrome
- Need 3/5 RF’s to be considered metabolic syndrome
- Glucose intolerance
- FBG 100 to 125 mg/dL
- Hgb A1c 5.7 to 6.4%
- Elevated Blood pressure
- SBP > 135
- DBP > 85
- Dyslipidemia (Trig and HDL are separate RF’s)
- Elevated triglyclerides > 150 mg/dL
- Low HDL <40 mg/dl
- Elevated apolipoprotein B
- Central obesity
- Waist circumference greater than 40 inches in men
- 35 inches in women
when initiating statin therapy it is important to check
baseline LFTs and CK
