CARDIO: CVD/ASCVD/CAD Flashcards
What are the three signs of becks triad?
Hypotension
Muffled heart sounds
Distended neck veins
What is Cardiac Tamponade?
A compression of the heart (especially the right ventricle) caused by pericardial effusion, which leads to circulatory insufficiency.
Recurrent substernal chest pain elicited by strong emotion and resolving after several minutes is suggestive of
stable angina
What are the major types of angina?
stable angina, unstable angina, and vasospastic angina
I’ve been getting a pain in my chest for about 3 months now,” DS explains. “But only while I’m running. It goes away when I stop and rest.” When you ask him to describe the pain, he tells you it feels like squeezing that goes from the left side of his chest down into his left arm and up into his jaw.
What is at the top of your diff dx?
Stable angina
You tell DS that his condition is known as stable angina. His coronary vessels contain plaque, and the plaque is obstructing blood flow. During exercise, the vessels cannot deliver enough blood to meet the oxygen demands of the heart. The tissues that aren’t getting enough oxygen stimulate cardiac nerves that relay pain signals, and that explains the pain. The pain stops during rest because that’s when the heart isn’t working as hard and doesn’t need as much oxygen. Sublingual nitroglycerin, aspirin, β-blockers, and cholesterol medications combined with a healthy diet are first-line treatments for stable angina.
What is angina?
chest pain that is caused by myocardial ischemia.
In __________angina, chest pain occurs with exertion and is promptly relieved by rest.
Stable
In ________ angina, chest pain occurs at rest or with increasing frequency and duration.
unstable
In ___________ angina pain occurs at rest, often while sleeping.
vasospastic
Both stable and unstable angina are caused by
Both stable and unstable angina are caused by coronary artery disease, or atherosclerosis, which decreases the vessel lumen diameter and reduces blood flow.
___________ angina is caused by coronary artery spasm and is most common in people who smoke cigarettes.
Vasospastic
Treatment for stable angina involves
β-blockers, statins, and aspirin.
Treatment of vasospastic angina is with
calcium channel blockers and smoking cessation.
What is the tx difference for STEMI vs NSTEMI?
non-ST elevation myocardial infarction, as evidenced by the presence of persistent chest pain at rest with ST-segment depressions on ECG. These patients require in-patient admission for monitoring and treatment with multiple drugs.
An emergency coronary artery catheterization would be required for a patient with an ST-elevation myocardial infarction.
How can a stable atherosclerotic plaque lead to MI?
Complete occlusion of the vessel can occur after the plaque ruptures leading to a myocardial infarction.
Stable angina is caused by atherosclerosis of the coronary arteries that narrow their lumen and reduce the flow of blood. On histopathologic examination, a narrowed vessel with atherosclerotic plaque will be found. The arteries do not have a normal caliber and diameter
In a pt with STABLE angina, which of the following medications increase life expectancy of pts?
A. Atorvastatin
B. Diltiazem
C. Nitroglycerin
D. Verapamil
Atorvastatin
The correct answer is atorvastatin (A). Statins work as primary prevention to reduce mortality risk and myocardial infarction. None of the other drugs reduces mortality risk. Diltiazem (B) and verapamil (D) are backup drugs to β-blockers that can reduce symptoms but not mortality risk. Nitroglycerin (C) reduces chest pain.
What diagnostic tests would you run to confirm dx of unstable angina?
Coronary angiography
What dx tests would you run to confirm stable angina?
History and physical
Exercise stress testing in uncertain cases
You can so pharmacologic stress testig with a coronary aa vasodialator (adenosine, dipyridamole). This testing causes a marked increase in blood flow ni normal coronary arteries and a relatively small increase in blood flow in stenotic coronary arteries. The difference in blood flow allows for the dx of obstructive coronary artery disease due to reduced uptake of rasioactive isotope in ischemic myocardium.
What would you expect on ECG in a pt with unstable angina?
Often shows ST-segment depression and ischemic T-waves
What would you expect on ECG in a pt with stable angina?
Normal when no pain
ST depressions during pain
_____________________involves placing a catheter in the coronary artery in the area of obstruction, inflating a balloon to unclog the artery, then placing a stent (a mesh device, often coated with mTOR inhibitor drugs) in the artery to keep it open.
Percutaneous Coronary Intervention. Also known as coronary artery angioplasty
Aspirin prevents unstable angina by inhibiting which coronary pathway?
Aspirin blocks the cyclooxygenase (COX) pathway, preventing platelet-determined clotting.
Why is aspirin prescribed in pts with a hx of ASCVD, MI, stroke, CABG?
Secondary prevention of future cardiac events by inhibiting platelet function through COX pathway to decrease thrombus formation
What is the MOA of nitroglycerin?
NTG produces a molecule (cyclic guanosine monophosphate [cGMP]) that relaxes vascular smooth muscles (ie, vasodilation). NTG targets veins more than arteries. Dilating the large veins that return to the heart decreases venous pressure. Decreased venous return means decreased left ventricular filling (decreased preload). Decreased preload means decreased contraction force and myocardial oxygen use, thereby reducing chest pain. In addition, NTG causes some direct coronary artery vasodilation that increases oxygen supply to the heart, also relieving the chest pain.
What drug therapies do we normally consider for stable angina?
Reduces the amount of work the heart does (eg, β-blockers)
Delivers more blood by dilating the arteries (eg, nitrates)
Helps reduce the progression of disease (eg, statins, antiplatelets).
How do beta blockers work?
These agents block myocyte β-adrenergic receptors. Cardiac cells express only β1 receptors, and stimulation of these increases contractility and heart rate. Direct inhibition of the β1 receptors decreases the work of the heart and myocardial oxygen demand, which drive angina symptoms.
Some β-blockers (eg, metoprolol, atenolol) are selective and only block the β1 receptor, whereas others are not selective. The advantage of selective agents is that they do not also cause extracardiac adverse effects (eg, bronchospasm with β2 receptors). Both selective and nonselective types work for treating stable angina.
Note that b blockers do not decrease overall mortality, they only decrease angina episodes
What are the cut offs for htn dx?
sustained bp over or + to 130 systolic or over = to 80 diastolic (some guidelines use 140/90)
You have a 46 yo male w/10 pack yr smonking hx and a new dx of htn. What labs/imaging may you order?
Routine labs to assess renal function, TSH to assess possible other causes of htn, lipid profile and fasting glucose/a1c to assess ASCVD risk factors!
How might you differentiate LE edema due to chronic venous insufficiency vs LE edema due to heart failure?
Jugular venous pressure
1-3 is normal
3+ may indicated R heart failure
Dyspnea and lung crackles are also signs of PE due to R heart failure. (NOTE that bilateral wheezes and prolong expirations are more likely COPD symptoms and not so much pulm edema)
The following are clinical features of what?
Chronic Venous Insufficiency
Risk factors include older age, obesity, tobacco use, sedentary lifestyle, previous LE trauma or venous thrombosis
What pharmacotherapies have been studied and demonstrate mortality benefits for those with HFrEF?
Angiotensin system inhibitors, beta blockers, mineralocorticoid receptor antagonists, and SGLT-2 inhibitors
Why would we give someone with HFrEF a mineralocorticoid receptor antagonist (ie spironolactone, eplerenone)?
They block the deleterious cardiac remodeling effects of aldosterone
What scoring system can we use to assess a pt’s risk for thromboembolic risk in nonvalvular afib?
CHA2DS2-VASc
What are the major secondary causes of htn?
Consider renal, renal vascular, renal endocrine, OSA, thyroid, and parathyroid, or anatomical causes (ie coarctation).
Suggestive findings of this condition include resistant htn, abdominal bruit, recurrent flash pulm edema, AKI following ACE initiation.
Renal Artery Stenosis
Hypocalcemia, elevated serum creatinine and abnormal urinalysis in the light of htn raises concern for…
Parenchymal renal disease (ie glomerulonephritis, polycystic kidney disease)
Presents initially as poorly demarcated erythematous plaques of the lower legs bilaterally, classically involving the medial malleolus. It is one of the spectrum of cutaneous findings that may result from______________________
Chronic Venous Stasis Dermatitis
Disorder characterized by chronic venous insufficiency following acute dvt
Post thrombotic syndrome
Why are thiazide diuretics preferred in pts with osteoperosis?
Thiazide diuretics increase Ca resorption in the distal tube thus reducing renal calcium wasting and slowing bone loss.
In DHF, what compensatory mechanisms are activated?
sympathetic nervous system mechanisms and RAAS mechanisms that together stimulate vasoconstriction and increase sodium retention to maintain organ and tissue perfusion in the light of decreased cardiac output. These mechanisms are ultimately maladaptive.
Presents age 30-40 with htn, possible flank pain and/or hematuria
PKD
Angina that happens sometimes at night and can show STMIS on ECG
Vasospastic
How do you treat vasospastic angina?
Calcium Channel blocker to dialate coronary arteries
-Diltiazem
-amlodipine
Smoking cessation
What valvular diseases contribute significantly to HFrEF?
Regurgitant valvular diseases ie mitral regurg and aortic regurg
What are some etiologies of eccentric LV hypertrophy?
Ischemic heart disease (like from infarction), dialated cardiomyopathy, aortic or mitral regurg
Causes of concentric LV hypertrophy
Chronic htn, aortic stenosis
Middiastolic/late diastolic murmur should always raise concern for _____________
MITRAL STENOSIS
How do you differentiate left vs right sided heart failure?
Left sided:
-most common
-pulmonary congestion
-tachy
-reduced GFR (increased sodium and water retention)
-Dyspnea, cough, orthopnea
Right sided:
-hepatojugular congestion
-hepatomegaly
-JVD
-Peripheral edema
Cor pulmonale= RV failure resulting from pulm path that leads to pulm htn (COPD,PE), pulm edema is not present with isolated R ventricular failure
What is a simple way to remember HFrEF vs HFpEF?
rEF=systolic, heart cant pump
pEF=diastolic, heart cant fill
Why is the stroke volume decreased in diastolic heart failure?
Stroke volume is decreased in diastolic heart failure due to decreased ventricular compliance, reduced ventricular filling, and therefore decreased preload, reducing stroke volume.
Note this is preserved EF
What are the 4 cardomyopathies?
Dialated, hypertrophic, restrictive, arrhythmogenic right ventricular
This is the most common cardiomyopathy. The ventricles are thinned and lose contractility, usually due to viral infection, myocarditis, or toxins (eg, heavy alcohol consumption or the chemotherapy drug doxorubicin). This causes systolic HF and can affect both ventricles.
Dilated cardiomyopathy
This is an uncommon genetic disorder that leads to left ventricle (LV) hypertrophy and diminished ventricular outflow, causing diastolic HF, dyspnea, and arrhythmias in young adults.
Hypertrophic Cardiomyopathy
In this uncommon disorder, the heart has a stiff, poorly functioning myocardium, caused either by fibrosis (eg, due to systemic sclerosis or radiation damage) or infiltrative disease (eg, sarcoidosis, amyloidosis).
Restrictive cardiomyopathy
This rare genetic disorder causes fatty infiltration of the right ventricle, leading to arrhythmias and systolic right heart failure.
Arrhythmogenic right ventricular cardiomyopathy
What toxins can cause dilated cardiomyopathy, the most common cardiomyopathy?
Alcohol or the chemotherapy drug doxorubicin can cause dilated cardiomyopathy, the most common cardiomyopathy.
Findings of “backward” left heart failure are due to________________ and include __________________, __________________, _____________________, _____________, and _______________
Findings of “backward” left heart failure are due to pulmonary congestion, and include dyspnea, orthopnea, cough, crackles on pulmonary exam, and paroxysmal nocturnal dyspnea.
Left-sided heart failure include findings of “forward failure” including ….
dizziness, tachycardia, confusion, and acute kidney injury.
When is screening for AAA warranted?
USPSTF recommends 1 time abdominal US in men age 65-75 who have ever smoked.
What is acute coronary syndrome?
Acute coronary syndrome (ACS) is the clinical manifestation of myocardial infarct and commonly the default working diagnosis in patients with new-onset chest pain suspected to be of cardiac ischemic origin. It can be divided into further diagnoses:
ST-Elevated ACS
Non-ST-elevated ACS
How do we clarify whether acute chest pain w/out ST elevation is an NSTEMI or unstable angina?
Cardiac troponin levels
What other vasospastic disorders might you see in a pt w/vasospastic angina?
Raynaud
What therapies should any pt who just underwent PTCA (percutaneous coronary angioplasty) be started on?
Long term dual antiplatelet therapy like clopidogrel or tricagrelor for 12 months, long term secondary prevention therapy includes ACE inhibitor, beta blocker, nitrate, and high-dose statin therapy. Low-dose aspirin therapy is continued lifelong.
Water hammer pulse is a classic finding for pts w/
Aortic regurg
Other findings of AR include pulse synchronous head nodding (de Musset’s sign) and, occasionally, a rumbling, low-pitched mid-diastolic murmur (Austin Flint murmur) that is caused by the regurgitant blood striking the anterior leaflet of the mitral valve,
Livedo reticularis and impaired renal output in the setting of recent cardiac catheterization should raise concern for…
cholesterol embolization syndrome
‘blue toe’ syndrome
patient presents with symptomatic, unstable sinus bradycardia. What is the first line tx?
Atropine is an anticholinergic agent that is used to increase heart rate. Intravenous atropine is the first-line treatment in patients who present with unstable bradycardia. Asymptomatic patients do not require treatment.
What markers are sensitive for heart failure?
Brain Natriuretic peptide
A hormone with vasodilator and diuretic properties that is secreted by cardiomyocytes. Production is increased during cardiomyocyte stretch and ventricular wall stress. Causes of elevated BNP include heart failure, renal failure, and atrial fibrillation.
Commonly implicated pathogens in myocarditis include
VIRUSES: coxsackie B, adenovirus, parvovirus B19, HIV, and HHV-6.
BACTERIA: Group A β-hemolytic Streptococcus (acute rheumatic fever)
Corynebacterium diphtheriae (diphtheria)
Borrelia burgdorferi (borreliosis)
Mycoplasma pneumoniae
PARASITIC: Toxoplasma gondii, Trypanosoma cruzi (Chagas disease, common in South America)
What clinical features might you look for when you suspect myocarditis?
Recent hx of illness, DCM and acute heart failure
SO
—Enlarged cardiac silouette on x-ray due to balloon like ventricular dialation
—dyspnea and inspiratory crackles and vascular markings on cxr consistent with pulm edema
—chest pain
In __________________________ defective venous valve leaflets result in reflux of venous blood back into the periphery, leading to increased venous pressure (hydrostatic pressure) and subsequent extravasation of venous blood into the interstitium. Plasma proteins in the interstitium in turn cause edema and tissue hypoperfusion, which results in inflammation, atrophy, and possibly ulcer formation.
Chronic venous insufficiency
What might you see in a venous vs arterial ulcer?
Venous= warm skin, pruritis, varicose veins, edema
Arterial= painful, cold skin, shiny skin w/reduced hair!!!! absent pulses
So look at pulses, hair, and skin temp!
How does mitral stenosis lead to a right axis deviation?
Mitral stenosis leads to elevated left atrial pressure, which can trigger atrial fibrillation and cause increased pulmonary capillary wedge pressure (PCWP). Over time, the increased PCWP leads to remodeling of the pulmonary arteries, increased pulmonary vascular resistance, an S2 split, and right ventricular hypertrophy (seen as right axis deviation). In MS, shorter interval between the opening snap and S2 indicates more severe disease. This is because left atrial pressure is greater than left ventricular end-diastolic pressure.
How does mitral stenosis lead to increased Pulm Capillary Wedge Pressure?
Mitral stenosis leads to elevated left atrial pressure, which can trigger atrial fibrillation and cause increased pulmonary capillary wedge pressure (PCWP). Over time, the increased PCWP leads to remodeling of the pulmonary arteries, increased pulmonary vascular resistance, an S2 split, and right ventricular hypertrophy (seen as right axis deviation).
What is pulmonary capillary wedge pressure
An indirect measure of left atrial pressure and, therefore, an estimation for preload. Measured by advancing a balloon catheter into a small pulmonary artery and then inflating the catheter. The PCWP is then measured distal to the inflated balloon. Normal: 4–12 mm Hg.
What are the major cardiac effects of alcohol abuse?
Alcohol has toxic effects on the myocardium, leading to ventricular dilation and reduced contractility. This can result in dialated cardiomyopathy. If detected early enough, consistent abstinence from alcohol leads to reversal of cardiomyopathy and is, therefore, the most important step in management. In patients with chronic alcohol use disorder, the shift to abstinence should be monitored closely to prevent complications of alcohol withdrawal.
Part of normal skin flora and may contaminate prosthetic hear valves in valve replacement surg
S. epidermidis is a novobiocin sensitive, coagulase-negative, catalase-positive, gram-positive coccus with the capability of biofilm formation. As S. epidermidis is part of the normal skin flora, contamination of prosthetic devices (e.g., heart valves and hip implants) may occur during surgery.
Staphylococcus aureus is another common causal pathogen of early prosthetic valve endocarditis (i.e., within 60 days after implantation).
Sedentery lifestyle, hyperlipidemia, hypertension, physical activity, smoking, diabetes. Out of all of these, which is the most significant risk factor for CEREBRAL INFARCTION?
Htn
Recall that for CAD, smoking is the most sig modifiable factor
What are the ‘statin benefits groups’ of pts as defined by ASCVD?
Current clinical ASCVD
LDL cholesterol > 190 mg/dL
Diabetes (type 1 or 2) age 40-75 years with LDL > 70 mg/dL
Estimated 10-year ASCVD risk by Pooled Cohort Equations > 7.5%.
What is the padua criteria?
Criteria for dx of ACM
What is duke’s criteria?
Its the criteria that we use to assess the liklihood of IE
When should pts be evaluated for secondary causes of dyslipidemias?
Patients with LDL cholesterol ≥ 190 should be evaluated for secondary causes of their dyslipidemia.
What medical conditions can lead to dyslipidemias?
Type 2 diabetes mellitus and insulin resistance are associated with hypertriglyceridemia and low HDL cholesterol.
Cholestatic or obstructive liver disease, such as primary biliary cirrhosis, may lead to elevated total cholesterol levels and xanthomata.
Nephrotic syndrome causes high serum total and LDL cholesterol concentrations as well as triglycerides due to increased hepatic production and diminished lipid catabolism.
Hypothyroidism causes high LDL cholesterol concentrations as well as hypertriglyceridemia.
Acute hepatitis can cause hypertriglyceridemia.
Alcohol can cause hypertriglyceridemia.
Thiazide diuretics, beta-blockers, oral estrogens, and protease inhibitors can cause modest changes in serum lipid concentrations.
Familial Dyslipidemia
What do you look for on eye exam to assess for hypertensive retinopathy?
Hemmorages, exudates, cotton wool spots (microstrokes)
What is papilledema and what does it indicate?
A swelling of the optic disc secondary to elevated intracranial pressure
This is seen in the setting of a htn emergency sometimes
What is the physiology behind renal artery stenosis and secondary htn?
Stenosis (likely from plaques/ASCVD)–> reduced flow to the glomeruli–>abnormal stimulation of juxtaglomerular apparatus–> overproduction of renin to compensate for the physiologically perceived hypotension
In renal artery stenosis, RENIN is the primary driver. All the components of the RAAS get involved but it all starts w/renin
Give breif overview of RAAS
Renin (from glomeruli)–> converts angiotensinogen to angiotensin I—> converted to angiotensin II by ACE in the pulmonary vasculature–> angiotensin II is potent vasoconstrictor, leads to Na resorption in renal tibules
aldosterone is released by adrenal cortex–> increase NA and fluid retention and hypokalemia, vasopressin release from posterior pitutitary leads to increase fluid retention
Renal artery stenosis is most commonly caused by ________________in older pts and ___________________in younger pts
atheroclerosis
fibromuscular dysplasia
