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).
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
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
What is a simple way to remember HFrEF vs HFpEF?
rEF=systolic, heart cant pump
pEF=diastolic, heart cant fill
When is screening for AAA warranted?
USPSTF recommends 1 time abdominal US in men age 65-75 who have ever smoked.
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!
What is duke’s criteria?
Its the criteria that we use to assess the liklihood of IE
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
