Medicine (Cardiovascular) Flashcards

1
Q

What is hypertension?

A

-Persistently elevated arterial blood pressure of 130/80 in adults.

-Diagnosed by 2 elevated readings of at least 130/80 on 2 or more visits

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2
Q

What are the stages/classification of HTN?

A

-Normotension: <120/80
-Elevated: 120-129/<80
-Stage I: 130-139/80-90
-Stage II: >140/90

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3
Q

What are the types of hypertention?

A

-Essential hypertension: No identifiable cause (most common). Assoc
-Secondary hypertension: From an identifiable cause (pheochromocytoma, renal artery stenosis, cushing syndrome, pregnancy)

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4
Q

What are the sequelae of HTN?

A

-Left ventricular hypertrophy
-Ischemic heart disease
-CVA
-CHF
-Renal insufficiency

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5
Q

How is HTN treated?

A

-Secondary HTN: Treat underlying cause.

-Lifestyle modification: Weight loss, smoking cessation, decreased sodium intake, exercise

-Pharmacologic: Ca channel blocker, Ace inhibitor, ARBs, beta blockers, thiazide diuretics, alpha 2 agonists

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6
Q

How do ACE inhibitors and ARBs work?

A

-ACE inhibitor: Block conversion of angiotensin I to angiotensin II. Angiotensin II responsible for vasoconstriction

-ARBs: Block angiotensin II receptors. Leads to decreased vasoconstriction and aldosterone secretion

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7
Q

How do beta blockers work?
What are examples of selective vs non-selective beta blockers?

A

-Block b-adrenergic receptors. Results in decrease in myocardial contractility and decrease in renin productino. Relaxes smooth muscles

-Selective beta 1 blockers: Atenolol, esmolol, metoprolol (A-M)

-Non selective beta blockers (b1, b2): L-P and carvedilol (propranolol, timolol, sotalol)

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8
Q

How does clonidine work?

A

-A2 agonist
-Central adrenergic receptors leading to decreased norepinephrine release (sedation, decreased BP, ADHD and other applications)

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9
Q

What are anesthetic considerations for HTN patients?

A

-Pre-op ECG, CBC, BMP
-Intraop monitoring of EKG and BP
-Limit epi in local to 0.4 mg
-Avoid ketamine
-Watch for intra-op hypotension due to meds pt is taking

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10
Q

What is atherosclerosis?

A

-Hardening of arteries due to lipid accumulation within arterial wall

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11
Q

What are risk factors for atherosclerosis?

A

-Genetics, dyslipidemia, tobacco, HTN, DM, metabolic syndrome

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12
Q

What are complications of atherosclerosis?

A

-Embolization of atherosclerotic plaque to distant site causing infarction (CVA)

-Weakening of vessel wall leading to aneurysm

-Peripheral artery disease

-Renal artery stenosis

-MI

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13
Q

What is ischemic heart disease?

A

-Disease process secondary to stenotic coronary arteries that leads to ischemic sequelae from a myocardial oxygen supply and demand imbalance

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14
Q

What is stable angina?

A

-Transient chest discomfort due to a fixed atheromatous plaque secondary to a myocardial oxygen supply and demand imbalance

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15
Q

What are symptoms of stable angina and how is it worked up?

A

-Dyspnea on exertion, chest pain. Symptoms occur at 70% stenosis

-EKG may show ST depression or wave inversion, stress test to assess cardiac reserve, echocardiogram to assess wall function, coronary angiography to assess stenotic coronary arteries

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16
Q

What is acute coronary syndrome?

A

-Disease process along a continuum secondary to a ruptured atherosclerotic plaque with subsequent formation of a thrombus within the coronary vessel

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17
Q

What is unstable angina?

A

-Chest pain not relieved by rest.
-Occurs secondary to a coronary thrombus that is partially occlusive
-May see ischemic changes on EKG

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18
Q

What is a STEMI and NSTEMI?

A

-NSTEMI: Partially occlusive thrombus results in a subendocardial infarction. Elevated biomarkers are seen

-STEMI: Occlusive thrombus resulting in a trasnmural infarct. Will see ST elevations and biomarkers

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19
Q

What are complications of an MI?

A

-Can lead to fatal arrhythmias, conduction blocks, cardiogenic shock, wall rupture, heart failure

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20
Q

How is ischemic heart disease treated?

A

-Nitrates: Cause venodilation and decrease preload, dilates coronary arteries

-beta blockers/calcium channel blockers: Decrease oxygen demand by decreasing heart rate and contractility

-Percutaneous coronary intervention (Cath lab): Stent placed at stenotic coronary vessel

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21
Q

What are drug eluding stents and bare metal stents?

A

-Used to increase patency of the coronary vessel

-Bare metal stents decrease rate of epithelialization but are thrombogenic (need longer anticoagulation)

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22
Q

When is a CABG completed?

A

-Coronary artery bypass grafting
-Graft done to bypass obstructive coronary vessels
-Preferred for multivessel disease

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23
Q

What is the acute treatment for an MI?

A

-Morphine: Analgesia/anxiolysis
-Oxygen: Increase oxygen supply to myocardium
-Nitrates: Improve coronary flow
-Aspirin: Decrease platelet aggregation
-Beta blocker: Decrease myocardial oxygen demand
-Transfer to hospital for PCI and stent deployment vs fibrinolytic therapy

24
Q

Why are clopidogrel, prasurgrel and ticagrelor used s/p MI?

A

-ADP receptor inhibitors (prevent platelet aggregation).
-Used to prevent coronary thrombosis

25
Q

What are METS and why are they important in pre-op work-up?

A

-Metabolic equivalents
-Helps with risk stratification of functional capacity.
-METS less than 4 concerning for treatment

26
Q

What are anesthetic considerations for IHD patients?

A

-Pre-op optimization, EKG, etc
-Non-cardiac surgery can be carried out 6 weeks after an episode of ACS
-Maintain HR and BP within 20% of pre-op

-Anxiolysis
-Limit epi 0.04 mg
-Avoid ketamine

27
Q

How much epi is in each mL of 1:100k anesthetic?

A

-0.01 mg/mL

28
Q

What is CHF?

A

-Condition characterized by the inability of the heart to pump enough blood to meet the metabolic demands of the body

-Compensatory: Body increases sympathetic tone to decrease pulmonary congestion and fluid retntion
-Decompensated: Pulmonary and systemic congestion

29
Q

What is the difference between systolic and diastolic heart failure?

A

-Systolic: Impaired contractility of the heart, high afterload. EF <40%

-Diastolic: Impaired diastolic relaxation or ventricular filling (left ventricular hypertrophy). EF >50%

30
Q

What are classifications of CHF?

A

-New York Heart Association

-Class I: Heart disease, no limitations on physical activity
-Class II: No symptoms at rest, slight limitation of activity
-Class III: Marked limitation of activity with minimal exertcion
-Class IV: Symptoms at rest. Severe limitation of activities

31
Q

What is the work-up of a CHF patient?

A

-EKG
-Echo
-CXR
-Clinical exam
-BNP, BMP, LFT, lipid pannel, glucose, CBC, TSH

32
Q

How is CHF treated?

A

-Diuretics: Decrease systemic and pulmonary congestion
-Beta blockers: Decrease myocardial oxygen consumption
-Digoxin: Increase cardiac contractility
-ACE inhibitor: Decrease afterload
-Nitrates: Decrease preload
-Ventricular assist devices

33
Q

What are anesthetic considerations of a CHF patient?

A

-Supplemental oxygen
-Pre-op labs
-Avoid NSAIDs (renal failure)
-Avoid fluid overload
-Avoid drugs that depress myocardial activity or increase myocardial oxygen consumption

34
Q

What is mitral stenosis?

A

-Decrease in the size of the mitral valve orfice resulting in decreased blood flow across the valve during diastole and increased arterial pressures and volume

35
Q

What is the treatment of mitral stenosis?

A

-Diuretics to decrease left atrial pressure
-Control heart rate

36
Q

What is mitral regurgitation?

A

-Backflow of blood across mitral valve during systole.
-Leads to increased atrial pressure and decreased stroke volume/cardiac output

37
Q

What is treatment for mitral regurgitation?

A

-ACE inhibitor, beta blockers, biventricular pacing
-Decrease afterload (with vasodilators)
-May need mitral valve surgery (repair vs replacement)

38
Q

What is mitral valve prolapse?

A

-Prolapse of one or more mitral leaflets into the atrium during systole.
-Can occur with or without regurgitation

39
Q

What is the treatment for MVP?

A

-Beta blockers and SSRIs
-Mitral valve repair

40
Q

What is aortic stenosis?

A

-Decrease in aortic valve resulting in obstruction of blood flow into the aorta and increased left ventricular pressures

41
Q

How is aortic stenosis managed/treated?

A

-Medical management
-Valve replacement if symptomatic or severe aortic stenosis (bioprosthetic or mechanical valves)

42
Q

What is aortic regurgitation?

A

-Disease of the aortic leaflets or root resulting in backflow of blood across the aortic valve into the left ventricle during diastole

43
Q

What is the treatment for aortic regurgitation?

A

-Reduce afterload
-Surgical replacement before permanent left ventricular dysfunction

44
Q

What is tricuspid regurgitation?

A

-Backflow into the right atrium during systole

45
Q

How is tricuspid regurgitation treated?

A

-Diuretics
-Medical management
-Rarely surgical

46
Q

What is tricuspid stenosis?

A

-Decreased blood flow across valve, increased right atrial pressure

47
Q

How is tricuspid stenosis treated?

A

-Relieve fluid congestion with diuretics
-Bioprosthetic valves preferred for surgical correction

48
Q

What is pulmonic regurgitation?

A

-Backflow across valve into right ventricle during diastole

49
Q

How is pulmonic regurgitation treated?

A

-Rarely needs treatment
-Sometimes valve replacement

50
Q

What is pulmonic stenosis?

A

-Obstruction of flow into pulmonary arteries, causes increased right ventricular pressures

51
Q

How is pulmonic stenosis treated?

A

-Balloon valvotomy

52
Q

What are general recommendations for patient management of valvulopathies?

A

-Consultation with cardiologist or PCP to understand underlying pathology and severity

-Fragile patient, decreased cardiac reserve

-Avoid tachycardia and anxiety

53
Q

What are anesthetic considerations for mitral valve stenosis?

A

-Avoid excessive fluid administration
-Avoid trendelenburg
-Avoid and manage tachycardia
-Avoid ketamine
-Control blood pressure to decrease afterload

Maintain fluid, HR, BP

54
Q

What are anesthetic considerations for mitral valve regurgitatino?

A

-Normal or slightly increased HR
-Bradycardia bad. Avoid increase in systemic vascular resistance.

Slightly increased HR, BP low to normal. Keep things moving forward

55
Q

What are anesthetic considerations for aortic stenosis?

A

-Avoid hypotension
-Preserve cardiac output
-Avoid ketamine and propofol

Need to be extremely careful with these patients

56
Q

What are anesthetic considerations for aortic regurgitation?

A

-HR above 80 bpm
-Avoid increase in systemic vascular resistance

-Keep things moving forward with HR and decreased BP

57
Q

What happens with a transplanted heart?

A

-Denervation

-Can’t use atropine, digoxin, glycopyrolate
-Ephedrine has decreased effect
-Need to use epinephrine, dopamine, norepinephrine or beta blockers