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OMS Board Review > 13. Cardiovascular Disease > Flashcards

13. Cardiovascular Disease Flashcards

1
Q

Define hypertension
How is it diagnosed?
How is it classified?

A

Persistently elevated arterial blood pressure of 130/80 or higher in adults

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

AHA and ACC update to JNC7 classification:
- Normotension <120/80
- Elevated 120-129/<80
- Stage I 130-139/80-89
- Stage II >140/90

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2
Q

Calcium channel blockers

A

Decrease influx of calcium ions resulting in vasodilation and reduction in blood pressure (amlodipine, felodipine, diltiazem, verapamil)

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3
Q

ACE inhibitors

A

Block conversion of angiotensin I to angiotensin II. (angiotensin II is responsible for vasoconstriction and liberating aldosterone). Inhibiting vasoconstriction and decreasing the effects of aldosterone results in a reduction of blood pressure (lisinopril, fosinopril, enalapril, captopril, ramipril).

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4
Q

Angiotensin II receptor blockers (ARBs)

A

Block effects of angiotensin II through antagonism of angiotensin II receptors leading to decreasing vasoconstriction and aldosterone secretion (losartan, valsartan, olmesartan, telmisartan).

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5
Q

Beta blockers

A

Block beta-adrenergic receptors resulting in a decrease in myocardial contractility, decrease in renin production, and relaxation of smooth muscles (metoprolol, atenolol, esmolol, carvedilol, labetalol)

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6
Q

Thiazide diuretics

A

Block reabsorption of NaCl in the distal convoluted tubule of the nephron leading to a contracted intravascular volume (hydrochlorothiazide, chlorthalidone).

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7
Q

Vasodilators

A

Work by decreasing vascular smooth muscle tone (hydralazine, sodium nitroprusside)

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8
Q

Alpha-2 adrenergic agonist

A

Works on central adrenergic receptors leading to decreased norepinephrine release (clonidine)

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9
Q

Direct renin inhibitor

A

Prevents renal release of renin with subsequent decrease in angiotensin II production (aliskiren)

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10
Q

What is hypertensive urgency

A

BP >180/120 with no signs/symptoms of end organ dysfunction

Refer to physician

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11
Q

How is hypotension treated intraoperatively

A

Ephedrine and phenylephrine. Be cautious of reflex bradycardia with phenylephrine usage.

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12
Q

Patients taking these medications are more prone to anesthesia-induced hypotension

A

ACE inhibitors and ARBs

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13
Q
A
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14
Q

AHA recommendation of epinephrine dose for “cardiac” patients

A

0.04mg of epinephrine(40 ug)

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15
Q

What is a hypertensive crisis?

A

BP 180/120 with signs/symptoms of myocardial ischemia, bradycardia, hypertensive encephalopathy, dyspnea, chest pain, confusion, nausea/vomiting, headache, seizures, and pulmonary edema.

Treatment is gradual reduction of BP to not lead to hypotension and subsequent myocardial ischemia and cerebrovascular ischemia.

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16
Q

What is atherosclerosis?
Pathophysiology

A

Hardening of the arteries due to lipid accumulation within the arterial wall.

Damage to endothelium
Lipoproteins traverse intima and leukocytes are recruited via chemotaxis
Macrophages imbibe LDL to form foam cells
Smooth muscle cells of media layer secrete exctracellular matrix that traps the lipoprotein and gives bulk to the lesion.
Matrix gives rise to fibrous cap. As lesion increases in size, fibrous cap thins. Rupturing of the fibrous cap exposes thrombotic lipid core, which may lead to ACS.

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17
Q

What is metabolic syndrome?

A

Cluster of HTN, hyperlipidemia, insulin resistance, and abdominal obesity

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18
Q

What is ischemic heart disease (IHD)?

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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19
Q

What is stable angina?

A

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

  • Dyspnea on exertion
  • Retrosternal chest pain that may radiate to arm or jaw
  • “Pressure” on chest
  • Symptoms appear when vessel is at least 70% stenotic and cease with rest
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20
Q

Diagnostic workup angina

A

EKG may show ST depression or T wave inversion.

Stress testing to assess cardiac reserve.

Pharmacologic testing with dipyridamole thallium in persons unable to exercise.

Echocardiogram used to assess wall function, EF, and valvular function.

Coronary angiography is used to assess stenotic coronary arteries (gold standard).

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21
Q

What is acute coronary syndrome (ACS)?

A

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

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22
Q

What is unstable angina?

A

Occurs secondary to a coronary thrombus that is partially occlusive. Patients have chest pain that is not relieved by rest. Can see signs of ischemic changes on an EKG with negative cardiac enzymes.

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23
Q

Non-ST segment elevation MI vs. ST segment elevation MI

A

Non-STEMI: due to a partially occlusive thrombus that results in a subendocardial infarction.

STEMI: occlusive thrombus that results in a transmural infarct

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24
Q

Nitrates

A

cause venodilation which decreases preload (determinant of wall stress) and dilates coronary arteries.

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25
Q

How are beta blockers and calcium channel blockers used to treat ischemic heart disease?

A

Decrease oxygen demand by decreasing HR and contractility

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26
Q

Treatment of MI

A

Morphine (analgesia, anxiolysis)
Oxygen (increases O2 supply to myocardium)
Nitrates (improve coronary flow)
Aspirin (decrease platelet aggregation)

Beta-blockers: decrease myocardial oxygen demand
Transfer to hospital for PCI with stent deployment or fibrinolytic therapy if hospital does not have interventional cardiology capabilities.

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27
Q

What is congestive heart failure (CHF)?

A

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

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28
Q

Contrast compensated heart failure to decompensated heart failure

A

Compensated heart failure: compensatory mechanisms such as increase in sympathetic tone that decreases pulmonary congestion and fluid retention.

Decompensated heart failure: acute or gradual onset of signs and symptoms of pulmonary and systemic congestion

29
Q

Systolic failure

A

Due to impaired contractility of the heart or high afterload (chronic volume overload from mitral and aortic regurgitation, dilated cardiomyopathies, HTN, aortic stenosis). EF <40%

30
Q

Diastolic failure

A

Due to impaired diastolic relaxation or ventricular filling of the heart (left ventricular hypertrophy, restrictive cardiomyopathy, myocardial fibrosis, myocardial infarction). Can have preservation of the EF >50%.

31
Q

Contrast Left-sided heart failure signs/symptoms to Right-sided heart failure signs/symptoms

A

Left-sided heart failure
- Dyspnea
- Paroxysmal nocturnal dyspnea
- Orthopnea
- Third heart sound (S3) and pulmonary rales. S4 sound with diastolic failure.

Right-sided heart failure
- Most common cause is left-sided heart failure
- Abdominal discomfort
- Anorexia
- Hepatomegaly
- Peripheral edema
- Jugular venous distension

32
Q

What lab is used to diagnose and monitor CHF progression?

A

Brain natriuretic peptide (BNP): used to diagnose and monitor CHF progression. BNP >35 pg/ml for diagnosis of non-acute onset CHF and >100 pg/ml for acute onset CHF.

33
Q

How is CHF treated?

A
  • Diuretics to treat systemic and pulmonary congestion (Lasix; consider spironolactone to prevent potassium wasting)
  • Beta-blockers to decrease myocardial oxygen consumption
  • Digoxin to increase cardiac contractility. Narrow therapeutic range. Toxicity = nausea, vomiting, confusion, paresthesias, PVCs, heart block, trigeminy, bigeminy.
  • ACE inhibitors to decrease afterload and prevent aberrant cardiac remodeling
  • Ventricular assist devices to maintain cardiac output.
34
Q

Mitral valve disorders

A

Mitral stenosis
Mitral regurgitation
Mitral valve prolapse

35
Q

What is mitral stenosis?
What is its most common cause?
What are some signs and symptoms?
How is it treated?

A

Decrease in size of mitral valve orifice resulting in decreased blood flow across the valve during diastole and increased atrial pressures and volume.

  • Most common cause is rheumatic heart disease
  • Also can be caused by congenital disease, SLE, RA, fenfluramine use, left atrial myxoma, carcinoid syndrome, prior mitral valve repair.
  • Dyspnea on exertion, chest pain, hemoptysis, low pitched early diastolic murmur over the apex, hoarseness due to left atrial enlargement and impinging on the recurrent laryngeal nerve (Ortner syndrome), atrial fibrillation, atrial thrombus formation.

Treatment with diuretics, control of heart rate with beta-blockers, calcium channel blockers, or digoxin. Baloon valvuloplasty or valve replacement.

36
Q

What is mitral regurgitation?
What are its causes?
Signs/symptoms?
Treatment?

A

An increase in size of the mitral valve orifice, resulting in the backflow of blood across the mitral valve during sytole. This causes an increase in left atrial pressure and a decrease in left ventricular stroke volume and cardiac output.

  • Ischemic heart disease, rheumatic heart disease, endocarditis, mitral valve prolapse, hypertrophic cardiomyopathy, congenital heart disease, among others can result in papillary muscle dysfunction, mitral annular dilation, or rupture of chordae tendinae leading to dilation of the mitral valve orifice.
  • Patients often asymptomatic for years, eventually leads to ventricular hypertrophy and increased compliance of left atrium. Volume overload results in decreased myocardial contractility and drop in EF. Afib may result.
  • DOE, fatigue, orthopnea, cough, heart palpitations, S3 heart sound, holosystolic blowing murmur at cardiac apex radiating to axilla. Afib.
  • Treated with ACE inhibitors, betablockers, biventricular pacing, mitral valve repair favored over replacement.
37
Q

What is mitral valve prolapse?
Risk factors?
Symptoms?
Treatment?

A

Prolapse of one or both mitral leaflets into the left atrium during systole, this may occur with or without regurgitation.

-Floppy or myxomatous mitral valve. Most common form of valvular heart disease.

  • Risk factors = Marfan’s syndrome, Ehlers-Danlos syndrome, rheumatic heart disease, myocarditis, osteogenesis imperfecta, thyrotoxicosis, and SLE
  • Can cause cerebral embolic events, infective endocarditis, dysrhythmias, and sudden death from rupture of chordae tendinae.

-Dyspnea on exertion, fatigue, anxiety, orthostatic hypotension, midsystolic click on auscultation, cardiac dysrhythmias

-Treated conservatively with beta blockers and SSRIs (to treat associated hyperadrenergic syndrome). Mitral valve repair favored over replacement.

38
Q

Aortic valve disorders

A

Aortic stenosis
Aortic regurgitation

39
Q

What is aortic stenosis?
Risk factors?
Symptoms?
Treatment?

A

Decrease in aortic valve area resulting in obstruction of blood flow into the aorta and increased left ventricular pressures.
- Congenital unicuspid or bicuspid aortic valve, hypertension, hypercholesterolemia, smoking, rheumatic heart disease, endocarditis, and certain genetic markers are risk factors.
- Increase in cardiac afterload, increase in myocardial work, left ventricular hypertrophy, increased myocardial oxygen demand.
- Angina pectoris despite absence of coronary artery disease.
- Fatigue, DOE, syncope, angina, sudden death, heart failure, severe LV disease, crescendo-decrescendo systolic murmur.

Tx: medical management in asymptomatic patients (blood pressure/cholesterol can be used).
-Valve replacement if symptoms arise.
- Severe aortic stenosis that is asymptomatic should be surgically managed.
- SAVR or TAVR

40
Q

What is aortic regurgitation?
Causes?
Symptoms?
Treatment?

A

Disease of aortic leaflets or aortic root resulting in back flow of blood across the aortic valve into the left ventricle during diastole.
- Leaflet abnormalities: Infective endocarditis, rheumatic fever, bicuspid aortic valve, and anorexigenic drugs.
- Aortic root abnormalities: aortic root dilation, hypertension induced aortic annular ectasia, aortic dissection, osteogenesis imperfecta, syphilitic aortitis, Marfan’s, Ehler’s Danlos, RA, ankylosing spondylitis, and psoriatic arthritis.
- Pressure and volume overload in left ventricle and decrease in cardiac output resulting in left ventricular hypertrophy.
- DOE, fatigue, angina, decrescendo high pitched diastolic murmur along left sternal border.
- Afterload reduction (ACE-i and CCBs), loop diuretics, surgical replacement before onset of permanent left ventricular dysfunction.

41
Q

What is tricuspid regurgitation?

A

Tricuspid annular dilation resulting in backflow of blood across the tricuspid valve into the right atrium during systole.
- Right ventricular enlargement, pulmonary hypertension, infective endocarditis, carcinoid syndrome, rheumatic heart disease, tricuspid prolapse, and Ebstein’s anomaly are associated.
- Often associated with mitral or aortic valve disease.
- DOE, fatigue, peripheral edema, hepatomegaly.
- Tx: mild disease with diuretics, improve lung function, treat left heart failure symptoms, reduce pulmonary HTN. Surgical management rarely performed for isolated tricuspid disease.

42
Q

What is tricuspid stenosis?

A

Decrease in the size of the tricuspid valve orifice resulting in decreased blood flow across the valve and increased right atrial pressure.
- Rare in adult population. Rheumatic heart disease with coexisting tricuspid regurgitation. Carcinoid syndrome and endomyocardial fibrosis are also causes.
-DOE, fatigue, peripheral edema, hepatomegaly.

43
Q

What is pulmonary regurgitation?

A

Annular dilation of the pulmonic valve resulting in backflow of blood across teh valve into the right ventricle during diastole.
- Caused by pulmonary hypertension, connective tissue disorders, congenital, post repair of tetralogy of fallot, carcinoid syndrome, infective endocarditis, rheumatic heart disease.
- Rarely symptomatic, right heart volume overload develops. DOE, fatigue, peripheral edema, hepatomegaly.
- Treat primary cause; sometimes bioprosthetic valve replacement is indicated.

44
Q

What is pulmonic stenosis?

A

Decrease in pulmonic valve area resulting in obstruction of blood flow and increased right ventricular pressures.
- Usually congenital, acquired causes include rheumatic heart disease, infective endocarditis, or previous surgeries.
-DOE, angina, peripheral edema, hepatomegaly, ejection click with split S2.
-Tx with surgical balloon valvotomy

45
Q

Anesthetic considerations for mitral stenosis

A

-Avoid excessive perioperative fluid administration
-Avoid Trendelenberg position
-Manage tachycardia aggressively
-Avoid ketamine due to effects on HR
-Control blood pressure to decrease afterload

46
Q

Anesthetic considerations for mitral regurgitation

A

-Maintain normal to slightly elevated HR
-Bradycardia may result in left ventricular volume overload. Increases in systemic vascular resistance should be avoided.

47
Q

Anesthetic considerations for mitral valve prolapse

A

-If there is associated regurgitation, patient should be treated the same as patient with regular MR
-Normal to slightly elevated HR
-Avoid bradycardia (left ventricular volume overload)
-Avoid increases in systemic vascular resistance

48
Q

Anesthetic considerations for aortic stenosis

A

Prevention of hypotension, preservation of cardiac output.
- Normal sinus rhythm must be maintained
- Avoid agents like ketamine (which increase HR) and propofol (which decreases SVR)

49
Q

Anesthetic considerations for aortic regurgitation

A

HR kept above 80 bpm
Bradycardia results in increased diastole = more time to regurg blood
Abrupt increases in systemic vascular resistance can precipitate left ventricular failure

50
Q

Anesthetic considerations for tricuspid regurgitation

A

Note that nitrous oxide can be a weak pulmonary artery vasoconstrictor and can increase the degree of regurgitation.

51
Q

Difference between native heart and transplanted heart

A

Denervation

-Efferent denervation ablates resting parasympathetic tone responsible for maintaining baseline HR (increased HR 90-100BPM)

-Loss of direct sympathetic innervation means cardiac response to physiologic stressors is mediated by circulating catecholamines and occurs much less quickly.

52
Q

Pharmacologic considerations with transplanted heart

A
  • Denervated heart no longer responds normally to indirect-acting medications (medications that mediate effects via autonomic nervous system).
  • Neostigmine, physostigmine, pyridostigmine, edrophonium, glycopyrrolate, atropine, digoxin, nifedipine no longer produce anticipated heart effects
  • Indirect acting drugs such as ephedrine have a decreased effect
  • Direct acting drugs such as glucagon, norepinephrine, epinephrine, isoproterenol, dopamine, and beta blockers are effective
53
Q

What is a normal ejection fraction?

A

> 55%

54
Q

What does S1 sound represent?
What does S2 sound represent?
What is an S3 sound?

A

S1: Closure of mitral and tricuspid valves
S2: Closure of aortic and pulmonic valves
S3: auscultated at left sternal border at fifth intercostal space, heard early in diastole and secondary to rapid ventricular filling in a dilated cardiac chamber.

55
Q

What is BNP?

A

Brain natriuretic peptide (normal less than 100pg/ml)
- With CHF, increased pressure and workload on the heart trigger myocardial cells to secrete natriuretic peptides.
- Work as natriuretic, diuretic, and vasodilator agents to reduce preload and afterload
- Plasma concentrations increased in asymptomatic and symptomatic CHF

56
Q

Most patients with heart failure are routinely managed with a combination of three types of drugs:

A
  1. Diuretic
  2. ACE inhibitor or angiotensin receptor blocker (ARB)
  3. Beta blocker

A fourth agent: digoxin, may be initiated to reduce symptoms, prevent hospitalization, control rhythm, and enhance exercise tolerance. (Increases contractile state of myocardium).

57
Q

What is atrovastatin?

A

HMG-CoA reductase inhibitor used to lower cholesterol

58
Q

What is lisinopril?

A

Angiotensin-converting enzyme (ACE) inhibitor

59
Q

S3 sound

A

Caused by left ventricular volume overloading or dilation as is present in heart failure

60
Q

S4 sound

A

Caused by poor compliance and stiffness of left ventricles

61
Q

Jugular venous distension

A

Sign of venous hypertension, most commonly secondary to right-sided heart failure

62
Q

How is a stress test performed?

A

Used to further risk-stratify higher risk patients undergoing intermediate to high-risk surgeries. Cardiovascular system is tested or “stressed” either with physical activity (walking on treadmill) or pharmacologically using sympathomimetic agents (Persantine or dobutamine) to test for myocardial ischemia (with electrocardiographic monitoring).

Duration of exercise, development of symptoms, and presence of ECG findings such as flipped T waves or ST-segment depression or elevation. May also include echocardiography or myocardial perfusion with labeled radioisotopes.

63
Q

Gold standard for evaluating coronary anatomy and assessing for presence of significant atherosclerosis

A

Cardiac catheterization

64
Q

ASA I monitors

A

ECG, blood pressure, heart rate, pulse oximeter monitoring

65
Q

Immediate treatment of MI

A
  • Supplemental O2 (to increase oxygen delivery)
  • 325mg aspirin (to inhibit platelet function and clot propagation)
  • Sublingual nitroglycerin (vasodilator to increase coronary blood flow and reduce cardiac ischemia and pain)
  • Morphine IV if chest pain not resolved

“MONA”

IV access
12 lead ECG
Serum cardiac markers
Serum electrolytes and coags
Chest XR
Rapid assessment and transport to cardiac cath lab (door-to-balloon time <90 mins)

66
Q

Initial treatment hypertension

A

Low dose hydrochlorothiazide (first-line antihypertensive)

Beta blocker may be better choice in patients with CAD due to post-myocardial infarction cardioprotective effect, migraine headaches, glaucoma, angina pectoris, essential tremor, and resting tachycardia.

67
Q

Initial treatment hypertension in diabetic patients with microproteinuria

A

ACE inhibitors

68
Q

Common side effect of ACE inhibitors

A

Dry cough (most likely due to buildup of bradykinins), often will change to ARBs as alternative

69
Q

Calcium channel blockers and CHF

A

Potent vasodilators. Not recommended for initial therapy for hypertension. Use in patients with CHF increases mortality. Also can exacerbate reflux in GERD.

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