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Internal Medicine TEHELKA OMELETTE > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What are the components of the aortic valve?

A

Three valve leaflets.
Three commissures.
One annulus.

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2
Q

What is the normal surface area of the aortic valve?

A

3–4 cm².

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3
Q

What is aortic stenosis (AS)?

A

Narrowing of the aortic valve orifice, leading to restricted blood flow from the left ventricle to the aorta.

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4
Q

What are the common causes of aortic stenosis by age?

A

Young age: Bicuspid aortic valve (BAV).
Elderly: Degenerative calcification and aortic sclerosis.
Rare cause: Rheumatic heart disease.

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5
Q

What is the prevalence of aortic stenosis in the elderly?

A

Ages 65–75: 2.4%.
Ages 75–85: 4%.
Ages >85: 10%.

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6
Q

What is the pathophysiology of aortic stenosis?

A

Valve myofibroblasts differentiate into osteoblasts → Calcium hydroxyapatite deposition.
Inflammation and lipoprotein activation.
RAAS activation.
Compensatory concentric left ventricular hypertrophy (LVH).

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7
Q

What are the stages of aortic stenosis based on severity?

A

Mild/Moderate AS: Asymptomatic with LVH.
Severe AS: Symptomatic with valve area <1 cm², mean gradient >40 mmHg, peak velocity >4 m/s.
Very Severe AS: LV systolic dysfunction with significant cardiac output reduction.

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8
Q

What are the symptoms of severe aortic stenosis, and what is the associated prognosis?

A

Symptoms: Angina, syncope, dyspnea.
Prognosis without treatment:
Angina: Death within 5 years.
Syncope: Death within 3 years.
Dyspnea: Death within 2 years.

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9
Q

What is the most common congenital valve defect, and what complications are associated with it?

A

Defect: Bicuspid aortic valve (BAV).
Complications: Aortic stenosis (75%), aortic regurgitation (20%), ascending aortic aneurysm, aortic dissection.

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10
Q

What are the key diagnostic features of severe aortic stenosis?

A

Slow-rising pulse (Pulsus tardus).
Narrow pulse pressure.
Harsh ejection systolic murmur radiating to the carotids.
S4 gallop.

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11
Q

How is aortic stenosis severity classified using echocardiography?

A

Mild AS:
Mean gradient <25 mmHg.
Peak velocity <2.5 m/s.
Severe AS:
Mean gradient >40 mmHg.
Peak velocity >4 m/s.
Valve area <1 cm².

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12
Q

What are the treatment options for aortic stenosis?

A

Medical management: For asymptomatic and mild AS.
Aortic Valve Replacement (AVR):
Indications: Symptomatic AS, EF <50%, or rapid disease progression.
Types:
Mechanical valves (lifelong warfarin therapy).
Bioprosthetic valves (last 12–15 years, no anticoagulation).
Transcatheter Aortic Valve Implantation (TAVI): For high-risk surgical patients.
Balloon Valvuloplasty: Temporary relief in select patients.

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13
Q

What is the role of a dobutamine stress echocardiogram in AS?

A

Differentiates true severe AS (low flow, low gradient) from pseudo-severe AS by assessing stroke volume and pressure gradient.

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14
Q

What are the complications associated with bicuspid aortic valves?

A

Aortic stenosis.
Aortic regurgitation.
Ascending aortic aneurysm.
Aortic dissection.

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15
Q

What are aortic stenosis mimickers?

A

Supravalvular AS: Seen in children with Williams syndrome.
Subvalvular AS: Associated with subvalvular membranes or hypertrophic cardiomyopathy.

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16
Q

What is the characteristic murmur of aortic stenosis?

A

Harsh, rasping, ejection systolic murmur.
Radiates to the carotids.
Best heard at the 2nd right intercostal space.

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17
Q

What are the root causes of chronic aortic regurgitation?

A

Aortic root diseases: Aortic dissection, Marfan syndrome, Syphilis, Ankylosing spondylitis, Reiter syndrome, Osteogenesis imperfecta.

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18
Q

What are the valvular causes of chronic aortic regurgitation?

A

Rheumatic heart disease (less common), Bicuspid aortic valve, Infective endocarditis, Trauma.

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19
Q

What happens during diastole in aortic regurgitation?

A

Blood flows back from the aorta into the left ventricle (LV), causing volume overload.

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20
Q

What compensatory mechanism occurs in chronic aortic regurgitation?

A

Eccentric hypertrophy (LV dilatation) to accommodate the increased end-diastolic volume. The LV increases stroke volume to maintain cardiac output.

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21
Q

What are the hemodynamic changes in chronic aortic regurgitation?

A

Increased preload and afterload.
High end-diastolic volume (EDV) and stroke volume.
Systolic BP increases, while diastolic BP decreases → Wide pulse pressure.

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22
Q

What occurs in very severe aortic regurgitation?

A

LV failure. Progressive reduction in cardiac output. Symptoms of heart failure (e.g., dyspnea, fatigue).

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23
Q

What are the key symptoms in mild-to-moderate aortic regurgitation?

A

Palpitations. Cardiomegaly (in moderate cases).

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24
Q

What symptoms occur in severe aortic regurgitation?

A

Wide pulse pressure due to high systolic and low diastolic pressure. Nocturnal angina due to reduced coronary perfusion during diastole.

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25
Q

What are the characteristic pulse findings in chronic aortic regurgitation?

A

Hyperkinetic pulse (Collapsing pulse/Water hammer pulse). Specific signs: Corrigan’s pulse, Hill’s sign.

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26
Q

What are other notable peripheral signs of aortic regurgitation?

A

Becker’s sign, Landolfi’s sign, Rosenbach’s sign, Quincke’s sign, De Musset’s sign, Traube’s sign, Duroziez’s sign.

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27
Q

What are the characteristics of the murmur in aortic regurgitation?

A

Early diastolic murmur: High-pitched, decrescendo, blowing murmur. Best heard in the 3rd intercostal space (left sternal border). Austin Flint murmur: Low-pitched mid-diastolic murmur at the apex.

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28
Q

What are the causes of acute aortic regurgitation?

A

Infective endocarditis, Aortic dissection, Trauma.

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29
Q

How does acute aortic regurgitation differ from chronic aortic regurgitation?

A

Acute AR: Rapid increase in left ventricular diastolic pressure, pulmonary edema, and cardiogenic shock. Chronic AR: Gradual LV dilatation and compensation.

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30
Q

What murmur is heard in acute aortic regurgitation?

A

Low-pitched early diastolic murmur.

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31
Q

What is the diagnostic modality of choice for aortic regurgitation?

A

Transthoracic echocardiography (TTE).

32
Q

How is the severity of aortic regurgitation assessed?

A

Left ventricular end-systolic dimension (LVESD), Regurgitant volume, Effective regurgitant orifice area (EROA). Severity grading: Mild, Moderate, Severe.

33
Q

What is the treatment for symptomatic chronic aortic regurgitation?

A

Definitive treatment: Aortic valve replacement (AVR).

34
Q

What are the indications for aortic valve replacement in asymptomatic aortic regurgitation?

A

EF <50%, LVESD >50 mm, Progressive LV dilatation on follow-up echocardiography.

35
Q

How is acute aortic regurgitation managed?

A

Emergency surgical intervention (AVR). Medical stabilization: Vasodilators (e.g., nitroprusside) and inotropes if required.

36
Q

How does Mitral Stenosis progress over time?

A

If left untreated, symptoms of MS may worsen and lead to right-sided heart failure, atrial fibrillation, and pulmonary hypertension.
Death typically occurs within 2-5 years if the disease is symptomatic and untreated

37
Q

What are the signs of pulmonary congestion in Mitral Stenosis?

A

Dyspnea (especially on exertion), orthopnea, and paroxysmal nocturnal dyspnea (PND).
Pulmonary hypertension leading to right-sided heart failure in severe cases

38
Q

What is the role of percutaneous mitral balloon valvotomy (PMBV) in Mitral Stenosis management?

A

PMBV is indicated in severe symptomatic mitral stenosis with a valve area <1 cm² and a systolic pulmonary artery pressure >50 mmHg, or in patients who are not surgical candidates.

39
Q

What are some potential complications of Mitral Stenosis?

A

Atrial fibrillation due to increased left atrial pressure.
Pulmonary hypertension due to high left atrial pressure.
Thromboembolism, often originating from the left atrial appendage.
Hemoptysis due to pulmonary congestion

40
Q

What is the treatment for atrial fibrillation in Mitral Stenosis?

A

Warfarin is prescribed to prevent thromboembolism, especially in patients with atrial fibrillation due to increased risk of stroke

41
Q

What are the X-ray findings in Mitral Stenosis (MS)?

A

Enlarged left atrium: Double density seen on the chest X-ray.
Splaying of the carina (left main bronchus lifted up).
Straightening of the left heart border.
Prominent upper lobar pulmonary veins.
Kerley B lines indicating pulmonary congestion.
Backward displacement of the esophagus

42
Q

What is the role of echocardiography in Mitral Stenosis?

A

Trans-thoracic echocardiography (TTE) assesses the valve area, calcification, and associated mitral regurgitation.
Trans-esophageal echocardiography (TEE) is used in cases with thrombus or when further detail is needed

43
Q

What is the management for symptomatic Mitral Stenosis?

A

Mitral valve replacement (MVR) is recommended for patients with severe MS.
Percutaneous mitral balloon valvuloplasty (PMBV) or commissurotomy is an option for symptomatic patients with severe MS (valve area <1 cm² or systolic pulmonary artery pressure >50 mmHg).

44
Q

What are associated murmurs in Mitral Stenosis (MS)?

A

Tricuspid regurgitation (TR): Pansystolic murmur, increases with inspiration (Caravalos sign).
Graham Steel murmur: High-pitched diastolic decrescendo murmur heard along the left sternal border.
Austin Flint murmur: Heard in Aortic regurgitation (AR), low-pitched murmur at the apex.

45
Q

What are the key auscultatory findings in Mitral Stenosis?

A

Mid-diastolic murmur (MDM) best heard at the apex with the bell of the stethoscope, characterized by a rough rumbling sound.
Opening snap: A distinctive sound due to the stiff mitral valve.
Associated thrill may be present

46
Q

What clinical findings are associated with Mitral Stenosis (MS)?

A

Pulse: May be weak due to low cardiac output. Atrial fibrillation is common.
BP: Narrow pulse pressure in severe MS.
JVP: Elevated, with a waves (pulmonary hypertension) and v waves (tricuspid regurgitation).
Apex: Lateral displaced, parasternal heave, epigastric pulsations.
S1: Loud.
S2: Loud P2 (due to pulmonary hypertension).
Opening snap.

47
Q

What are the symptoms of Severe Mitral Stenosis?

A

Fatigue, cachexia (wasting), narrow pulse pressure.
Decreased blood supply to brain and kidneys, leading to mitral facies (bluish-purple cheeks).
Systolic pulmonary artery pressure >50 mmHg.
Orthopnea and paroxysmal nocturnal dyspnea (PND).
Risk of atrial fibrillation

48
Q

What are the symptoms of Moderate Mitral Stenosis?

A

Dyspnea even with mild activity.
Increased left atrial pressure (>25 mmHg), leading to pulmonary venous congestion and right ventricular hypertrophy.
Loud P2, palpable P2, parasternal heave, tricuspid regurgitation (TR), and a waves on JVP

49
Q

What are the symptoms of Mild Mitral Stenosis?

A

No symptoms at rest.
Dyspnea on exertion due to increased left atrial pressure during physical activity

50
Q

What are the common causes of Mitral Stenosis (MS)?

A

Rheumatic fever (most common cause).
Congenital parachute valve.
Myxoma (rare)

51
Q

What is the pathophysiology of Mitral Stenosis (MS)?

A

Chronic inflammation and thickening of the mitral valve leaflets, often due to rheumatic fever.
This leads to fibrous tissue formation, commissural fusion, and shortening of chordae tendineae, resulting in a fish-mouth deformity.
Calcification of the valve worsens stenosis and increases the risk of thromboembolism, especially from the left atrial appendage

52
Q

What is the blood supply to the papillary muscles?

A

Lateral papillary muscle: Dual blood supply.
Medial papillary muscle: Blood supply from the right coronary artery (RCA) only. Rupture of the posterior papillary muscle is common after inferior wall myocardial infarction (MI), leading to acute mitral regurgitation (MR).

53
Q

What are the components of the mitral valve?

A

Anterior leaflet
Posterior leaflet (with three lobes)
Two annuli (anterior and posterior)
25 chordae tendineae
Papillary muscles (lateral and medial

54
Q

What are the key clinical features of severe MR?

A

Severe dyspnea, orthopnea, and fatigue.
Palpitations due to atrial fibrillation.
Pulsus alternans and narrow pulse pressure in advanced stages.
Soft S1, wide S2, and possible S3 in severe cases.

55
Q

What is the role of percutaneous mitral valve repair in MR?

A

Percutaneous mitral valve repair (such as the MitraClip procedure) may be considered for high-risk surgical candidates with symptomatic severe MR

56
Q

What are the indications for mitral valve surgery in MR?

A

Symptomatic patients.
Severe MR with evidence of LV dysfunction (EF < 60% or LV end-systolic diameter > 40 mm).
Pulmonary hypertension or severe symptoms despite medical therapy

57
Q

How does dynamic auscultation affect the murmur in MVP?

A

The timing of the click and murmur varies with LV cavity size. As LV cavity size decreases, the click moves closer to S1, and the murmur duration increases

58
Q

How is mitral valve prolapse (MVP) diagnosed and managed?

A

MVP is often diagnosed by echocardiography. Management depends on severity: asymptomatic MVP requires no treatment, while symptomatic MVP may require beta-blockers or surgical intervention for severe cases

59
Q

What are the benefits of mitral valve repair in MR compared to replacement?

A

Mitral valve repair offers better outcomes, including a lower risk of complications, reduced mortality, and better preservation of LV function

60
Q

What is the most common cause of acute mitral regurgitation?

A

Acute papillary muscle rupture, commonly seen in inferior wall myocardial infarction (MI).

61
Q

What is the difference between primary and secondary chronic mitral regurgitation (MR)?

A

Primary MR: A defect in the mitral valve leaflets or chordae tendineae (organic MR).
Secondary MR: Caused by left ventricular dysfunction leading to mitral annular dilatation (functional MR)

62
Q

What are the causes of primary MR?

A

Mitral Valve Prolapse (MVP)
Rheumatic Heart Disease (RHD)
Endocarditis
Myxomatous degeneration

63
Q

How does the body compensate for chronic mitral regurgitation?

A

Chronic MR is compensated by left ventricular dilatation (increased preload). This increases LV end-diastolic volume and stroke volume while maintaining normal filling pressures in the early stages

64
Q

What symptoms occur in chronic MR before it becomes severe?

A

Palpitations are common, and symptoms often appear only when the LV dysfunction becomes significant

65
Q

What are the common clinical symptoms seen in chronic MR?

A

Palpitations
Dyspnea on exertion (due to decreased cardiac output in advanced stages)
Fatigue
Orthopnea (in severe cases)

66
Q

What physical examination findings are common in chronic MR?

A

Pulse: Hypokinetic pulse (in severe MR with LV failure)
Blood Pressure: Narrow pulse pressure (severe MR)
JVP: Typically not elevated unless there is right heart failure
Apex: Hyperkinetic, displaced downward and laterally (in severe MR)
Heart Sounds: Soft S1, wide and variably split S2; S3 in moderate/severe MR

67
Q

What is the most characteristic murmur in chronic MR?

A

A soft, musical, pansystolic murmur best heard at the apex, radiating to the axilla. It is high-pitched and heard with the diaphragm of the stethoscope

68
Q

What autoimmune diseases are commonly associated with MR?

A

Systemic Lupus Erythematosus (SLE) and Rheumatoid Arthritis (RA)

69
Q

What is the normal ejection fraction in MR, and when does the prognosis worsen?

A

Normal EF in MR is 70%.
Prognosis worsens when EF drops below 60%.

70
Q

What is the primary hemodynamic change in acute MR?

A

In acute MR, there is a sudden increase in left atrial pressure due to regurgitation, leading to acute pulmonary edema

71
Q

An early systolic decrescendo murmur, heard best at the apex

A

acute MR

72
Q

What are the common causes of a soft S1?

A

• Mitral regurgitation: Reduced valve closure.
• Long PR interval: Delayed ventricular contraction (e.g., first-degree heart block).
• Severe mitral stenosis: Stiff valve causing incomplete closure.
• Ventricular septal defect: Regurgitant flow reducing sound intensity.
• Myocardial depression: Reduced heart muscle contractility (e.g., in myocardial infarction).

73
Q

What conditions lead to a loud S1?

A

• Mitral stenosis: Forceful valve closure due to narrowed mitral valve.
• Short PR interval: Rapid atrioventricular contraction (e.g., WPW syndrome).
• Hyperdynamic states: Increased cardiac output (e.g., fever, pregnancy, hyperthyroidism).
• Tachycardia: Faster heart rate causing enhanced valve closure.

74
Q

What are the typical echocardiogram (Echo) findings in Dilated Cardiomyopathy (DCM)?

A

• Left Ventricular Dilation: Increased size of the left ventricle (especially in end-diastole), a hallmark of DCM.
• Decreased Ejection Fraction (EF): Typically <40%, indicating systolic dysfunction.
• Mitral and/or Tricuspid Regurgitation: Due to dilation of the atrioventricular annuli, causing valvular incompetence.
• Global Hypokinesis: Reduced contractility of the entire left ventricle (uniform wall motion abnormality), though regional wall motion abnormalities may also be seen.
• Thin, Dilated Walls: Thinning of the left ventricular walls, often with reduced myocardial contractility.
• Increased Left Ventricular End-Diastolic Pressure: Seen in the setting of heart failure.
• Atrial Enlargement: Left atrial dilation, which occurs secondary to the increased volume load from mitral regurgitation.
• Systolic Dysfunction: The hallmark finding, which is characterized by a reduced left ventricular systolic function and impaired myocardial contractility.

75
Q

What are the ECG findings in Dilated Cardiomyopathy (DCM)?

A

Small voltage complex in limb leads (chest leads: high voltage)
Sinus tachycardia
Poor R wave progression

76
Q

Angina with normal coronaries?

A

Myocarditis
HCM
Takotsubo cardiomyopathy

Internal Medicine TEHELKA OMELETTE (3 decks)

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