Cards Test 4 Flashcards

1
Q

What is the second most common cause of valvular heart disease?

A

Aortic Stenosis

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2
Q

What is the most common congenital cardiac abnormality?

A

Bicuspid Aortic Valve

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3
Q

What are the 3 major manifestations of AS?

A

Angina, Exertional Syncope, and Heart Failure

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4
Q

T/F: Aortic Stenosis is atrial kick dependent

A

True; Atrial kick contributes more than 25% of the stroke volume in AS

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5
Q

Valsalva will increase/decrease the intensity of an AS murmur?

A

Valsalva decreases intensity of murmur in AS But increases intensity of murmur in HOCM

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6
Q

Fixed splitting of S2 corresponds to what?

A

ASD

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7
Q

Paradoxical splitting corresponds to what?

A

AS or LBBB

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8
Q

What diagnostic study confirms AS?

A

Echo

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9
Q

What is the ONLY effective treatment for AS?

A

Surgical Replacement

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10
Q

What are the indications for AVR in AS?

A

Symptoms develop or Evidence of progressive LV dysfunction (loss of contractility, low EF), in absence of symptoms

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11
Q

A widened pulse pressure is associated with acute/chronic AR?

A

hallmark of chronic AR; the combo of high LV stroke volume (and therefore high systolic arterial pressure) with a reduced aortic diastolic pressure produces a widened pulse pressure

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12
Q

How does aR clinically present?

A

• Patients with chronic AR remain asymptomatic for a long time.
• When symptoms do develop they are from decreased CO and development of HF
• Patients with chronic AR remain asymptomatic for a long time.
• When symptoms do develop they are from decreased CO and development of HF
Other sx: DOE, Fatigue, Decreased exercise tolerance, palpitations, and angina (failure to perfuse the coronaries)

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13
Q

Bisferiens Pulse

A

Double systolic impulse in carotid or brachial artery

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14
Q

Corrigan Pulse

A

“Water-hammer” pulses with marked distention and collapse

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15
Q

De Musset Sign

A

Head-bobbing with each systole

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16
Q

Duroziez Sign

A

To-and-fro murmur heard over femoral artery with light compression

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17
Q

Hill Sign

A

Popliteal systolic pressure more than 60 mm Hg greater than brachial systolic pressure

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18
Q

Muller sign

A

Systolic pulsations of the uvula

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19
Q

Quincke Sign

A

Capillary pulsations visible at lip or proximal nail bed

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20
Q

Traube Sign

A

“Pistol-shot” sound auscultated over femoral artery

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21
Q

Describe the Austin Flint murmur and what valvular disorder is it associated with?

A

– Low-frequency mid-diastolic rumbling at apex. It reflects turbulence across MV during diastole. It is associated with AR.

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22
Q

What is the diagnostic study that confirms AR?

A

Echo

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23
Q

What is the Tx for Acute AR?

A
  • Emergent Surgical Replacement
  • IV vasodilator: Sodium Nitroprusside: reduces both afterload and preload;
  • IV Dobutamine: positive inotropic agent
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24
Q

What is the Tx for Chronic AR?

A
  • Afterload reduction-vasodilators
  • Nifedipine (Procardia XL) (CCB)
  • Symptomatic patients, or asymptomatic patients with severe AR and impaired LV will require SURGICAL CORRECTION.
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25
Q

What have studies revealed about Nifedipine?

A

Studies shown to reduce LV enlargement, inc LVEF, and delay need for valve surgery

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26
Q

What are the Sx of Tricuspid Valve disorders?

A

Dominant symptoms usually not considered cardiac in origin
– Abdominal discomfort
– Jaundice
– Wasting

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27
Q

What are some causes of TR?

A
  1. Functional problem rather than structural problem of the tricuspid valve
    – Result of RV enlargement, usually secondary PHTN (pressure or volume overload)
  2. Tricuspid valve endocarditis
    – IV drug users (Staph aureus)
  3. Carcinoid tumors (rare)
    – Higher serum levels of serotonin
    – Metabolites form plaques
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28
Q

What are some causes of TS?

A

Rare, usually consequence of rheumatic heart disease
– Almost exclusively accompanies MS
– Isolated rheumatic TR is very rare

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29
Q

A prominent v wave in jugular vein is associated with TR or TS?

A

TR

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30
Q

A prominent A wave in jugular vein is associated with TR or TS?

A

TS

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31
Q

How does PR develop?

A
  • Most commonly develops in setting of severe pulmonary hypertension; this leads to regurge back to the RV
  • Results from dilatation of valve ring by enlarged pulmonary artery
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32
Q

How does PS develop?

A
  • Rare; congenital deformity in 95% cases
  • Carcinoid syndrome
  • Only patients with moderate to severe cases are symptomatic
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33
Q

Mid systolic click is associated with what disorder?

A

MVP syndrome

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34
Q

What disorder is commonly found in young thin females who often feel “anxious?”

A

MVP

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35
Q

Marfan’s is associated with what two valvular disorders?

A

MVP and AR

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36
Q

What are the 2 reasons to fix a valve?

A
  1. Fix if you have sx

2. If you don’t have sx but you have LV dysfunction.

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37
Q

Describe mechanical valves in terms of coagulation therapy & durability?

A

-Durable
- Foreigh thrombogenic surfaces
- Require lifelong anticoagulation (Coumadin)
• Target INR 2.5 – 3.5
Once you get to therapeutic INR, you will stop the Heparin

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38
Q

Describe Bioprosthetic valves in terms of coagulation therapy & durability?

A

– Limited durability
– Structural failure up to 50% at 10 years
• Leaflet tears
• Calcification
– Very low rate of thromboembolism
– NO lifelong coagulation. You are on it for 6 mos and then taken off

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39
Q

If patient is elderly, and has a high risk for falling with intracranial bleeding, what valve would you recommend?

A

Bioprosthetic valve

40
Q

Why would you not give Vitamin K to a patient who has undergone a valve replacement? What would be your treatment of choice?

A

Because the patient may develop rebound thrombosis over that valve; GIVE FRESH FROZEN PLASMA

41
Q

What are the indications for a Mechanical valve?

A

– Younger patients

– Those tolerant of, and compliant with long term oral anticoagulation

42
Q

What are the indications for a Bioprosthetic valve?

A

– Patients 65 years or older (geriatric)

– Contraindications to chronic anticoagulation therapy

43
Q

How do you tell apart Infective Carditis from Rheumatic Fever?

A

Infective carditis is INFECTIOUS. There is an actual problem with the valves. It is defined as • Infection of endocardial surface of the heart, including the cardiac valves, can lead to extensive tissue damage, often fatal.

44
Q

Native valve endocarditis accounts for what % of cases?

A

60-80%

45
Q

Infective Endocarditis: Rank the valves in order of frequency of infection

A

Mitral – aortic – tricuspid – pulmonic

46
Q

What pathogen/bacteria is the common cause for endocarditis of prosthetic valves?

A

– Staphylococcus epidermidis,

47
Q

IV drug users have high propensity for endocarditis of right-sided valves, especially which one? What is the name of the pathogen/bacteria that forms 70% of cases?

A

Tricuspid valve; Staphylococcus aureus

48
Q

What are some of the causes of Infective Endocarditis?

A
  • Most common cause endothelial injury is turbulent blood flow resulting from preexisting valvular disease (50-70%) (Either AS or MR as the preexisting valve disease)
  • Endothelial injury may be incited by foreign material within circulation (indwelling catheters, prosthetic heart valves)
  • Gram-positive organisms account for approx 90% cases
49
Q

What is the common pathogen for Acute Bacterial Endocarditis?

A

Staph aureus

50
Q

What is the most common pathogen in subacute endocarditis?

A

Viridans streptococci

51
Q

Splinter hemorrhages are associated with what?

A

Infective endocarditis

52
Q

What are Janeway lesions?

A

PAINLESS, flat, irregular discoloration on palms/soles

53
Q

What are osler nodes?

A

Tender, (PAINFUL), pea-sized, erythematous nodules pulp space of finger/toes

54
Q

What are Roth spots?

A

Emboli to retina, hemorrhages

55
Q

What is the Tx for Infective Endocarditis?

A

• 4-6 weeks high-dose IV abx therapy
• Surgical intervention – valve replacement
– Persistent bacteremia
– Severe valvular dysfuntion causing heart failure
– Myocardial abscess
– Recurrent thromboembolic events

56
Q

What are the conditions for which antibiotic prophylaxis is reasonable?

A
  1. Presence of prosthetic heart valve, or prior repair with prosthetic material
  2. Prior h/o endocarditis
  3. Certain Congental Heart Diseases
  4. Cardiac transplant recipients who develop cardiac valve abnormalities
57
Q

What oral meds do you give to a patient for AHA-IEP Dental Procedures? Allergic to Penicillin?

A

Amoxicillin; If alllergic give Clindamycin or Cephalexin or Azithromycin or Clarithromycin

58
Q

What parenteral meds do you give to a patient for AHA-IEP Dental Procedures? Allergic to Penicillin?

A

Ampicillin; If allergic to PCN give: Clindamycin or Cefazolin

59
Q

Trisomy 21 is associated with what CHD?

A

ASD, VSD

60
Q

Turner Syndrome is associated with what CHD?

A

Coarction of the aorta

61
Q

Marfan Syndrome is associated with what CHD?

A

Aortic dilation, AR, MR

62
Q

Kartagener’s syndrome is associated with what CHD?

A

Dextrocardia

63
Q

What is the most common congenital cardiac abnormality?

A

Bicuspid Aortic Valve

64
Q

The presence of a diastolic murmur of AR in a patient with a febrile illness should alert you to the possibility of what?

A

Endocarditis

65
Q

The Finding of upper extremity HTN in Bicuspid Aortic valve should all you to what?

A

Concomitant aortic coarction

66
Q

Most common site of ASD?

A

Secundum (75%)

67
Q

Decreased stamina, palpitations and paradoxical emoboli are associated mostly in what adult CHD?

A

ASD

68
Q

T/F:

ASD can have systolic murmur at ULSB and middiastolic murmur at LLSB

A

True; this is due to increased flow from the shunted blood.

69
Q

What is the Tx for ASD?

A

Elective surgical repair

  • if large volume of shunted blood
  • If evidence of RV volume overload on echo
  • Prevent development of HF or pulmonary vascular disease
  • These patient will get Eisenmenger much quicker due to a larger hole.
Percutaneous closure
- Only for secundum (contraindicated in others)
- No right-left shunting (no reversal)
Surgical closure: Good prognosis
Closure age < 40 mm Hg
70
Q

How do you distinguish VSD from MR and TR, the other holosystolic murmurs?

A

VSD does not radiate to axilla like MR; VSD does not increase with inspiration like MR;

71
Q

True/False: Smaller defects tend to have loudest murmurs b/c of greater turbulence of flow

A

True

72
Q

If pulmonary vascular disease develops in VSD, what can you expect?

A
  • Holosystolic murmur diminishes as pressure gradient decreases
  • RV heave (due to volume overload)
  • Loud pulmonic closure (P2)
  • Cyanosis
73
Q

Do VSD patients receive endocarditis prophylaxis?

A

Yes for all patients

74
Q

T/F: Once a patient get pulmonary changes, it is IRREVERSIBLE! YOU CANNOT FIX THAT. They will need a heart and lung transplant.

A

True

75
Q

What are the risk factors for PDA?

A
  • First trimester maternal rubella infection
  • Prematurity
  • Birth at high altitude – due to low oxygen concentration and ductus will not close
76
Q

True/False: Usually ductus constricts after birth (first 10-15 hrs) due to sudden rise in blood oxygen tension and reduction in level of circulating prostaglandins

A

True; Low PGEs =closure of ductus arteriosus

High PGE’s= open DA

77
Q

In PDA what chambers become volume overloaded?

A

LA and LV

78
Q

What is the flow of blood in PDA?

A

blood flows from descending aorta to pulmonary artery

79
Q

If pulmonary vascular disease ensues, Eisenmenger syndrome results. What happens?

A
  • reversal of the shunt causing blood to flow from the PA through ductus to descending aorta
  • Resulting flow of desaturated blood to LE results in cyanosis of feet.
  • UE not cyanotic b/c they receive normally saturated blood from proximal aorta
80
Q

What are some physical exam findings in PDA?

A
  • Continuous, machine-like murmur
  • Heard best left subclavian region
  • Present throughout entire cardiac cycle (systole and diastole)
  • If Eisenmenger syndrome develops, you will notice lower extremity cyanosis and clubbing may develop: clubbing due to chronic hypoxia
81
Q

Do PDA patients require Endocarditis prophylaxis?

A

Yes until 6 months post repair

82
Q

How do you Tx a neonate/premature infant with PDA and HF

A

Trial of prostaglandin synthesis inhibitors in an attempt to close PDA; Low PGEs = closure of Ductus arteriosus

83
Q

T/F: 50% of coarctation of the aorta cases are associated bicuspid aortic valve

A

True

84
Q

What is the most usual presentation of coarctation of the aorta?

A

systemic HTN

85
Q

What are some physical exam findings in a patient with coarctation of the aorta

A
  • Femoral pulses weak and delayed compared to brachial pulses
  • Elevated BP in upper body
86
Q

What would you expect to auscultate in a patient with coarctation of the aorta?

A
  • Mid to late systolic ejection murmur; heard left subclavian area
  • Longer/almost continuous murmur RADIATING TO THE BACK
  • if associated bicuspid aortic valve: expect to see ejection click, systolic ejection murmur and blowing diastolic murmur
87
Q

What would you expect to see on a chest X-Ray of a patient with Coarctation of the aorta?

A

The “3” SIGN: Notching (scalloping) of inferior surface of the posterior ribs.

88
Q

What would you expect to see on an EKG of a patient with Coarctation of the aorta?

A

LVH and Left atrial enlargement (late finding)

89
Q

What is the Tx for a patient with Coarctation of the aorta?

A

Neonates with severe obstruction:
- Prostaglandin infusion to keep ductus arteriosus open to maintain flow to the descending aorta

Children:

  • Elective repair to prevent systolic HTN
  • HTN persists in 1/3 of patients operated on after age 14
  • Antibiotic prophylaxis: to prevent endarteritis : Even after repair
90
Q

Describe EISENMENGER SYNDROME

A
  • Condition of severe pulmonary vascular obstruction that results from chronic left-to-right shunting through a congenital cardiac defect
  • Elevated pulmonary vascular resistance causes reversal of the original shunt and development of systemic cyanosis
  • Change from left-to-right shunt to a right-to-left shunt due to increased pressures in the right. You will bypass the lungs. (Remember: if you bypass the lungs, you become cyanotic)
91
Q

Physical exam findings in a patient with Eisenmenger Syndrome

A
  • Cyanosis:- DIFFERENTIAL with PDA
  • Clubbing digits
  • Murmur of left-to-right shunt absent
  • Loud P2
  • RV heave
  • RV failure – edema, hepatomegaly, ascites
92
Q

What are the four anomalies that arise in Tetralology of Fallot?

A
  1. VSD
  2. Subvalvular pulmonic stenosis (Beneath the pulmonic valve we have tissue that is blocking outflow kind of like HOCM)
  3. Overriding aorta
  4. RVH
93
Q

What is the most common form of cyanotic congenital heart disease?

A

Tetralogy of Fallot

94
Q

What is the major problem in Tetralogy of fallot?

A

It’s the RV outflow obstruction of the Subpulmonic valve. This is the major problem!!! The magnitude of the shunt is related to the subpulmonic valve.
Deoxygenated blood out the shunt to the body and you will bypass the lungs. Causing cyanosis.

95
Q

True/False? In the Tetralogy of Fallot Squatting increases systemic vascular resistance by “kinking” femoral arteries, thereby decreasing right-to-left shunt and directing more blood from RV to lungs

A

True

96
Q

How do you Tx Tetralogy of Fallot?

A

Surgical correction:

  • Closure of VSD
  • Enlargement of subpulmonary infundibulum
97
Q

Do you give antibiotic prophylaxis to patients with Tetralogy of Fallot?

A

Antibiotic prophylaxis prevent endocarditis and 6 mos post surgery