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CV 2 Exam 3 > Chest Pain, stenosis, regurgitation etc. > Flashcards

Chest Pain, stenosis, regurgitation etc. Flashcards

1
Q

what to do with chest pain

A

first decide if it is ischemic, based on the history

non ischemic requires another pathway

Things that make you think ischemic:

  • brought on by exertion or emotional upset, etc.
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2
Q

Ischemic pain, 4 symptomatic types

A

1-Stable angina
2-unstable angina
3- NSTMI
4- STMI

note that 2-4 above are acute coronary syndromes

Duration of pain will be the mainstay of the discrimination, angina lasts 2-10 minutes, unstable u pto 20 minutes, acute MI 20 minutes-6 hours but may studder over 24 hours

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3
Q

Stable angina

A

occurs on exertion or emotional upset
lasts 2-10 minutes, usually 4-6
reliably occurs with the same amount of exertion
relievedby rest or nitro
may be present for many years
remember, new onset angina that occurs within 4 weeks is UNSTABLE

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4
Q

unstable angina

A

pain may last up to 20 minutes, longer is usually an MI
defined as any change for the worse in pre-existing angina, or new onset angina

MEDICAL EMERGENCY

usually little or no EKG changes but the sentinel finding is normal cardiac markers (no necrosis)

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5
Q

2 types of acute MI

A

NSTMI- without ST elevatino

STMI- with ST elevation

use troponin levels, etc.

can have elevated markers without necrosis (clearance issues!- renal)

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6
Q

Aortic Stenosis in Adults

A

The most common cause of LV outflow obstruction.

Etiology has changed over the past 40 years with Bicuspid AV and Senile AS taking over from RF (RHD). (pre-antibiotic era)

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7
Q

Bicuspid AV

A
  • 20% of people with bicuspid aortic valve have aortopathy as well, which often kills

The most common congenital abnormality of the heart
Occurs in 1-2% of the population
Men out number women 4:1
Two cusps instead of three, unequal size, presents in adulthood, younger (35-55 years old) then Senile

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8
Q

Senile AS

A

Many names, AS of aged, etc.
Seems to be associated with atherothrombotic degeneration of the AV (trileaflet)
Much older patients, likely in their 80s and 90s.

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9
Q

Aortic Stenosis: what happens? 3 symptoms

A

The obstruction to outflow from the LV causes LVH first, then LA dilatation, finally LV dilatation CHF and death

3 cardinal symptoms are DOE (dyspnea on exertion), syncope (near syncope, exertional lightheadedness, etc) and angina of effort.

Any one of these symptoms are indications for valve replacement as life expectancy is reduced to less than 3 years.

TAVr- transcutaneous aortic valve replacement

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10
Q

what happens in muscle mechanics with increased afterload?

A

fiber shortening decreases
(when you release the afterload, the EF normalizes)

preload increases fiber shortening
–> hyper ejection fractions, 65, 85% . When that patient drops their EF, they will die fast.

in stenotic valve disease, the EF drops but you can fix it. In regurgitant valve disease, by the time the EF drops it’s too late.

the heart tolerates regurgitant disease well, but not stenotic.

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11
Q

Aortic Stenosis PE

A

PE is diagnostic if done correctly.

Echocardiography is indicated if significant AS is suspected.
Look for other causes of symptoms, especially in the aged.

Coupling the symptoms with echo findings helps lead to proper care. It is usually difficult.

Inspection may find JVD with right heart failure (late finding)
There is LVH (non displaced large apex impulse, LV dilatation is late)
A precordial thrill, 3rd interspace, LSB may be felt.
S1 normal, SEM at base, radiates into neck and onto the clavicles (much easier to hear)- if you don’t hear it on the clavicles, it’s very likely not AS
Murmur that stops at base of heart and doesn’t radiate into neck is usually not AS, it may be HOCM
AS almost always radiates onto the clavicle, it is my “ace in the hole”
Severe AS radiates a “shudder” into the carotid, like a cat purring in the neck. You can diagnose AS by careful palpation of the carotids, before you listen to the heart.

(should be able to feel a carotid shudder– a transmitted murmur)– how long have you had aortic stenosis?

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12
Q

degree of AS symptoms

A

The degree of symptoms varies widely from patient to patient.

There is a long asymptomatic period in each patient.

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13
Q

AS echo

A

AVA= aortic valve area
Pressure gradients, mean and max, flow velocity above (distal) to AV and calculated outflow tract dimensions are all utilized to stratify the severity of AS.
You must correlate the signs symptoms and echo findings in each patient.

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14
Q

Aortic regurgitation

A

AR is a volume problem like MR. These are well tolerated and the vast majority of patients with AR remain compensated for life. Only when the LV dilates and the EF starts to decrease is your patient in trouble.
When this happens intense med Rx may be used but it should just be a bridge to AVR.

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15
Q

AR etiology

A

aortic regurgitation

Valvular disease:

  1. RF
  2. Senile AV
  3. IE (infective endocardities)
  4. Trauma
  5. Myxomatous degeneration
  6. Degeneration of a Bioprosthetic AVR (aortic valve replacement)

Aortic Root Dilatation

  1. Marfans, can also involve the leaflets
  2. Dissecting AA (aortic aneurysm)
  3. Non dissecting AA
  4. Ankylosing Spondylitis
  5. Becet’s, syphilis, Osteogenesis Imperfecta, Psoriatic Arthritis, etc
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16
Q

AR PE

A
  1. Bounding pulse, large pressure-pulse and pulse-pressure lead to many signs like Demecet’s, Traub’s, Quinke pulse, etc
  2. Early diastolic decresendo murmur, LSB (left sternal border), 4-5th ICS, or RSB in AA

Vasodilation can decrease the excess preload

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17
Q

chronic vs acute aortic regurge

A

almost always chronic

sometimes trauma can cause acute

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18
Q

Mitral stenosis- causes?

A

Clinically significant MS is only due to Inactive Rheumatic Heart Disease in the adult. Rarely mitral annular calcifications leads to MS, not usually of great significance.

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19
Q

Rheumatic Fever

A

is a disease of childhood and young adults. The first onset is almost always in childhood. 50% of patients with RF have no history of same. RF is a disease of populations deprived of antibiotics (3rd world, abused populations, etc).

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20
Q

Rheumatic Heart Disease

A

affects 1 in 3 patients with RF.
The mitral valve is involved almost 100% in Rheumatic Heart Disease.
40% of patients with RHD have isolated MV involvement, 40% more have aortic involvement.

RF is a late sequelae of Group B strep infections, usually the throat, not treated with effective antibiotics. It is an autoimmune disease, requiring weeks to develop.

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21
Q

congenital vs rheumatic

A

pulmonic is very common in congenital, very rare in rheumatic fever

can have pulmonic valvular insufficiency from pulmonic htn of any cause. Graham-Steele murmur is from pulmonic valve stenosis.

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22
Q

Symptoms of Mitral Valve Stenosis

A

Etiology= RHD
Symptoms are DOE, PND, orthopnea and fatigue.
Symptoms are due to the obstruction of flow from the LA to the LV through the MV. This increases the pressure in the LA, pulmonary vasculature back into the RV and RA. It is the resistance to blood flow that increases the pressure.; The heart always tries to maintain the flow (CO), and thus the pressure rises secondarily. The LV is relatively protected from the problem with normal or low LV pressures.

Other symptoms are hemoptysis, atrial fibrillation, thromboembolism, chest pain (from pulmonary hypertension).

23
Q

MS-Atrial Fibrillation

A

A very common Sequalea of MS, a fib reduces CO by two mechanisms. The loss of atrial contribution to LV filling and the increase in HR both of which reduce LV filling (passive early and active late). This will frequently precipitate APE.

24
Q

PE in MS

A 
Mitral facies-pink purple cheeks (maxillary) from decrease in CO and vasoconstriction
Pulmonary Hypertension leads to Right Heart Failure with RV enlargement, loud P2, etc
Cardiac auscultation (after inspection and palpation) findings:
25
Q

Sydenham chorea is a major diagnosis of

A

rheumatic fever

26
Q

Cardiac auscultation in Mitral stenosis

A

Increased S1
Single S2
Opening Snap, follows S2, severe shortens the A2-OS interval
Mid diastolic murmur (rumble), heard at apex, with pre systolic accentuation (if in NSR).

27
Q

MS testing

A

EKG-P mitrale (= left atrial enlargement), a fib, RVH
CXR-LAE, RVH, pulmonary congestion, enlarged PA (hypertension)
Echocardiography is now the gold standard. PA pressures, mitral gradients (mean and peak), CO, SV and MVA are all standard.

28
Q

Patients with acute mitral regurgitation

A

are often gravely ill with significant hemodynamic abnormalities that require urgent medical and usually surgical treatment”. Otto, Up to Date, July 2015.

29
Q

mitral regurg etiology

A

Only 2 basic mechanisms:

  1. Ruptured mitral chordae tendinae due to myxomatous disease (was called MVP), infective endocarditis, trauma, rheumatic heart disease (either acute or chronic) or spontaneous rupture.
  2. Papillary muscle rupture due to acute MI or trauma or pap muscle displacement due to ischemia or MI.
30
Q

mitral regurge Etiology Prosthetic Valves

A

Tissue valve leaflet rupture due to degeneration, calcification or endocarditis
Impaired closure of mechanical valve due to thrombosis, infection, pannus (scar tissue).
Paravalvular regurgitation

St. Jude’s valve is the most common one used right now.

31
Q

mitral regurg pathophysiology

A

LA compliance (remember physics) is usually normal, causing an immediate and severe reflection of high pressure from the LA to the pulmonary circulation, causing pulmonary edema. In chronic MR the LA dilates and becomes very compliant, there is no time for LA dilatation in acute MR.

Also, because the LV is not dilated, much of the cardiac output is diverted into the LA, causing a decrease in effective CO. This causes cardiogenic shock

32
Q

warm and cool, wet and dry

A

warm– normal cardiac output
cool– bad CO

wet or dry– wet if heart failure

33
Q

clinical manifestations of mitral regurg

A

Patients present as the moniker “Acute Severe MR” would suggest with pulmonary edema and cardiogenic shock, they are dying. Only rapid correctly directed care will save their life.

34
Q

PE of mitral regurg

A

Signs of both APE and Cardiogenic Shock prevail, fast thready pulse, hypotension with hypoperfusion (cold), wet lungs (crackles), extreme air hunger and orthopnea (can’t lay down).

There is usually a murmur of MR, but many patients will have a soft or inaudible murmur due to increase in LA pressure diminishing the noise.

35
Q

mitral regurg testing

A

The diagnosis is made with echocardiography, along with the EKG, CXR and cardiac catheterization

Many of these patients will need to be intubated and placed on an ET tube to obtain these tests as their clinical state is as above.

36
Q

Medical Stabilization of mitral regurg

A

Most texts mention vasodilators first, but in my experience you need an IABP first, after endotracheal intubation and sedation, often in the Cardiac Cath lab, followed by coronary arteriography. It only takes 2-3 minutes to place an IABP, once the lab and equipment are ready. Also an LVAD will work nicely (but nowhere as available as IABP.

37
Q

Acute MR Endocarditis

A

This is one of the absolute indications for surgery in SBE, or ABE.

38
Q

Ischemic Acute MR

A

PCI works well, but may require IABP support.
If papillary muscle rupture occurs, only surgery will save your patient’s life. IABP, LVAD may be life saving prior to going to the OR.

39
Q

Chronic mitral valve regurgtation management topics

A 
Pathophysiology and Natural History
Severity of Valve Lesion
Presence of Atrial Fibrillation
Effectiveness of Vasodilator Therapy
Endocardial Prophylaxis
Indications for MV Replacement or Repair
40
Q

Pathophysiology and Natural History of chronic mitral valve disease

A

Most elusive is the transition from compensated to decompensated state
This transition is dependent on the mechanisms of compensation and the severity of the valvular regurgitant volume
LV chamber size and function are very important determinants of outcome, both with and without surgery

41
Q

Pathophysiology Phases of chronic MR

A
  • Compensated Phase
    LVEDD less than 6 cm, LV LVESD less than 4 cm
  • Transitional Phase
    Worsening symptoms (usually)
    LVEF decreasing from normal or hyperdynamic to slightly depressed (ie, EF less than 55%)
  • Decompensated Phase
    LVEF less than 40%, LVEDD>7 cm, LVESD>4.5cm.
    Very important to recommend surgery prior to decompensation as surgical results are very poor in these patients.
42
Q

5 “parts” of the MV apparatus

A
  1. Leaflets
  2. Mitral Annulus
  3. Chordae Tendinae
  4. LA
  5. LV (papillary muscle, regional LV dysfunction at the origin of the muscle, etc)
43
Q

MV Leaflets and MR

A

MR may occur due to:

  1. Myxomatous MV (MV Prolapse)
  2. Rheumatic changes (underdeveloped countries)
  3. SBE
44
Q

Mitral annulus and MR

A

MR may occur due to calcification “fixing” the apparatus open, usually not severe, very difficult or impossible to surgically repair (I’ve never seen an attempt to repair surgically)

45
Q

Chordae Tendinae and MR

A

Rupture-usually acute
Fixation from RF
Disruption from SBE-usually acute

46
Q

Left Atrium and MR

A

MR begets MR

Progressive LA dilatation leads to valve being “pulled apart” as there is continuity of the LA with the leaflets

47
Q

Left Ventricle and MR

A

Dilatation of the LV leads to some level of MR in most cases.

48
Q

Atrial Fibrillation and MR

A

May decompensate patient rapidly

Due to decreased filling of LV from increased HR (encroaching on diastole when the LV fills, early and mid diastole, passive filling phase) and loss of atrial contribution to LV filling in late diastole

49
Q

Ischemic Heart Disease and MR

A

The papillary muscles contract late in the cardiac cycle, “end circulation” of the muscles can lead to MR by loss of “holding down” the leaflets due to ischemia of the papillary muscles. Chronic MR may develop, and it usually is reversible with revascularization techniques (PCI or CABG).

50
Q

Signs and Symptoms of MR

A

Dyspnea on Exertion (DOE)
Fatigue
Palpitations- especially with atrial fibrillation
CHF decompensation, orthopnea, PND, Functional Class III or IV

Precordial Exam:
LV heave
Holosystolic Murmur, or Pan Systolic Murmur (PSM, HSM), at the apex, radiates in direction of MR jet, anterior or posterior (opposite leaflet).

Decreased S1, wide split S2 from early A2, occasional S3
Rapid rising and falling bounding pulse-volume problem like AR

51
Q

Echocardiography signs of MR

A 
Chamber size (LA, LV) and function (EF increased at first)
Doppler measurements of Flow, regurgitant volume (fraction), direction and volume of jet in LA, etc.
52
Q

Treatment of MR

A

SVR (systemic vascular resistance determined by arteriolar resistance) is the resistance to LV ejection (with a normal AV and LVOT)
There is a competition between the periphery and the LA for blood flow in systole. LA resistance is determined by LA size and compliance.

Vasodilators such as ACE or ARB, hydralazine, nitrates (venular dilator) may be usefull
If LV systolic dysfunction is present, general CHF meds do apply

53
Q

Surgery for MR

A

Mitral Valve Repair favored over Replacement

Percutaneous Mitral “Clip”

CV 2 Exam 3 (23 decks)

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