1
Q
When do ventricles begin to contract- what are the sequence of events
A
- begin to contract during systole (onset of systole)
- AV valve closes
- pressure rises in ventricles but not transmitted to atrium
- AV valve closed thoughout systole
- upstream flow (from systemic or pulmonary veins into atrium begins to increase atrial volume
- semilunar valves open when ventricular pressure = pressure in root of great vessel and ejection begins
- both ventricle and great vessel pressure rise in concert
- approaching end of systole both ventricle and great vessel pressures fall in concert
- ventricle pressure falls below great vessel pressure and semilunar valve close (lowest volume of ventricle)
- ventricular pressure falls below atrial pressure and AV valve opens - diastole begins
2
Q
Sequence of events diastole
A
- blood flows from atrium to ventricle
- ventricle and atrium are in continuity during diastole and pressure are equal
- atrium contracts near end of diastole and reaches its least volume
3
Q
Valve types (2+2)
A
- Atrioventricular valves (complex)
- bicuspid (mitral)
- tricuspid - Semilunar valves (simple)
- aortic
- pulmonic
4
Q
Requirements of atrioventricular valves
A
- complex
- functionally dependent on contraction of papillary muscles and attachments via chordae tendinae
5
Q
Valve ring in atrioventricular valve during systole
A
-deformed during systole
6
Q
Atrioventricular valve during systole
A
- closed
- high ventricular pressure but low atrial pressure
- allowing no backward flow
7
Q
Atrioventricular valve during diastole
A
- open
- low ventricular pressure
- forward flow with no resistance
- ventricular and atrial pressures equal
8
Q
Semilunar valve requirements
A
-intrinsic support (lunulae and nodules)
9
Q
Semilunar valve ring
A
Fairly fixed contour during systole
10
Q
Semilunar valve during systole
A
- open
- high ventricular pressure
- forward flow iwth no resistance
- ventricular and great vessel pressures equal
11
Q
Semilunar valve during diastole
A
- closed
- high great vessel pressure
- low ventricular pressure
- no backward flow
12
Q
Stenosis
a) definition
b) direct consequence
c) compensation
A
- narrowing of open orifice
- resistance to flow while valve is open (increases pressure distal to stenosis)
- maintenance of forward flow requires that pressure in the chamber proximal to stenotic valve exceed pressure in the distal chamber or vessel (gradient)
13
Q
Effect of gradually developing stenosis on SV
a) at rest
b) with exercise
A
- likely no decrease in SV at rest
- exercise reserve may be decreased
14
Q
Regurgitation/insufficiency/incompetence
a) definition
b) direct consequences (2, when they occur)
c) indirect consequence (2)
A
- abnormal functional anatomy of closed orifice
- leads to leak (backflow) when valve is closed
- leak occurs in systole with AV valves and in diastole with semilunar valves
- end diastolic volume of the ventricles is increased (in both types of valves) –_> increased total SV (total SV= forward SV + regurgitant volume)
15
Q
Effect of gradually developing regurgitation on SV
a) at rest
b) with exercise
A
- the increase in total SV is sufficient to allow forward SV to be maintained near normal at rest
- may be decreased with exercise
16
Q
Common valve lesions (2)
A
1) Aortic stenosis and regurgitation
2) Mitral stenosis and regurgitation
17
Q
Pathophysiology of stenotic semilunar valve
a) what must happen for flow to be maintained
b) consequences of this.. (4 points)
A
For flow to be maintained pressure in upstream camber must rise -i.e. proximal ventricle
1) Increased pressure in ventricle = increased wall stress
2) Ventricle will undergo hypertrophy (concentric) to reduce wall stress
3) Hypertrophy causes diastolic compliance (volume change/pressure change) to fall -takes more pressure to change the volume of the ventricle (i.e. harder for ventricle to relax)
4) End diastolic pressure rises (as well as atrial pressure -leading to dilation of atria -check??)
18
Q
Pathophysiology of stenotic AV valve
a) direct consequence
b) secondary consequences (2)
A
Goal: Proximal atria must develop greater pressure than normal
- increased pressure is transmitted to proximal circulation (pulmonary or systemic venous) because are no valves proximal to the atrim
- atrium hypertrophies
19
Q
Consequences of stenosis as progresses over time -end stage
a) output..
b) back ups (2)
A
- limitation to CO with exercise and eventually at rest
- in left side of heart –> increased pressure in pulmonary capillaries and pulmonary edema
- in right side of heart –> increased systemic venous pressure and peripheral edema
20
Q
Consequence if valve is regurgitant
a) where is the blood regurgitating from and into where (2)
b) consequence
A
- some of the blood pumped in the ventricle during systole returns during diastole from
a) the great vessel -if regurgitation in semilunar valve
b) from the proximal atrium - if regurgitation of AV valve - causes increased ventricular preload
21
Q
Changes to SV with regurgitant valve and consequences of that
A
- total SV must increase so that when the regurgitant volume is subtracted the forwad SV is close to normal
- larger total SV = larger EDV (afterload) = ventricular wall stress (afterload) is increased (laplaces law)
22
Q
Consequences of slow developing regurgitation
A
- time for increase in compliance (starling effect)
- therefore little increase in EDP
23
Q
Consequence of increased EDV from regurgitation
a) how the heart compensates
b) later on what does this lead to
A
- ventricle dilates
- increase r = increased wall stress
- ventricle undergoes hypertrophy (eccentric) to reduce wall stress (afterload)
- as EDV continues to increase and ventricle continues to thicken (decreased compliance-pressure increases more per given volume) the EDP will rise and pressures begin to rise in chambers/circulation proximal to the affected chamber
24
Q
Consequences of severe regurgitation
A
A) limitation to CO with exercise and eventually rest
B) Ventricular dysfunction:
-ventricle develops systolic dysfunction which may become severe
-dysfunctional ventricle causes high proximal pressure and low forward SV
25
Detecting stenosis/regurgitation (what is fist sign of abnormality usually)
- usually abnormality present for many years without any symptoms (with the exception of severe congenital abnormalities and acute onset regurgitation, rarely stenosis)
- often first sign of abnormality is murmur
26
Heart murmur
Audible sound resulting from turbulent blood flow
27
Types of turbulent blood flow (3)
1) normal flow through narrow passage
2) increased flow through normal passage
3) flow from high to low pressure chamber
28
Describing murmurs (7)
- described as to intensity (grade 1-6)
- frequency/pitch
- timing (systolic, diastolic, continuous)
- shape
- location (maximal intensity)
- radiation
- response to maneuvers
29
Innocent murmur -features (2 main)
-usually systolic and brief
(may be continuous, but not purely diastolic)
-with no other cardiac abnormalities and normal ECG, chest x-ray, and echo
30
What may ECG show over time with valvular lesion
-show changes due to hypertrophy of the chambers required to develop increased pressure or volume
31
What may chest x-ray show over time (2)
- increased Ca2+ deposition
| - eventually chamber enlargement (especially with regurgitant valve ma show chamber enlargement earlier on)
32
Management of patient with pathological murmur (4)
- regular follow-ups
- endocarditis prophylaxis (primarily oral/dental hygiene)
- valve repair or replacement if indicated
- medication generally only adjunctive to surgery (although may improve symptoms/delay repair/replacement somewhat)
33
When valve repair/replacement should be delayed
1) Until significant symptoms are present (sometimes -depends on what type valve lesion)
2) Check LV function to do repair at optimal time --> when the LV is volume overloaded LV dysfunction may precede the development of significant symptoms and compromise long-term outcomes
34
Aortic stenosis pathophysiology
a) what is pathological
b) adaptation to sustain forward flow
c) consequneces of this adaptation
Narrow AV orifice
1) LV must generate more pressure during systole to sustain forward flow
2) increase in LV chamber pressure increases LV wall stress (afterload)
2) LVH (concentric) develops to reduce wall stress
3) eventually contractile performance declines (decreasing SV) and LVEDP rises excessively (as blood builds up in ventricle)
35
Clinical course of aortic stenosis
a) what is first abnormality detected (usually)
b) describe the murmur
- location
- radiation
- change as stenosis progresses
c) carotid pulse (2)
d) Echo (2)
e) ECG (1)
f) Chest x ray (3)
1) Usually asymptomatic for many years
2) Systolic ejection murmur - first abnormality normally
- maximal at R2ics at sternal edge
- radiating to the carotids
3) murmur increases in intensity and duration as severity of stenosis progresses (accompanied by thrill if grade 4)
4) murmur diminishes in late stages as CO falls
5) carotid pulse contour gradually becomes delayed and diminishes (pulsus tardus and parvus)
6) early echo shows abnormal AV morphology and increased peak ejection velocity
7) ECG will eventually show LVH
8) Chest x ray will show enlarged aorta and possibly AV calcification. Visibly enlarged LV occurs late in course.
36
Symptoms and associated prognosis for aortic stenosis (2)
- angina (5 years)
| - syncope (3 years)
37
Pathophysioloy of aortic regurgitation
1) AV leaks during diastole -allows ejected blood to reenter the LV
2) LVED rises (increasing preload)
3) increase of SV to allow forwward CO to be close to normal (Starling effectO
4) usually seveity of LV increases gradually -gives time for LV ompliance to increase and increase in LVEDV may not result in significant rise in LVEDP
5) LV contractility declines -rising LVEDP results in increased LA and pulmonary capillary pressures and exertional dyspnea and CHF
38
Consequence of acute AR
- increase in LVEDV may result in significant increase in LVEDP
- result in increase of LA and pulmonary capillary pressure
- dyspnea on exertion or at rest with pulmonary edema
- may be impossible to sustain normal CO at rest
39
Clinical course of aortic regurgitation: what can find on physical exam
- usually asymptomatic for years
- first sign is usually diastolic decrescendo murmur heard best down the left sternal border (accentuated by leaning forward with held expiration)
- often also an aortic systolic murmur
- apex beat usually forceful and will eventually be displaced (due to LV enlargement and hypertrophy)
- widened pulse pressure (difference between systolic and diastolic BP)
40
Aortic regurgitation - findings on echo
- abnormal AV morphology
- regurgitant jet Ao to LV
- LV dimension increased
- LVH is increasingly marked
41
Aortic regurgitation -findings on ECG
-LVH (diastolic overload pattern)
42
Aortic regurgitation - findings on chest x ray
- aorta enlarged
- LV enlarged
- later signs of CHF
43
Prognosis AR with onset of symptoms
-poor (first signs usually exertional dyspnea)
44
Management of AR
1) beta blockers for symptomatic improvement
2) Moderate exercise is safe as long as no symptoms occur
3) Systemic hypertension should be managed aggresively to decrease afterload on LV
4) Monitor LV function - replace or repair AV when LV dysfunction is detected but before significant symptoms occur
5) Onset symptoms of exertional dyspnea or low CO require surgical valve replacement or repair
6) Acute onset or sudden progression AR is generaly a surgical emergency
45
Mitral stenosis pathophysiology
1) MV orifice narrows
2) LA pressure rises to maintain normal forward blood flow (usually orifice must reduce considerably before the is an increase LA pressure)
3) Increase LA pressure leads to increase pressure in pulmonary capillaries, PA, RV and RA (back up)
46
Consequence of increased LA pressure due to mitral stenosis (3)
1) RV dysfunction may occur
2) people with particularly reactive pulmonary arterioles and pressures in the PA, RV, RA may rise more than anticipated - if pulmonary cap pressure sufficiently high, interstitial and alveolar pulmonary edema may occur
3) CO may become limited with exercise and eventually at rest (because effective atrial contraction and diastolic filling time important to sustain CO and development of AF or other atrial tachyarrhythmias can precipitate a marked fall in CO and increase in LA pressure)
47
In what gender is MS more common
Much more common in women
48
Signs of MS on physical exam - characteristics of murmur
Characteristic murmur:
-apical
-preceded by opening snap (presystolic)
-then early diastolic rumble
-then eventually heard through most of diastole
(murmur occurs early in the disease course)
49
Features of MS on echo
- abnormal MV morphophogy
- high velocity transmitral flow
- eventually elevated PA pressure and RV dysfunction
50
Features of MS on ECG
- LA hypertrophy
| - eventually RA hypertrophy
51
Features of MS on chest x ray
- LA enlargement
- MV calcification
- pulmonary venous redistribution
- RV enlargement
- pulmonary congestion
52
Signs of MS on exam -other than murmur
- exertional dyspnea (likely first symptom)
- may be brought on by pregnancy (increase in CO results in rise LA pressure)
- rales, JVD and edema may develop
- evidence low CO
- atrial thrombus may form (particularly in AF) and may cause stroke or peripheral embolus
53
Management of MS
- tends to progress more rapidly than AS -intervention may be required at young age
- intervene before onset pulmonary congestion and RVF
- percutaneous mitral valvultomy good but eventually will need surgical repair or replacement (somtimes required initially)
- medication to manage tachyarrhythmias and CHF (adjuvant therapy only)
- anticoag for AF or previous stroke or peripheral embolus
54
Pathophysiology of mitral regurgitation
1) MV leaks during systole
2) LVEDV increases (because allow and increase in SV to maintain CO at near normal) and LA volume increases (which may worsen MR)
3) Increase LVEDV raises LV wall stress and LVH (eccentric) develops to reduce wall stress
4) Eventually LV dysfunction develops (initially with exertion but later at rest with fall in EF and SV)
5) Rising LA pressure result back up to pulmonary cap, PA, RV and RA
55
Consequences of acute MR
- marked rise in LAP and LVEDP
- causes elevation pulmonary capillary pressure sufficient to cause interstitial or pulmonary edema and forward CO can be quite low
56
First finding in MR (may be asymptomatic for many years)
Blowing pansystolic murmur maximal at apex and radiating into the left axilla
57
Findings of MR on echo
- abnormal MR morphology
- increased LA dimension
- increased LV internal dimension
- MV regurgitant jet
58
Findings of MR on ECG
-eventually show LA hypertrophy and LVH (volume overload)
59
Findings of MR on chest x ray
- eventually show LA and LV enlargement
| - in later stage may show RV enlargement or pulmonary vascular redistribution and eventual congestion
60
First and most prominent symptom + conditions that complicate symtpms of MR
- dyspnea (first on exertion and then eventually at rest)
- fatigue from low CO
- symptoms of L and R congestive heart failure
- atrial arrhythmias and pregnancy likley to bring on symptoms
61
When surgery is needed for MR + other principles management of MR
Will eventually require MV repair or replacement
-refer to surgery when LV dysfunction is documented on echo vs when get symptoms
(significant symptoms result in poorer prognosis)
-medical management tachyarrhythmias and CHF
62
Etiology of Aortic stenosis (3)
- degenerative
- biscupid AV
- rheumatic fever
63
Etiology of Aortic regurgitation (5)
- rheumatic fever
- congenital
- traumatic
- endocarditis
- aortic root
64
Etiology of Mitral Stenosis (3)
- rheumatic fever
- rarely congenital
- LA tumor or thrombus
65
Etiology of mitral regurgitation (7)
- myxomatous degeneration or MV prolapse
- LV dysfunction and enlargement
- rheumatic fever
- disrupted chordae tendinae or papillary muscle
- annular calcification
- endocarditis
- hypertrophic cardiomyopathy
