Cardiac Function 1: Le Grice

Question 1

Describe LV hypertrophy

Answer 1

Chamber is smaller, muscle is thicker

Question 2

What do echocardiograms test for?

Answer 2

Supplement what you have found in the physical exam.
e.g. murmur, displaced apex beat etc.

This one has found

• Inc thickness of LV wall
• LV cavity of normal size
• LA enlargement

Question 3

What is a normal EF?

Answer 3

at rest about 55% form min,

Question 4

What are the important clinical signs?

Answer 4

murmur, heave, gallop rhythm, displaced apex beat, peripheral edema, ascites and abdominal enema, liver pulses.

Question 5

But is the diagnosis HF?

Answer 5

EF 70%,
Is diastolic HF
HFnEF (heart failure with normal ejection fraction)
HFpEF (Heart failure with preserved ejection fraction)

Question 6

What are the dominant symptoms in each?

• Right heart failure
• Reverse heart failure
• Forward heart failure

Answer 6

• abdominal edema, ascites, liver problems
• Lung problems
• fatigue

Right sided failure docent mean peripheral oedema

Question 7

What is systolic Heart failure

Answer 7

heart failure with reduced ejection fraction

EF < 40-50%, eccentric remodelling = wall dilated in one direction

Question 8

Diastolic HF

Answer 8

(50% of HF patients) Concentric remodelling = wall thickened on both sides so hasn’t dilated out one way.
Heart failure with preserved EF e.g. > 40-50%
the problem is filling, ventricle is too stiff to fill properly. therefore the effects are the same in terms of pressure back to the lung.
Older, female, hypertensive, diabetic, AF, CKD
Symptoms usually with exercise rather than rest
20-30% mortality each year.
No effective treatment. unless you treat the hypertension, cant actually fix the heart problems (lusiotropic treatment)

Question 9

Mechanisms of HFpEF

Answer 9

poorly understood
Diastolie is quite an active process.
Muscle relaxation requires release of contractile proteins, which requires ATP, so in people with ischaemia this can be slow

Question 10

relaxation and compliance

Answer 10

relaxation: 
X bridge detachement 
Ca2+ removal 
ATP 
Elastic recoil 

Compliance:
Titin (phosphorylation by PKA reduces stiffness), pulls things back into line to connect sarcomere together

Remodelling of collagen can contribute to stiffness and diatonic dysfunction.

Question 11

LV diastolic dysfunction determined by both active and passive processes a the level of?

Answer 11

myocyte
ECM
LV chamber
Forces extrinsic to the myocardium (right heart, pericardial and extra cardiac, preload, after load)

Question 12

Relaxation (lusitropy)

Answer 12

Tension is released when Ca dissociates from TnC
Ca decline results in reduced Ca-Tn C binding
Ca decline due to: NCX

Question 13

Passive stretch

Answer 13

AV pressure gradient

Chamber stiffness
- Collagen (amount, type, X-links, organisation)
- Titin
- chamber geometry: diameter, wall thickness, la place law.
Atrial contraction
- atrial structure and function

Question 14

what is the formula for mean arterial pressure

Answer 14

MAP = Pd + 1/3(Ps-Pd)

Question 15

Why does the diastolic heart failure patient have hypertension?

Answer 15

inc peripheral resistance (impaired systemic vasorelaxation in HFpEF) and thus
Increased MAP
Though her cardiac output is likely to be relatively normal
pulse pressure is large because proximal conduit arteries have reduced compliance (stiff)
These blood vessels initially store much of the blood ejected from the LV during systole and discharge it relatively uniformly towards the periphery throughout the cardiac cycle

HIGH RESISTANCE, LOW COMPLIANCE VASCULATURE

Question 16

How would the pressure volume loop be different

Answer 16

In diastolic dysfunction the diastolic pressure volume line is displaced upwards and to the left, there is diminished capacity to fill at low left atrial pressures. In diastolic dysfunction the ejection fraction is normal and the end diastolic pressure is elevated.

Question 17

Why does the HFpEF patient have pulmonary oedema?

Answer 17

Increased passive stiffness of the LV leads to an increase of the left atrial volume and pressure. As a result, blood volume in the pulmonary circulation increases and pulmonary pressures become elevated. Thus causing pulmonary edema.

Question 18

Why is the HFpEF patients Sob worse at night and why is she more comfortable sleeping with her upper body raised?

Answer 18

less venous pooling in the legs. which raises the starling pressure in the lungs so theyre a lot harder to move.
paroxysmal nocturnal dyspnea

effective BV increased by recumbency
When we are standing
- blood is stored in the lower extremities (superficial veins in these regions dilate when exposed to hydrostatic pressures associated with gravity)
when we are horizontal:
- BV is transferred to central venous compartment
- right heart filling increased

Question 19

Speculate on possible treatment for the HFpEF patient

Answer 19

Reduce congestive state - low salt, diuretics
Reduce HR (longer filling times) beta blockers (treat AF if present)
Control hypertension
Reduce / reverse remodelling - ACE inhibitors, AgII blockers, spironolactone

Question 20

CRT: what might be the pathophysiological background to the electrical problem

Answer 20

30-50% of patients with CHF have intraventricular conduction defects
These abnormalities progress over time
Indépendant predictor of mortality
Inflammation / fibrosis in myocardium and conduction system in HF
Leads to
Discoordinated conduction
Leads to
Dysynchronous contraction and relaxation, systolic impairment and reduced LV filling time

Question 21

How might the mechanical function of the heart be affected by this cardiac electrical function?

Answer 21

poor contraction and relaxation, part of the wall can actually bulge during systolie. possibility that part of the wall cant contract because of scarring and another reason the the part of the wall is still waiting for a contraction signal as the purkingie fibres to that area have been damaged
poor activation can also affect cardiac FILLING e.g.
- RV/LV values sequence changes
- Slow LV relaxation
- LV systole prolonged
- LV filling time shortened

Question 22

SPECT?

Answer 22

Single photon emission computed tomography - way of looking at blood flow. different colours for strength of blood flow.

Question 23

Given the patient is on optimal pharmacotherapy is there any other treatment option available to help this patient?

Answer 23

Difference between CRT treatments and standard pacemakers for standard bradycardia conditions. Here we are prescribing CRT for someone who doesnt have a standard antibradycardic condition e.g. sinus node dysfunction, AV node conduction issues.
Compared to a standard pacemaker which normally implants leads to the right atrium and ventricle. you can place leads to the left ventricle epicardially, tend not to place them endocardially because of the worries about thrombus and stroke. (some methods now do with fancy techniques)

Question 24

What sort of patients do we give CRT to?

Answer 24

Patients who continue to have symptoms despite being on maximal medical therapy and who fit certain criteria, because of the success rates of the implantation therapy, and there are some examples of people getting this therapy who shouldn’t e.g. patients with RBBB, or LBBB but normal QRS. and they are expensive, also in terms of expensive complications. Pacing from an energetics point of view is quite cheap whereas using medications to help the heart can make it consume more energy than is safe to do.

Question 25

Benefits of CRT therapy compared to conventional drugs use

Answer 25

Something for nothing? No extra energy/O2 demand (unlike dobutamine) may even lower energy /O2 demand
Improved EF symptoms, quality of life and survival
Reverse remodelling in patients with moderate to severe HF.

Question 26

What factors do you need to consider to optimise CRT therapy?

Answer 26

ECG
Electrical mapping
Echo
MRI