Cardiac Function II Flashcards

1
Q

Cor pulmonale

A

right sided heart failure, enragement of the right ventricle due to high blood pressure in the lungs, usually caused by chronic lung disease

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2
Q

Pulmonary hypertension my be caused by?

A
  • Loss of capillary beds (e.g. due to bullous changes in COPD or thrombosis in pulmonary embolism)
  • Vasoconstriction caused by hypoxia, hypercapnia, or both
  • Increased alveolar pressure (e.g. in COPD during mechanical ventilation)
  • Medial hypertrophy in arterioles (response to pulmonary hypertension due to other mechanisms)
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3
Q

What does smoking do to the lungs long term?

A

Causes obstructive airway disease, loss of elastin etc, all of which inc work of breathing

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4
Q

What is the 2nd heart sound related to

A

Normally split, splitting increases during inspiration (reduced intrathoracic pressures during inspiration = more fluid into right side of heart so emptying of right heart takes a bit longer)and decreases during expiration

In order for the ventricle to eject blood against a higher pressure than used too it takes longer, so splitting might be increased, and because inc pressure in the pulmonary artery, when the valve closes the sound is a lot more accentuated than normal

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5
Q

Explain back pressure in right sided heart failure

A

Neck vein distension (raised JVP), hepatomegaly and peripheral oedema due to elevated systemic venous pressures as a result of right heart dysfunction

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6
Q

What may occur in the heart late in disease as a result of RV dilatation

A

tricuspid regurgitation

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7
Q

Cor pulmonale, what might you see on an ECG

A

Right axis deviation

increase in right ventricle size?

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8
Q

What does COPD do to ECG signals

A

expanded chest may reduced ECG potentials

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9
Q

Cor pulmonale why the intraventricular septum displaced to the left during diastolie?

A

During diastole pressure is higher on the right than on the left, because you have back pressure on the right side of the heart through the periphery which turns out to be filling pressure when the heart is relaxed

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10
Q

Childhood rheumatic fever and mitral stenosis

A

yes.
Thickening of valve leaflets with fibrous obliteration
May be calcium deposition in the leaflets, chord and the annulus with commissural and chordal fusion
Eventually get funnel shaped metal valve with fish - mouth orifice

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11
Q

mitral valve stenosis - Sob and fatigue with exercise

A

high pressures in the lungs, pulmonary vascular engorgement, reduced lung complaince and increased work of breathing
Lack of atrial contraction –> reduced ventricular pre load
at rest may be fine but during exercise, heart unable to increase output sufficiently to get increased demand

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12
Q

Ortner’s syndrome

A

vocal cord paralysis

impression of left recurrent laryngeal nerve by enlarged LA or pulmonary artery

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13
Q

Severe mitral valve stenosis, explain attenuated first heart sound

A

Greater excursion of leaflets during closure, since elevated LA pressure has kept the leaflets relatively wide apart
except when valve gets super calcified and hardly moves, sound gets soft again,

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14
Q

mitral valve stenosis: explain the opening snap

A

Under a high pressure gradient the abnormal valves billow into the LV and are rapidly arrested by the chordae, causing sudden vibrations

No heard when significantly calcified

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15
Q

mitral stenosis: explain prolonged diastolic murmur

A

turbulent blood flow through narrowed valve opening, best heard over the apex of the heart with the bell of the stethoscope

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16
Q

Treatments for mitral valve stenosis

A

percutaneous mitral valvuloplasty
Mitral valve replacement surgery

Mechanical valve clots so have to take anticoagulants, if still of childbearing age, not ideal.

17
Q

Why are patients with mitral stenosis typically at risk of developing atrial arrhythmas such as atrial fib

A

structural remodelling of left atrium
Manifested by LA distention and hypertrophy as well as extensive diffuse fibrosis
LA enlargement increases atrial electrical path lengths and the distention also increases the probability of ectopic activation in the sleves in the base of the pulmonary veins where they enter the roof of the LA
The inflammation and fibrosis contribute to tortuous conduction and activation delays to facilitate unstable electrical activity
- regional varying of ANS remodelling, changing excitability of some regions of the atria
said changes markedly increase the probability of re entrant arrhythmia in atria, and in extreme cases lead to AF

18
Q

What treatments are possible for the atrial fibrillation

A

Rate control

  • Ca channel blocker
  • Beta-blocker
  • Digoxin

Rhythm control

  • amiodarone
  • sotalol- nonspecific beta blocker
  • dc conversion
  • ablation therapy
19
Q

What other drugs are important in Atrial Fib and why?

A

Anticoagulant - risk of stroke, thrombi from the left atria and left atrial appendage

Dabigatran > warfarin (less blood tests and interactions with other drugs and food)

20
Q

aortic stenosis risk factors

A

hypertension, smoking, smile sex, age, increased LDL, diabetes

21
Q

pathogenesis following aortic stenosis

A

LV must generate higher pressure to eject blood
Leads to development of LV hypertrophy (concentric) impaired diastolic function (HFpEF) over time this can progress to LV dilatation, wall thinning and systolic failure (HFrEF)

22
Q

Where would you expect to hear aortic stenosis and what characteristics?

A

systolic, ‘crescendo, decrescendo’ pattern. right parasternal edge 2nd ribspace, radiating to the neck bilaterally
Feel for a thrill in the sternal notch

23
Q

Explain lack of splitting of second heart sound

A

Aortic component of 2nd heart sound tends to become decreased and softer as the aortic stenosis becomes more severe.
This is a result of the increasing calcification of the valve preventing it from “snapping” shut, producing a sharp, loud sound.

24
Q

Aortic stenosis - ECG findings

A

left axis deviation

enlarged QRS complexes

25
Q

aortic stenosis, cause of mild chest discomfort during exercise?

A

Angina
Increased LV muscle mass, without soncomitatnt increase in vasculature, reduces coronary reserve
Increased HR and ventricular wall tension during exercise (demand) cannot be met but increased coronary perfusion (supply) because of aortic stenosis.
Coronary ostia are outside the aortic valve where pressure is low - increased flow rate here will also reduce pressure.

26
Q

Aortic stenosis - heart failure basis

A

Initially thick, stiffened ventricle, HFpEF
over time
wall thickens progressive ischaemia to tissue, chamber dilates and get HFrEF

27
Q

Speculate on long term treatment

A

balloon valvuloplasty just palliative procedure, valves still thick and calcified

Definitive treatment is aortic valve replacement
Decision on when to treat is based on severity:
- Primarily based on transaortic pressure gradient (using doppler US) and blood flow velocity across the aortic valve