Heart intrusions Flashcards

1
Q

Left heart failure

A

• Failure in the left side of the heart reduces cardiac output – the ventricle is not contracting as well as it should and therefore stroke volume and cardiac output is reduced • This leads to activity intolerance & signs of decreased tissue perfusion (paleness and organ impairment)

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2
Q

Tissue perfusion:

A

The volume of blood that flows through a unit quantity of the tissue
• They may also suffer from pulmonary congestion (fluid in the lungs)

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3
Q

Pulmonary edema:

A

fluid in the alveoli causes problems with breathing lying down,paroxysmia (breathlessness) and coughing up frothy sputum

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4
Q

Impaired gas exchange:

A

can causes cyanosis (skin or lips turn blue) and hypoxia (low oxygen levels in the blood)

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5
Q

Right heart failure, Congestion in peripheral tissues

A

can cause problems with the liver, GI tract and edema & ascites (build up of fluid in the abdomen)

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6
Q

Pulmonary congestion

A

breathlessness was one of the main signs and symptoms of left sided heart failure
• It tends to occur when end diastolic volume increases towards the upper limits of whats possible

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7
Q

Why?- Ejection fraction and consequences of reduced ejection fraction in a failing heart

A

more blood returns and the left ventricle fills up even more and starts to stretch – this causes pressure buildup
• This pressure buildup forces the blood back into the left atrium
• The increase in pressure in the left atrium feeds back up the pulmonary vein to the venous end of the capillaries in the lungs
• The venous end of the capillaries are seeing a much higher hydrostatic pressure (blood pressure) than normal

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8
Q

The way in which fluids

A

ases and nutrients can pass out of the cardiovascular system is through capillaries into tissues
• This movement of fluid is driven by differences in the hydrostatic pressure (blood pressure) and the osmotic pressure (pressure exerted by proteins in the blood that hold onto the fluid and try to stop it leaving the capillary)
• Whereas hydrostatic pressure forces fluid out of the capillary, osmotic pressure draws fluid back in
• At the arterial end, hydrostatic pressure is greater than osmotic pressure and therefore fluid gets pushed out of the capillary into the intracellular space to take the oxygen and nutrients to the cells
• In the middle of the capillary, the osmotic pressure is the same but the hydrostatic pressure has decreased – no net movement of fluid
• At the venous end, hydrostatic pressure is lower than osmotic pressure therefore fluid is drawn back into the capillary

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9
Q

Capillary exchange

A

In the case of a patient with heart failure, we said that there was an increase in hydrostatic pressure (blood pressure) at the venous end of the capillary due to this backlog of blood
• If hydrostatic pressure is increased at the venous end of the capillary, then less fluid is going to be reabsorbed
• That fluid that remains in the intracellular space and eventually gets into the alveoli is what causes the pulmonary congestion, impaired gaseous exchange and shortness of breath

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10
Q

In a patient with heart failure, what is the mechanism by which fluid appears in the lungs?

A

Signs and symptoms of left sided failure
• The patient has pitting edema up to the calves – fluid that is sitting in the intracellular space
• As he lies down, some of that fluid (due to changes in pressure by lying down) will move back into his cardiovascular system
• This will increase blood volume, which will increase venous return
• If we increase venous return, the additional blood that is returning to the heart will cause an increase in pressure in the left ventricle, the left atrium, the pulmonary veins and the capillaries of the lungs
• This will drive fluid into the lungs
• Coupled with that, if we’re lying down, our cardiovascular doesn’t have to work against gravity to return blood to the heart
• So just the art of lying down is going to increase venous return, which is going to increase pressure in the left side of the heart which once again will eventually cause fluid to move out into the lungs
• An easy way around this problem (breathlessness while lying down) is to not lie down lol • The level of severity of a patients heart failure can sometimes be “measured” by how many pillows they need to be propped up a sufficient amount to get a good nights sleep
• Mr Holmbush therefore sleeps sitting up
• Crackles: bubbling sound that the lungs make when you inhale because there is fluid in the lungs
• Cardiomegaly: enlarged heart

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11
Q

Signs and symptoms of right sided failure

A
  • If the right side of the heart has failed, then blood returning to the right side will pool in the right ventricle
  • More blood returns = increase in pressure in the right ventricle = increase in pressure in the right atrium
  • This increases pressure in the vena cava
  • Due to the build up of pressure, there is a build up of pressure in the abdomen and that can cause ascites
  • It can also cause a build up of the capillaries in the periphery and cause pitting oedema (see picture)
  • Raised jugular venous pulse due to elevated pressures in the right atrium, causing the pulse of the jugular vein to appear higher up than the jugular vein
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12
Q

Why do the conditions listed in the patients PMH contribute to heart failure?
-Causes of heart failure in order from most likely to least likely

A

Acute MI and associated cardiovascular risk factors (obesity, diabetes, cigarette smoking) – heart attack damages muscle fibres in the left ventricle of the heart and therefore the heart cant work as well
• Hypertension – heart is having to work much harder to pump the blood and over time that increase in work is going to increase the size of the muscle fibres in the heart (kinda like going to the gym). When these muscle cells become larger, the volume of the ventricular chamber gets reduced and therefore cardiac output decreases. In addition, although the muscle cells are now bigger, they are less efficient
• Valve disease – Aortic valve stenosis occurs when the heart’s aortic valve narrows. The valve doesn’t open fully, which reduces or blocks blood flow from your heart into the body. This causes the heart to work much harder, which will once again increase muscle size etc. Mitral valve regurgitation (leaky valve) is when your heart’s mitral valve doesn’t close tightly, allowing blood to flow backward into the atria, therefore cardiac output is impaired and the heart will have to work harder, which will once again increase muscle size etc.
• Cardiomyopathies – genetic conditions that can lead to changes in the ability of the muscle cells to contract
• Toxins (alcohol, cytotoxics; doxorubicin) – can damage heart muscle cells
• Viruses/bacteria (e.g. viral myocarditis HIV and SLE; systemic lupus erythematosus)
• Arrhythmias (AF) – heart is working harder than normal

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13
Q

Right-sided failure:

A

Chronic pulmonary problems – anything that causes pulmonary hypertension, people can get these by COPD or lung cancer etc.
• Gaseous exchange gets impaired in part of the lung
• If a piece of tissue is not receiving enough oxygen, the blood vessels constrict so the blood supply to that damaged area is reduced
• The blood going to the lungs is then redistributed to part of the lungs that are healthy • But since part of the lung now doesn’t receive any blood, you’ve increased blood pressure in the lungs, which can lead to damage in the right side of the heart

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14
Q

Diagnosis

A
  • Signs and Symptoms
  • 2D Doppler Echocardiography to monitor the amount of blood that is pumped out of the ventricles per beat (Ejection fraction <35%)
  • Raised JVP
  • Brain natriuretic peptide (BNP) levels >100 pg/mL suggest heart failure. Levels >400pg/ mL poor prognosis. The higher the value, the poorer the prognosis. (Hormone secreted by cardiomyocytes in the heart ventricles in response to stretching caused by increased ventricular blood volume)
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15
Q

Use of BNP to diagnose heart failure

A
  • Can measure brain natriuretic peptide (BNP) or NT pro-BNP in the heart
  • Both released when the heart muscle cells become abnormally stretched
  • Increasing end diastolic volume will stretch the ventricles, and when it does BNP and ANP are released
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16
Q

BNP vs ANP (atrial natriuretic peptides)

A
  • These peptides reduce renin secretion, which decreases the production of angiotensin and aldosterone
  • Reduction of these causes loss of salt and water, reducing blood volume
  • Reduced blood volume decreases venous return and end diastolic volume and blood pressure as a result
  • These peptides also have some direct vasodilatory actions which will also decrease blood pressure
  • Measured using an immunoassay, primarily BNP because it has a longer half life
17
Q

Summary

A
  • Heart failure is a serious condition which if not treated can lead to death.
  • Main causes Left-sided failure MI; right sided failure pulmonary hypertension • Symptoms: oedema, fatigue, breathlessness.
  • Diagnosis, history, 2D doppler echo., raised JVP, BNP levels.
18
Q

Pharmacology of drugs used to treat heart failure

A

• Cardiac output is decreased, which results in a decrease
in blood flow in the aorta
• This activates the sympathetic nervous system – activated
by baroreceptors, which signal the medulla
• In order to try and increase cardiac output, noradrenaline will
work on beta 1 receptors in the heart to increase the frequency
and force of contraction
• This increases cardiac output
• Noradrenaline also constricts arteries by acting on alpha 1 receptors
• This causes total peripheral resistance to go up, which causes blood pressure to go up, this once again causes the heart to work harder
• Noradrenaline also constricts veins, more blood comes back into the heart and the heart has to work harder again to pump this extra blood out
• Remember: blood pressure = cardiac output x peripheral resistance

19
Q

Angiontensin II

A

constricts arteries and veins, which increases blood pressure, which increases cardiac output – heart has to work harder

20
Q

Aldosterone

A

causes salt and water retention, which increases blood volume, which increases blood returning to the heart – heart has to work harder

21
Q

natriuretic peptides

A

When the walls of the ventricles stretch, it releases natriuretic peptides in the heart (BNP and ANP)

22
Q

dilate arteries and veins

A

These peptides dilate arteries and veins and cause salt and water excretion (they work against the changes that have been caused by the sympathetic and renin angiotension system) – these peptides try to protect your heart
• The higher the natriuretic peptides, the worse the heart failure

23
Q

fibrosis

A

Connective tissue builds up in the heart muscle

24
Q

cardiomyocyte hypertrophy

A

Heart muscle get bigger, which decreases ventricle size

25
Q

Problems with prolonged compensation

A
  • Starlings law (overstretch leads to loss of function) – that’s why the line trails off at the end, because the heart muscle cells are too damaged
  • Desensitisation of beta receptors – due to constant exposure of the receptors to the noradrenaline of the sympathetic system, the receptors will be removed
  • Increased angoiotensin secretion leads to increased afterload can drive remodelling of the heart.
  • Abnormally high levels of NA/A causes increases in heart rate (catecholamines) leads to arrhythmias
26
Q

Myocardial hypertrophy

A

– Make heart stiffer
– Muscle growth can decrease chamber size
– Muscle growth can occur faster than blood vessel supply