Unit 12 Week 4 Flashcards

1
Q

Pitting oedema

A

Excessive interstitial fluid in which when pressure is applied leaves an indentation

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2
Q

Common causes of pitting oedema

A

Heart valve issues

Low protein levels

DVT

Congestive heart failure

Venous insufficiency

Infections

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3
Q

How does HF lead to pitting oedema

A

In heart failure with low CO state, kidneys are sensitive to changes in BP so macula densa cells of the juxtaglomerular apparatus detect a fall in BP, releases renin, renin leads to angiotensinogen –> ANG1 –> ANG2 via ACE. increases BP

Sodium is reabsorbed via various transporters in the nephron

As pressure builds up in the central venous system, ECF is forced out into the legs, abdomen, ankles and feet

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4
Q

How does a raised JVP relate to HF?

A

Jugular venous pressure provides an indirect measure for central venous pressure.

Low output HF leads to a reductio in the volume of blood ejected with each beat, leading to a rise in central venous pressure. This blood backs up into the vena cava, raising the pressure in the jugular vein subsequently.

Has a biphasic wavefront pattern

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5
Q

How does HF cause hepatomegaly?

A

Increased central venous pressure in the IVC leads to blood backing up into the hepatic veins, causing the liver to become congested and grow larger.

This is sometimes tender upon examination.

In severe cases might cause jaundice or ascites.

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6
Q

What is a gallop rhythm?

A

A third heart sound that occurs in HF- 3rd heart soundsoccur in early ventricular filling and represent the tensing of the chordae tendinae and atrioventricular ring.

Results in increased atrial pressure –> ↑ flow rates and large amounts of blood striking the compliant lect ventricle –> therefore often associated with ventricular dilation

Produces a sound like a galloping horse.

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7
Q

Symptoms of HF

A

Dyspnoea + orthopnoea (worse when lying down)

Fatigue

Fluid retention- peripheral oedema –> ascites

Nocturnal cough or wheeze

Light headedness or syncope

Anorexia

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8
Q

Signs of HF

A

Displaced apex or RV heave

Narrow pulse pressure

Raised JVP

Gallop rhythm

Inspiratory crackles

Tachypnoea

Pleural effusions

Cyanosed

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9
Q

Definition of heart failure

A

– complex clinical syndrome where the heart is incapable of maintaining a cardiac output that is adequate to meet metabolic requirements and accommodate venous return

It is the common end stage of many forms of chronic heart disease, developing from the cumulative effects of chronic cardiac work overload (e.g. valve disease or hypertension), or ischemic heart disease (e.g. following myocardial infarction)

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10
Q

Which acute haemodynamic stressors can precede HF

A

Fluid overload

Abrupt valvular dysfunction

Myocardial infarction

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11
Q

Symptoms of left ventricular heart failure

A
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12
Q

Symptoms of right sided heart failure

A

peripheral and abdominal fluid accumulation

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13
Q

Systolic HF

A

Heart is not able to eject enough blood in systole

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14
Q

Diastolic HF

A

Chambers aren’t filling sufficiently so therfore reduced preload and↓ contractility (frank-starling mechanism)

Stroke volume is too low - ejection fraction is preserved

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15
Q

Frank-starling mechanism

A

ability of the heart to change its force of contraction and therefore stroke volume in response to changes in venous return

“strength of the heart’s systolic contraction is directly proportional to its diastolic expansion, with the result that under normal physiological conditions the heart pumps out of the right atrium all the blood returned to it without letting any back up in the veins”

A higher preload sufficiently stretches the walls of the ventricles meaning that there is more overlapping actin and myosin filaments. Therefore, more cross bridges can form and there is greater contractility.

If the walls are stretched too far- less overlapping filaments and therefore less contractility.

Means that CO=VR

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16
Q

Left sided heart failure

A

Usually due to systolic dysfunction

CO from the left ventricle does not match VR from pulmonary vein

Therefore blood backs up in the pulmonary circulation.

Can cause RSHF via cor pulmonale

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17
Q

Cause of LSHF: ischaemic heart disease

A

Artherosclerosis leads to emboli in coronary artery (most commonly LAD). Occludes artery and no perfusion to downstream cardiac tissue. Ischaemia that leaves a scar on the myocardium.

MI causes myocardial stunning, myocyte necrosis, decompensation of existing HF, restructuring of heart walls (thinning?) and acute mitral regurgitation due to papillary muscle dysfunction

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18
Q

Causes of left sided heart failure

A

Ischaemic heart disease (MI to myocardium of left V)

Long-standing hypertension

Dilated cardiomyopathy

Diastolic filling dysfunction

Restrictive cardiomyopathies

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19
Q

Cause of RSHF: Chronic hypertension

A

As arterial pressure in the systemic circulation increases it increases afterload.

To compensate left v hypertrophies so it can contract with more force.

This increase in muscle mass also means that there is a greater demand for oxygen.

Extra muscle also squeezes down on the coronary arteries, meaning that even less blood is delivered to the myocardium.

Ultimate result is that the myocardium has weaker contractions.

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20
Q

Dilated cardiomyopathy as a cause of LSHF

A

In hypertension, myocardium undergoes concentric hypertrophy

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21
Q

concentric hypertrophy

A

new sarcomeres are generated in parallel with the old ones

As the ventricular wall enlarges, it therefore crowds into the ventricular chamber space, leaving less room for filling.

can also be caused by aortic stenosis (narrowing of the aortic lumen) and by hypertrophic cardiomyopathy (abnormal ventricular wall thickening often from a genetic cause).

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22
Q

Cause of LSHF: restrictive cardiomyopathies

A

Myocardium becomes stioffer and less compliant and therefore, can’t easily stretch and fill.

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23
Q

Role of RAAS in symptoms

A

With a lower CO, detected renal baroreceptors and activates the RAAS

Causes a gretaer BV –> more pressure in vessels –> water forced out into peripheral tissues

Ultimately causes increased fluid retention via sodium retention

Compensatory sytem as increased BV –> increased filling and preload –> increased contractility

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24
Q

Signs of LSHF

A

Inability to pump blood means it backs up into the pulmonary circulation via the pulmonary vein. Increased P over cap beds and pul artery.

Water forced out of caps into pulmonary interstitium and alveoli making gas exchange slower –> blood not as high oxygen content –> detected in brain –> tachypnoea

Fluid is heard as crackles and pops

Enough fluid can rupture these caps and bleed into alveoli

25
Q

Treatment for left sided heart failure

A

Medications to increase blood flow

e.g. ACE inhibitors to heklp dilate blood vessels

Diuretics reduce fluid build up

Prevent hypertension from making hF worse

26
Q

Right sided heart failure

A

Often caused by left sided HF (biventricular HF)

Increased pulmonary BP makes it harder for the RSH to pump.

27
Q

Causes of right sided heart failure

A

left sided heart failure

Left to right cardiac shunt (isolated RSHF)

Chronic lung disease (isolated RSHF)

28
Q

Cause of isolated RSHF: left to right cardiac shunt

A

May be an atrial or ventricular defect allowing blood to flow from the higher pressure left side to the lower pressure right side

This ↑ volume on the right side of the heart, leads to concentric hypertrophy

Makes it more prone to ischaemia, a systolic dysfunction

and also a smaller volume, a diastolic function

29
Q

Cause of RSHF: chronic lung disease

A

Makes it hard to exchange oxygen. In response to hypoxia, the pulmonary arterioles constrict, increasing pulmonary BP and causing hypertrophy and heart failure—– this is COR PULMONALE

30
Q

Right sided congestion

A

Jugular venous distension

Hepatosplenomegaly- painful

Liver congestion can cause cirrhosis

Exces fluid near organ surface–> peritoneal space–> ascites

Leg –> oedema

Sacrum –> oedema

31
Q

3 determinants of stroke volume

A

myocardial contraction

preload

afterload

Frank-starling mechanism and laplace law influence these factors

32
Q

laplace law

A

pressure insde an inflated elastic container with a curved face (e.g., blood vessel or chamber) is inversely proportional to the radius

33
Q

Wall stress

A

(cavity pressure x radius) / (2 x wall thickness)

increase to ventricular wall stress and therefore increased oxygen demand:

increased LV pressure

increased LV radius

increased LV wall thickness

myocardial infarction

34
Q

Causes of HF general

A

Corronary heart disease

hypertension

valvular heart disease

obesity

high output states (e.g., thyrotoxicosis)

Volume overload (end stage chornic kidney disease)

obesity

drugs (e.g., cocoaine, alcohol)

35
Q

Stages of heart failure

A

by fucntional limitation

class 1- No limitation. Normal physical exercise does not cause fatigue, dyspnea or palpitations.

class 2- Mild limitation. Comfortable at rest but normal physical activity produces fatigue, dyspnoea or palpitations.

class 3- marked limitation. comfortable at rest but gentle physical acitivity produces marked symptoms of heart failure

class 4- Symptoms of HF occur at rest and are exacerbated by any physical activity.

36
Q

Types of heart failure

biventricular

congestive

left sided

HF w reduced ejection fraction

HR w preserved ejection fraction

HPmrEF - mid range

Right sided

cor-pulmonale

low output

high output

valvular

arrhythmic

acute

A
37
Q

Arrhytmic HF

A

Prolonged period od your heart pumping ineffectively die to bradycardia or tachycardia (like atrial fibrillation) can lead to heart failure.

38
Q

valvular heart failure

A

one or more of valves in your heart doesn’t work properly (don’t open or close properly). This can cause the blood flow through your heart to your body to be disrupted.

39
Q

High output HF

A

normally functioning heart can’t keep up with an unusually high demand for blood to one or more organs in the body. The heart may be working well otherwise, but it cannot pump out enough blood to keep up with this extra need. o High output

40
Q

Low output HF

A

decreased CO accompanied by end organ hypoperfusion.

41
Q

o Heart failure with reduced ejection fraction (HFrEF)

A

also called systolic failure when LV loses ability to contract normally. Heart cant pump with enough force to push enough blood into circulation.

42
Q

Heart failure with preserved ejection fraction

A

also called diastolic failure = LV loses its ability to relax normally (because muscle become stiff). Heart cant properly fill with blood during resting period between each beat.

43
Q

Link between atrial fibrillation + tachycardia to heart failure

A

Risk factor for HR, stroke and sudden MI

Improper filling of atria means that ventricles don’t fill properly and therefore CO drops transiently.

44
Q
A
45
Q

Cardiac remodelling

A

1) pathopysiological stimuli (e.g. cardiac injury, neurohormonal stim.)
2) Remodelling pathways
a) CMs loss- autophagy, necrosis, apoptosis
b) CMs hypertrophy- Ca2+ influx stimulates hypertrophic response
c) myocardial fibrosis- MIs cause release of DAMPS that bond to PRR’s that cause fibrosis
3) Cardiac remodelling- changes in geometry of the ventricles from eliptical to spherical

46
Q

Neurohormonal response to heart failure

A

SNS

RAAS

ADH

Endothelin system

natriuretic peptides

47
Q

Role of SNS in heart failure

A

Activated in HF via low and high-pressure baroreceptors

Provides inotropic support and maintains cardiac ouput

chronic activation is harmful

activates RAAS–> increased venous and arterial tone, reabsorption of salt and increasing noradrenaline concs

gradual desensitisation to catecholamines

48
Q

Role of RAAS in heart failure

A

Ang II is a vasoconstrictor and stimulates the release of noradrenaline from sympathetic nerve terminals and inhibits vagal tone (therefore increasing HR)

leads to sodium and therefore water retention and increased potassium excretion

Aldosterone, ang II and SNSN are potent stimulants for myocardial hypertrophy and fibrosis as well as vascular remodelling

49
Q

ADH levels are increased in severe chronic HF

HF = paradoxical increase in ADH

contributes to the enhanced renal retention of fluid

A
50
Q

Endothelin system

A

endothelin is secreted by vascular endothelial cells and is a potent vasoconstrictor peptide, especially on renal vasculature so promotes retention of sodium

51
Q
A
52
Q

Natriuretic peptides

A

3 of them and they lead to the excretion of sodium in urine:

Atrial NP- released from atria, responds to stretch –> natriuresis and vasodilation

Brain NP- released from the ventricles

C-tyoe NP- limited to vascular endothelium and CNS- limited effects on. natriuresis

ANP ans BNP both increase in response to volume expansion and pressure overload of the heart and act as antagonists to the effects of ANG II on vascular tone, aldosterone secretion and renal-tubule reabsorption

As HF progresses, NPs fail to compensate

53
Q

Digestive link to HF

A

Splanchnic circulation receives nearly 25% of CO

High SNS concentration

Even small reductions in splanchnic perfusion leads to intestinal iscahemia

54
Q

BNP

A

nowadays measure the NT-proBNP

increases GFR- filtered laod of sodium and water via dilatinf afferent and constricting efferent

Decreases sodium reabsorption

inhibits renin secretion

promotes urination

inhibits effects of catecholamines

55
Q

Basal crepitations

A

Crepitous sounds caused by excess fluid in the airaways having a bubbling/ crackling sound

can either be exudate or infection

56
Q

Cardiothoracic ratio

A

Allows you to confirm cardiomegaly (enlargement of the heart) on CXR.

CT ratio: A=B/C

Possible causes of a ratio greater than 50% include:

cardiac failure

pericardial effusion

left or right ventricular hypertrophy

57
Q

A doctor might use echocardiograms in HF to find out:

A

The size of your heart. An enlarged heart might be the result of high blood pressure, leaky heart valves, or heart failure. Echo also can detect increased thickness of the ventricles. Increased thickness may be due to high blood pressure, heart valve disease, or congenital heart defects.

  • Heart muscles that are weak and aren’t pumping well. Damage from a heart attack may cause weak areas of heart muscle. Weakening also might mean that the area isn’t getting enough blood supply, a sign of coronary heart disease.
  • Heart valve problems, can show whether any of your heart valves aren’t operating normally (regurgitation ect)
  • Problems with your heart’s structure. Echo can detect congenital heart defects, such as holes in the heart.
  • Blood clots or tumors.
58
Q

Heart failure clinics

A

Aims to reduce symptom trouble

each patient has their own plan

often works with heart failure specialist nurses

patient education

pathway to get involved in research