Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

SA Cardiovascular system > S9) Heart Failure > Flashcards

S9) Heart Failure Flashcards

1
Q

What is heart failure?

A

Heart failure is a state in which the heart fails to maintain an adequate circulation for the needs of the body despite an adequate filling pressure

either due to an inibility of the heart muscle to contract properly or due to heart not being able to fill properly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Outline the aetiology (causes) of heart failure

A
  • Ischaemic Heart Disease - heart becomes stiff and doesnt contract properly
  • Hypertension
  • Dilated/hypertrophic Cardiomyopathy
  • Valvular/Congenital Heart Disease
  • Pericardial disease
  • Arrhythmias

= remodelling of cardiac muscles = changes ventricular size and shape = impair ventricular filling and ventricular ejection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the clinical signs of chronic heart failure?

A
  • Pulmonary congestion
  • Venous congestion
  • Dependent oedema
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the symptoms of chronic heart disease?

A
  • Dyspnoea (waking up suddenly gasping for breath)
  • Lethargy
  • Orthopnoea (breathlessness worse when they are lying flat)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Describe the clinical features of Class I heart failure

A

No symptomatic limitation of physical activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe the clinical features of Class II heart failure

A
  • Slight limitation of physical activity
  • Ordinary physical activity results in symptoms
  • No symptoms at rest
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe the clinical features of Class III heart failure

A
  • Marked limitation of physical activity
  • Less than ordinary physical activity results in symptoms
  • No symptoms at rest
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe the clinical features of Class IV heart failure

A
  • Inability to carry out any physical activity without symptoms
  • May have symptoms at rest
  • Discomfort increases with any degree of physical activity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are the factors affecting cardiac output?

A
  • Heart rate
  • Venous capacity (preload - how much the ventricles can expand)
  • Myocardial contractility
  • Arterial and peripheral impedance (afterload - how much ventricles contract)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is Starling’s Law of the Heart?

A

“The force developed in a muscle fibre depends on the degree to which the fibre is stretched.”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe the pathophysiology of Left Ventricular Systolic Dysfunction

A
  • Increased LV capacity
  • Reduced LV cardiac output
  • Thinning of the myocardial wall

I. Fibrosis and necrosis of myocardium

II. Activity of matrix proteinases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the causes of Left Ventricular Systolic Dysfunction?

A
  • Mitral valve incompetence or tricupid valve stenosis
  • Neuro-hormonal activation
  • Cardiac Arrhythmias
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Which structural heart changes occur after Left Ventricular Systolic Dysfunction?

A
  • Loss of muscle
  • Uncoordinated myocardial contraction
  • Changes to the ECM (increase in collagen)
  • Change of cellular structure and function (myocyte hypertrophy)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe ventricular remodeling after acute infarction

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe ventricular remodeling in diastolic and systolic heart failure

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Label the following images:

A

concentric hypertrophy - to do with dialation of the left ventricle wall

eccentric hypertrophy - dialtion of the lumen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Identify the 5 different pathways for neuro-hormonal activation

A
  • Sympathetic Nervous System
  • Renin-Angiotensin-Aldosterone System
  • Natriuretic Hormones
  • Anti-Diuretic Hormone
  • Endothelin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Why is SNS stimulated in heart failure?

A

Early compensatory mechanism to improve cardiac output:

  • Cardiac contractility
  • Arterial and venous vasoconstriction
  • Tachycardia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Outline the long-term deleterious effects of the SNS in heart failure

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

When is RAAS commonly activated in heart failure?

A
  • Reduced renal blood flow
  • SNS induction of renin from macula densa
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Outline the action of RAAS in heart failure

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

In terms of the brain, blood vessels, heart and kidney, explain how Angiotensin II plays a key role in organ damage

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

When are natriuretic peptides released in heart failure?

A
  • Atrial distension (atria remains in diastole and the valves wont open so their is a build up of blood)
  • Increased blood volume and pressure
24
Q

Outline the action of natriuretic peptides in heart failure

A
25
Q

Outline the effect of ADH (vasopressin) in heart failure

A

ADH is increased in heart failure:

  • Increased H2O retention
  • Tachycardia and increased TPR → increased CO
26
Q

Outline the action of endothelin in heart failure

A
  • Endothelin is secreted by vascular endothelial cells resulting in renal vasoconstriction via autocrine activity
  • Activates RAAS (increased levels in some patients with heart failure)
27
Q

Outline the effect of other chemicals in heart failure:

  • Prostaglandin E2 and I2
  • Nitric oxide
  • Bradykinin
A
  • Prostaglandins: vasodilators stimulated by NA and RAAS to counter their effects
  • Nitric oxide: potent vasodilator produced by endothelial cells via NO synthase (NO synthase may be blunted in HF)
  • Bradykinin: promotes natriuresis, vasodilatation and stimulates production of PGs
28
Q

What is oedema?

A
  • Oedema is the excessive volume of fluid within the tissues (interstitial / intracellular) which can occur due to changes in capillary dynamics
  • It is often seen in heart failure as there is increased capillary hydrostatic pressure
29
Q

Vascular endothelium increases in peripheral arterial resistance.
Why is this?

A
  • SNS
  • RAAS
  • Reduced NO
  • Increased endothelin
30
Q

Changes in vascular endothelium leads to skeletal muscle changes.

Identify some

A
  • Reduced skeletal muscle blood flow
  • Reduction in skeletal muscle mass (cachexia)
  • Abnormalities of structure and function
31
Q

Describe the renal effects associated with changes in the vascular endothelium

A
  • GFR (glomerular filtration rate) is maintained in early HF by haemodynamic changes at the glomerulus – increased Na+ /H2O retention due to neurohormonal activation
  • GFR falls in severe HF due to reduced renal blood flow leading to a subsequent rise in serum urea and creatinine
32
Q

Describe the multi-factorial aetiology of anaemia associated with vascular endothelium changes

A
  • Chronic inflammatory disease
  • Expanded plasma volume
  • Drug therapy (ACEi / Aspirin)
  • Iron malabsorption
  • Chronic renal failure
33
Q

Heart Failure with Preserved Ejection Fraction (HFpEF) occurs in almost 50% of heart failure patients.

Describe the clinical features of this condition

A
  • Frequently elderly and female
  • Often history of hypertension / diabetes / obesity
  • Normal LV function with concentric remodelling
34
Q

In four steps, describe the pathophysiology of HFpEF

A

⇒ Reduced LV compliance and impaired myocardial relaxation

⇒ Impaired diastolic LV filling (dependent on high LA pressure)

⇒ RV dysfunction results from high LA and PA pressure

⇒ Triggers neuro-hormonal activation as per systolic heart failure

35
Q

Identify the 5 clinical syndromes of heart failure

A
  • Left Sided Heart Failure
  • Right Sided Heart Failure
  • Congestive cardiac failure
  • LVSD (left ventricular systolic dysfunction - pump failure)
  • HFpEF (failure of LV relaxation)
36
Q

Identify the symptoms of Left Sided Heart Failure

A
  • Fatigue
  • Exertional dyspnoea (difficulty breathing)
  • Orthopnoea (breathlessness while lying down but relieved when standing or sitting)
  • Paroxysmal nocturnal dyspnoea (PND)
37
Q

What are the clinical signs of Left Sided Heart Failure?

A
  • Tachycardia
  • Cardiomegaly (displaced apex beat)
  • 3rd or 4th heart sound (‘Gallop rhythm’)
  • Functional murmur of mitral regurgitation
  • Basal pulmonary crackles (fluid in the lungs)
  • Peripheral oedema
38
Q

Describe the aetiology of Right Sided Heart Failure

A
  • Chronic lung disease
  • Pulmonary embolism / pulmonary hypertension
  • Pulmonary/tricuspid valvular disease
  • Left-to-right shunts (ASD/VSD)
  • Secondary to left heart failure (most frequent)
39
Q

What are the signs and symptoms of Right Heart Failure?

A
  • Fatigue
  • ↑ JVP
  • Pitting oedema (when the are is pressed and relieved the skin stays pitted for a while)
  • Ascites (build up of fluid in abdomen)
  • Pleural effusion (when there is a build up of fluid in abdomen)
  • Dyspnoea
40
Q

What is congestive (biventricular) heart failure?

A
  • Congestive heart failure is a chronic progressive condition in which the heart’s function as a pump is inadequate to meet the body’s needs
  • Both the right and left sides of the heart fail to pump adequately, hence, the signs and symptoms of both right and left heart failure develop
41
Q

timeline of an organ system failure

A

dips because they catch infections or something bad happens

42
Q

heart failure classification

A

1) no symptomatic limitation of physical activity
2) slight limitation of ordinary physical activity and symptoms
3) marked limitation of physical activity, less than ordinary physical activity - symptoms
4) cant carry out any physical activity without symptoms and have symptoms at rest, any movement = discomfort

43
Q

Investigations

A

does patient have heart failure?

history (breathlessness, ankle odema, sleeping upright in bed), clinical examination (elevation of JVP, 3rd heart sound, crepatations in the chest), investigation (mt probe vmp) differential diagnosis

What sort of heart failure do they have?

  • HFrEF
  • HFpEF
  • valvular/ structural heart failure
  • right ventricular failure
  • high output cardiac failure

whats causing the heart failure?

ischaemic heart disease

hypertension

viral

alochol

44
Q

managment

A

symptomatic treatment - Furosemide (makes you urinate more and is a venodialator, lower prelaod and heart doesnt struggle to push it out)

prognostic treatment - HFrEF only

  • cardiac rehabilitation
  • ACE/ARB
  • mineral corticoid receptor antagonist
  • sacubitril valsarta
  • ICD +/- biventricular pacemaker
45
Q

what do crepitations suggest

A

fluid in lungs

46
Q

blood tests to help classify heart failure

A
  • NTpro-BNP (natriuretic peptide) ANP and BNP - oppose neurohormonal effects, promote vasodialation and renin secretion
  • FBC - full blood count tells you if they are anemic
  • U+Es - urea and electrolytes so tests kidney function
  • LFTs - liver function test (may be elevated)
  • clotting - anticoagulation
  • thyroid function, vit D level, CRP
47
Q

light and dark side of heart failure

A

left = dark (the body doesnt understand that the heart is weak so it makes it work harder to try and get more blood arounf the body)

right = light (but only occurs when the heart is severely weak) damps down sympathetic nervous system and drains out some fluid

48
Q

common prognostic treatments to learn for OSCE

A
  • ACE inhibitor and ARB (angiotensin 2 receptor blockers)
  • Beta blockers - reduce contractility
  • mineralcorticoid receptor antagonist - aldosterone antagonist so reduces sympathetic system
  • biventricular ICD - pacemaker in right ventricle
49
Q

what is ejection fraction

A

stroke vol

end diastolic volume (amount of blood just before systole)

normally between 50-70%

a normal value still might mean thet have heart failure because ventricle may be fine at contracting there is just reduced filling as the ventricle is stiff, so diastolic vol is reduced

50
Q

compare HFrEF and HFpEF → classification

A
  • HFrEF - heart failure with reduced ejection fraction
  • HFpEF - heart failure with preserved ejection fraction

problems with both

  • HFrEF - contractility problem (not enough force) but there is enough space
  • HFpEF - not a contractility problem but less filling due to stiff ventricle walls (preload is reduced slightly as there is less space)

value on echocardiogram for ejection fraction

  • HFrEF - <40%
  • HFpEF - >50%

symptoms

  • dyspnoea
  • fatigue
  • oedema (pulmonary or peripheral)
51
Q

which side of the ventricle is commonly effected

A

left = pulmonary odema

but sometimes it can be so bad that

52
Q

rough pathophysiology of heart failure

A

B1 → tachycardia

A1 → renin

53
Q

what are some lifestyle factors to reduce heart failure

A

reduce salt intake and liquid intake

54
Q

how do ACEi and ARBS treat hypertension and heart failure?

what are some adverse effects

A
  • it inhibits vasoconstriction and aldosterone, so there is reduced resistance on blood vessels and a lower volume
  • dry cough, angioedema (bradykinin increases vascular permeability, if it can’t be broken down then permeability increases), hypotension, renal impairment
  • people to avoid: people who already have angioedema
55
Q

what are sacubitril/valsartan

A
  • neprilysin inhibitor
  • neprilysin breaks down natriuretic peptides
  • natriuretic peptides → cause natriuresis (Na out into urine)
  • so if we inhibit the breakdown then the peptides have a longer lasting effect and then more Na out and more urination and so helps reduce heart workload

SA Cardiovascular system (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions