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Cardiovascular Health > Patho & Treatment - Chronic Heart Failure > Flashcards

Patho & Treatment - Chronic Heart Failure Flashcards

1
Q

Define chronic heart failure

A

An inability of the heart to pump sufficient blood to meet the metabolic demands of the tissues
It is a defect of filling or of emptying

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2
Q

Outline the 2 different type of heart failure

A

Heart failure may be acute or chronic. Acute heart failure may occur in significant haemorrhage where a lack of blood in the vascular system prevents the heart from adequately providing blood to tissues. Another example of acute heart failure might be secondary to septicaemia where toxins plus the inflammatory response to them result in significant capillary permeability shifting fluids from the vascular spaces into the interstitial spaces

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3
Q

What does diastolic heart failure cause?

A

Failing to fill and ejection fraction is preserved

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4
Q

What does systolic heart failure cause?

A

Failing to empty and EJ is reduced

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5
Q

What is ejection fraction (EF)?

A

Each ventricle ejects 70mls (SV)
Volume of blood ejected per ventricle per contraction as a % of available blood (i.e. EDVV) e.g. 70/120ml = ~ 68%
Normal EDVV = 120mls
Its a measure of ventricular pumping efficiency

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6
Q

How is EF measured?

A

Echocardiogram

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7
Q

What is a normal, moderate and poor ventricular function in terms of ejection fraction?
What EF is indicative of heart failure?

A

normal: > 50 - 70%
moderate: 40 - 49%
poor: < 40% (indicative of heart failure)

Low EF and symptoms can mean heart failure.
EF can be normal and CO be low and the patient still has heart failure i.e. heart failure preserved ejection fraction (HFpEF)

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8
Q

What causes heart failure preserved ejection fraction (HFpEF)?

A

Fibrosis and hypertrophy which limit compliance and end diastolic ventricular volume (EDVV) - heart will need higher than normal filling pressures so the ventricles can adequately fill. If it cannot achieve higher filling pressures then EDVV will be reduced.
Cardiac output is low in HFpEF as filling is poor

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9
Q

What is heart failure reduced ejection fraction (HFrEF)?

A

Usually occurs after a heart attack

  1. Myocardial remodelling post-AMI ventricular dilation – enlarged low mm mass ventricles
  2. Post-AMI – loss of myocardial contractile mass

• Filling not a problem so EDVV is preserved.
• Contraction limited (due to loss of myocardial muscle mass) - a reduced SV
So (SV (ejection)) / (a relatively low % of EDV (filling)) = (reduced EF)
• Due to poor force production - despite reasonable filling CO is low.

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10
Q

What is another name for systolic heart failure and what is the main cause of it?

A

Reduced ejection fraction heart failure due to impaired contractility
Most common type of HF

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11
Q

What is another name for diastolic heart failure and what is the main cause of it?

A

Preserved ejection fraction heart failure due to fibrosis, stiff, non-complaint ventricular walls

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12
Q

What happens to blood pressure in chronic heart failure?

A

BP = CO x TPR
In chronic heart failure BP will fall but the body compensates with a neuro-endocrine responses but in the long term this mechanism fails and organs eventually fail

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13
Q

How would you know if a patient is in heart failure?

A

A patient is in chronic heart failure if;

  1. CO is low regardless of EF
  2. They are symptomatic

Use the New York Heart Association (NYHA) Classification of Heart Failure Severity
- Has 4 classes of HF from asymptomatic to severe

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14
Q

Explain how volume over-load causes chronic heart failure (CHF).

A
  1. Thyrotoxicosis = hyperactivity of the thyroid gland meaning there is too much thyroid hormone in the body, it causes expansion of blood volume leading to CHF
  2. Mitral (bicuspid) valve incompetence (i.e. regurgitation (exists between left atria and ventricle (closes at beginning of ventricular systole & is supposed to stay closed until ejection has occurred) - when there is a build up of pressure there is when l. ventricle contracts it causes build up of blood in l.atria
  3. Renal failure - fluid retention
  4. Paget’s disease - the hyper-growth of bone which causes the growth of new blood vessels to help supple the excess bone
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15
Q

What are the 3 main causes of CHF?

A
  1. Volume overload
  2. Pressure overload
  3. Disorders of myocardial function
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16
Q

Explain how pressure over-load causes chronic heart failure (CHF).

A

Disorders which increase resistance to ventricular outflow i.e. ventricles work consistently harder than normal

LV: - e.g. systemic HTN,
aortic valve stenosis (narrowing) due to fibrosis and calcification of the valves - higher forces needed to be generated by the left ventricle to push blood out through these narrowed valves

RV: e.g. pulmonary HTN, pulmonary valve stenosis

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17
Q

Explain how disorders of myocardial function cause chronic heart failure (CHF).

A
  1. diminished contractility e.g. post AMI
    • loss of contractile tissue
    • paradoxical scar tissue movement
  2. a type of cardiomyopathy
    • dilated cardiomyopathy - most common type of cardiomyopathy -ventricles are enlarged - sarcomeres a have abnormal length-tension relationship
    • restrictive cardiomyopathy - stiff and non-compliant walls but no hypertrophy i.e. storage diseases like a defective enzyme which means a nutrient cannot be fully broken down
    • hypertrophic obstructive cardiomyopathy (HOCM) - genetically inherited
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18
Q

Define systemic hypoperfusion

A

Inadequate cardiac output

19
Q

Define pulmonary hyperperfusion

A

cardiogenic pulmonary oedema

20
Q

What is LVF?

What are the signs/symptoms of hyper-perfusion in left ventricular failure (LVF)?

A

Preceding system is hyperperfused (lung) and the succeeding system is hypoperfused (the systemic circulation)

  • gas exchange
  • dyspnoea (the sensation of SOB)
  • Orthopnoea (inability to lie flat - there is redistribution of blood if they lie flat there will be an overload in the heart and blood will backlog into the lungs)
  • paroxysmal nocturnal dyspnoea (waking up during the night with anxiety and breathlessness)
  • pulmonary crackles upon auscultation (which indicate pulmonary oedema)
  • pulmonary oedema at the alveoli and bronchioles
  • pleural effusions
  • Coughing
  • Wheezy
21
Q

What is LVF?

What are the signs/symptoms of hypo-perfusion in left ventricular failure (LVF)?

A

The preceding system is overloaded (the lungs) and the succeeding system is underloaded (systemic circulation)

Fatigue and reduced exercise tolerance

Dyspnoea - SOB driven by congestion of pulmonary circulation, skeletal muscles are inadequately perfused so they go into anaerobic metabolism quickly - blood becomes acidic (H+ ions & lactate) quickly which is detected by peripheral chemoreceptors and they signals go to respiratory centres in the medulla which increases respiratory rate in the lungs. Type 2 (glycolytic) skeletal muscle fibres will be used instead of type 1 (aerobic) skeletal muscle fibres

Confusion - reduced cerebral perfusion

22
Q

What would be seen in a chest x-ray in chronic heart failure?

A

Cardiomegaly - expansion of the heart to take up 60-75% instead of 50% of the available thoracic dimensions, enlargement of LV in LVF which can cause basal collapse of LLL (left lower lobe) which can cause dyspnea, in RVF the RV will be enlarged

Pulmonary oedema

Pulmonary effusions

23
Q

What is RVF?

A

Congestion of the preceding system (systemic circulation) and hypo-perfusion of the succeeding system (lungs)

24
Q

What are the clinical signs of RVF?

A

Systemic venous congestion
• systemic oedema - in the feet
• hepatomegaly - (megaly = enlargement) (hepat = liver)
• Ascites - increased fluid between abdominal structures
• Nocturia - passing a lot of urine at night
• Pleural effusions

Pulmonary hypoperfusion (severe cases)
• dyspnoea - exercise intolerance - fatigue
25
Q

What compensatory mechanism occur in response to heart failure?

A
  1. neuro-endocrine responses - help maintain BP, CO and TPR (blood volume)
  2. Ventricular hypertrophy & remodelling
26
Q

Describe the neuro-endocrine response

A
  1. Sympathetic nervous system activation
    CO, TPR (via constriction of arterioles) and BP are all increased
    Venoconstriction of vein which increases VR which increases stroke volume
2. RAAS (renin-angiotensin-aldosterone system) - increases blood volume
angiotensin 2 (a vasoconstrictor of arterioles) -> increases TPR and BP
angiotensin 2 promotes the release of aldosterone and ADH (which both act on kidney to preserve water increasing blood volume)
  1. Naturetic peptide (secretions by RA cardiomyocytes)
27
Q

What are the negative consequences of a prolonged neuro-endocrine response?

A

Pre-load is continuously increased (due to increased circulatory volume (caused by RAAS) and increase venoconstriction (caused by sympathetics)

  • This places increased demand on the heart causing increased congestion in the preceding systems & hypoperfusion on the succeeding systems

SNS and angiotensin 2 act on arterioles by causing them to constrict. This increases TPR which increases afterload which decreases SV and CO
(left ventricle has to work harder to eject blood into the systemic circulation via the aorta)

Sustained high SNS activity decreases SNS receptor sensitivity which overall decreases contractility and CO

28
Q

What are is the normal response to the heart when it is placed under physiological pressure?

A
  1. Dilation of ventricular chambers -> larger SV at lower HRs & larger COs on exercise
  2. Hypertrophy -> larger ventricular mm mass - larger SV at lower HRs & larger COs on exercise
29
Q

What are the pathophysiological changes that occur in the body response to cardiac heart failure?

A

Sustained angiotensin II & aldosterone

Activation of macrophages -> cytokine release & activation of fibroblasts

Dysregulated /uncontrolled cardiac remodelling (which occurs in a non-uniform pattern within the myocardium). It causes death of myocytes, distruption of structural and contractile proteins, inflammatory mediators disturb Ca2+ homeostasis

30
Q

What are the ventricular remodelling changes that occur in heart failure?

A
  1. Excessive & irregular hypertrophy -> small chambers
  2. Failure of myocardial vasculature to proportionally proliferate
  3. Increased fibrosis -> stiff chambers & electrical challenges. Chambers fail to relax during diastole
  4. Fibre elongation -> adverse length/tension relationship
  5. Changes may include associated vasculature – where smooth muscle hypertrophy and fibrosis may increase vascular resistance (coronary and pulmonary circulation)
31
Q

What is decompensation? What causes it and how would you treat it?

A

An exacerbation of current symptoms of CHF which will be an exacerbation shortness of breath
Can be cause by a change in medication/not taking medication, systemic infection, AMI, PE, taking excessive fluid, salt, alcohol or drugs

Treatment: supplemental O2, eliminate new causes, IV diuretics

32
Q

How would you manage CHF?

A
  1. General management
  2. Pharmacological management
  3. Physical management
  4. Surgical management
33
Q

What is involved in general management of CHF patients?

A

Fluid restriction - drinking more fluid will overload the heart
Physical exercise
Lifestyle - smoking alcohol
Diet - low in salt, fat and sugar

34
Q

What is the main aim of the pharmacological management in CHF?

A

Main aim= to reduce cardiac workload

  1. Reduce pre-load (blood volume)
  2. Reduce after-load -> TPR
  3. Reduce contractility and HR

Patients will usually be on a combination of 2 of the above group - its unlikely they would be on all 3

35
Q

What drugs reduce pre-load?

A
  1. Diuretics (e.g. furosemide) - act on kidney to create more urine output which reduces blood volume
  2. Angiotensin receptor blockers (ARBs) (e.g. valsartan) - block binding site for angiotensin 2 (which stimulates release of aldosterone (acts on kidneys to conserve water).
  3. ACE inhibitors reduce aldosterone production (e.g. ramipril) - takes angiotensin converting enzyme (ACE) out of the equation so if angiotensin 1 is produced very little angiotensin 2 is produced as ACE is not present to convert angiotensin 1 to angiotensin 2 and hence water is not conserved in the kidneys
  4. Selective aldosterone receptor blockers (SARAs) (e.g. Eplerenone) - selectively blocks aldosterone receptor site
  5. SLGT2 inhibitors ( -flozin: e.g. dapagliflozin) - encourage loss of glucose from blood into the urine and brings water with it so it reduces blood volume
  6. Venodilators (e.g. nitrate (GTN)) - encourages veins to act as reservoirs for blood rather than returners
36
Q

What drugs reduce after-load?

A

ACE inhibitors - reduces venoconstriction and TPR

ARBs

Arterial Vasodilators - targets smooth muscle of arterioles to dilate them

37
Q

What drugs reduce contractility and HR?

A

Reducing contractility -> reduces SV
Reducing HR -> reduces CO (as HR and SV are both reduced)

Beta blockers (e.g. propoanolol, bisoprolol)
Beta blockers do the following in CHF:
1. Artificially lower HR at rest, on exercise meaning diastole is longer - this means blood has more time to perfuse the myocardium (as the myocardium is perfused during diastole)
  1. Limits the force of contraction (ionotropy)
    which can be done as pre-load and after-load have been lowered (by other 2 medications?)
  2. Diastole is longer
  3. Boosts cardiac filling
38
Q

How would you address the physical management of patients with chronic heart failure?

A
  1. Supervised group exercise-based rehab designed specifically for patients with CHF - could be incorporated into an existing CR programme
  2. Patients may not wish to attend PR/CR classes – ensure you can devise an appropriate home exercise programme for them.
39
Q

What are the skeletal muscle adaptations seen post-exercise

A

Typically type I aerobic fibres are targeted.
• Increased aerobic efficiency in terms of providing, extracting & utilising O2 to manufacture ATP aerobically results in a reduction in the demands placed upon the ailing heart to do work.

40
Q

What is the most common surgical technique used for CHF?

A

Heart transplantation: bi-caval technique

Some of the heart is removed and part of the left atrium is left behind
New heart is anatomised onto the left atrium and joined up with the major blood vessels.
The new SA node functions independently of the autonomic nervous system (i.e. the brain). The new heart has no parasympathetic activity so their resting heart rate will be 100 bpm (they are denervated)

41
Q

What is a contraindication to exercise?

A

Tachycardia of 100 or greater beats per minute but in heart transplant patients this contraindication does not apply

42
Q

What are the 2 types of LVAD devices?

How do left ventricular assist devices (LVAD) work?

A
  1. Pulsatile
  2. Apulsatile - continuous flow devices. There will be no pulse in their radial artery in the patient as the pump is continuously supplying blood to the heart

Blood enters heart as normal, drains into the pump, pumps it into the aorta.
The pump acts as a left ventricle

43
Q

What are the indications for ventricular assist devices (VAD)?

A
  • Immediately post cardiotomy or other cardiac surgery (short-term device) if they have very low cardiac output
  • Bridge to transplantation
  • Bridge to recovery
  • Destination therapy

Cardiovascular Health (9 decks)

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