Patho & Treatment - Chronic Heart Failure

Question 1

Define chronic heart failure

Answer 1

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

Question 2

Outline the 2 different type of heart failure

Answer 2

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

Question 3

What does diastolic heart failure cause?

Answer 3

Failing to fill and ejection fraction is preserved

Question 4

What does systolic heart failure cause?

Answer 4

Failing to empty and EJ is reduced

Question 5

What is ejection fraction (EF)?

Answer 5

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

Question 6

How is EF measured?

Answer 6

Echocardiogram

Question 7

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

Answer 7

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)

Question 8

What causes heart failure preserved ejection fraction (HFpEF)?

Answer 8

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

Question 9

What is heart failure reduced ejection fraction (HFrEF)?

Answer 9

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.

Question 10

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

Answer 10

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

Question 11

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

Answer 11

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

Question 12

What happens to blood pressure in chronic heart failure?

Answer 12

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

Question 13

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

Answer 13

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

Question 14

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

Answer 14

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

Question 15

What are the 3 main causes of CHF?

Answer 15

1. Volume overload
2. Pressure overload
3. Disorders of myocardial function

Question 16

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

Answer 16

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

Question 17

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

Answer 17

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

Question 18

Define systemic hypoperfusion

Answer 18

Inadequate cardiac output

Question 19

Define pulmonary hyperperfusion

Answer 19

cardiogenic pulmonary oedema

Question 20

What is LVF?

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

Answer 20

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

Question 21

What is LVF?

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

Answer 21

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

Question 22

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

Answer 22

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

Question 23

What is RVF?

Answer 23

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

Question 24

What are the clinical signs of RVF?

Answer 24

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

Question 25

What compensatory mechanism occur in response to heart failure?

Answer 25

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

Question 26

Describe the neuro-endocrine response

Answer 26

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) ``` 3. Naturetic peptide (secretions by RA cardiomyocytes)

Question 27

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

Answer 27

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

Question 28

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

Answer 28

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

Question 29

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

Answer 29

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

Question 30

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

Answer 30

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)

Question 31

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

Answer 31

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

Question 32

How would you manage CHF?

Answer 32

1. General management 2. Pharmacological management 3. Physical management 4. Surgical management

Question 33

What is involved in general management of CHF patients?

Answer 33

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

Question 34

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

Answer 34

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

Question 35

What drugs reduce pre-load?

Answer 35

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

Question 36

What drugs reduce after-load?

Answer 36

ACE inhibitors - reduces venoconstriction and TPR ARBs Arterial Vasodilators - targets smooth muscle of arterioles to dilate them

Question 37

What drugs reduce contractility and HR?

Answer 37

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) ``` 2. Limits the force of contraction (ionotropy) which can be done as pre-load and after-load have been lowered (by other 2 medications?) 3. Diastole is longer 4. Boosts cardiac filling

Question 38

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

Answer 38

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.

Question 39

What are the skeletal muscle adaptations seen post-exercise

Answer 39

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.

Question 40

What is the most common surgical technique used for CHF?

Answer 40

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)

Question 41

What is a contraindication to exercise?

Answer 41

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

Question 42

What are the 2 types of LVAD devices? | How do left ventricular assist devices (LVAD) work?

Answer 42

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

Question 43

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

Answer 43

- 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