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Cardiovascular diseases > Heart failure > Flashcards

Heart failure Flashcards

1
Q

What is heart failure?

A

Failure of the pumping mechanism of the heart.

The later stages of heart failure, severely affect the quality of life of the patient and has a poor prognosis associated with it.

You can get right sided heart failure, left sided heart failure or a combination of both (most common)

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2
Q

How does the heart work? (review)

A

The heart is 2 pumps that work together
- Deoxygenated blood from the body comes to the right side of the heart where it is then pumped to the lungs to be oxygenated (takes up oxygen and eliminated carbon dioxide) and then the oxygen rich blood returns back to the left side of the heart which then pumps oxygenated blood to the rest of the body through arteries to orange and tissues.

The heart is regulated by a system of valves
- To ensure the blood flows in the correct direction

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3
Q

What is the cardiac output in health?

A

Around 5l/min

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4
Q

What is the mean heart rate in health?

A

Around 70 beats per minute

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5
Q

What is the stroke volume in health?

A

Stroke volume is the volume of blood pumped out of the left ventricle during systole (when the heart contracts)

Around 70ml

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6
Q

How much will our filled ventricle hold in health?

A

Your filled ventricle will hold a volume of 130ml.

The stroke volume (the volume ejected-70ml), the fraction therefore ejected every time your heart contracts, is more than 50% of the ventricle contents.

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7
Q

What are the 2 reasons as to why heart failure can occur?

A
  1. Results from structural (congenital (from birth) or inherited) and/or functional cardiac disorders
    - Usually of gradual onset
  2. The ability of the heart to function as a pump is implied
    - Blood is not cleared from the heart
    - Unstable to sustain an adequate delivery of blood therefore starved of oxygen and nutrients to the tissues.
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8
Q

What are the main causes of death within heart failure?

A
  • Recurrent pump failure
  • Sudden cardiac death
  • Recurrent myocardial infarction
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9
Q

What are the 2 underlying problems leading to heart failure?

A
  1. Pump failure
  • Damage to the heart muscle itself has resulted in reduction in myocardial contractility
  1. Overloading

When theres excessive load on the heart which it can’t cope then it’ll go into heart failure.

Extra workload on the heart can lead to:
- Decreased force and velocity of contraction and delayed relaxation
- Excessive after load (pressure overload)
- Excessive preload (volume overload)

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10
Q

What is the definition of afterload?

A

The pressure that the chamber of the heart has to generate in order to eject blood out of the chamber
- i.e. total peripheral resistance

“Hence the effort that the heart has to produce when contracting to push the blood out and into the circulation”

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11
Q

What is the definition of preload?

A

Volume of blood present in a ventricle of the heart, after passive filling and atrial contraction
- i.e. left ventricular end diastolic volume (amount of stretch of left ventricle)

“It represents the volume of blood that is coming into the heart, hence what comes into the heart and not after the heart”

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12
Q

What is pump failure?

A
  • It is damage to the heart and leads to systolic failure (the failure of the heart to contract)
  • The most common cause of systolic failure is ischaemic heart disease.
  • It can occur acutely/immediately for example after having myocardial infarction or can be progressively (chronically) as a consequence of diffuse fibrosis of the myocardial tissue.
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13
Q

What are the causes of pump failure?

A
  • Ischaemic heart disease
  • Myocardial infarction
  • Cardiomyopathy (heart muscle disease - malfunctioning muscle-can be congenital/inherited or viral cause)
  • Arrhythmias
  • Viruses & infection
  • Inflammation of the heart muscle
  • Excessive alcohol consumption
  • Diffuse fibrosis (formation of excessive fibrotic connective tissue making the heart muscle stiff hence difficult for the heart to pump)
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13
Q

What is overloading?

A
  • Overwork and overstretch of the cardiac muscle can cause structural and biochemical abnormalities in the cells.
  • This eventually leads to decreased force, velocity of contraction and delayed relaxation
  • Unfortunately the effects at this stage are usually irreversible
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14
Q

How does excessive afterload cause overloading?

A

Excessive afterload can occur in multiple occasions:

  1. If systemic vascular resistance is high
    - E.g. In a patient with hypertension
    - Which results in raised afterload on left ventricle and causes it to fail
  2. If pulmonary vascular resistance is high
    - E.g. when theres pulmonary hypertension secondary to chronic lung disease
    - This will cause right ventricular failure (Known as cor pulmonale)
  3. Valve dysfunction
    - Stenosis (narrowing) or incompetence of one of the valves
    - Therefore the pressure the chambers of the heart has to generate to push the blood through those stenosed valved increases, hence increasing the afterload.
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15
Q

How does excessive preload cause overloading?

A

Less common cause of heart failure.

But usually caused by situations where theres hypervolaemia (increased volume of blood). These situations include:
- Fluid retention e.g. in renal failure
- Excessive intravenous (IV) infusions
- Polycythaemia (condition where theres over production of red blood cells, increasing the volume of blood, increasing the preload on the heart)
- Drugs e.g. NSAIDs, steroids (side effects include increasing sodium and water retention, increasing the volume of blood, therefore increasing the preload on the heart)

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16
Q
A
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16
Q

What are some other causes of overloading apart from preload and afterload?

A
  1. Excessive demand on the heart. This could be because:
  • The patient is anaemic (anaemia- The oxygen carrying capacity of the blood is reduced hence resulting on an increase demand on the heart to pump more blood)
  • Hyperthyroidism or thyrotoxicosis (excessive thyroid hormones circulating in the blood, increasing the metabolic rate of the body, therefore increasing the demand on the heart)
  • Valve dysfunction
  • Arrythmias - Bradycardia or Tachycardia (both will increase demand on the heart)
  • Widespread vasodilation, e.g. in septic shock. Cardiac output in increased in an attempt to raise blood pressure when theres vasodilation, which drops your blood pressure, hence the nature response is for the heart to increase its output and the excessive demand will put the patient into heart failure.
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17
Q

What are the 2 classifications heart failure?

A
  • Acute heart failure
  • Chronic heart failure
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17
Q

What is acute heart failure?

A
  • Rapid in onset
  • Example when this might occur is straight after myocardial infarction, where the contractility of the heart immediately drops due to the damage to the heart muscle caused by the MI
  • This contractility will cause cardiac output to fall but then this results in simulation of a process of compensation in order to try and maintain cardiac output and peripheral perfusion

This is known as compensatory heart failure

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17
Q

What happens if a myocardial infarction is very severe?

A

If MI is very severe and there has been extensive damage to the heart muscle, cardiac output dramatically drops. Because of the severe damage to the heart, there is no cardiac reserve and the cardiovascular system is unable to compensate and is overwhelmed.

This is known as decompensated heart failure

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18
Q

What is chronic heart failure?

A

The underlying pathophysiology is the same as acute heart failure but the decline is progressive rather than a sudden fall

Patients can remain in compensated failure indefinitely but with chronic heart failure some sudden acute issues may present e.g. infection, sudden fluid overload, exertion or anaemia, and this can cause severe stress and drive them into decompensated heart failure.

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19
Q

What is the Starling’s Law of the Heart?

A

The greater the volume of blood entering the heart during diastole (heart muscle related and allows to fill with blood), the great the volume of blood ejected during systolic contraction.

  • In a normal functioning heart this effect is achieved by increased stretching of muscle fibres and increased force of contraction.
  • In heart failure, as the heart starts to fail, the overstretched muscle is unable to respond to the increase in preload. There’s a drop in cardiac output and the initial compensatory process eventually leads to decompensation.
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20
Q

What is happening during compensation?

A

In the failing heart, as a result of reduction in cardiac output and reduction in tissue perfusion, the body tempts to maintain cardiac output by the following compensatory processes:

  • Cardiac enlargement
  • Arterial constriction
  • Increased sympathetic drive
  • Salt and water retention
21
Q

What is cardiac enlargement?

A

As the heart starts to fail, in order to maintain the cardiac output, theres a progressive alteration of ventricular size, shape and function:

  • The cardiac muscle stretches as a result from increased residual volume after contraction and this gives the heart an appearance of being enlarged with extra muscle.
  • Although this is a short term compensatory mechanism, this extra muscle is actually ineffectual (ineffective)
  • Which then eventually becomes responsible for significant impairment of the heart as a pump

*Known as Left Ventricular Hypertrophy (LVH) *

22
Q

What is arterial constriction?

A

When cardiac output starts to fall in a patient with heart failure:

  • The arteries constrict to divert blood to the essential organs but away from skin and GI tract
  • But this arterial constriction will eventually cause a raise in systemic vascular resistance, this then has a consequence of increasing the afterload on the heart
23
Q

What is increased sympathetic drive?

A

When you get a failing heart and reduction in tissue perfusion, this then stimulates the sympathetic nervous system via baroreceptors in the blood vessel walls:

  • This then exposes the heart to catecholamines which have a positive inotropic (increases force of contraction) and chronotrophic (increases rate of contraction) effects in an attempt to maintain cardiac output.
  • This leads to an increase in levels of noradrenaline, angiotensin, aldosterone and vasopressin.
  • It promotes excessive stimulation of the heart and widespread vasoconstriction, to initially help maintain cardiac output but long term will affect the heart negatively.
  • Increases contractility
24
Q

What is salt and water retention?

A

Reduced cardiac output; at any stage when the heart is failing, there is reduced cardiac output which as a consequence you get reduced renal perfusion which:

  • Releases renin
  • Renin leads to formation of angiotensin I and II which are vasoconstrictors.
  • Which ultimately leads to adrenal aldosterone release.
  • Purpose of aldosterone is to retain salt and water at distal renal tubule.
  • This then expands blood volume and increases preload.
  • Promotes the release of Atrial Natriuretic Peptide (ANP), which is a compound designed to be a vasodilator to counteract the increased preload
25
Q

What are the 3 classical symptoms of heart failure?

A
  1. Exercise limitation (fatigue)
    - Due to decreased cardiac output, impaired oxygenation and decreased blood flow to exercising muscles.
  2. Shortness of breath
    - ‘Back pressure’ from the failing heart, as if the left side of the heart starts to fail, you get backlog of blood and fluid into the lungs and accumulation in the lungs.
    - Mostly occurs when exercising or lying down due to gravitational forces
    - Can be accompanied by a cough as a consequence
  3. Oedema (fluid accumulation)
    - Very common feature of heart failure due to the lack of clearance of fluid
    - Swelling of ankles and feet due to retention of salt and water and ankles tend to be the first areas due to gravitational forces.
26
Q

What is hypoperfusion?

A

A reduction in perfusion caused by forward component (hence going on forward from the heart). It is caused by a reduction of blood flow leaving a failing heart.

Symptoms include:
- Peripheral vasoconstriction (main cause- increase in afterload of the heart hence reduction in blood supply)
- Fatigue and exercise intolerance (lack of oxygen and nutrients to the tissues)
- Cold and pale extremities
- Fluid and electrolyte retention
- Tachycardia and tachypnoea

27
Q

Why is congestion/oedema known as the backward component?

A

Blood entering a failing heart or lack/excessive blood that can’t be cleared.

Right-sided heart failure symptoms:
(Pathophysiology: The right side of the heart receives deoxygenated blood from the body which is then pumped onto the lungs)

  • Peripheral oedema (swollen ankles)
  • Hepatomegaly (enlargement of the liver)
  • Raised jugular venous pressure
  • Peripheral cyanosis
  • Fluid and electrolyte retention

Left-sided heart failure symptoms:
(Most common form of heart failure and usually more serious)
(Pathophysiology: Left side receives oxygenated blood from the lungs, if the left side fails you get backlog into ur fluid and blood into the lungs - hence the lung type symptoms)

  • Pulmonary oedema (accumulation of fluid in the lungs)
  • Dyspnoea (shortness of breath)
  • Orthopnoea (shortness of breath that occurs when lying down)
  • Paroxysmal nocturnal dyspnoea (wake up at night with sever short of breath)
  • Cough/wheeze
  • Central cyanosis
  • Tiredness
  • Breathlessness
28
Q

What is seen in a patient with Class I New York Heart Association Classification?

A

No limitations. ordinary physical activity does not cause fatigue, breathlessness or palpitation.

29
Q

What is seen in a patient with Class II New York Heart Association Classification?

A

Slight limitation of physical activity. Such patients are comfortable at rest. Ordinary physical activity results in fatigue, palpitation, breathlessness or angina pectoris (mild)

30
Q

What is seen in a patient with Class III New York Heart Association Classification?

A

Marked limitation of physical activity. Although patients are comfortable at rest, less than ordinary physical activity will lead to symptoms (Moderate)

31
Q

What is seen in a patient with Class IV New York Heart Association Classification?

A

Inability to carry on any physical activity without discomfort. Symptoms of congestive cardiac failure are present even at rest. With any physical activity increased discomfort is experienced (Severe).

32
Q

How do we diagnose heart failure?

A
  • Symptoms of heart failure alone cannot be relied upon to make a diagnosis.
  • We need evidence of cardiac dysfunction which will come from investigations and measurements of left ventricular structure and function.
  • The underlying cause should be established in all patients and to investigate whether there are any reversible or correctable causes, hence aiding treatment.
33
Q

What investigations are done to diagnose heart failure?

A

Review of signs and symptoms which includes:

  1. Looking for a raised jugular vein (on the side of your neck, becomes visible for somebody with heart failure due to venous distension. The more visible the jugular vein is, it reflects the greater degree of fluid accumulation in that patient)
  2. Lung sounds are checked using a stethoscope (Crackles at bases (crepitations))
  3. Swelling of ankles and legs (signs of peripheral oedema)
34
Q

What tests are done in order to diagnose heart failure?

A
  1. Natriuretic peptides (BNP & NTproBNP).
    - Natriuretic peptides are secreted from the ventricle in somebody who has heart failure as part of the compensatory process, and these natriuretic peptides has a vasodilatory effect.
  2. Echocardiography (most important test)
    - Main state of diagnosis of somebody with heart failure.
    - It is an imaging technique that allows us to see the heart in motion and assess the performance as a pump
    - Can measure ejection fraction (contents ejected)
35
Q

What does the results of the ejection fraction indicate?

A

The results of the ejection fraction allows us to classify heart failure.

HFrEF - (less than or 40%) Heart failure with reduced ejection fraction. NICE Guidelines suggest drug treatment for.

HFpEF - (50% or more) Heart failure with preserved/mainted ejection fraction

HFmrRF - (41-50%) Heart failure with mid range ejection fraction

36
Q

What other investigations are carried out in order to identify the underlying causes of heart failure?

A
  1. Chest X-ray
    - To assess size of the heart and to look for lung consolidation (sign of infection)
  2. Heart rate, rhythm and sounds measured
  3. Electrocardiogram (ECG)
    - Specifically looking for any arrhythmias such as atrial fibrillation (AF)
  4. Blood pressure (Hypertension is associated with the development of heart failure)
  5. Blood tests
    - Looking for underlying causes such as anaemia, renal failure and thyroid disease.
37
Q

What are the aims of drug treatment in heart failure?

A
  1. Reduce morbidity
    - Relieve symptoms
    - Improve exercise tolerance
  2. Reduce mortality
38
Q

If the underlying cause of heart failure is due to disease of the myocardium, what is the aim of drug treatment?

A

To increase inotrophy (increase the force of contraction)

39
Q

If the underlying cause of heart failure is due to excessive load, what is the aim of drug treatment?

A

Depending on whether its excessive pre-load or after-load:

  • Reduce pre-load
  • Reduce after-load
  • Or potentially reduce both
40
Q

What are the drugs used in heart failure and what are they used for?

A
  • Diuretics (To reduce preload)
  • ACEIs/AII receptor antagonists (To reduce pre-load and after-load)
  • B-blockers (To reduce preload and after-load)
  • Aldosterone antagonists (To reduce pre-load and block the effect of aldosterone on the heart)
  • Digoxin (To improve myocardial stimulation)
  • Isosorbide dinitrate (To reduce preload) and Hydralazine (To reduce after-load) - Used as combination
  • Ivabradine (Improves myocardial stimulation)
  • ARNI - Combination drug called Sacubitril- Valsartan (To reduce preload and after-load)
  • SGLT2 inhibitors (To reduce preload and after-load)
41
Q

What does the NICE guidelines recommend for acute heart failure - first line treatment?

A

Intravenous (IV) diuretics - For fluid removal and reduce preload on the heart an d reduce fluid and congestion symptoms.

42
Q

What are diuretics used for?

A
  • Used in acute heart failure for fluid removal and reduce preload
  • In anyone that have chronic heart failure is likely to continue to take diuretics to provide ongoing control of their fluid symptoms
  • Reduce symptoms of heart failure, mainly pulmonary (causes shortness of breath) and peripheral oedema (causes swelling of ankles)
  • Use of diuretics known to reduce hospital admission and improve exercise performance
43
Q

What are the different types of diuretics available?

A
  1. Thiazide diuretics
    - Less potent hence tend to only be used for mild heart failure.
    - E.g. Bendroflumethiazide - can be up to 5mg OM
    - They are not as effective when you get to a significant level of renal impairment so if you have an eGFR of less that 20ml/min, then thiazide diuretics will not work at all.
  2. Lood diuretics
    -Mainstay of treatment
    - Extremely Potent
    - E.g. furosemide,bumetanide
    - Can use high doses in severe HF
    - Can be used IV - hence forms first line treatment for first line treatment
  3. Metolazone
    - Although it has a thiazide like structure, it is a atypical thiazide diuretic
    - It IS EFFECTIVE in reduced renal function
    - It is used in combination with loop diuretics in patients who have resistant heart failure
    - Very potent
    - STAT dose of 2.5-5mg is enough to kickstart diuresis in somebody with resistant heart failure
    - Can be used short term - 2.5mg / 5mg OD for 2 or 3 days
    - Occasionally in severe heart failure, might be seen used as long term maintenance strategy for fluid removal - 2.5mg/5mg 2 or 3 times a week
44
Q

What are the pharmaceutical care issues associated with using diuretics?

A
  • Hypotension
  • Dehydration
  • Renal impairment
  • Electrolyte disturbances
  • Rate of administration of IV furosemide
45
Q

What are ACE inhibitors used for in the treatment of heart failure?

A
  • Considered to be first line evidence based treatment for patients with chronic heart failure.
  • They reduce the pre-load and after-load on the heart
  • They improve symptoms and long term survival
  • We start at a low dose and then uptitrate to maximum dose a patient can tolerate.
46
Q

What are angiotensin II antagonists used for in the treatment of heart failure?

A
  • Used as an alternative to patients who are intolerant to ACE inhibitors
47
Q

What are B-blockers used for in the treatment of heart failure?

A
  • They are joint first line treatment with ACE inhibitors
  • Only B-blockers licensed for heart failure can be used (UK: Bisoprolol, Carvedilol, Nebivolol)
  • Reduces pre-load and after-load
  • CAUTION: Can cause worsening of symptoms initially especially if you got a patient with unstable acute heart failure as beta blockers slow the heart rate down. So have to “Start low, go slow” - start patients on very low doses and slowly uptitrate and need to be used in STABLE PATIENTS ONLY
48
Q

What are aldosterone antagonists (MRAs) used for in the treatment of heart failure?

A
  • Examples are Spironolactone, Eplerenone
  • These are also joint first line treatment with ACE inhibitors and B blockers
  • Low dose used - they have some diuretic effect - but the main benefit in heart failure patients is the blocking of action of aldosterone in development of LVH (left ventricular hyertrophy)
  • Known to increase long term survival and reduce hospital admissions.
49
Q

What medications are recommended by NICE guidelines as add-on therapy in patients who are not improving or intolerant to first line therapy?

A
  • Combination of Hydralazine and Nitrates
  • Ivabradine
  • ARNI- Angiotensin receptor - neprilysin inhibitor - Sacubitril - Valsartan
  • Digoxin
  • SGLT2 inhibitors
50
Q

What are the combination drugs Hydralazine and nitrates used for in the treatment of heart failure?

A
  • For patients intolerant or contraindicated to ACEIs and/or Angiotensin II antagonists
  • Add on therapy
  • Strong evidence for patients of African or Caribbean origin
51
Q

What is Ivabradine used for in the treatment of heart failure?

A
  • It lowers heart rate by selectively and specifically inhibiting If channels in the SA node
  • Recommended for add-on therapy in worsening heart failure in patients on optimal first line therapy.
52
Q

What is ARNI (Sacubitril-Valsartan) used for in the treatment of heart failure?

A
  • Sacubitril is a neprilysin inhibitor (neprilysin is the enzyme responsible for the breakdown of natriuretic peptides)
  • Valsartan is an angiotensin II antagonist which is a benefit in patients with heart failure
  • NICE recommends it is a consideration of add on therapy in worsening heart failure in patients in optimal first line therapy. FIRST LINE THERAPY OF ACEI or ARB NEEDS TO BE STOPPED 36HRS BEFORE STARTING ARNI. This is to reduce any chance of sever action for example angioedema which is more likely to occur if you are taking both an ACE inhibitor or ARB along side an ARNI.
53
Q

What is digoxin used for in the treatment of heart failure?

A
  • Mainly used in AF but can be used as add on therapy for heart failure.
  • Improves symptoms, exercise tolerance and hospital admissions but NOT mortality
  • Add on therapy for patients who remain symptomatic despite optimal treatment with other drugs
54
Q

What is SGLT2 inhibitors used for in the treatment of heart failure?

A
  • Examples: Dapagliflozin or Empaglifloazin
  • Add on therapy in worsening heart failure in patients on optimal first line therapy WHETHER DIABETIC OR NOT.

Cardiovascular diseases (18 decks)

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