10. Heart Failure Flashcards
What is heart failure?
—> The inability of the heart to pump adequate blood to meet the body’s metabolic demands
Systolic heart failure
- Systolic heart failure: inability of the heart to contract efficiently to eject enough blood to meet the metabolic demand from tissues. Also known as heart failure with reduced ejection fraction (HFrEF)
- Lv is not contracting efficiently
Diastolic heart failure
- Diastolic heart failure: reduced compliance leading to poor filling of the ventricles. Contraction is unaffected therefore LV ejection fraction is preserved (heart failure with preserved ejection fraction – HFpEF)
- Reduced compliance, stretching of LV it is more stiff and so it can’t fill properly
• Left heart failure
• Left heart failure: left ventricle cannot pump enough blood leading to congestion in the pulmonary circulation blood backs up back through pulmonary vein and pulmonary oedema
Right heart failure
• Right heart failure: right ventricle cannot pump enough blood through pulmonary circulation leading to systemic congestion of the venous system – peripheral oedema and liver congestion. Usually from respiratory disease. Note – left heart failure usually leads to right heart failure due to pulmonary hypertension.
• Congestive heart failure:
• Congestive heart failure: failure of both left and right ventricles
Heart failure with reduced ejection fraction (HFrEF)
heart failure from reduced cardiac output
Associated with Lv and systolic heart failure
Heart failure with preserved ejection fraction (HFpEF)
heart failure occurring with normal cardiac output due to a mismatch between supply of blood and metabolic demand. Can be caused by anaemia or increased metabolic demand (e.g. thyrotoxicosis).
Causes of Heart Failure
- Ischaemic Heart Disease (commonest cause in Western world)
- Dilated cardiomyopathies
- Hypertension
- Valvular Disease
• Many others:
– ASD/VSD, restrictive cardiomyopathy, hyperdynamic circulation, pericardial disease, myocarditis
Bp formula
• Blood pressure = cardiac output x total peripheral resistance
○ BP (MAP) = CO x TPR
Co formula
• Cardiac output = stroke volume x heart rate
○ CO = SV x HR
Sv formula
• Stroke volume = end diastolic volume (volume of blood in ventricles before contraction) – end systolic volume (after contraction)
○ SV = EDV – ESV
Preload
—> Stretch experienced by cardiac muscle cell (cardiomyocyte) immediately after ventricular filling in diastole (proportional to end diastolic volume)
• Preload is increased by
– Increased central venous pressure (sympathetic activation of venous smooth muscle) or increased venous return
– Increased ventricular compliance – ability to stretch
– Reduced heart rate (increased ventricular filling time)
Increased EDV = increased preload
Frank-Starling Law
- Increasing the venous return to the heart -> increased LV end-diastolic pressure -> increased sarcomere length -> increased sensitivity to Ca2+ -> stronger contraction -> stroke volume increases (more forceful contraction of LV)
- The ability of the heart to change stroke volume in response to venous return is called Frank-Starling mechanism
Frank-Starling Law in the failing myocardium
What should happen
- Reduced blood volume ejected from each contraction results in higher ‘end-diastolic volume’ in the left ventricle after filling
- According to Frank-Starling Law, a normally functioning heart should increase contractility and restore function of the myocardium (i.e. pump more blood out from LV by a more forceful contraction)
Frank-Starling Law in the failing myocardium
What actually happens
- In a failing myocardium – this does not happen. There is a physical limit to the relationship between cardiac stretch and contractility.
- Beyond this limit – further increases in preload have a negative effect on stroke volume
2 Compensatory mechanisms to increase cardiac output
- Renin-angiotensin-aldosterone system
2. Sympathetic activation
Renin-angiotensin-aldosterone system: renin
What is it
- Regulation of blood volume and vascular resistance to help regulate cardiac output
- Drop in cardiac output leads to a reduction in renal perfusion
- Reduced renal perfusion (amount of blood going through kidneys) = reduced blood pressure within kidney.
Renin-angiotensin-aldosterone system: renin
Steps
- Juxtaglomerular cells line the afferent arteriole of the kidney. - detect drop in blood pressure within kidney
- They produce renin in response to reduced renal perfusion
- Renin which is produced by juxtaglomerular cells of the kidney converts and cleaves angiotensinogen from the liver to angiotensin I
- Angiotensin I is converted to angiotensin II in the lungs by angiotensin converting enzyme (ACE) which is made by the lungs
- Angiotensin II is a POWERFUL VASOCONSTRICTOR!
• increased vasoconstriction = increases resistance = increase blood pressure = increase venous return = improve preload = improve cardiac output
Renin-angiotensin-aldosterone system: angiotensin
- Vasoconstriction increases total peripheral resistance and blood pressure increases
- Venoconstriction leads to increased venous return
- Increased venous return improves preload -> improved cardiac output
- Increased BP means renin production from kidney is reduced (negative feedback)
Renin-angiotensin-aldosterone system: aldosterone
- Angiotensin II also has an effect on the adrenal glands to increase aldosterone production
- This leads to increased reabsorption of sodium and water in the renal tubules
- This reduces excretion of water and sodium in the urine which increases blood volume
- This increases venous return which increases preload -> increasing cardiac output
Sympathetic activation
Sympathetic activation - how is it activated
- Cardiac output is falling in chronic heart failure -> drop in blood pressure
- In carotid sinus (and aortic sinus) baroreceptors pick up this fall in pressure
- Signals are transmitted to the medulla
Sympathetic activation - what does it do
• Medullary activation via sympathetic nervous system to increase blood pressure
– stimulation of SA node to increase heart rate (-> tachycardia) increase CO
– increased contractility via noradrenaline release to B1 receptors on myocardium= more forceful contractions
– noradrenaline release to arterioles (alpha-1 adrenergic receptors) for vasoconstriction (increased TPR) – and venoconstriction via same pathway to increase preload
– Renin is also released from juxtaglomerular cells in response to noradrenaline stimulation -> activating RAAS
Signs and Symptoms of left heart failure
– Problem with ejection of blood from the left ventricle
– Blood will accumulate in the left atrium and pulmonary veins and pulmonary venous circulation
– Pulmonary venous pressure increases due to accumulation of blood
– Fluid leaks out into interstitial fluid of pulmonary tissues = pulmonary oedema
– Decreased ventilation across the alveoli -> hypoxemia (with exertion)
– LV has to pump harder against increasing afterload -(LV may get bigger) -> cardiomegaly
Symptoms of left ventricular heart failure
• Dyspnoea (breathlessness – often exertional)
– impaired gas exchange
• Cough
– Often dry
– Can have frothy white or pink sputum
• Fluid leaks into pulmonary tissues, irritates alveoli = cough
• Orthopnoea
– Difficulty lying flat
• Ask patient how they sleep, can they sleep lying down or do they have to be sat up in armchair
• Paroxysmal nocturnal dyspnoea
– Waking up breathless at night
Signs of left ventricular heart failure
- Crackles on auscultation (bi-basal) - bottom of the lung on both sides, where fluid has accumulated
- Tachycardia – to increase co
- Cardiomegaly – bigger heart
- 3rd and 4th heart sounds
What are symptoms
Symptoms = what the patient experiences and tells you about
What are signs
Signs = what you pick up on through examination
Right sided heart failure
- Increased pressure in pulmonary veins causes difficulty of RV to pump through the pulmonary circulation
- Either caused by left ventricular failure or respiratory disease
- If caused by respiratory disease (common cause) – it is termed ‘cor pulmonale’ -> increase in pulmonary circulation pressure due to chronic hypoxia (from diseases like copd and cystic fibrosis)
- Blood has to back up and accumulate into the systemic venous circulation
Signs of right heart failure
- Increased jugular venous pressure (raised JVP)
- Hepatic congestion
- Peripheral oedema
- Ascites
Congestive heart failure - signs and symptoms
• Both the right and left ventricles affected
combination of signs and symptoms
– Dyspnoea – Cough – Orthopnoea – Cardiomegaly – Peripheral oedema – Raised JVP – Hepatic congestion
Heart failure with preserved ejection fraction (HFpEF)
- The end-diastolic volume is reduced in HFpEF as left ventricle does not fill properly
- The left ventricle is however able to maintain normal contractility
- Ejection fraction is normal – but the heart is unable to pump effectively enough to meet metabolic demand of body as overall the cardiac output would be lower- edv is much lower as lv isn’t being filled properly in diastole
Ejection fraction
- Ejection fraction: (stroke volume / end-diastolic volume) * 100
- Amount of blood pumped out from LV as proportion of what is normally left in lv
- Stroke volume will be decreased due to problem with pumping
History taking - heart failure
– Exercise tolerance:
• how far can they walk before becoming breathless? Has this changed?
– Orthopnoea:
• how many pillows do they need to sleep? Do they sleep upright in an armchair?
– PND:
• do they wake up in the middle of the night feeling breathless?
• Paratismal nocturnal dyspnea – wake up brethless
– Cough:
• presence of cough (often dry – textbooks mention ‘pink, frothy sputum’ but this is rare
– Weight change:
• Decrease appetite in heart failure
• Increase – due to fluid overload
Examination - heart failure
• General
– Lower limb swelling
• Specific shoes like crocs worn to help swelling
– Breathlessness (especially after stairs) - more out of breathe than normal
– Tachycardia
Examination - heart failure
• Cardiovascular/Respiratory
– Displaced apex beat – normally in 5th intercostal space, but hypertrophy of LV can displace it more laterally
– Bibasal crackles – instead of being normally scattered, due to pulmonary odeoma accumulation of fluid
– Sacral oedema – fluid accumulates at sacrum base of spine
Bedside investigations - heart failure
• Temperature
– Should be normal
• Oxygen Saturations
– Hypoxia
• Blood pressure
– Likely elevated: hypertension can result in heart failure
• Respiratory rate
– Can be elevated: especially R heart failure / after exertion
• Heart rate
– Likely elevated: effect of noradrenaline to maintain CO. Irregular pulse?
Af can can give irregualry irregular pulse due to changed shape of heart
Investigations – heart failure
• 12-lead ECG
– All patients with suspected chronic heart failure should have an ECG
• Blood tests
– N-terminal pro-B-type natriuretic peptide level = neurohormone in bluid
– Urea and electrolytes, eGFR, FBC, iron studies, TFT, LFT, HbA1c, fasting lipids
– Urine dipstick
– Chest X-ray
ECG - heart failure
– All patients with suspected chronic heart failure should have an ECG
• See old myocardial infarction – q waves showing that part of heart tissue has been damaged indicating a cause of heart failure
• Hypertophy of LV – left axis deviation
N-terminal pro-B-type natriuretic peptide level (NT-pro-BNP)
- Cardiac neurohormone
- Synthesised in ventricular cardiomyocytes in response to increased stress on ventricular wall
- Inactive peptide released alongside BNP (active hormone) when there is increased pressure on the ventricular wall
- Released in equal amounts to BNP but degrades less quickly – BNP due to fast degragation is a bad marker
- Low levels of NT-pro-BNP (<4000ng/L) have strong negative predictive value for heart failure (97%)
- Low NT pro BNP = unlikely that patient has high BP
Blood tests
U&E and eGFR
• U&E and eGFR: markers of kidney function = low renal perfusion
Blood tests
FBC and iron studies
• FBC and iron studies: anaemia (presence of anaemia with HF has poorer prognosis) - worse outcomes
Blood tests
Lft
• LFT: marker of hepatic congestion – liver fucntion test
Blood tests
TFT
• TFT: marker of increased metabolic demand – hyperthyroid
Blood tests
HbA1c and lipids
• HbA1c and lipids: presence of diabetes/hyperlipidaemia associated with poorer outcomes
Chest X-ray - heart failure
- Sensitive marker of cardiomegaly
- The heart width should not make up more than 50% of the thoracic window = if it does than it I too big = hf
• Other features include
– Upper lobe diversion = more whitness in upper lumbs as blood is diverted
– Kerley B-lines = thin white lines
NT-pro-BNP as a marker -values
- < 400ng/L: unlikely heart failure. Consider a different cause of the symptoms
- 400-2000ng/L: cardiology referral + echocardiogram within 6 weeks
- > 2000ng/L: urgent cardiology referral + echocardiogram within 6 weeks
Echocardiogram
—> ultrasound of the heart = shows blood flwoign through heart in real time
• Will also identify valvular abnormalities, filling abnormalities and changes in contraction (regional wall motion abnormalities) = areas of heart may have been ischaemic in the past
• Transthoracic echocardiogram (TTE)
• Identifies the ejection fraction to differentiate heart failure into different groups
• Assess heart valve problems
– HF reduced EF: LVEF < 40%
– HF minimally reduced EF: LVEF 40-49% (contentious) – HF preserved EF: LVEF > 50%
Other possible investigations: non-routine
Heart failure
- Cardiac MRI (cMRI)
- Coronary angiogram
- Lung function tests
- Holter monitoring
• Cardiac MRI (cMRI)
– Useful if TTE is non-diagnostic
If you can’t see certain things on echocardiogram – if patient is overwieght
• Coronary angiogram
– Identification (and treatment) of coronary artery disease – and can treat with stents
• Lung function tests
– If right sided heart failure is suspected (e.g. cor pulmonale from COPD)
• Holter monitoring
– Arrhythmia idenfitication
24 hours – 7 days patient keeps device in pocket, tracks heart for as long as patient wears ut
Management - heart failure
- Patient education and lifestyle changes are vital parts of overall management = changes at patient level
- Several effective drug therapies have been developed which reduced the progression of heart failure – but it cannot be ‘cured
Lifestyle changes + modifiable risk factors
Heart failure
- Stop smoking
- Adaptations in the home e.g. install stair lift, movement wheelchair
- Annual flu vaccine, one-off pneumococcal vaccination
- Supervised exercise-based rehabilitation
- Depression and anxiety screening = psychosocial consequences
- Ensure co-morbidities are optimally managed
Drug therapies -
Heart failure
• Think about compensatory mechanisms – these are the targets of drug therapies
RAAS system
– ACE-inhibitors
– Angiotensin receptor blockers
– Mineralocorticoid receptor antagonists
– Beta blockers
– Loop diuretics
– Drug management of co-morbidities
- These are specifically for heart failure with reduced ejection fraction
- There is insufficient evidence for common drug classes in HFrEF – heart failyre with reduced ejection fracture
ACE-I + Angiotensin receptor blockers
- ACE inhibitors = angiotensin converting enzyme inhibitors made in lung
- Prevent the conversion of angiotensin I to the potent vasoconstrictor angiotensin II
– Reduce preload
ACE-I + Angiotensin receptor blockers
Problem
• Produces bradykinin -> dry cough in ~20% of patients – problesm with adherence
- If problematic: consider ARB
- Examples: ramipril, lisinopril, enalapril, captopril - all end in ril
- Stop in acute kidney injury
Beta-blockers
Olol drugs
- Prevent stimulation of beta adrenergic receptors
- Reduce heart rate – longer time for ventricular filling
- Consider cardiac selective beta blockers: bisoprolol is often first line
- -olol drugs
• Avoid in asthmatic or bradycardic patients
Mineralocorticoid receptor antagonists
- Can be considered as add-on therapy if ACE-I and beta-blockers are insufficient (aldosterone antagonists)
- Reduce sodium reabsorption (increase water excretion by the kidney)
- Reduces blood pressure and circulating volume
- Careful with electrolyte levels
• Spironolactone, eplerenone – one drugs
Mineralocorticoid receptor antagonists
Examples
• Spironolactone, eplerenone – one drugs
Beta-blockers
Example
• Consider cardiac selective beta blockers: bisoprolol is often first line
ACE-I + Angiotensin receptor blockers
Examples
• Examples: ramipril, lisinopril, enalapril, captopril - all end in ril
Loop diuretics
- No effect on heart failure prognosis but offers symptomatic benefit
- Promote excretion of water from the kidney to reduce circulating volume and reduce pulmonary and peripheral oedema
- Highly effective
Loop diuretics
Examples
- Furosemide, bumetanide – remove a lot of water from body to treat odeoma and breathlessness
- IV preparation of furosemide can be used in acute heart failure
Second-line treatment - heart failure
- Sacubitril/valsartan (Entresto)
- Ivabradine
- Hydralazine
- Digoxin
- Can only be initiated under specialist advice
- Listed here out of interest – not expected to know MoA of these drugs for this lecture (may come up elsewhere)
Device therapy
Very severe HF
• Implantable cardiac defibrillator
• Cardiac resynchronisation therapy
• Cardiac transplant
• Implantable cardiac defibrillator
– Has very specific indications
– Heart failure associated with arrhythmia
• Cardiac resynchronisation therapy
– Pacing of both ventricles in HFrEF with prolonged QRS
– Often has defibrillator alongside CRT
Machine is used to trigger contractions of t the heart
