Heart Failure Flashcards
1
Q
What is an acute decompensated heart Failure?
A
In heart failure, cardiac output is not able to meet metabolic demands of the body.
Acute decompensated heart failure can occur as either new-onset (de-novo) heart failure, without any previous cardiac dysfunction or, more commonly, due to decompensation of chronic heart failure.
2
Q
What is the epidemiology of an acute decompensated heart failure?
A
- In the UK, heart failure is responsible for over 67,000 hospital admissions per year.
- > 65 years of age
3
Q
What are the risk factors of an acute decompensated heart failure?
A
- Increasing age
- Coronary artery disease
- Hypertension
- Valvular disease: commonly senile calcification of the aortic valve
- Diabetes
- Atrial fibrillation
- Renal insufficiency
4
Q
What is the pathophysiology of decompensated heart failure?
A
Acute decompensated heart failure can occur as either new-onset (de-novo) heart failure without any previous cardiac dysfunction or as an acute decompensation of chronic heart failure.
In heart failure, cardiac output is not able to meet the metabolic demands of the body.
Common causes of heart failure include coronary artery disease and hypertension.
General pathophysiology:
- In response to reduced cardiac output, thesympathetic nervous systemis activated
- This results intachycardia, increasedmyocardial contractility, peripheralvasoconstriction, andRAASactivation, causing salt and water retention
- Patients with heart failure are generally hypervolemic → brain natriuretic peptide (BNP) release by ventricular myocytes in response to stretch
- These processes lead topulmonary and/or venous congestion
- Pulmonary oedemapresents with shortness of breath, whilst venous congestion causesperipheral oedema
5
Q
What are the causes of de-novo heart failure?
A
Cardiac causes: myocardial dysfunction
- myocardial infarct
- ventricular rupture
- myocarditis
- high-output states, e.g. sepsis, thyroid storm
- drug-induced cardiomyopathy
- takotsubo cardiomyopathy
Valvular dysfunction:
- Infective endocarditis
- valvular dysfunction post - MI, e.g. mitral regurgitation
Arrythmias
Extracardiac causes: pericardial effusion -> tamponade
- aortic dissection
- pulmonary embolism
- tension pneumothorax
6
Q
What are the signs of acute de compensated heart failure?
A
- Cool peripheries
- Signs of congestive heart failure: peripheral, pitting oedema and raised JVP
- Displaced apex beat
- Hypotension
- Crackles on auscultation: left-sided failure; usually coarse bi-basal crackles
- Third heart sound (S3)
- Stony dull percussion: if an effusion is present
7
Q
What are the symptoms of acute decompensated heart failure?
A
-
Dyspnoea: due to pulmonary oedema
- Often a history of orthopnea and paroxysmal nocturnal dyspnoea
- Fatigue and weakness
- Cardiogenic wheeze
- Symptoms of congestive heart failure: swelling of the peripheries and ascites
8
Q
What are the investigations to acute decompensated heart failure?
A
-
FBC:anaemia can be an underlying cause of heart failure
- U&Es: to investigate renal failureas an underlying cause of heart failure. Renal function should be monitored because loop diuretics such as furosemide are nephrotoxic.
- Arterial blood gas: demonstrates type 1 respiratory failure; degree of acidosis helps to determine which patients may require non-invasive ventilation
- BNP or NT-proBNP:BNP <100 pg/ml or NT‑proBNP <300 pg/ml suggest an alternative diagnosis
- ECG: assess for abnormalities such as arrhythmias; may be AF; left ventricular hypertrophy
-
CXR:**pulmonary congestion features include:
- A-Alveolar oedema (batwing opacities)
- B- KerleyBlines
- C-Cardiomegaly
- D-Dilated upper lobe vessels
- E- PleuralEffusion
- Transthoracic echocardiogram:**important to **assess for systolic and diastolic function, ejection fraction and valvular disease (NICE defines a reduced left ventricular ejection fraction as < 40%)
9
Q
What is the acute management of acute decompensated heart failure?
A
If there is anunderlying cause, e.g. myocardial infarction, this should be treated in the first instance.
10
Q
What is the acute management of acute decompensated heart failure?
A
If there is anunderlying cause, e.g. myocardial infarction, this should be treated in the first instance.
- Stabilise the patient: administer oxygen to maintain a SpO2≥94%
- Fluid restriction: fluid intake is usually limited to <1.5L/day
- IV diuretic: usually a loop diuretic e.g. furosemide is administered as a bolus or infusion to relieve fluid overload
- Inotropes or vasopressors e.g. dobutamine: only offer to patients with heart failure and cardiogenic shock (i.e. haemodynamically unstable)
- Non-invasive ventilation (NIV): consider NIV if the patient does not stabilise with initial medical management, as evidenced by desaturation or increasing respiratory distress
- Continuous positive airway pressure (CPAP) is commonly used.
- Bilevel positive airway pressure (BiPAP) can also be given
- Continuous positive airway pressure (CPAP) is commonly used.
- Intubation and ventilation: if CPAP is unsuccessful
11
Q
What should not be given for acute management of Acute decompensated heart failure (ADHF)?
A
DO NOT GIVE:
- According to NICE,nitrates and opiates should not be routinely given.
- An example of a nitrate isglyceryl trinitrate. Sodium nitroprusside shouldnot be given according to NICE
12
Q
What is the surgical management of ADHF?
A
- If acute heart failure is due to aortic stenosis: offersurgical aortic valve replacement
- Mechanical assist device: pump that can temporarily help the pumping action of the heart
13
Q
What is the long-term management of ADHF?
A
1st line: ACE-inhibitor e.g. ramiprilanda cardioselective β-blocker e.g. bisoprolol
- Offer if the patient has a reduced left ventricular ejection fraction (< 40%)
- Generally,one drug should be started at a time
- Improved prognosisby slowing, or even reversing, ventricular remodelling
- Fluid restriction: fluid intake is usually limited to <1.5L/day
- Loop diuretic (e.g. furosemide) forsymptomaticrelief of oedema
14
Q
What are the complications of ADHF?
A
- Arrhythmias: can both precipitate acute heart failure and occur as a result of it.
- Atrial fibrillation is one of the most common arrhythmias associated with heart failure.
15
Q
What is the prognosis of ADHF?
A
- Mortality for acute heart failure ranges from 2-20%.
- Poor prognostic factors include old age, hypotension, male sex, ischaemic congestive heart failure, renal dysfunction, previous chronic heart failure, a respiratory rate on admission > 30 and an elevated BNP.
16
Q
What is congestive heart failure?
A
In heart failure, cardiac failure describes when cardiac output cannot meet metabolic demands of the body.
Congestive cardiac failure describes a combination of left and right-sided ventricular failure.
17
Q
What is the epidemiology of Congestive HF?
A
- M>F
- More prevalent with increasing age
18
Q
What are general Risk factors for Congestive HF?
A
General:
- Male
- Increasing age
- Obesity
- Smoking
19
Q
What is the cardiovascular risk factors for HF?
A
Cardiovascular
- Previous myocardial infarction: the single greatest risk factor
- Ischaemic heart disease
- Hypertension
- Hypercholesterolaemia
- Valvular heart disease
- Cardiac arrhythmias: Atrial fibrillation
- Cardiomyopathy
20
Q
What are the respiratory Risk Factors for congestive HF?
A
Respiratory
- Cor pulmonale
- Respiratory conditions such as COPD cause pulmonary hypertension and subsequent right-sided heart failure.
21
Q
What are the other risk factors for congestive HF?
A
Other
- Diabetes mellitus
- Renal failure: causes ‘high-output’ heart failure due to fluid overload
-
Anaemia
- Poor oxygen carrying capacity results in the heart having to pump more blood resulting in ‘high-output’ failure.
- Hyperthyroidismresults in ‘high-output’ failure
22
Q
What is the causes congestive HF?
A
In heart failure, cardiac output struggles to meet the metabolic demands of the body.
It results when there is an insult to the heart resulting in compromise in systolic and/or diastolic function.
Heart failure can happen one of two ways: systolic failure or diastolic failure
Congestive cardiac failure describes a combination of left and right-sided ventricular failure (biventricular failure). Right-sided heart failure usually occurs as a result of left-sided heart failure. Blood starts backing up into the lungs causing pulmonary oedema and congestion. The pulmonary hypertension puts pressure on the right ventricle (cor pulmonale) and causes right-sided heart failure. The pulmonary congestion is responsible for the respiratory symptoms seen in heart failure.
MISSED IMAGE
23
Q
What is systolic HF?
A
- Cardiac output = stroke volume x heart rate
- The ejection fraction is not preserved: an ejection fraction of 40% or less would indicate systolic heart failure.
- The low stroke volume is due to the ventricles not pumping enough blood out.
The model on the left is a normal heart during systole, whilst the model on the right shows a dilated and hypertrophied heart, as seen in heart failure.
Left-sided ventricular dysfunction results in backflow into the pulmonary circulation, eventually causing right ventricular failure (congestive cardiac failure).
24
Q
What is diastolic HF?
A
- Cardiac output = stroke volume x heart rate
- In this case, the stroke volume is low but the ejection fraction is preserved. The reason for the low stroke volume is due to reduced filling of the ventricle (reduced preload)
25
What does congestive refer to?
The term ‘congestive’ refers to sodium and water retention.
26
What are the causes of systolic failure?
- **Systolic failure:**
- **Ischaemic heart disease**: as less blood and oxygen get to the myocardium, the myocytes start to die
- **Hypertension**: as arterial pressure increases in the systemic circulation, it gets harder for the left ventricle to pump blood out into that hypertensive systemic circulation.
- Left ventricular hypertrophy: increased muscle mass requires increased oxygen supply - making it more likely for that the muscle will die
- Dilated cardiomyopathy: heart chambers dilate and thin out, leading to weaker contractions.
27
What are the causes of diastolic failure?
- **Diastolic failure:**
- Left ventricular hypertrophy: causes the ventricular chamber to decrease in size which means less blood can enter.
- Restrictive cardiomyopathy: ventricle can't stretch enough to accommodate the blood
- **Valvular disease**: e.g. aortic stenosis causes LVH or mitral regurgitation means blood doesn't enter the ventricles in the right amount as it leaks back into atria
- Arrhythmias e.g. **atrial fibrillation**
28
What is the pathophysiology of Congestive HF?
- In a normal heart, increased ventricular filling results in increased contraction via the Frank-Starling law → increased cardiac output
- In patients with heart failure, this mechanism fails ****due to the ****
systolic and/or diastolic compromise → inadequate cardiac output
- As the heart continues to fail → **compensatory mechanisms** are activated to maintain cardiac output, including an **increase** in heart rate, **catecholamine release** and **RAAS activation** (due to decreased blood flow to kidneys)
- These mechanisms are useful in the **initial** period,
- but are usually overexpressed, thus instigating a vicious cycle → eventually lead to cardiac remodelling, which further exacerbate the heart failure
- Compensatory mechanisms are usually responsible for the fluid retention and fluid overload symptoms experienced by the patient
- **Medications** such as ACE inhibitors aim to target these compensatory pathways
29
What is the heart failure classification?
Heart failure can be classified according to the ejection fraction or the side of the heart affected:
1. Heart failure with reduced ejection fraction
- reduced ventricular contractility leading to systolic dysfunction
- causes: damage to Myocytes (e.g. ischaemic heart disease)
2. Heart failure with preserved ejection fraction
- reduced ventricular compliance leading diastolic dysfunction and reduced filling pressures
- causes: increased ventricular stiffness (e.g. HTN) or reduced relaxation (e.g. constrictive pericarditis)
3. Left sided Heart failure
- Backflow into the pulmonary circulation
- causes: increased LV afterload (e.g. HTN) or increased LV preload (e.g. aortic regurgitation)
4. Right sided HF
- backflow into systemic veins
- causes: increased RV afterload (e.g. pulmonary HTN) or increased RV preload (e.g. tricuspid regurgitation)
30
What is left sided heart failure?
Heart failure and a reduced ejection fraction. Usually caused by systolic (pumping) dysfunction.
**Left sided cardiac failure →**pulmonary congestion (heart is not able to pump efficiently so blood backs up in the veins that take blood through the lungs. Pressure in these vessels increases and fluid is pushed into the alveoli) and then overload of right side.
31
What is the aetiology of left sided heart Failure?
- IHD
- Hypertension
- As arterial pressure increases, harder for LV to pump blood out → LV hypertrophy → greater demand for oxygen
- Coronaries squeezed by extra muscle → less blood delivered to tissue
- Cardiomyopathy
- Dilated – heart chamber dilates (grows in size) in order to fill ventricle with more blood (increased preload)
- Over time, muscle wall gets thinner and weaker → systolic HF
- Restrictive – heart wall becomes stiff → less compliant → can’t stretch
- Aortic stenosis – narrowing of aortic valve
32
What is the pathophysiology of LSHF?
Systolic: Ischaemic heart disease, MI, cardiomyopathy
Diastolic: Tamponade, constrictive pericarditis, systemic hypertension
33
What is the epidemiology of LSHF?
- Annual incidence of 10% in patients over 65
- 50% of patients die within 5 years
34
What are some common clinical manifestation of HF?
It is important to note that approximately 15% of patients experience weight loss (‘cardiac cachexia’), which is often masked by the weight gain associated with fluid retention.
35
What are the symptoms of LSHF?
Dyspnoea: particularly exertional
Orthopnoea and paroxysmal nocturnal dyspnoea
Fatigue and weakness
Cough with pink frothy sputum
Cardiogenic wheeze
36
What are the signs of LSHF?
Trachypnoea and tachycardia
Cool peripheries
Peripheral or central cyanosis
Displaced apex beat
Stony dull percussion; if an effusion is present
Crackles on auscultation; coarse bi-basal crackles
Third heart sounds (S3)
37
What are the symptoms of Right sided HF?
Swelling in legs
Distended abdomen
Fatigue and weakness
38
What are the signs of RSHF?
Raised JVP
Peripheral pitting oedema
Hepatosplenomegaly
Ascites
39
What are the importantly signs and symptoms associated with congestive HF?
Coughing
Tiredness
Shortness of breath
Pulmonary edema (excess fluid in lungs)
Pumping action of the heart grows weaker
Pleural effusion (excess fluid around lungs)
Swelling in abdomen
Swelling in ankles and legs
40
What are the symptoms of LSHF?
- Exertional dyspnoea
- Fatigue
- **Weight loss**
- Paroxysmal nocturnal dyspnoea – attacks of severe SOB and coughing at night
- **Nocturnal cough – pink, frothy sputum**
- Orthopnoea – dyspnoea (SOB) that occurs when lying down
41
What are the signs of LSHF?
- **Cardiomegaly (displaced apex beat)**
- **Pulmonary Oedema**
- **3rd and 4th heart sounds**
- **Pleural effusion**
- **Crepitations in lung bases**
- **Tachycardia**
- Reduced BP
- Cool peripheries
- Heart murmur
42
What is the first line of investigations of LSHF?
**FIRST LINE:**
- NT-proBNP: should be done in all patients with suspected HF as a first-line investigation. If NT-proBNP is normal then heart failure is unlikely, but if it is positive then it does not necessarily confirm diagnosis of HF. Other investigations are required.
- ECG: should be done in all patients with suspected HF. Identifies potential aetiological factors (MI/arrhythmias) but is also necessary for treatment decisions eg rate control/anticoagulation for AF/pacing for bradycardia. A normal ECG makes HF very unlikely.
- CXR: classic ABCDE findings of alveolar oedema, Kerley B lines, cardiomegaly, dilated upper lobe vessels, pleural effusion.
43
What is the diagnostic investigations for LSHF?
**DIAGNOSTIC:**
- Echocardiography is the definitive diagnostic investigation. All patients should have transthoracic echocardiogram done within 2-6 weeks depending on NT-proBNP level in suspected chronic HF.
If acute HF suspected then should be done within 48hrs of admission
44
What are managements for LSHF grouped into?
Lifestyle
ACE inhibitors
Beta blockers
Diuretics
- Calcium glycoside – digoxin (inhibits Na/K pump) 🡪 slower HR
- Ventricular Assist Device
- Surgery
- **Heart transplant**
45
What is the lifestyle management of LSHF?
- Lifestyle
- Education
- Obesity control
- Diet
- Smoking cessation
- Cardiac rehab
46
What are the ACE inhibitors management for LSHF?
- **ACE** **inhibitors** – dilates blood vessels
- Ramipril, enalapril
- Side effects
- Cough - due to accumulation of bradykinin
- Hypotension
- Hyperkalaemia
- Renal dysfunction
- If cough is a problem then give angiotensin-II-receptor blocker e.g. candesartan, losartan
47
What are BB management for LSHF?
- **Beta blockers** - must give a lose dose 🡪 slow up titration
- Bisoprolol, metoprolol, propranolol
- Contraindicated in asthma and 3rd degree heart block
-
48
What are the diuretics for LSHF?
- **Diuretics –** promote Na+ and water loss 🡪 reducing ventricular filling (preload) 🡪 decreasing congestion
- Loop diuretic – furosemide
- Thiazide diuretic – Bendroflumethiazide (inhibits Na+ reabsorption in DCT)
- Aldosterone antagonist – spironolactone
49
What are the risk factors for life sided heart failure?
- Hypertension
- Hypercholesterolaemia
- Diabetes
- Obesity
- Smoking
- Physical inactivity
50
What is the differential diagnosis for LSHF?
- Acute respiratory distress syndrome
- Acute kidney injury AKI
- Bacterial pneumonia
- COPD
- Cardiomyopathies
51
What is heart failure?
Heart failure is a clinical syndrome rather than one specific disease.
52
What are the types of HF?
1. Right sided heart failure
2. Left sided heart failure
3. Systolic heart failure
4. Diastolic heart failure
53
Define HF?
Heart failure is a condition in which the heart is unable to generate a cardiac output sufficient to meet the demands of metabolising tissues without increasing diastolic pressure.
54
Define HF?
Heart failure is a condition in which the heart is unable to generate a cardiac output sufficient to meet the demands of metabolising tissues without increasing diastolic pressure.
55
What is the aetiology of Right sided Heart Failure?
- Left ventricular failure
- Fluid build up causes increased pressure in the pulmonary artery making it harder for the right side to pump blood into it.
- Cor pulmonale
- (This is a lung disease that causes right side of the heart to fail).
- This is a condition the essentially makes it harder to exchange oxygen.
- The pulmonary arterioles constrict, leading to an increase in pulmonary blood pressure.
- This makes it harder for the right valve to pump against resulting in hypertrophy (enlargement/thickening of heart wall) and heart failure.
- Pulmonary hypertension
- Pulmonary stenosis
- Atrial / Ventricular shunt
- Blood moves from the left to right side leading to Right ventricular hypertrophy.
56
What causes RSHF?
Note: Right sided heart failure is often caused by left sided heart failure and it can be developed acutely or chronically.
57
What is the pathophysiology of RSHF?
-
- When the heart starts to fail many bodily systems are involved in initiating physiological compensatory changes.
- Sympathetic nervous system
- Renin angiotensin aldosterone system
- The changes try to maintain cardiac output and peripheral perfusion in order to negate the effects of heart failure.
- But as heart failure progresses the compensenstary changes become pathological.
58
What is the epidemiology of RSHF?
Womens incidence increases at a later age.
59
What are the symptoms for RSHF?
- Shortness of breath
- Peripheral oedema
- Nausea
- Anorexia
- Ascites (fluid collects in the spaces within your abdomen)
- Fatigue
60
What are the signs of RSHF?
- Raised jugular venous pressure - JVP distension
- Hepatosplenomegaly (a disorder where both the liver and spleen swell beyond their normal size).
- Pitting oedema
- sacral/leg oedema in bed bound patients which causes a pit when pressed.
- Ascites
- Weight gain (fluid)
- Pleural effusion (“water on the lungs,” is the **build-up of excess fluid between the layers of the pleura outside the lungs**.)
61
What are the investigations for RSHF?
1. Chest X Ray - ABCDE:
- Alveolar oedema (bat wings)
- kerley B lines (interstitial oedema)
- Cardiomegaly
- Dilated upper lobe vessels of lung
- Effusion (pleural)
2. Bloods:
- B-type Natriuretic Peptide
- It is increased in patients with heart failure and is secreted by ventricles in response to increased myocardial wall stress.
- The levels of it correlate with ventricular wall stress and severity of heart failure.
- But it is not specific as it may be raised in acute pulmonary embolism.
- FBC
- LFTs
- U&Es
- TFTs
3. ECG - May show evidence of underlying causes.
4. Transthoracic echocardiogram - If the ECG and BNP is abnormal an echocardiogram needs to happen
62
What is the management for Acute RSHF?
- Acute heart failure
- Oxygen
- Pain relief - Opiates e.g., Diamorphine IV
- Diuretic - Furosemide IV
- Nitrates - GTN spray
63
What are the lifestyle managements for RSHF?
Education
- Obesity control
- Diet
- Smoking Cessation
- Cardiac rehab
64
What are the pharmaceutical managements for RSHF?
- ACE inhibitors - Ramipril
- Beta blockers - Bisoprolol
- Diuretics - Thiazide diuretic (Bendroflumethiazide), Loop diuretic (Furosemide)
- Calcium glycoside - digoxin
Transplantation
65
What are the complications for RSHF?
- Arrhythmias
- Renal dysfunction
66
What are the Risk factors for RSHF?
Over the age of 65
- Male gender
- Obesity
- Family history of MI
- Those who have had previous MI
67
What is Brain natriuretic peptide?
Brain natriuretic peptide (BNP) is a natriuretic hormone released primarily from the heart, particularly the ventricles.
68
How does BNP work?
- Cleavage of the prohormone proBNP produces biologically-active **BNP** and biologically inert, **NT-proBNP**
- Both would be expected to be **increased** in heart failure as ventricular cells secrete BNP in response to high ventricular filling pressure
- A very high BNP level is associated with a **poor prognosis**
69
What are BNP results values?
An urgent echocardiogram should be considered in patients with acute heart failure within 48 hours of admission.
Acute HF: BNP= <100 pg/ml|NT-proBNP=<300pg/ml
= suggests an alternative diagnosis?
For patients with suspected chronic heart failure, NICE recommends NT-proBNP as the first-line investigation.
Chronic HF:
BNP - NT-proBNP
- Normal: <100pg/ml | <400pg/ml
- Raised: 100-400 pg/ml | 400-2000pg/ml
- High: >400pg/ml | >2000 pg/ml
70
What do BNP results mean?
Normal: rules out decompensated heart failure
- Raised: arrange a specialist assessment and transthoracic echocardiogram within 6 weeks
- High: arrange a specialist assessment and transthoracic echocardiogram within 2 weeks
71
What cardiac causes increase BNP?
- Left ventricular hypertrophy
- Right ventricular overload
- Diastolic dysfunction
- Atrial fibrillation
- Acute coronary syndrome
- Valvular heart disease (e.g., aortic stenosis)
72
What are the non-cardiac causes of BNP?
**Non-cardiac causes**
- Acute pulmonary embolism
- Pulmonary hypertension
- COPD with cor pulmonale
- Hyperthyroidism
- Sepsis
- Acute kidney injury or chronic kidney disease
- Diabetes
Other
- Age > 70
73
What can decrease BNP levels?
- ACE-inhibitors and ARBs
- Aldosterone antagonists
- Diuretics
- Obesity
74
What is the severity criteria of HF?
The New York Heart Association (NYHA) classification system is reflective of functional limitations associated with heart failure.
Class 1: mild - no limitation of physical activity
- ordinary physical activity does not cause fatigue, palpitations or dyspnoea
Class 2: mild - slight limitation of physical activity
- comfortable at rest, but ordinary physical activity results in fatigue, palpitations or dyspnoea
Class 3: moderate - marked limitation of physical activity
- comfortable at rest, but mild activity causes fatigue palpitations or dyspnoea
Class 4: severe - cannot carry out physical activity without discomfort
- symptoms of cardiac insufficiency at rest
75
What are the primary investigations for congestive HF?
- Primary investigations
- **NT-proBNP:** increased in chronic heart failure
- **ECG:** broad QRS complexes; evidence of left ventricular hypertrophy
- **CXR:**
- **A** - **A**lveolar oedema (batwing opacities)
- **B** - Kerley **B** lines
- **C** - **C**ardiomegaly
- **D** - **D**ilated upper lobe vessels
- **E** - Pleural **e**ffusion
- **Transthoracic echocardiogram:** determine left ventricular ejection fraction (LVEF), diastolic function, and valvular abnormalities
76
What are some other investigations for congestive HF?
- Other investigations to consider in chronic congestive heart failure:
- **FBC:** anaemia may be a cause of ‘high-output’ heart failure
- **U&Es**: to investigate for renal failure as an underlying cause of heart failure; also U&Es monitored as ACEi's and aldosterone antagonists can cause electrolyte abnormalities
- **Blood lipids and fasting blood glucose:** screen for hypercholesterolaemia and evidence of diabetes
- **Loop diuretic (e.g. furosemide):** symptomatic relief of fluid overload but no improvement in prognosis.
77
What is the 1st line management for Congestive hF?
- 1st line
- **Beta-blocker e.g. bisoprolol and ACE inhibitor e.g. ramipril**: start one drug at a time.
- *Beta-blockers and ACE inhibitors shown to improve mortality but not in heart failure with preserved ejection fraction*
- Beta-blockers **licensed** in the UK for heart failure include bisoprolol, carvedilol, and nebivolol
- If ACE inhibitor is not tolerated: **angiotensin receptor blocker** (e.g losartan) or **hydralazine with nitrate** (particularly in Afro-Caribbean patients)
78
What is the 2nd line management for Congestive HF?
- 2nd line
- **Aldosterone antagonist** (e.g. spironolactone) if symptoms not controlled with 1st line management
79
What is the 3rd line management for congestive HF?
- 3rd line
- **Cardiac resynchronisation therapy** **(CRT):** involves biventricular pacing and forces both ventricles to contract in synchrony, thereby improving cardiac output
OR
- **Implantable cardioverter-defibrillator (ICD):** able to perform cardioversion, defibrillation and, in some cases, pacing
- **CRT or an ICD** is generally indicated in: **symptomatic** patients with an ECG indicating **ventricular dyssynchrony** (e.g. QRS >120ms) **AND** LVEF **<35%**
- **Digoxin**: an alternative option, particularly for patients with Atrial fibrillation and heart failure due to its inotropic effects.
- It does not improve prognosis in patients with heart failure.
- **Ivabradine**: an alternative option if HR >75 bpm,**NHYA class II-IV,** and LVEF <35%, and the patient is already on suitable medication (i.e.. bisoprolol, ramipril and spironolactone).
- It slows the heart rate so the heart can pump more blood through the body each time it beats.
80
What are some other considerations for management of congestive HF?
- Smoking cessation, diet changes, exercise
- **Fluid restriction**: usually limited to <1.5L/day
- **Annual influenza vaccine** and **one-off pneumococcal vaccine**
- **Sacubitril-valsartan (Entresto):** consider if the patient is symptomatic on an ACE inhibitor or ARB **AND** has a reduced LVEF; works by relaxing blood vessels so that blood can flow more easily, making it easier for heart to pump blood. Initiate **after** ARB/ACEi ‘wash-out’ period.
- **Cardiac transplantation**: considered for patients with severe refractory symptoms or refractory cardiogenic shock
- **Surgical replacement of valve** if valvular disease
- **Avoid** verapamil, diltiazem and short-acting dihydropyridine agents in people who have heart failure with a reduced LVEF
81
What are some complications of Congestive HF?
- **Pleural effusion:** heart failure causes an elevated pulmonary capillary pressure, usually resulting in bilateral transudative pleural effusions
- **Acute decompensation of chronic heart failure:** patients usually present with acute respiratory distress due to significant pulmonary oedema
- **Acute renal failure:** reduced cardiac output and drug overuse (ACE inhibitors, aldosterone antagonists, diuretics) results in poor renal perfusion
- Arrhythmias ****
82
What is the prognosis of Congestive HF?
- In general, the survival of patients with end-stage heart failure is poor.
- For example, 65% of patients in NYHA class IV are alive at 17-month follow-up.
83
What is ischaemic HF?
Ischaemia is the insufficient supply of blood to an organ or tissue, usually as a result of narrowing or blockage of an artery.
84
What is the aetiology of HF?
- Coronary artery disease (atherosclerosis)
- Blood clot-due to plaque rupturing
85
What is the pathophysiology of ischaemic HF?
- Pathophysiology
- Myocardial ischemia occurs when blood flow to your heart is reduced, preventing the heart muscle from receiving enough oxygen.
- The reduced blood flow is usually the result of a partial or complete blockage of your heart's arteries (coronary arteries).
- Reduces the heart muscle's ability to pump blood.
86
What is the pathophysiology of ischaemic HF?
- Pathophysiology
- Myocardial ischemia occurs when blood flow to your heart is reduced, preventing the heart muscle from receiving enough oxygen.
- The reduced blood flow is usually the result of a partial or complete blockage of your heart's arteries (coronary arteries).
- Reduces the heart muscle's ability to pump blood.
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What are the signs and symptoms of ischaemic HF?
- Signs & Symptoms
- Neck or jaw pain.
- Shoulder or arm pain.
- A fast heartbeat.
- Shortness of breath when you are physically active.
- Nausea and vomiting.
- Sweating.
- Fatigue.
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What are the investigations of Ischaemic HF?
- ECG
- Bloods
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What is the management of Ischaemic HF?
Lifestyle changes
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What are the complications of Ischaemic HF?
- Heart attack
- Heart failure
- Arrythmia-irregular heart rythm
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What are the complications of Ischaemic HF?
- Heart attack
- Heart failure
- Arrythmia-irregular heart rythm
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What are the risk factors of Ischaemic HF?
- Obesity
- Lack of exercise
- Smoking
- Diabetes
- High blood pressure
- High cholesterol
- Hyperlipidaemia
