Cardiac Failure Flashcards
Explain how the RAAS system usually works [+]
Angiotensinogen is converted to angiotensin I under the action of renin
Angiotensin I is then converted to angiotensin II under the act of angiotensin converting enzyme (ACE)
Angiotensin II then:
i) proximal tubule: Increases Na+ reabsorbtion, which increases blood flow, which increases BP
ii) adrenal cortex: increases aldosterone, which causes increase Na+ & H20 reabsorbtion in distal tubule, increase bloodflow and BP
iii) systemic arterioles: binds to GPCR = artriolar vasoconstriction = increases BP
iv) brain: stimules release of ADH = increase Na reabsorbtion
This results in the increased volume of the blood which in turn increases blood pressure and thus venous pressure which in turn increases pre-load thereby increasing the stretching of the heart and thus force of contraction and thus stroke volume and thus cardiac output
Describe what is meant by the term acute heart failure [1]
What is the general aetiological cause of HF? [1]
Acute heart failure (AHF) is life-threatening emergency. AHF is a term used to describe the sudden onset or worsening of the symptoms of heart failure.
AHF is usually caused by a reduced cardiac output that results from a functional or structural abnormality.
Describe the pathophysiology of acute onset HF [2]
AHF involves the acute failure of the heart to pump blood to meet the body’s demand.
As a result, two courses of pathology develop:
Congestion in the pulmonary or systemic circulation.
* Pulmonary oedema develops when the left ventricle is unable to empty, which increases the hydrostatic pressure in pulmonary vasculature leading to pulmonary oedema and hypoxia.
These patients are ‘WET’.
Hypoperfusion
* of vital organs as the cardiac output is reduced.
* These patients are ‘COLD’.
What is de-novo acute heart failure caused by? [4]
Describe pathophysiology of de-novo acute heart failure [3]
De-novo acute HF: caused by and increased cardiac filling pressures and myocardial dysfunction usually as a result of ischaemia.
This causes reduced cardiac output & therefore hypoperfusion.
This, in turn can cause pulmonary oedema.
Caused by:
* Ischaemia
* Viral myopathy
* Toxins
* Valve dysfunction
Decompensated heart failure accounts for most cases of AHF.
What are the most common precipitating causes of acute AHF? [4]
- Acute coronary syndrome
- Hypertensive crisis: e.g. bilateral renal artery stenosis
- Acute arrhythmia
- Valvular disease
There is generally a history of pre-existing cardiomyopathy. It usually presents with signs of fluid congestion, weight gain, orthopnoea and breathlessness.
CHAMP
Acute coronary syndrome (ACS)
Hypertensive crisis
Arrhythmias, e.g. atrial fibrillation, ventricular tachycardia, bradyarrhythmia
Mechanical problems, e.g. myocardial rupture as a complication of ACS, valve dysfunction
Pulmonary embolism
50% of patients will show signs of congestion without signs of hypoperfusion (WET-WARM).
45% of patients will show signs of congestion with signs of hypoperfusion (WET-COLD).
5% of patients will show no signs of congestion (DRY-WARM or DRY-COLD).
Describe how you manage an acute heart failure patient [+]
Oxygen
- Patients often require 15L/minute with a reservoir mask.
- reassess and down-titrate oxygen to avoid hyper-oxygenation which is associated with worsening myocardial ischaemia and other pathology.
Loop diuretics:
- All ‘WET’ patients will require diuretics as the cornerstone of their management.
- 40 milligrams furosemide intravenously initially to improve symptoms of congestion fluid overload.
Nitrates:
- sublingual glyceryl trinitrate or intravenous nitrates
- Do not use nitrates in those with SBP < 90mmHg or aortic stenosis, who rely on sufficient preload to overcome their pressure gradient.
NIV:
- for those with cardiogenic pulmonary oedema or dyspnoea
- improves ventilation to reduce respiratory distress and drives fluid out of alveoli
What are the signs [6] and symptoms [4] of AHF?
How does blood pressure present with regards to AHF? [1]
Symptoms:
* Breathlessness
* Reduced exercise tolerance
* Oedema
* Fatigue
Signs
* Cyanosis
* Tachycardia
* Elevated jugular venous pressure
* Displaced apex beat
* Chest signs: classically bibasal crackles but may also cause a wheeze
* S3-heart sound
Over 90% of patients with AHF have a normal or increased blood pressure (mmHg).
What is the difference between Low and High Output Failure?
low output failure:
- Traditional concept of heart failure where the heart cannot maintain an adequate cardiac output to meet the demands of the body.
- results in increased systemic vascular resistance in an attempt to maintain mean arterial pressure
High output failure:
- high cardiac output (i.e. > 8L/min)
- heart is unable to meet the increased demand for perfusion despite normal cardiac function.
- The problem is with reduced systemic vascular resistance, often due to diffuse arteriole vasodilatation or shunting
- It is generally due to states of increased metabolic demand (e.g. hyperthyroidism), reduced vascular resistance (e.g. thiamine deficiency, sepsis) or significant shunting (e.g. large arteriovenosu fistula).
Describe what is meant by the Frank-Starling principle [1]
Essentially stretching of cardiac muscle (within physiological limits) will increase the force of contraction.
Increased venous pressures lead to increased venous return and raised end diastolic volume (EDV)
This increased EDV means an increase in the preload as there is increased stretch on the cardiomyocytes
This increased stretching - an increase in the length of the sarcomere - leads to a more forceful contraction. In turn, this increase in contractility leads to an increase in the stroke volume.
Describe the pathophsiology of chronic heart failure [+]
Chronic heart failure refers to the clinical features of impaired heart function, specifically the function of the left ventricle to pump blood out of the heart and around the body - i.e. the ejection fraction decreases
This increased end-systolic volume (ESV) means the myocardium experiences greater stretch.
In a normal heart, this would lead to an increase in myocardial contractility by the Frank-Starling principle. However, in a failing heart, this causes a reduction in stroke volume (and thus cardiac output). This is because the relationship between cardiomyocyte stretch and contractility cannot continue unfettered.
Impaired left ventricular function results in a chronic backlog of blood waiting to flow into and through the left side of the heart
The left atrium, pulmonary veins and lungs experience an increased volume and pressure of blood.
They start to leak fluid and cannot reabsorb excess fluid from the surrounding tissues, resulting in pulmonary oedema.
Explain how the heart tries to compensate for a failing heart [4]
Increasing preload (increasing venous pressures):
* Increases end-diastolic volume (EDV) compensating for the reduced ejection fraction, thus maintaining cardiac output.
* In severe disease, large increases result in pulmonary oedema, ascites and peripheral oedema.
Increasing heart rate (a sinus tachycardia)
Activation of the renin-angiotensin-aldosterone system (RAAS)
* due to renal hypoperfusion from the reduced cardiac output.
* contributes to increased venous pressures through vasoconstriction and there is retention of water and sodium that contributes to oedema.
Sympathetic nervous system activation
* via baroreceptors; increasing myocardial contractility and heart rate
How do you calculate cardiac output? [1]
cardiac output = stroke volume x heart rate
- Heart rate: number of times the heart beats each minute
- Stroke volume: the amount of blood pumped by the left ventricle with each contraction
How do you work out MAP? [1]
MAP = diastolic blood pressure + 1/3rd of the pulse pressure
MAP is dependent on the cardiac output and systemic vascular resistance
* Cardiac output: the amount of blood pumped out the heart each minute. Measured in litres per minute (L/min).
* Systemic vascular resistance: resistance to blood flow offered by all of the systemic vasculatures, excluding the pulmonary vasculature.
Describe why right sided heart failure may occur [4]
Right-sided heart failure commonly occurs as a result of advanced left-sided failure.
Primary right-sided heart failure is uncommon and broadly related to three categories:
* Pulmonary hypertension
* Pulmonary/Tricuspid valve disease
* Pericardial disease
Also:
* Pneumonia
* Pulmonary embolism (PE)
* Mechanical ventilation
* Acute respiratory distress syndrome (ARDS)
Pulmonary hypertension may occur secondary to left-sided heart disease, primary pulmonary hypertension or significant pulmonary disease (e.g. COPD).
What are the five overarching causes of chronic heart failure? [5]
State common causes for each [+]
Vascular
* Ischaemic heart disease
* Hypertension
Muscular
* Dilated cardiomyopathy (30%)
* Hypertrophic cardiomyopathy
* Congenital heart disease
Valvular
* Commonly aortic stenosis
Arrhythmias
* commonly atrial fibrillation
High-output failures
* Anaemia
* Septicaemia
* Thyrotoxicosis
* Liver failure
High output failures:
- Typically heart failure is caused by a reduced cardiac output. In some cases, however, the cardiac output may be raised but the systemic vascular resistance very low
What is a normal EF? [1]
An ejection fraction above 50% is considered normal.
Describe what is meant by heart failure with reduced ejection fraction? [1]
Describe what is meant by heart failure withpreserved ejection fraction? [1]
HFrEF:
* ejection fraction is less than 50%.
HFpEF:
* when someone has the clinical features of heart failure but an ejection fraction greater than 50%.
* result of diastolic dysfunction, where there is an issue with the left ventricle filling with blood during diastole (the ventricle relaxing).
Describe the different NYHA classifications for the severity of HF [4]
NYHA Class I
* no symptoms
* no limitation: ordinary physical exercise does not cause undue fatigue, dyspnoea or palpitations
NYHA Class II
* mild symptoms
* slight limitation of physical activity: comfortable at rest but ordinary activity results in fatigue, palpitations or dyspnoea
NYHA Class III
* moderate symptoms
* marked limitation of physical activity: comfortable at rest but less than ordinary activity results in symptoms
NYHA Class IV
* severe symptoms
* unable to carry out any physical activity without discomfort: symptoms of heart failure are present even at rest with increased discomfort with any physical activity
What are the symptoms of HF? [6]
- Breathlessness, worsened by exertion
- Cough, which may produce frothy white/pink sputum
- Orthopnoea, which is breathlessness when lying flat, relieved by sitting or standing (ask how many pillows they use)
- Paroxysmal nocturnal dyspnoea (suddenly waking at night with a severe attack of shortness of breath, cough and wheeze.)
- Peripheral oedema
- Fatigue
Describe the signs of HF [+]
- Tachycardia (raised heart rate)
- Tachypnoea (raised respiratory rate)
- Hypertension
- Murmurs on auscultation indicating valvular heart disease
- Peripheral oedema of the ankles, legs and sacrum
- Raised JVP
- Displaced apex
- Heart sounds S3/S4
- Pulsus alternans
- Hepatomegaly
- Ascites
Describe what is meant by Paroxysmal Nocturnal Dyspnoea (PND) [2]
Explain why this occurs [3]
Experience that patients have of suddenly waking at night with a severe attack of shortness of breath, cough and wheeze.
They may describe having to sit on the side of the bed or walk around the room, gasping for breath
Pathophysiology:
- Fluid settles across a large surface area of the lungs as they lie flat to sleep, causing breathlessness. As they stand up, the fluid sinks to the lung bases, and the upper lung areas function more effectively
AND
- respiratory centre in the brain becomes less responsive. the respiratory rate and effort do not increase in response to reduced oxygen saturation like they would when awake.
AND
- there is less adrenalin circulating during sleep. Less adrenalin means the myocardium is more relaxed, reducing cardiac output.
Describe how you investigate for HF [+]
All patients given N-terminal pro-B-type natriuretic peptide (NT‑proBNP) blood test first-line:
- If high: arrange specialist assessment (including transthoracic echocardiography) within 2 weeks
- if levels are ‘raised’ arrange specialist assessment (including transthoracic echocardiography) echocardiogram within 6 weeks
Other investigations include:
* ECG
* Bloods for anaemia, renal function, thyroid function, liver function, lipids and diabetes
* Chest x-ray and lung function tests to exclude lung pathology
B-type natriuretic peptide (BNP) is a protein released by cardiomyocytes in response to excessive stretching
What are you looking for to that might indicate HF in an ECHO [3] or CXR [5]
Echocardiogram:
* Evidence of previous MI
* Left ventricular strain / hypertrophy
* Conduction abnormalities / AF
CXR:
* Cardiomegaly (Cardiothoracic ratio > 50% on PA film)
* Alveolar shadowing oedema
* Kerley B lines (fluid in septae of secondary lobules)
* Pleural effusion
* Upper lobe diversion
What are normal, raised and high levels of BNP and NTproBNP? [9]
Explan your answer [1]
Left ventricular aneurysm
The ischaemic damage sustained may weaken the myocardium resulting in aneurysm formation. This is typically associated with persistent ST elevation and left ventricular failure. Thrombus may form within the aneurysm increasing the risk of stroke. Patients are therefore anticoagulated.
A patient has chronic heart failure. You trial and ACEI but the patient is intolerant.
You then trial an ARB, but the patient is still intolerant.
What treatment should you consider nexr? [1]
Hydralazine and nitrate
A patient has chronic heart failure.
You iniate an ACEin and a BB as first line treatment. This does not resolve their EF.
You next trial and aldosterone antagonist. This does also not help.
They are Afro-Carribean.
What is the appropriate third line treatment?
- Ivabradine
- sacubitril-valsartan
- digoxin
- hydralazine in combination with nitrate
- cardiac resynchronisation therapy
- hydralazine in combination with nitrate
A patient has chronic heart failure.
You iniate an ACEin and a BB as first line treatment. This does not resolve their EF.
You next trial and aldosterone antagonist. This does also not help.
They have LVEF < 35% and symptomatic
What is the appropriate third line treatment?
- Ivabradine
- sacubitril-valsartan
- digoxin
- hydralazine in combination with nitrate
- cardiac resynchronisation therapy
A patient has chronic heart failure.
You iniate an ACEin and a BB as first line treatment. This does not resolve their EF.
You next trial and aldosterone antagonist. This does also not help.
They have LVEF < 35% and symptomatic
What is the appropriate third line treatment?
sacubitril-valsartan
