Cardiovascular Disease 2 PDF

Cardiovascular Disease 2 Within this study block we will expand upon the learning from the cardiovascular disease 1 section and look into other heart conditions as well as some medications used for these. We will begin by reviewing the learning on the heart from last year to ensure that you remembe...

Cardiovascular Disease 2 Within this study block we will expand upon the learning from the cardiovascular disease 1 section and look into other heart conditions as well as some medications used for these. We will begin by reviewing the learning on the heart from last year to ensure that you remember how the heart works- you may want to revisit CVD1 to re-familiarise yourself with the heart and circulatory system. Arrhythmia will be described and the different types of arrhythmia, their presentations and treatments will be reviewed before looking at management of arrhythmia and the risk factors caused by arrhythmia. We will then look at Heart failure; expanding upon what it is, why it occurs and how it can be treated- both pharmacologically and non-pharmacologically. Deep-vein thrombosis is another condition relating to the cardiovascular system that can cause major issues if not treated promptly. We will learn what it is, how it occurs and how to treat as well as prevent it. In relation to this will will explore the various anticoagulants that are available and consider the approaches to treatment with these drugs. This will include Warfarin- for which we will learn about the INR test and the importance of appropriate management in patient care. We will explore anaemia and understand what the signs/symptoms are, the types of anaemia that exist and ways to treat the more common forms of anaemia, before finally reviewing kidney failure. Patients with kidney failure require extra consideration in drug dosing and general patient care, having an knowledge of what kidney failure is and how it may affect medication can ensure that you understand the extra risks associated with these patients. By the end of this section you will be able to: Explain how the body controls the heart rate Describe the different types of arrhythmia List the symptoms of arrhythmia Discuss the pharmacological and non-pharmacological treatments of arrhythmia Describe the causes of heart failure Compare acute vs chronic heart failure Describe the clinical features (symptoms) of heart failure Detail how patients are diagnosed with heart failure Outline the guidance for medicines used in heart failure Give appropriate non-pharmacological advice to patients with heart failure. Describe the processes of blood clotting. Explain the differences between certain types of blood clot, such as pulmonary embolisms and deep-vein thromboses. Articulate the medical approaches to identifying and managing deep-vein thromboses. List the common treatments for for deep-vein thromboses. Summarise the method of action of common anticoagulants Distinguish between the different groups of anticoagulants Describe how INR can be altered and the importance of monitoring Define anaemia and list the common signs/symptoms Describe the treatments of iron deficiency and folate deficiency anaemia Describe what kidney failure is and the how it can occur Outline the treatments and considerations that need to be taken into account in patients with kidney failure Learning Outcomes Review of the heart Arrythmias Heart Failure Deep-vein thrombosis Anticoagulants and Fibrinolytics Anaemia Acute Kidney Injury Kidney failure Summary Lesson 1 of 10 Learning Outcomes  GPhC Learning Outcomes This study block of medicines, diseases and health will support development in the following GPhC learning outcomes: 13. Apply professional judgement in best interests of people 14. Recognise and work within the limits of their knowledge and skills, and refer to others when needed 15. Understand how to work within local, regional and national guidelines and policies 17. Use information to make effective decisions 28. Understand the basic, principles of biology, microbiology and chemistry 29. Understand the basic pharmacological principles that apply to the use of medicines in relation to disease processes and the treatment of identified clinical condition 30. Confirm the suitability of a person’s medicines for use 42. Recognise adverse drug reactions and interactions and respond appropriately 44. Respond appropriately to medical emergencies, including providing first aid  Apprenticeship Standards In addition this learning will cover the following apprenticeship standards for England: K3: Understand the science of pharmacy, basic pharmacological principles, actions and use of drugs K6: How to apply professional judgement in the best interests of people K15: Understand the importance of effective methods of communication to different audiences K16: Know how to manage a person’s diverse needs and what is important to them K17: Know how to provide and promote advice on healthy lifestyles and initiatives, using available resources and evidence-based techniques K18: Understand how to effectively collaborate and work with colleagues and health care professionals K23: Know how to work within any local, regional and national guidelines and policies S1: Recognise and work within their scope of practice and skills, S2: Use relevant data and information to make effective decisions S11: Provide a safe, effective and responsive pharmacy service S30: Respond to medical emergencies B4: Respect all individual’s values and confidentiality B5: Value diversity and respect cultural differences – making sure that every person is treated fairly and with respect Complete the content above before moving on. Lesson 2 of 10 Review of the heart Review of the heart We looked at the heart and its role in blood pressure last year. If you need a refresher the interactive video is shown below, you may also want to revisit the previous cardiovascular disease module to refresh your knowledge as many of the medications will be discussed within this section too. Thumbnail the heart intro transcript.docx 13.8 KB Review As you can see, the heart is made up of two pumps working together. - Blood from muscles & organs enters right side - Heart pumps the blood to the lungs - Takes up oxygen & eliminates carbon dioxide - Oxygen rich blood enters left side of the heart - Pumped through arteries to organs & tissues - Regulated by a system of valves which ensures blood flows in correct direction Average readings It can be useful to have an awareness of some of the average monitoring parameters which for a healthy adult. You do not need to remember these. Monitoring Parameter Average reading Cardiac output ~5l/min Mean heart rate ~70bpm Stroke volume ~70ml Filled ventricle ~130ml > 50% of ventricle ⇒ fraction ejected contents Before you continue... Please ensure you take a moment to review the cardiovascular material and medicines from Year 1 before continuing with the study block. Lesson 3 of 10 Arrythmias Normal heart rate Most adults have a resting heart rate between 60 and 100bpm (beats per minute). The fitter you are, the lower your resting heart rate is likely to be. For example, athletes may have a resting heart rate of 40 to 60bpm, or lower. If someone thinks that their heart rate is continuously below 60 or above 120bpm then they should be advised to see their healthcare professional. Normal heart rhythm The normal heart rhythm is called sinus rhythm; although the rate will vary between patients, the pulse should be regular. Although it is very common to have occasional irregular heartbeats, such as missed beats, an irregular pulse may be a sign of cardiac disease and the patient should be referred to their GP. Normal electrical control of the heart The rhythmic contraction of the heart is controlled by electrical signals within the heart. A chamber of the heart beats when an electrical impulse passes across it and causes it to contract. The electrical signals are generated from an area of nerve tissue in the right atrium called the sinoatrial (SA) node - it is sometimes referred to as the heart's pacemaker. Each time an electrical signal is generated in the SA node and passes around the rest of the heart, this causes the heart to beat once. The video below shows this happening: Basic Heart Function: Electrical Activity (Part 3) What is an arrhythmia? An arrhythmia is when the normal rate or rhythm of the heart changes. Some are benign (cause no harm) and some can be fatal. Arrhythmias are described in terms of where they occur: Supraventricular arrhythmias occur in the area above the ventricles ("supra" = above) - the atria, the junction between the atria and ventricles (atrio-ventricular junction) or the AV node. Ventricular arrhythmias occur within the ventricles and the effect they have on the heart rate:  Bradycardia - slow heart rate - less than 60bpm Tachycardia - fast heart rate - greater than 100bpm Symptoms of arrhythmias Symptoms will vary in severity from patient to patient, and can include: palpitations dizziness/feeling light headed fainting shortness of breath chest pain fatigue pounding sensation in neck Some patients may lose consciousness, and in a small number the arrhythmia will lead to a cardiac arrest. Some patients have no symptoms at all and are diagnosed by chance when being investigated for something else. How are arrhythmias diagnosed? PH YS ICA L E X A MIN A T IO N E L E CT R O CA R DIO GR A M (E CG) Examining the patient physically won't diagnose the specific type of arrhythmia but will help decide if the patient needs further investigations. A clinician will check: Pulse - is it too slow, too fast or irregular? Listening to the heart - are there irregular heart sounds? PH YS ICA L E X A MIN A T IO N E L E CT R O CA R DIO GR A M (E CG) This records the electrical activity of the heart, and can therefore detect an abnormal heart rate or rhythm. Each type of arrhythmia will show a characteristic pattern on an ECG, which will help diagnosis. Note: You do not need to know about ECGs in detail. The video below shows a patient having an ECG. There are various types of ECG - you can find more information here.  British Heart Foundation - Your guide to ECG (electrocardi… (electrocardi… Types of arrhythmias Bradycardias Sinus bradycardia Decreased heart rate but with normal rhythm Heart block This is failure to conduct electrical signals across the entire heart. The most common type of heart block is AV block which is where the electrical impulse generated by the SA node travels across the atria but is blocked at the AV node before it can reach the ventricles. Can be caused by acute MI, infection and some drugs e.g. beta-blockers, digoxin, verapamil Tachycardias Sinus tachycardia Increased heart rate but with normal rhythm - this is the normal response to exercise. Other causes include infection, hypotension, anaemia, hyperthyroidism. It is a side effect of several drugs, e.g. nicotine, beta-agonists (salbutamol), levothyroxine, theophylline Treatment involves treating the underlying cause or stopping the drug that has caused it. Atrial fibrillation (AF) In AF, the heart's electrical signal doesn't begin in the SA node but instead begins in another part of the atrium or the nearby pulmonary veins. The signals spread in a disorganized way through the atria which causes them to quiver, or fibrillate rapidly (300-600 bpm). The irregular rhythm is transmitted to the ventricles, causing the heart to beat too fast (100-180 bpm). AF is covered in more detail below. Ventricular fibrillation (VF) Rapid and uncoordinated contraction of the ventricles which severely reduces cardiac output (the amount of blood the heart is able to pump round the body). People with VF will lose consciousness within 20-30 seconds. It is the most common cause of death due to acute myocardial infarction. Ventricular tachycardias (VT) Lots of people experience occasional palpitations caused by extra ventricular beats - these are called 'ectopics'. Frequent runs of ectopic beats indicates that something more serious is going on. Causes include: Acute MI, IHD, myocarditis (inflammation of the heart tissue), diseases of the valves within the heart. Torsade de pointes is a specific type of VT which is due to QT prolongation - this is named after a change on the patient's ECG, and you may have heard the term before as it can be caused by many different drugs. The risk is increased if a patient is taking more than one drug which has the potential to cause QT prolongation. Examples include: macrolide antibiotics tricyclic antidepressants other antidepressants - citalopram, venlafaxine lithium fluconazole NOTE: you are not expected to remember this list, it is provided to illustrate how a serious side effect can be caused by several common medicines. The video below shows how the common types of arrhythmia affect the heart. Heart arrhythmias: what are the common types? | Bupa H… H… Non-drug management of arrhythmias Although we don't get involved in these treatments, it might be useful for you to be aware of them in case a patient refers to them in a consultation. Permanent Pacemaker (PPM) A small electrical device is inserted in “skin-pocket” below collar bone and leads are inserted into heart which sense electrical activity within heart. It delivers a small electrical impulses to myocardial tissue if detect inappropriate rhythm, which puts the heart back into sinus rhythm. Defibrillation Delivery of an electric shock to the myocardium (heart tissue) across the chest wall; this is used in conjunction with CPR when someone is in cardiac arrest. Cardioversion This is the process of restoring the heart's normal rhythm by applying a controlled electric shock (defibrillation) across the chest wall while the patient is anaesthetised. Ablation The precise part of the heart tissue which is generating the arrhythmia is destroyed, which disrupts the conduction pathway and stops the arrhythmia from occurring. You can find more about these procedures here. Atrial fibrillation (AF) We are focusing specifically on AF because it is the most common supraventricular tachycardia, affecting about 1 in 20 of people over 65yrs in UK. It is more common in men than women but women respond less well to treatment and have an increased risk of mortality. A person with AF is five times more likely to have a stroke than someone without AF. It also increases the risk of a person developing heart failure, angina and thromboembolism (blood clots). There are several factors which increase the risk of developing AF, and they can be divided into cardiac and non-cardiac. Move the cards onto the correct piles depending on whether its a cardiac or non cardiac risk factor: Cardiac risk factors  Hypertension Ischaemic heart disease Structural heart problems Non-cardiac risk factors Diabetes Thyrotoxicosis Increased alcohol COPD  Management of AF If the AF is due to a treatable cause, then this should be addressed, e.g. an infection, treating hyperthyroidism, reducing alcohol intake. If this isn't successful or there are no treatable causes, there are three main ways in which AF is managed. Please note that there are drugs that are used to treat arrhythmias that we are not covering here because they are uncommon and used under specialist supervision. Should you wish to find out more, there are some references provided at the end of the learning material. 1 Stroke prevention 2 Rate control 3 Rhythm control Stroke prevention We use anticoagulants to reduce the risk of stroke in someone with AF. The anticoagulants used in AF are discussed in detail in the 'anticoagulants & fibrinolytics' section - click the button to go there now. ANTICOAGULANTS &... Although they are very effective drugs at reducing stroke risk, they are associated with some serious adverse effects, in particular bleeding. To help a clinician decide whether a patient  should be started on an anticoagulant, they need to assess the patient's risk of stroke versus their risk of bleeding and then make a judgement about whether the risk of stroke outweighs the risk of bleeding or vice versa. Assessing the stroke risk The CHA₂DS₂-VASc (pronounced "chadz-vasc") Score for Atrial Fibrillation is used to determine the risk of a particular person having a stroke. It takes into account the persons gender, their age and their medical history and gives them a score based on these factors. The higher the score, the more likely the patient is to have a stroke. You can see it in action here. Assessing the bleeding risk The ORBIT bleeding risk score is used to determine the risk of someone bleeding if they take an anticoagulant. It takes into account the person's age, gender, whether they have a history of bleeding, their renal function and whether they are taking antiplatelet drugs. You can see it in action here. Making the decision Once the clinician has assessed the patient's stroke risk and bleeding risk, they need to weigh up both risks and decide if the benefit of using an anticoagulant outweighs the bleeding risks or vice versa. DOACs are recommended as first line treatment, with Edoxaban the preferred option, then rivaroxaban (more details here). In some clinical situations, warfarin may be used. A LMWH might also be used although this will only happen in hospital and it will be for short term use. Please visit the 'anticoagulants & fibrinolytics' section for detailed information about these drugs.  Rate control This means using a treatment which reduces the patient's heart rate to within the normal range, but without affecting the heart rhythm. The drugs which can be used are: Standard β-blockers, e.g. metoprolol, bisoprolol The calcium channel blockers diltiazem & verapamil Digoxin If monotherapy (one drug alone) does not control the AF, patients may take a combination of 2 from the different groups. Beta-blockers All standard beta-blockers (not sotalol) can be used to treat arrhythmias. We covered beta- blockers in the cardiovascular material in year 1. Let's see what you can remember: What is the mechanism of action of beta-blockers? They stimulate beta-receptors in the cardiac muscle They antagonise beta-receptors in the cardiac muscle  SUBMIT Which of the following are recognised adverse effects of beta-blockers? Bradycardia Bronchospasm Constipation Warm hands & feet Dry skin Tiredness SUBMIT  Complete the content above before moving on. If you feel that you need a refresher on beta-blockers, please revisit the cardiovascular study block from year 1 (block 5). Calcium channel blockers We also covered this drug group in year 1. The drugs from this group that are used to treat arrhythmias are the non-dihydropyridine ones: verapamil and diltiazem (although this isn't licensed for AF so you won't see a recommended dose in the BNF). In year 1 we learnt that calcium channel blockers block the influx of calcium ions into muscle cells, leading to relaxation of the smooth muscle in the wall of blood vessels which results in lowering of blood pressure. Verapamil and diltiazem also block the influx of calcium ions into cardiac muscle cells, leading to relaxation of the cardiac muscle and a reduction in the force with which the heart contracts. They also reduce electrical conduction in the SA node and the AV node, leading to a reduction in heart rate. Adverse effects There are some side effects that are common to all calcium channel blockers, and then some which are specific to individual drugs.  Information taken from the BNF about side effects for all calcium channel blockers. In addition, specific adverse effects for the individual drugs include: Diltiazem - hypotension, malaise, constipation, hepatitis Verapamil - hypotension, constipation, hepatic impairment (dark urine, pale stools, yellowing skin or whites of eyes) Patient information and advice Patients taking verapamil should be advised to avoid grapefruit juice, which is an enzyme inhibitor and can increase verapamil levels. Patient taking modified-release preparations containing more than 60 mg of diltiazem should ideally stay on the same brand. This is because the different brands may have different bioavailability and therefore may not have the same clinical effect. To avoid any confusion the prescriber should specify the brand to be dispensed.  Digoxin Digoxin is a cardiac glycoside drug which is derived from the leaves of the purple foxglove. It can be used to treat AF in patients who have a sedentary life-style. This is because is doesn't control the heart rate as well during exercise as beta blockers or calcium-channel blockers do. Digoxin works by slowing down electrical conduction within the AV node. It also increases the force of contraction of the heart and is particularly useful in patients who have both AF and heart failure. Pharmacokinetics of digoxin Digoxin has a narrow therapeutic index - we learnt what this means at the start of year 1: let's revisit it now: The therapeutic index (or therapeutic window) is the concentrations of drug over which the drug will work safely. If the concentration of drug in the blood is below the therapeutic index the drug won’t work, above the therapeutic index and the patient will be at risk of toxic effects. So when a drug is being developed, the dose is designed to give a concentration that is within the therapeutic index. Some drugs have a narrow therapeutic index; the gap between the minimum and maximum concentrations is small and toxic levels can develop more easily. Digoxin also has a very long half-life, which is the time taken for the concentration of drug in the blood to fall by half. As we learnt in year 1, this means that it will take a long time to be completely eliminated once the patient stops taking it and therefore side effects will hang around for a long time. Adverse effects Below you can see the information about adverse effects of digoxin from the BNF. Some of the side effects (confusion, nausea, anorexia, or disturbance of colour vision) are more likely to occur if the digoxin levels in the blood are too high, so it is important to advise patients to speak to their doctor. Patient information sources British Heart Foundation: Digoxin - Drug cabinet About digoxin - NHS (www.nhs.uk) Rhythm control This can be achieved by either non-drug or drug treatment. Non-drug treatment Electrical cardioversion (DCCV: Direct current cardioversion) - this is application of a controlled electric shock across chest wall. The video below explains more:  British Heart Foundation - Your guide to cardioversion trea… trea… Drug treatment This involves using a drug which controls both the heart rate and rhythm. First-line: standard beta-blocker (any but sotalol) - although beta-blockers are also used for rate control they can have a positive impact on the heart's rhythm too. Others: Amiodarone (especially if the patient also has heart failure) Dronedarone Amiodarone This drug works by reducing electrical activity in the heart, this reduces the heart rate and helps to control the rhythm.  It has a long half-life and therefore has to be given as a loading dose on initiation. This is usually 200mg three times a day for 1 week, then 200mg twice a day for 1 week then 200mg once a day to continue. Some clinicians use different (unlicensed) loading doses. It has several serious side effects which limit it's use, and it is always initiated in hospital. Adverse effects BNF information about amiodarone adverse effects Other side effects include: Arrhythmias; nausea; constipation; skin reactions; headache; angioedema; confusion; delirium; pancreatitis; severe cutaneous adverse reactions (SCARs); myopathy (usually reversible on discontinuation); peripheral neuropathy (usually reversible on discontinuation); photosensitivity reaction - this can result in a blue-grey skin discolouration as seen in the picture on the right; movement disorders; sleep disorders; taste altered; vomiting. Amiodarone has a very long half-life which means that adverse effects can persist long after the drug has been stopped (often for several weeks or months).  Disorders of Pigmentation Fischer, Andrew, Dermatology Secrets, Chapter 18, 156-166 Amiodarone-induced photodistributed blue-gray hyperpigmentation. (Courtesy Fitzsimons Army Medical Center teaching files.) Copyright © 2021 Copyright © 2021 by Elsevier, Inc. All rights reserved. Patient monitoring Because of the serious side effects which amiodarone can cause, patients must undergo the following tests: Thyroid function tests should be performed before treatment and then every 6 months. Liver function tests required before treatment and then every 6 months.  Chest x-ray required before treatment. Patient information and counselling It is important that patients know to look out for symptoms of the serious adverse effects: Patients and carers should be cautioned on the effects on driving and performance of skilled tasks—corneal microdeposits may be associated with blurred vision Hepatotoxicity - nausea, yellow skin discolouration, fatigue, dark urine & pale stools. Shortness of breath or a cough may indicate pulmonary toxicity Because of the possibility of phototoxic reactions, patients should be advised to shield the skin from light during treatment and for several months after discontinuing amiodarone; a wide-spectrum sunscreen to protect against both long-wave ultraviolet and visible light should be used. Dronedarone This works in a similar way to amiodarone and is also initiated under specialist supervision. It doesn't have quite an many safety concerns but there are still some important points to remember about it. Adverse effects Asthenia; bradycardia; congestive heart failure; diarrhoea; gastrointestinal discomfort; nausea; QT interval prolongation; skin reactions; vomiting, photosensitivity reaction; respiratory disorders; taste altered, hepatic disorders; vasculitis Important adverse effects to be aware of: Liver injury including life-threatening acute liver failure has been reported rarely; Patients should have their liver function monitored before treatment, 1 week and 1 month after initiation of treatment, then monthly for 6 months, then every 3 months for 6 months and periodically thereafter. Patients or their carers should be told how to recognise signs of liver disorder and advised to seek prompt medical attention if symptoms such as abdominal pain, anorexia, nausea, vomiting, fever, malaise, itching, dark urine, or jaundice develop. New onset or worsening heart failure has been reported reported. Patients or their carers should be told how to recognise signs of heart failure and advised to seek prompt medical attention if symptoms such as weight gain, dependent oedema, or dyspnoea develop or worsen. If heart failure or develops, discontinue treatment. Pulmonary toxicity has been reported. Patients should be advised to report symptoms such as dyspnoea or dry cough. Paroxysmal AF This is AF that terminates spontaneously - the management strategies depend on the frequency of the episodes but can include: Abstinence from precipitating factors e.g. alcohol/caffeine “Pill-in-the-pocket” (eg flecainide) – if the patient is aware of attacks (they can detect 'palpitations') and they are infrequent, the patient may use a drug on an 'as required' basis. If episodes are frequent then aim to reduce frequency/prevent episodes with rate/rhythm control Anticoagulant therapy should be considered as patient will be at increased risk of thromboembolism during the episodes Test your knowledge Try the following questions to test your knowledge from this section. If there are any areas you struggle with please revisit them above Which of the following is true regarding Amiodarone? A loading dose of 200mg twice daily is needed for five days It can lower or raise the thyroid levels It is safe to use in liver disease It only has a few side effect, all of which are mild SUBMIT Which of the following calcium channel blockers can be used to treat arrhythmia? Amlodipine  Lercanidipine Nifedipine Verapamil SUBMIT Which of the following drugs may be used to control the hearts rhythm? Amiodarone Dronaderone Metoprolol Ramipril  Sotalol SUBMIT Which of the following heart rates is considered tachycardia? 38 62 98 120 SUBMIT Which of the following conditions is a form of bradycardia? Atrial fibrillation Heart Block Torsade de pointes arrhythmia Ventricular fibrillation SUBMIT Patient information resources Home - AF Association - United Kingdom (heartrhythmalliance.org) Stroke Association | Home British Heart Foundation: Drug cabinet antiarrhythmics Useful resources for further information NICE Clinical knowledge summaries NHS: Atrial fibrillation Pharmacology : an essential textbook / Mark A. Simmons. Medical Pharmacology at a Glance / Michael J. Neal Lesson 4 of 10 Heart Failure Introduction Heart failure is a fairly common condition, in which the risk increases with age, and it can complicate other conditions in the elderly. It has a high mortality rate, with 50% of patients dying within 5 years of diagnosis. Heart failure accounts for 5% of admissions to hospital medical wards and 10% of patients with heart failure have atrial fibrillation as a contributory factor (more on this later in the study block). Heart failure also increases the risk of thrombo-embolic conditions occuring. C O NT I NU E Heart failure results from structural and/or functional cardiac disorders Causes Heart failure is usually of gradual onset and many people will be unaware of any issues in the early stages. The ability of the heart to function as a pump is impaired and so it is unable to sustain an adequate delivery of blood (and therefore oxygen & nutrients) to the tissues (tissue perfusion). This can be caused by either one or both of: 1) PUMP FAILURE Damage to the heart muscle so there is a reduction in myocardial contractility. 2) OVERLOADING Extra workload on the heart, so there is decreased force and velocity of contraction and delayed relaxation, excessive afterload (pressure overload), and/or excessive preload (volume overload). Flip the cards below for some definitions. The pressure that the chamber of the heart has to generate in Afterload order to eject blood out of the chamber, i.e. total peripheral resistance  Volume of blood present in a ventricle of the heart, after passive filling and atrial Preload contraction, i.e. left ventricular end diastolic volume (amount of stretch of left ventricle) 1) Pump Failure Damage to the heart leads to systolic failure. Ischaemic heart disease is a common cause. It can occur acutely after a myocardial infarction, for example, or progressively (chronically). Causes of pump failure include: Ischaemic heart disease (e.g. angina) Myocardial infarction Arrhythmias Viruses & infection  Inflammation Excessive alcohol consumption 2) Overloading Overwork & overstretch of the cardiac muscle can cause structural & biochemical abnormalities in the cells. This can lead to decreased force, decreased velocity of contraction and delayed relaxation. These effects are usually irreversible. Causes of overloading are either excessive afterload or excessive preload. Excessive afterload If systemic vascular resistance is high, e.g. due to hypertension, then this will raise the afterload on the left ventricle and cause it to fail. If pulmonary vascular resistance is high, e.g. in pulmonary hypertension secondary to chronic lung disease, then this will cause right ventricular failure (cor pulmonale). If there is valve dysfunction, e.g. from stenosis or weak valves, then this can also cause excessive afterload Excessive preload Excessive preload is an uncommon cause of failure. Hypervolaemia (too much fluid in the body) is usual cause. Examples that cause this include: renal failure, excessive intravenous infusions or certain medications. Other causes of overloading include: - Anaemia - Hyperthyroidism or thyrotoxicosis - Valve dysfunction - Bradycardia or tachycardia - Widespread vasodilation e.g. septic shock and cardiac output is increased to raise BP Precipitating Factors are anything thing that increases the heart's workload!! (Arrhythmias, anaemia, hyperthyroidism, pregnancy, obesity, infections, changes in drug therapy - including poor compliance!) C O NT I NU E Pathophysiology The pathophysiology of heart failure is very complicated as the heart can compensate for a fair amount of damage. Heat failure can be classed as either: Acute or Chronic Acute  For example, after a myocardial infarction (MI). Contractility of the heart immediately drops > Cardiac output falls > Cardiovascular system initiates compensation in order to maintain cardiac output & peripheral perfusion. This leads to: ► Compensated Heart Failure If MI is very severe there may be extensive damage to heart muscle > Cardiac output dramatically drops > There is no cardiac reserve and the cardiovascular system is unable to compensate and is overwhelmed. This leads to: ► Decompensated Heart Failure Chronic Chronic heart failure is the same as acute, howevert the decline is progressive rather than a sudden fall. Patients can remain in compensated failure indefinitely. Severe stress can drive them into decompensation, for example if there is infection, fluid overload, exertion or anaemia. Compensation In the failing heart, as a result of a reduction in cardiac output & tissue perfusion, the heart adapts. The changes below can occur to compensate. 1. CA R DIA C 2. A R T E R IA L 3. IN CR E A S E D 4. S AL T AND W AT E R E N L A R GE ME N T CO N S T R ICT IO N S YMPA T H E T IC DR IV E R E T E N T IO N Progressive alteration of ventricular size, shape & function. Cardiac muscle stretched and thickened from increased residual volume after contraction. Muscle eventually becomes ineffectual. This is responsible for significant impairment of the heart as a pump - it is given the term: ► Left Ventricular Hypertrophy (LVH - often seen in patient notes)  1. CA R DIA C 2. A R T E R IA L 3. IN CR E A S E D 4. S AL T AND W AT E R E N L A R GE ME N T CO N S T R ICT IO N S YMPA T H E T IC DR IV E R E T E N T IO N When cardiac output is reduced: ► Arteries constrict to divert blood to organs from skin & GI tract BUT can also raise systemic vascular resistance ► Increase afterload on the heart 1. CA R DIA C 2. A R T E R IA L 3. IN CR E A S E D 4. S AL T AND W AT E R E N L A R GE ME N T CO N S T R ICT IO N S YMPA T H E T IC DR IV E R E T E N T IO N Failing heart & reduced tissue perfusion stimulates the sympathetic nervous system (triggering the fight or flight mechanism). This promotes excessive stimulation of the heart & widespread vasoconstriction, and increases contractility. 1. CA R DIA C 2. A R T E R IA L 3. IN CR E A S E D 4. S AL T AND W AT E R E N L A R GE ME N T CO N S T R ICT IO N S YMPA T H E T IC DR IV E R E T E N T IO N Reduced cardiac output leads to reduced renal perfusion and a retention of salt and water - This causes increased renin - Renin leads to formation of angiotensin I & II (vasoconstrictors) - Leads to adrenal aldosterone release - Aldosterone retains salt & water at distal renal tubule which expands blood volume & increases preload - This promotes the release of Atrial Natriuretic Peptide (ANP) (see diagnosis & investigations)  C O NT I NU E Clinical Features There are THREE classic symptoms of heart failure: 1) Exercise limitation (fatigue) Due to decreased cardiac output, impaired oxygenation & decreased blood flow to exercising muscles 2) Shortness of breath ‘Back pressure’ from failing heart causes fluid to accumulate in lungs Mostly occurs when exercising or lying down Can be accompanied by a cough 3) Oedema Swelling of ankles & feet Due to retention of salt & water and lack of clearance of fluid  Most clinical features result from either: Hypoperfusion (Forward component) - Impaired flow ahead of the heart or the chamber affected OR; Congestion/Oedema (Backward component) - Increase in pressure in veins draining into the heart Both conditions usually co-exist. They are different aspects of heart failure, not different forms of heart failure. The conditions cause different features and these may vary according to which side of the heart is affected. Flip the cards below for how the two conditions present. Fatigue & exercise intolerance Cold & pale extremities Hypoperfusion (Forward component) Fluid & electrolyte retention Fast heart rate Rapid breathing  Right-sided heart failure (remember - right side receives the Congestion/Oedema deoxygenated blood) Symptoms (Backward Peripheral oedema (swollen Component) ankles) Enlarged liver Raised jugular venous pressure Bluish discoloration of the New York Heart Association Classification of Heart Failure Symptoms Below is the class system which you will often see written in patient's notes. Heart failure, myocardial and pericardial disease Evans, Jonathan D.W., BMedSci, Crash Course Cardiovascular System Updated, 8, 99-107 NYHA functional classification for heart failure. Copyright © 2015 © 2015 Elsevier Ltd. All rights reserved.  C O NT I NU E Diagnosis Symptoms alone cannot be relied upon to make a diagnosis. There needs to be evidence of cardiac dysfunction. This can be through investigations and measures of left ventricular structure & function. The cause of heart failure should be established in ALL patients. This is because it may be reversible or correctable! Signs and symptoms will be reviewed, particularly looking for the raised jugular vein, the swelling of ankles and legs, and listening to lung sounds. Tests that may be performed include: Presence of Natriuretic Peptides (BNP & NTproBNP) Echocardiography (where you can see the heart in motion and assess it's performance as a pump - the ejection fraction can also be measured) Chest x-ray to see the size of heart and review lungs Checking heart rate, rhythms and sounds Electrocardiogram (ECG) to check the heart's rhythm and electrical activity  Blood tests including renal function, thyroid function, liver function, lipids etc. to rule out other issues or aggrevating factors Breathing tests to check lung for problems (spirometry and peak flow) C O NT I NU E Treatment of Heart Failure The aims of treatment are to reduce morbidity, relieve symptoms, improve exercise tolerance and reduce mortality. Treatment for the patient will be dependent on cause: If there is pump failure due to disease of the myocardium, we need to increase muscle contraction force. If there is excessive load, we need to reduce pre-load and/or reduce after-load. NICE guidance on heart failure recommends a loop diuretic on initial diagnosis and first line treatment of an ACE inhibitor and beta blocker combination. This is summarised with some useful flow charts in a BMJ article here (you will need to log in on open athens or via the uea) Some patients may require a heart transplant depending on the severity of the condition and if it is possible to do so. The drugs used in heart failure are summarised below. You will need to ensure you have refreshed your knowledge on these drugs from year 1. Links to the BNF are included throughout the section.  1 1. ACE Inhibitors There is significant evidence that using ACE inhibitors improves patient symptoms and increases long term survival. All patients with heart failure should be using an ACE inhibitor. The dose will be initiated at a low dose, and then uptitrated (increased). Angiotensin II antagonists are an alternative in patients intolerant to ACE inhibitors. There is good evidence for improvement in long term survival, but it is not as good evidence as ACE inhibitors. ACE Inhibitors are the first line therapy in heart failure. They reduce both pre-load and afterload.  2 2. Diuretics Diuretics are used extensively in acute heart failure, but also in chronic heart failure. They reduce the preload, and reduce symptoms like fluid on the lungs (and therefore shortness of breath) and swollen ankles. When used appropriately, they reduce hospital admissions and increase exercise performance. Pharmaceutical care problems include hypotension, dehydration, renal impairment and electrolyte disturbances (low potassium and sodium). There are different classes of diuretics which can be used: Loop diuretics: Mainstay of acute treatment They are more potent than other diuretics. E.g. furosemide, bumetanide and can be used at much higher doses than seen in the BNF (unlicensed). Can be used IV - but must not be given too quickly. Thiazides: Less potent – used for mild heart failure E.g. bendroflumethiazide up to 5mg in the morning. Not effective with renal impairment of eGFR40 less than baseline Yes =2 Sepsis - temp 38, WBC 8, RR >20, PCO2