Case 2- illness Flashcards
(137 cards)
1
Q
Ischaemia causes
A
Most common cause is the occlusion of blood vessels, occlusion can either be partial or complete. Complete is more severe and can lead to infarction. Affects any blood vessel
2
Q
Ischaemia- causes of occlusion
A
Atheroma- fatty deposits
Thrombosis- local clot formation
Embolism- clot is carried somewhere other then where it originated
Spasm- contraction of the muscle within the blood vessel
3
Q
Factors that make tissue more susceptible to ischaemia
A
- Previous damage to organ tissues- e.g. from a previous myocardial infraction
- Single blood supply- there is no alterntive supply for the tissue.
- Onset of blood supply affected- if the occclusion develops more gradually then the body has time to adapt and create more blood vessels
- Type of tissue affected- brain and heart tissue is more susceptible
4
Q
Venous and capillary ischaemia
A
Venous ischaemia is less common then ischaemia in the arteries, due to a blockage i.e. a hernia. Capillary ischaemia can be due to frostbite
5
Q
The two non vascular reasons why ischaemia can occur
A
Reason 1- Decrease in oxygenated blood flow, when the oxygen supply is less than the tissues demand. This could be due to Hypotension due to low blood volume (hypovolaemia) or the patient isnt getting blood around the body i.e. from trauma or sepsis. It can also be due to anaemia as the oxygen carrying capacity is reduced. Carbon monoxide could be lowering the oxygen carrying capacity of the blood.
Reason 2- increases tissue demand, this could be because of thyrotoxicosis (an overative thyroid), Tachyarrhythmias (the heart is beating faster so needs more oxygen to meet its demands).
6
Q
Causes of infarction
A
It is cell death due to an insufficient supply of oxygen, the causes are the same as in ischaemai
7
Q
Types of myocardial infarction
A
Acute coronary syndrome is an umbrella term for the clinical manifestations of myocardial ischaemia/infarctions. The three conditions are unstable angina, non-ST elevation myocardial infarctions (NSTEMIs), or ST elevation myocardial infarctions (STEMIs). They are caused by acute disruption of a coronary artery plaque which leads to sudden occlusion of the artery via platelet aggregation. Unstable angina is the least severe then NSTEMI and STEMI
8
Q
Symptoms of ACS
A
Central chest pain, dyspnoea and nausea
9
Q
Cause of ACS
A
There is an atherosclerotic plaque within the coronary arteries, this plaque then ruptures exposing the soft centre of the plaque. This material is thrombogenic, platelets aggregate and enhance the clotting process which forms a thrombus which blocks the coronary artery.
10
Q
Blood markers of ACS
A
Troponin T is released in necrosis so is present in NSTEMI or STEMI but not unstable angina as there is no necrosis
11
Q
ECG changes in unstable angina
A
Can be normal. Sometimes has ST depression, T wave inversion
12
Q
Unstable angina pathophysiology
A
Incomplete occlusion of the coronary artery which causes myocardial ischaemia without infarction. It occurs at rest, partial occlusion with no necrosis
13
Q
NSTEMI pathophysiology
A
Partial occlusion of a coronary artery. Partial thickness necrosis through the heart muscle. There will be raised Troponin
14
Q
ECG NSTEMI
A
Can be normal. Might have an ST depression and a T wave inversion
15
Q
STEMI pathophysiology
A
Complete occlusion of the coronary artery causing full thickness necrosis through the heart muscle. Troponin will be raised and there will be an ST elevation on the ECG
16
Q
Signs and symptoms of ACS
A
Signs- pale and clammy, hypotension, may be bradycardic or tachycardic
Symptoms- central precordial chest pain which often radiates to the arms/jaw, presyncope/syncope (fainting or feeling like you are about to), dyspnoea (breathlessness), nausea and vomiting
17
Q
Immediate management of ACS
A
This includes giving oxygen, a vasodilator (dilates blood vessels) and analgesia (painkillers)
18
Q
Acute management (revascularisation) of ACS
A
Meant to improve passage of blood through the arteries affected by occlusion. This can be done by inserting a stent into the coronary artery or a bypass grant (attaching a vessel which essentially bypasses the area of blockage within the artery)
19
Q
Long term management of ACS
A
All patients need it. Includes controlling modifiable risk factors, medication to reduce platelet aggregation (clumping), medication to control blood pressure and cholesterol levels
20
Q
Complications following a myocardial infarction (DARTH VADAR)
A
- Death
- Arrhythmias- e.g. ventricular fibrillation
- Rupture- of ventricular septum or papillary muscle
- Tampanode- accumulation of fluid within the pericardium leading to compression of the heart
- Heart failure- damage to the heart muscle due to necrosis
- Valve disease- mitral regurgitation
- Aneurysm- of the ventricles
- Dressler’s syndrome- pericarditis (inflammation of the pericardium)
- Thrombo Embolism
- Recurrence
21
Q
Inferior myocardial infarction
A
An infarction of the right coronary artery territory, affects the inferior parts of the heart. Can effect the AV node leading to heart block
22
Q
Causes of hypoxic damage in the heart
A
Most likely due to atherosclerosis, narrowing of arteries leads to less oxygen getting to the heart. Switches from aerobic to anaerobic respiration. This leads to lactic acid accumulation, a fall in pH and less ATP. Due to the rise in lactic acid and fall in ATP, there is a rise in intracellular sodium concentration. As without the ATP the sodium-potassium pump can not work so sodium and water accumulate within the cell. This coupled with a rise intracellular calcium concentration leads to cell oedema. This causes activation of degradative lysosomes and proteases, which release digestive enzymes which can lead to cell death.
23
Q
How hypoxic damage effects the heart
A
Decreases myocardial function. Contractile proteins need ATP and when they are not getting enough there will be impaired contraction and less force in the heart. If repurfusion does not occur within 20-40 minutes then there is irreversible necrosis. The dead cells are replaced by fibrous tissues, as the necrotic tissue is cleared and thinned it leads to structural weakness
24
Q
Stunned myocardium
A
After ischaemia when there is repurfusion to the heart. The heart will not contract as well and you will get prolonged systolic dysfunction. The contractile function will gradually recover but can take hours or days. If its a large enough area it may not be able to sustain life
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Epidemiology of ischaemic heart disease
Leading cause of death in the world. It is more slow progressing due to atherosclerosis, ACS is more rapid presenting as there is acute plaque disruption which leads to rapid occlusion of the coronary arteries
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Risk factors of ischaemic heart disease
Age, male, south Asians, family history of IHD, social deprivation, type 2 diabetes, smoking, reduced physical activity, obesity, high blood pressure, high cholesterol, excess alcohol consumption and excess stress. Diet can also make a difference if you eat a high level of saturated fat, salt and sugar.
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What can ischaemic heart disease also be called
Coronary heart disease (CHD) and coronary artery disease (CAD)
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Types of chronic ischaemic heart disease
Stable angina, variant angina, silent angina
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Stable angina
Most common presentation, how symptomatic it is varies. When the patient is under stress the metabolic demands of their heart increase, but due to narrowed coronary arteries, it is not possible to get enough blood to the heart for its metabolic demand. This leads to a build up of metabolites which leads to chest pain. This chest pain can be relieved by rest and nitroglycerins e.g. GTN spray which cause dilation of the blood vessels which increase the amount of blood which can get to the heart.
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Stable angina symptoms
Central precordial chest pain which may radiate to the arms/jaw, pain can be 'heavy, gripping, tight.' Can cause dyspnoea and palpitations
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Variant angina
Same symptoms as stable angina. Seen more frequently in females. It is caused by a spasm of the coronary arteries, this spasm can occur at rest. Due to this spasm the coronary arteries are narrowed, it is not possible to get enough blood to the heart for its metabolic demand. This leads to a build up of metabolites which leads to chest pain.
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Silent angina
Angina in which there is no chest pain or other symptoms. Shares the same pathophysiology as other types of angina. So impaired coronary blood flow or vasopasm leads to a blood supply not being able to meet the metabolic demands of the heart leads to a build up of metabolites. Reasons for why there may be no chest pain is due to autonomic neuropathy when the nerves are damages. It may not involve enough myocardium to produce pain.
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Management of angina
Lifestyle managements such as controlling risks factors like stopping smoking, dieting and exercise. Can be controlled though medication, this improves blood flow by dilating the blood vessels, it may also slow the heart rate or reduce its contractility to reduce the demands from the heart. You may need surgical intervention, for example, cardiac revascularisation i.e. stenting or bypass graft. This will improve the passage of blood through arteries affected by occlusion. Secondary prevention management is also used which reduces the patients risk of going on to have a myocardial infarction (heart attack). This may be medication to reduce platelet aggregation (clumping of platelets). Or medication to control the patients blood pressure, could also be to reduce/control patients blood cholesterol level.
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Types of valvular heart disease
4 valves- aortic, pulmonary, tricuspid, mitral (All Physicians Take Money)
2 abnormalities- stenosis or regurgitation. Affects the left side more
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Aortic stenosis
Narrowing of the aortic valve, causes turbulent flow through the aortic valve during systole. This causes a systolic murmur, its a crescendo-decrescendo murmur as it builds in intensity then reduces
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Symptoms of aortic stenosis
Chest pain (due to reduced flow to the coronary arteries), breathlessness, syncope (fainting) and fatigue. Aortic stenosis makes the ventricle work harder (increases afterload) and can cause left ventricular heart failure.
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Causes of aortic stenosis
* Age related calcification- an inflammatory process causes thickening of the aortic valve with lipoproteins, which become calcified, increasing leaflet stiffness.
* Bicuspid aortic valve- tends to present at a younger age. The normal aortic valve is tricuspid but 2% of people have a bicuspid aortic valve.
* Rheumatic heart disease- can also cause thickening and calcification of the aortic valve in addition to the mitral valve.
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Pulmonary stenosis
Narrowing of the pulmonary valve causing a systolic murmur. Normally congenital but can also be caused by rheumatic heart disease of carcinoid syndrome
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Mitral regurgitation
Regurgitation is abnormal backflow of blood through a valve that should be fully closed. Regurgitation through the mitral valve happens during systole when the ventricles contract. Causes a pan-systolic murmur, lasts all of systole at the same volume throughout. The heart has to work harder resulting in an enlarged left ventricle, causing a displaced, forceful apex beat and there may be signs of heart failure. Regurgitation happens because when the left ventricle becomes dilated, the mitral valve annulus dilates too much so the cusps cannot meet properly
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Symptoms of mitral regurgitation
Shortness of breath, fatigue, palpitations. It increases the risk of atrial fibrillation and heart attack
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Causes of mitral regurgitation
* Annular calcification: calcification of the mitral valve annulus can occur with increasing age
* Infective endocarditis: infection of the endocardium, usually involving blood vessels
* Mitral valve prolapse: when closed the leaflets (cups) of the mitral valve prolapse abnormally back into the left atrium.
* Myocardial infarction: can damage/rupture the chordae tendinae or papillary muscle
* Rheumatic heart disease: the mitral valve is the valve most affected. Rheumatic fever is caused by an immune to a Streptococcus infection. Rheumatic heart disease occurs when these antibodies damage the cardiac valves.
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Tricuspid regurgitation
Also causes a systolic murmur. Can occur due to right ventricular dilation, rheumatic fever, infective endocarditis, congenital abnormalities or carcinoid syndrome (due to a tumour which secretes plaques into the venous system which settle on the tricuspid valve).
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Aortic regurgitation
Blood flows backwards through the aortic valve during diastole. Causes a murmur which can be heard in early diastole. This increases the end diastolic volume in the left ventricle. The left ventricle then needs to pump out more blood in systole, this can cause LVH and is less efficient. Perfusion to the coronary arteries is reduced leading to ischaemia and left ventricular heart failure. There is a collapsing pulse. Large diggerence in systolic and diastolic blood pressure
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Causes of aortic regurgitation
* Dilation of the aortic valve leaflets: this can be due to rheumatic heart disease, infective endocarditis, bicuspid aortic valve or age related degeneration
* Dilation of the aortic root: connective tissue disorder e.g. Marfan’s syndrome and Ehlers-Danlos syndrome. Can also be due to an untreated syphilis infection or aortic dissection.
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Pulmonary regurgitation
Causes an early diastolic murmur can be due to any cause of pulmonary hypotension
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Mitral stenosis
Less blood through it at the end of diastole, reducing blood flow from the left ventricle to left atrium. You hear a mid-diastolic murmur. The left atrium gets larger as it has to work harder increasing the risk of atrial fibrillation. The enlarged left atrium can press on nearby structures causing difficulty swallowing. Causes high pressure in primary circulation leading to shortness of breath and right heart failure, Normally caused by rheumatic fever
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Detecting mitral stenosis
Malar flush, signs of atrial fibrillation are the same as RVH i.e. left parasternal heave
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Tricuspid stenosis
Causes mid-diastolic murmur, mainly caused by rheumatic disease
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Cardiomyopathy
A myocardial disorder in which the heart muscle is structurally and functionally abnormal without any underlying heart condition to explain it. Often genetic, can occur alone or as part of a multi-system disease
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Types of cardiomyopathy
Dilated cardiomyopathy, hypertrophic cardiomyopathy, restrictive cardiomyopathy, arrhythmoegnic right ventricular cardiomyopathy (ARVT)
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Dilated cardiomyopathy
Ventricular enlargement and loss of contractility in the heart muscle without any thickening. Tends to affect men between 20-60 especially those of African descent. You get sporadic and familial DCM. When presented acutely it can lead to arrhythmias, sudden cardiac death and stroke. When chronic it presents as heart failure is may be symptomless
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Familial DCM
Autosomal dominant inheritance, is associated with lots of different gene mutations. Many of these abnormal genes encode cytoskeletal or myocyte proteins. Some are associated with skeletal myopathies (progressive muscle atrophy and weakness) and conduction system disease.
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Sporadic DCM
Happens in a person with a normal heart in response to an insult. The insult could be myocarditis (inflammation of the heart) due to a virus or bacteria. It can also be due to toxins from chemotherapy or alcohol. It may also be due to an autoimmune response such as rheumatoid or systemic lupus erythematosus.
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Investigations of dilated cardiomyopathy
Chest x-ray will show signs of heart failure. ECG shows arrhythmias, conduction abnormalities or non specific ST segment changes
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Dilated cardiomyopathy management
Treated the same way as heart failure by any other cause. You will be given diuretics, ace inhibitors and beta blockers. Some patients may need anticoagulation if they have atrial fibrilation or a history of thromboembolism. Some patients need pacemakers and others choose to have implantable defibrillators fitted. It is the most common reason for a heart transplant.
Dilated cardiomyopathy is not curable- treatment aims to improve symptoms and cardiac function and prevent complications.
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Hypertrophic cardiomyopathy
Causes left ventricular hypertrophy, most prominent in the interventricular septum. The large septum can get in the way of the left ventricular outflow tract during systole, this is known as dynamic left ventricular outflow tract obstruction. Autosomal dominant, some sporadic but mostly familial. Tends to affect men and people from African origin more, most common cardiac death in young people
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Cause of hypertrophic cardiomyopathy
The most common mutation affects the beta myosin heavy chain and myosin binding protein C. The obstructive form of the disease is present in about a quarter of cases. The anterior leaflet of the mitral valve moves anteriorly, towards the left ventricular outflow tract during systole. This is known as systolic anterior motion of the mitral valve or “SAM” due to the large drag force of the hypertrophies septum.
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Symptoms of hypertrophic cardiomyopathy
Most are asymptomatic, some have chest pain, dyspnoea and syncope.
Signs= Ejection systolic murmur, jerky carotid pulse, fourth heart sound, double apical pulse and a pan-systolic murmur if there is systolic anterior motion of the mitral valve.
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Risk factors for Hypertrophic cardiomyopathy
Massive left ventricular hypertrophy, family history of sudden cardiac death before 50, non-sustained ventricular tachycardia (high heart rate at rest), prior unexplained syncope and abnormal blood pressure response on exercise (flat or hypotensive).
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Investigations for Hypertrophic cardiomyopathy
ECG shows left ventricular hypertrophy and ST and T wave changes. The echocardiography can be diagnostic, you can also use a cardiac MRI and a genetic analysis.
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Management for Hypertrophic cardiomyopaphy
About alleviating symptoms and preventing sudden death. Patients with 2 or more risk factors for sudden death should be considered for implantable cardioverter defibrillator (ICD). Potentially heart transplant. If someone has hypertrophic cardiomyopathy there first degree relatives need to be closely monitored with ECG’s and echocardiograms to ensure they do not develop it themselves. Prognosis is variable, while some can be asymptomatic others can end up dying.
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Restrictive cardiomyopathy
The size of the left and right ventricle and the thickness of their walls is normal, they are just stiffer then normal. Systolic function is near normal but the stiff myocardium impairs ventricular filling. It is the least common of the cardiomyopathies. It tends to affect the elderly. In most cases, no cause is found
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Causes of restrictive cardiomyopathy
Most common cause is amyloidosis which is the extracellular deposition of amyloid. Other causes are sarcoidosis, Loffler's endocarditis and endomyocardial fibrosis.
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Symptoms of restrictive cardiomyopathy
Signs of right sided heart failure i.e. oedema, ascites and raised JVP. Associated with Kussmaul's sign which is a raised JVP on inspiration
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Investigations into restrictive cardiomyopathy
ECG, in an echocardiography you will see myocardial thickening, and impaired diastolic filling. You can also see it in an cardiac MRI, a cardiac catheterisation. A endomyocardial biopsy is more useful than in other types of cardiomyopathy as it permits a specific diagnosis.
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Management of restrictive cardiomyopathy
There is no specific treatment instead they aim to treat the heart failure. Some patients may go on to need a heart transplant. Prognosis depends on underlying cause. Restrictive cardiomyopathy caused by amyloids tend to have the worst prognosis.
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Arrhythmogenic right ventricular cardiomyopathy (ARVT)
The cardiac myocyte is replaced with fibro-fatty material either due to apoptosis, inflammation or a genetic cause. Normally affects right ventricle but can affect the left, leaving it prone to arrhythmias which can cause sudden death. Less common then dilated and hypertrophic cardiomyopathy. Causes sudden death in young people from northern Italy and Greece. Familial in half of cases, different inheritance paaterns
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Arrhythmogenic right ventricular cardiomyopathy (ARVT) clinical features
Most patients are asymptomatic, but some can be symptomatic, sudden death may be the first presentation. Patients may present with signs and symptoms of right sided heart failure however; this is only seen in later stages of the disease.
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ARVT investigations
The ECG is usually normal. In the echocardiography it is frequently normal but may show dilation in later stages. You can also have a cardiac MRI and genetic testing.
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ARVT management
If arrhythmias are non life-threatening, beta blockers can be used. An ICD is required with life threatening or refractory arrhythmias. Management of heart failure if present, a heart transplant may need to be considered. ARVC is progressive and not curable. The prognosis varies from individual to individual
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Infective endocarditis
Infection of the endocardial surface (inner layer of the heart including the valves), can cause extensive damage and is often fatal. Endocardial damage exposes the sub-endocardial matrix, platelets and fibrin attach to the matrix causing a thrombus on the myocardial surface. Bacteria sticks to the thrombus and are protected by being coated with fibrin
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Causes of infective endocarditis
It can be caused by turbulent blood flow from valve problems (e.g. rheumatic heart disease, mitral regurgitation and aortic stenosis), congenital heart disease or cardiomyopathy. Can also be due to cardiothoracic surgery or implanted foreign material e.g. prosthetic heart valves and pacemaker leads.
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Infective endcarditis, how can bacteria enter the circulation?
When someone has poor dental hygiene, uses IV drugs, sepsis and has has surgery or a catheter. Immunosuppressed people are more a risk
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Infective endocarditis- why are the valves on the left more affected?
The high pressure blood on the left causes a more turbulent blood flow so more potential for damage. The higher oxygen content promotes bacterial growth
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Bacterial endocarditis- microbiology
Staphylococcus aureus is the most common causes. Streptococus is often due to poor dental hygiene. 5% of cases are due to gram negative bacteria called the HACEK group. This is Haemophilius, Aggregatiabacter, Cardiobacterium, Eikenella, and Kingella.
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Bacterial endocarditis presentation
Subacute endocarditis has a more gradual onset with fever, tiredness, night sweats and weight loss. Acute endocarditis presents over a few days with more severe symptoms, including severe febrile illness, prominent/changing heart murmurs, embolic events, cardiac and renal failure. Subacute endocarditis can progress to acute endocarditis
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Bacterial endocarditis- vascular phenomenon
Bacteria from the myocardial embolism can break off and travel through the circulation, these are called septic emboli. Small septic emboli can deposit in the skin and mucous membranes and cause micro-abscesses and small haemorrhages. In the hands and feet, this can cause red, painless spots called Janeway lesions. Haemorrhages might also be seen in the mucous membranes, subconjunctiva of the eyes and in the nails as splinter haemorrhages. Larger septic emboli can block blood vessels, preventing blood flow and causing severe complications such as ischaemic stroke, limb ischaemia, pulmonary embolism and spleen infarcts.
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Bacterial endocarditis- immunological phenomena
When lots of immune complexes are made (e.g. in infective endocarditis), they may be deposited in tissues around the body, causing inflammation. Immune complexes can deposit in the hands, causing Osler’s nodes. Immune complex deposition can also cause kidney damage. They can cause damage to retinal capillaries.
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Bacterial endocarditis- investigation
Diagnosis can be difficult, it is based on the Duke criteria, which includes evidence from blood cultures, echocardiogram and clinical presentation. The blood culture detects the bacteria and the echocardiography detect vegetation and can assess valve damage
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Bacterial endocarditis's- treatment
Prolonged antibiotic treatment and some patients require surgery
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Bacterial endocarditis- prevention
People at risk receive antibiotic prophylaxis to reduce the risk when they have complex surgery
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Systolic heart failure
Ventricles cannot eject blood during systole, affects left ventricle first. The poor contractions lead to a reduced stroke volume. As less blood is ejected and more is left in the ventricle there will be an increased preload. The ventricle has reduced contractility and is unable to compensate for the increased preload. This increases pressure in the left atrium and pulmonary veins. This causes an increase in hydrostatic pressure, fluid is pushed into the lung tissue leading to pulmonary oedema, which leads to heart failure.
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What causes systolic heart failure
Contractility can be reduced if the heart muscle is damaged, either from a heart attach, myocardial infarction or cardiomyopathy
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Preload
The blood in the ventricle at the end of diastole, represents the degree of stretch in the ventricles at the end of diastole
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After load
The pressure needed to eject blood from the ventricle
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Diastolic heart failure
Happens when the heart chambers are unable to fill with blood during diastole. Compliance is how easy a chamber is to fill. Ventricular compliance is reduced in impaired ventricular relaxation (old age and increased collagen fibres) as well as in Hypertrophy (when afterload is high).Reduced compliance also reduces the amount of blood in the ventricles, this reduces end diastolic volume. This reduces the preload meaning there is a reduced stroke volume. Because of the reduced compliance, there is higher end diastolic pressure. This is transmitted back into the venous system causing increased venous pressure. This increases the hydrostatic pressure and pushes fluid back into the tissues. This can cause pulmonary odemia and breathlessness.
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Causes of diastolic heart failure
There are other non-cardiac causes of heart failure: anaemia, sepsis, hyperthyroidism, liver failure and volume overload (excess fluid) either blood or intravenous fluid. Both systolic and diastolic heart failure can cause left and right heart failure.
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Left ventricular failure
When the left ventricle fails it is transmitted to the left atrium and onto the pulmonary veins and capillaries. This causes higher hydrostatic pressure, and fluid leaks into the pulmonary tissue causing pulmonary odema. This causes shortness of breath, its worse when lying down (orthnopnoea), it can be worse at night (paroxysmal nocturnal dyspnoea).
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Right ventricular failure
In right ventricular failure, the increase in end-diastolic pressure causes increased right atrium pressure and pressure in the systemic veins. This causes a raised jugular venous pressure (JVP) and the elevated hydrostatic pressure causes a leaking of fluid into the tissues, causing pitting peripheral oedema, hepatomegaly and kidney congestion leading to kidney injury.
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Causes of right heart failure
Most common cause is left sided heart failure. The high pulmonary pressure caused by LV failure leads to excessive afterload in the RV. Isolated RV failure can occur due to a MI of the right ventricle, as well as diseases of the lung which increase the afterload. Right ventricular failure caused by lung disease is called cor pulmonale and happens in COPD, pulmonary hypertension and pulmonary embolism.
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Heart failure history
Ask about risk factors, if they have a history of ischaemic heart disease, MI or valvular disease. Ak about hypertension, diabetes (increases risk of hypertension and ischaemic heart disease/MI), alcohol excess and smoking. Ask about symptoms will depend on what side of the heart is affected
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The New York Heart association (NHYA) of heart failure
Class 1 -No symptoms with ordinary activity 5-10% on year mortality
Class 2- symptoms (e.g. breathlessness) during ordinary activity with light limitation of activity 15% one year mortality
Class 3- symptoms with less then ordinary activity, limitation on physical activity 30% one year mortality
Class 4- symptoms at rest, severe limitations, 50-60% one year mortality
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Examination of heart failure
May be clinical signs of fluid over the lungs from left ventricular failure (crackles) or right ventricular failure (pitting odema, raised JVP). There could be signs of the underlying cause of heart failure (high blood pressure or a murmur from a valve problem). There may be abnormal heart sounds (S3 and S4), a displaced apex beat (due to cardiomegaly-an enlarged heart).
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Investigations heart failure
Echocardiogram provides the best information about heart function. ECG and blood tests. A chest X-ray can show signs of heart failure.
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Treatment of heart failure general
Balanced diet, exercise and stopping smoking. Most drug treatments are aimed at reducing the compensatory Renin-Angiotensin-Aldosterone system, as this increases afterload. This includes drugs that help the heart function or assist the kidneys in removing excess fluid. Severe heart failure can cause disorganised left and right ventricular contraction or abnormal heart rhythms, so some patients require a pacemaker or implantable defibrillator.
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Treatment for heart failure at the start
Start with IV diuretic therapy. Closely monitor renal function, weight and urine output. Once stabilised start or re-start beta blocker treatment. If its acute heart failure due to left ventricular systolic dysfunction prescribe an Ace inhibitor and treat as chronic heart failure. In chronic heart failure prescribe diuretics or titrate dose. If in a sinus rhythm or risk of thrombosis anticoagulants should be considered. Avoid calcium channel blockers. Consider loop diuretics
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Loop diuretics (furosemide, bumetanide, torasemide)
Used in pulmonary odema due to acute left ventricular failure, also used in patients with chronic heart failure. Increases vasodilator effect and is administered intravenously, reduces pre-load. Promotes urinary excretion of Na+, Cl-, K+ and H2O by stopping their reabsorption in the thick ascending loop of Henle
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Loop diuretics pharmokinetics
Administered orally with GI absorption, 50% bioavailability. Peak effect after 30 mins with a 2 hour half life. Action lasts 4-6hr. If taken in I.V. it has rapid onset of 10 minutes. It undergoes liver cytochrome P450 metabolism.
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Loop diuretics contra-indications
Anuria (failure of the kidneys to produce urine), comatose and precomatose states associated with liver disease, drug induced renal disease, severe hypokalaemia and sever hyponatraemia.
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Loop diuretics cautions
May exacerbate diabetes and gout. Risk of urinary retention if an enlarged prostate. Risk of hypovolaemia, hypotension, hypokalaemia. The risk of hypokalaemia is reduced by combining with a K+ sparing diuretic. You should use lower doses in the elderly.
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Loop diuretic side effects
Dizziness, electrolyte imbalance, fatigue, headache, metabolic alkalosis, muscle spasms or nausea.
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Digoxin
Used to treat heart failure with reduced ejection fraction. It is an antiarrhythmic drug used to increase vagal tone in the heart. It is a positive inotrope that increases intracellular Ca. It should be used in supraventricular arrhythmias, chronic atrial fibrillation and chronic heart failure (improves symptoms but not mortality rate)
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Digoxin pharmokinetics
It has an oral administration bioavailability of 75%. Its onset of action is 30 minutes and its peak effect is between 1-5 hours. It has a half life of 36 hours. 70% of the elimination is renal, depends on glomular filtration rate. The volume distribution is 640L/70kg, it is so high because it binds to skeletal muscle. It has a narrow therapeutic index so a high risk of toxicity.
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Digoxin contra-indications
Heart block, heart arrhythmias and ectopic beat
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Digoxin caution
Risk of digitalis toxicity (build-up of drug Digitalis in the body) with electrolyte imbalance, recent myocardial infarctions.
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Digoxin side-effects
Arrhythmias, cardiac conduction problems, cerebral impairment, diarrhoea, dizziness, nausea, skin reactions, vision disorders, vomiting.
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Ivabradine
A cardiotonic agent. It selectively inhibits the pacemaker “If” current, this slows the heart rate allowing more time for blood to flow to the myocardium. Treatment for angina and mild to severe chronic heart failure. It is an alternative to beta blockers and may be used alongside them.
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Ivabradine contra-indications
Acute myocardial infarctions, cardiogenic shock, patients with pacemakers or in heart block, unstable angina, unstable or acute heart failure.
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Ivabradine cautions
Arrhythmias, elderly, hypotension
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Ivabradine side effects
Headaches, dizziness, arrhythmias, hypertension and blurred vision
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Hydralazine and nitrate
Acts as a vasodilator to reduce pre-load and reduce the risk of pulmonary congestion. It also acts as an arterial vasodilator, to reduce after-load and increase stroke volume. The side effects are headaches, tachycardia or irregular heartbeat
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Spironolactone (heart failure)
It is a potassium sparing diuretic which prevents your body from absorbing too much salt and keeps your potassium levels from getting too low. It is used if the patient does not respond to first line treatment. It is an aldosterone antagonist , blocking sodium transport proteins in the DCT, which improves survival in chronic heart failure. Contraindicated if the patient has hyperkalaemia or renal impairment. Causes Na+ and water loss but K+ retention. Makes its effect via the metabolite canrenone which has a much longer half life
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Inotrope
An agent that alters the force or energy of a muscular contraction
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Mild haemorrhage
Under 750ml. Then you will feel slightly anxious, your heart rate will increase to <100/min, Your urine production will be 30ml/h so will decrease. Your blood pressure will stay the same as well as respiratory rate at 14-20/min.
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Moderate haemorrhage
Between 750-1500ml. The patient will feel mildly anxious. Urine production will decrease to 20-30ml/h, heart rate will slightly increase to >100/min. Respiration rate will increase to 20-30/min. Blood pressure will stay the same, but pulse pressure will decrease.
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Severe haemorrhage
Between 1500-2000ml. The patient will fell confused and anxious. Urine production will fall (5-15ml/h), heart rate will increase to >120/min. Respiration will increase to 30-40/min. Blood pressure and pulse pressure will fall by a lot.
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Very-severe / life threatening haemorrhage
Above 2000ml. The patient will feel confused and lethargic. Their heart rate will increase to 140>min and their urine production will be negligible. Respiration rate will drop to >35/min and their blood pressure and pulse rate will fall further
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Auto-transfusion of fluid during a haemorrhage
Up to 500ml of fluid moves from the interstitium into the circulation following a severe haemorrhage to help maintain circulating blood volumes. There is increased sympathetic activity in the liver, which increases glucose production. This increases plasma and interstitial osmolarity. This drives the absorption of water from the interstitial space.
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The 4 types of shock
Hypovolaemic, cardiogenic, septic, anaphylactic
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Hypovolaemic shock
Due to a fall in circulating blood volume. Could be because of a haemorrhage, loosing blood plasma in sever burns and fluid loss due to vomiting or diarrhoea. 30% of plasma can be lost and then compensated for. Ability to compensate is reduced in age, medication (beta blockers), and myocardial or respiratory disease
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Cardiogenic shock
Mechanical or electrical failure of the ventricles. May be due to Cardiac Tampanode where fluid or gas builds up in the pericardial space, this can physically compress the heart reducing cardiac function.
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Septic shock
Vasodilation due to bacterial toxins (polysaccharides/protein) resulting in a drop in blood pressure.
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Anaphylactic shock
Exaggerated immune response i.e. bee sting
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Symptoms of shock
They may be anxious, tired, or show signs of apathy or exhaustion. They may have an intense thirst. There may be decreases arterial systole, diastole and pulse pressures with a rapid and weak pulse. Veins will appear compressed and will take a long time to fill if compressed. Appear pale, cold and with moist skin due to sympathetic activation
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What is shock?
When the control mechanisms fail and there is an acute failure of the cardiovascular system to supply nutritional blood flow to all tissues. If the shock is severe there may be an irreversible reduction in blood pressure
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What can irreversible shock lead to (VHAC)
• Vascular failure- desensitisation of adrenergic receptors, depletion of neurotransmitters. The result of action from local metabolites. Fall in BP
• Heart failure- reduction in [Ca+2] therefore less contractility
- Acidosis- retention and increase in CO2
• Depression of the CNS- prolonged ischaemia leads to a general decrease in neuronal activity in the brain which leads to a decreased sympathetic output
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Presentation of typical angina
Precipitated by physical exertion. A constricted discomfort in the front chest, neck, shoulders, jaw or arm. Relieved by rest or GTN
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Atypical angina presentation
Contains at least two of the same symptoms as typical angina. Also includes gastrointestinal discomfort, might have breathlessness and nausea
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BNP test for heart failure
You do a BNP (B-type natriuretic peptide) test for heart failure, will be a raised proBNP in heart failure. You will also have an enlarged heart and fluid in the lungs. Ejection fraction is normally 70% in heart failure it will be below 70%.
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The cardinal symptoms of heart disease
Dyspnoea, chest pain. Cough, palpations, coughing up blood (haemoptysis), expectoration (coughing up phlegm) and syncopal attacks (fainting).
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Class 1 antiarrhythmic drugs
Include Lidocaine/ lignocaine. They target sodium channels changing the shape of the action potentials to weaken heart rate. Treat fast tachycardia.
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Class 2 antiarrhythmic drugs
Beta blockers. Include atenolol, metoprolol, sotalol. Block the effects of beta agonists and the sympathetic nervous system. Decreases phase 4 in an action potential.
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Class 3 antiarrhythmic drugs
Potassium channel blockers including amiodarone, causes a prolonged repolarisation. Treats tachycardia
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Class 4 antiarrhythmic drugs
Potassium channel blockers, pacemaker cells fire less frequently
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Treating bradycardia
Atropine switch of Vagus nerves. Isoproterenol activates beta receptors causing a greater degree of depolarisation and increasing heart rate.
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Treatment for ventricular fibrilation
Amiodarone and Lignocaine
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Treatment for cardiac arrest
Adrenaline/ epinephrine
