Case 2- illness Flashcards
Ischaemia causes
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
Ischaemia- causes of occlusion
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
Factors that make tissue more susceptible to ischaemia
- 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
Venous and capillary ischaemia
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
The two non vascular reasons why ischaemia can occur
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).
Causes of infarction
It is cell death due to an insufficient supply of oxygen, the causes are the same as in ischaemai
Types of myocardial infarction
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
Symptoms of ACS
Central chest pain, dyspnoea and nausea
Cause of ACS
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.
Blood markers of ACS
Troponin T is released in necrosis so is present in NSTEMI or STEMI but not unstable angina as there is no necrosis
ECG changes in unstable angina
Can be normal. Sometimes has ST depression, T wave inversion
Unstable angina pathophysiology
Incomplete occlusion of the coronary artery which causes myocardial ischaemia without infarction. It occurs at rest, partial occlusion with no necrosis
NSTEMI pathophysiology
Partial occlusion of a coronary artery. Partial thickness necrosis through the heart muscle. There will be raised Troponin
ECG NSTEMI
Can be normal. Might have an ST depression and a T wave inversion
STEMI pathophysiology
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
Signs and symptoms of ACS
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
Immediate management of ACS
This includes giving oxygen, a vasodilator (dilates blood vessels) and analgesia (painkillers)
Acute management (revascularisation) of ACS
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)
Long term management of ACS
All patients need it. Includes controlling modifiable risk factors, medication to reduce platelet aggregation (clumping), medication to control blood pressure and cholesterol levels
Complications following a myocardial infarction (DARTH VADAR)
- 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
Inferior myocardial infarction
An infarction of the right coronary artery territory, affects the inferior parts of the heart. Can effect the AV node leading to heart block
Causes of hypoxic damage in the heart
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.
How hypoxic damage effects the heart
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
Stunned myocardium
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
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
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.
What can ischaemic heart disease also be called
Coronary heart disease (CHD) and coronary artery disease (CAD)
Types of chronic ischaemic heart disease
Stable angina, variant angina, silent angina
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.
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
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.
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.
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.
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
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
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.
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.
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
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
Symptoms of mitral regurgitation
Shortness of breath, fatigue, palpitations. It increases the risk of atrial fibrillation and heart attack
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.
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).
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
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.
Pulmonary regurgitation
Causes an early diastolic murmur can be due to any cause of pulmonary hypotension
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
Detecting mitral stenosis
Malar flush, signs of atrial fibrillation are the same as RVH i.e. left parasternal heave
Tricuspid stenosis
Causes mid-diastolic murmur, mainly caused by rheumatic disease
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
Types of cardiomyopathy
Dilated cardiomyopathy, hypertrophic cardiomyopathy, restrictive cardiomyopathy, arrhythmoegnic right ventricular cardiomyopathy (ARVT)
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
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.
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.
Investigations of dilated cardiomyopathy
Chest x-ray will show signs of heart failure. ECG shows arrhythmias, conduction abnormalities or non specific ST segment changes