Escolar Documentos
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Overview
Review of basics Ischaemic heart diseases
Coronary artery occlusions Myocardial infarction
Shock
Hypovoleamic shock Cardiogenic shock Septiceamic shock Anaphylactic shock
Review
Atherosclerosis Epidemiology of coronary artery disease Physiology of the cardiac cycle Anatomy of the myocardium Vascular supply of the myocardium
Coronary Angiography
Areas of perfusion
Left anterior descending (LAD) supplies most of the apex of the heart, the anterior wall of the left ventricle and the anterior two-thirds of the ventricular septum. Left circumflex branch supplies the lateral wall of the left ventricle. The right coronary artery in 80% of the population supplies the right ventricle, the posterior third of the ventricular septum and the posterior-basal wall of the left ventricle. (Right dominant circulation)
Coronary atherosclerosis
Coronary atherosclerosis
Coronary atherosclerosis
Coronary atherosclerosis
Clinical Manifestations
Angina Pectoris Myocardial Infarction Chronic ischaemic heart disease
Progressive heart failure consequent to previous myocardial infarction.
Angina Pectoris
This is a symptom complex. Symptoms caused by transient myocardial ischaemia that falls short of inducing the cellular necrosis that defines myocardial infarction. Three variants: Stable angina Prinzmental angina Unstable angina
Angina Pectoris
Stable Angina Most common form. Chronic stenosing coronary atherosclerosis, reaching a critical level, leaving the heart vulnerable to increased demand. Typically relieved by rest or a vasodilator
Prinzmental Angina
Uncommon pattern Occurs at rest Documented to be due to arterial spasm Unrelated to physical activity, heart rate or blood pressure. Generally responds to vasodilators.
Unstable Angina
Pattern here is the pain occurs with progressively increasing frequency and tends to be more prolonged Associated with disruption of the atherosclerotic plaque, with superimposed thrombosis, embolisation or spasm. Predictor of Myocardial Infarction
Myocardial Infarction
Transmural Infarction
The ischaemic necrosis involves the full or nearly the full thickness of the ventricular wall in the distribution of a single coronary artery. Usually associated with chronic coronary atherosclerosis, acute plaque change and superimposed completely obstructive thrombosis.
Myocardial Infarction
Subendocardial infarct
Limited to the inner one-third or at most one half of the ventricular wall May extend laterally beyond the perfusion territory of a single coronary artery In a majority of cases, there is diffuse stenosing coronary atherosclerosis.
Hypereosinophilia
Coagulative necrosis
Infarct extension
Old myocardial infarct showing evidence of thinning of ventricular wall replaced by fibrous scar
Aortic Valves
Mitral Valves
Pulmonary Valves
Tricuspid Valves
Response to injury
Mechanical injury superficial fibrous thickening over preserved architecture. Inflammation invariably leads to vascularisation of structure, fibrosis leads to decrease in size/surface area. Degenerative changes distortion and increase in size due to deposits of material such as calcium salts, cholesterol, etc.
Atrial thrombus
Aortic Valve Inlet Looking into the left ventricular outlet Note the three valvular cusps and the three distinct commissures (arrows)
Mitral Valve Inlet Viewed from the left atrium. Note bicuspid valve leaflets. Slight tenting of the valve leaflets suggestive of early mitral valve prolapse.
Rheumatic fever
Once the most common cause of valvular heart disease in Hong Kong. It is an acute immunologically mediated , multi-system inflammatory disease that occurs a few weeks after an episode of Group A (-hemolytic) streptococcal pharyngitis.
Rheumatic Valvulitis
Infective Endocarditis
Colonisation or invasion of heart valves by microbiologic agent. Formation of friable vegetations (composed of thrombotic debris and organisms. Leads to destruction of underlying cardiac tissue. Source of infective embolisation
Infective endocarditis
Most common sites involve the left heart valves Tricuspid valves typically involved in intravenous drug abusers Development of infective endocarditis preventable in patients with valvular diseases by provision of antibiotic cover for any surgical or dental procedures.
Bacteria Endocarditis
(The heart)
Effective venous and lymphatic return Intact and unblocked blood vessels
Veins
Pulmonary vessels
64%
9%
3.0L
11.0L
Intracellular fluid
28.L
Blood volume contains both extracellular fluid (plasma) and intracellular fluid (fluid in RBC). Average blood volume is about 8% of body weight, approximately 5L (60% plasma 40% RBC)
What is shock?
A state of generalised hypoperfusion of all cells and tissues due to reduction in blood volume or cardiac output or redistribution of blood resulting in an inadequate effective circulating volume A systemic (whole body) event resulting from failure of the circulatory system It is at first reversible, but if protracted leads to irreversible injury and death.
Causes of shock
Hypovoleamia Cardiogenic (pump failure) Anaphylactic (peripheral pooling) (return failure) Septic (Septiceamic) Complex reasons
Hypovoleamic shock
Haemorrhage
External (Chop wounds, Gastro-intestinal bleeding, etc) Internal (Hemoperitoneum due to ruptured aortic aneurysm, ruptured ectopic pregnancy, etc.
Fluid loss
Dehydration (low intake or excessive loss)
External loss
Internal Bleeding
Taken from Guyton & Hall Human Physiology and Mechanisms of Disease
Progressive/Advance Stage
Results when no therapeutic intervention is given for the early stage, compensatory mechanisms become harmful. Autoregulation mechanisms breakdown.
Irreversible shock
Irreversible hypoxic injury to vital organs
Compensated hypotension
Hypotension (low volume or low cardiac output) Sympathetico-adrenal stimulation (fight or fright) Release of catecholamines resulting in peripheral vasoconstriction maintain BP Activation of renin-angiotensin-aldosterone system and increased anti-diuretic hormone release Fluid retention by kidneys, further vasoconstriction Impaired renal perfusion and perfusion to other organs with every effort made to maintain perfusion to brain and heart (auto-regulation)
Taken from Guyton & Hall Human Physiology and Mechanisms of Disease
Splenic Infarct
Infarct of kidney
Cardiogenic shock
Failure of myocardial pump.
Intrinsic due to myocardial damage Extrinsic
Due to external pressure e.g. cardiac tamponade Due to obstructed flow e.g. thrombosis
Anaphylactic shock
Usually due to prior sensitisation Exposure to specific antigens Mediated by histamines, complements and prostaglandins Vasodilatation of micro-circulation associated with pooling and fluid extravasation
Septic shock
Commonly due to gram-negative endotoxin producing bacteria. May also accompany gram-ve bacteria. Predisposing factors include: Debilitating diseases Complications of instrumentation and treatment Burns
Septic shock
Pathogenesis include: Inflammatory reaction vasodilatation mediated by histamines and complements Disseminated intravascular coagulopathy activation of clotting factors and platelets together with consumption of clotting factors Endothelial damage extensive due to endotoxins Release of interleukin-1 and TNF-alpha (Tumor necrosis factor alpha) from macrophages
Taken from Guyton & Hall Human Physiology and Mechanisms of Disease
Pathological changes
Hypoxic injury to vital organs infarction Necrosis of tissues Lysis of cells
The extent of pathological changes is dependent on the duration of decompensation before death. In acute deaths, often no significant findings are found.
Pathological changes
Brain
Hypoxic and ischaemic damage Initially found at boundary zones May also be associated with marked cerebral oedema.
Pathological changes
Heart
Focal myocardial necrosis Subendocardial infarction (vulnerable region of blood supply) If there is pre-existing coronary artery diseases, may also lead to acute transmural myocardial infarction
Pathological changes
In cardiogenic shock
Due to previous ischaemic heart diseases the ventricular chambers may well be dilated and distended. The walls are often thin and may be replaced by non-elastic fibrous scars In intrinsic myocardial diseases leading to pump failure, the myocardium may be unusually thickened and rigid.
Pathological changes
Lungs
Diffuse alveolar damage (adult respiratory distress syndrome) Damage to Type 1 pneumocytes and to endothelial cells oedema as well as hyaline membrane due to decreased surfactant production Haemorrhages, fibrosis, atelectasis and infection
Pathological changes
Kidneys
Acute tubular necrosis often associated with remarkably well preserved glomeruli
Pathophysiology of
Taken from Guyton & Hall Human Physiology and Mechanisms of Disease
Pathological changes
Gastrointestinal tract
Mucosal ischaemia, haemorrhage, necrosis, gangrene
Liver
Centrilobular necrosis, fatty degeneration
Adrenal glands
Focal necrosis Diffuse haemorrhagic destruction
Pump Failure
Cardiogenic Shock
Vessel injury
Physical injuries such as wounds, ruptures of aneurysms, etc (Hypovoleamic)
Peripheral Pooling
Hypoalbumineamia, Ascites, Renal failure, (Hypovoleamic) Septiceamic, Anaphylaxis (Capillary pooling)