CHI335 Cardiovascular System Lecture II PDF

CHI335 Diagnosis I Cardiovascular System Lecture II  Outline diseases of each layer of the heart Explain classes of HTN, its management and complications Describe the process of atherosclerosis, its risk factors and outcome in line with ischaemic heart disease and peripheral vascu...

CHI335 Diagnosis I Cardiovascular System Lecture II  Outline diseases of each layer of the heart Explain classes of HTN, its management and complications Describe the process of atherosclerosis, its risk factors and outcome in line with ischaemic heart disease and peripheral vascular diseases Outline types of angina pectoris and MI Describe heart failure and its clinical manifestations and describe the influence of compensatory responses on heart failure progression Describe the three main types of cardiomyopathies, and outline their relationship to heart failure Briefly describe types of congenital heart defects Outline heart dysrhythmia, and describe the common and deadly ones  Inflammation of the innermost lining of the heart and the valves Bacterial infections are the most common cause S & S: Weakness, fever, excessive sweating, general body aches, difficulty breathing, and blood in the urine Treatment addresses the underlying cause  Inflammation of the muscular layer of the heart The most common cause is viral infections ▪ Especially Group B Coxsackie virus S & S: Unexplained fever, chest pain, dyspnoea, fatigue, and fainting Treatment normally includes steroids, bed rest, and a low-sodium diet  Inflammation of the pericardium Most commonly caused by complications of viral or bacterial infections S & S: Sharp, stabbing chest pains, fever, fatigue, and orthopnoea ▪ “Friction rub” may be heard over the heart Treatment includes analgesics for pain, and diuretics are used to remove excess fluids around the heart  Essential or primary or idiopathic Secondary Malignant ▪ Severely high blood pressure (generally >180/120 mmHg) ▪ It is a medical emergency ▪ Must be treated immediately with medications ▪ May complicate hypertension of any aetiology ▪ Characterized by acute, ongoing target-organ damage ▪ Accelerated macro- and microvascular complications ▪ Next slide…  Non-Modifiable Modifiable ▪ Age ▪ Smoking ▪ Sex ▪ Hypercholesterolaemia ▪ Family history ▪ HTN ▪ DM ▪ Physical inactivity ▪ Overweight/Obesity  Atherosclerosis can be complicated by ▪ Embolus (mostly thromboembolism) ▪ Thrombosis → Therefore, a significant decrease in blood flow and increase in the risk of: ▪ Ischaemic heart disease (IHD) ▪ Stable angina pectoris ▪ Unstable angina pectoris (ACS*) ▪ MI (ACS) ▪ Cerebrovascular accidents (CVA) ▪ Stroke / TIA ▪ Peripheral arterial disease (PAD) *Acute Coronary Syndrome   Blood flow to the myocardium Leads to Deficits in oxygen and nutrients and A failure to remove metabolic waste from the tissue Leads to Inadequate resources to meet the needs of the heart Leads to The injury and, ultimately, death of heart muscle Stable angina (known as exertional angina) Causes ▪ An atherosclerotic plaque Characteristics ▪ Blood flow is adequate at rest but is compromised when the person exerts themselves, causing pain that lasts 5–15 minutes and is relieved by rest ▪ Usually, no other symptoms Unstable angina (ACS) Causes ▪ A huge atherosclerotic plaque, or a plaque complicated by vasoconstriction, or thrombus formation on top of it or thromboembolism (less likely) Characteristics ▪ Compromised blood flow at rest, leading to chest pain even without exertion ▪ Patient may also experience palpitation, shortness of breath, sweating, anxiety, pallor, nausea, and possibly vomiting Variant (Prinzmetal’s) angina Causes ▪ Unexplained vasospasms rather than atherosclerotic plaque formation Characteristics ▪ Individuals can experience this anginal pain at any time, even when sleeping, and there is no recognised trigger for their attacks  In stable angina, the flow is only insufficient when the person exerts themselves In unstable angina, the presence of an associated thrombus makes the blood flow insufficient even at rest Variant angina is the result of as- yet unexplained vasospasms (red arrows) aka Heart attack Cardiac muscle sustains permanent damage as a result of severe ischaemia ▪ Heart tissue that dies in an MI does not regenerate ▪ Caused by complete obstruction of coronary arteries due to atherosclerosis, a thrombus, or an embolus ▪ Severe squeezing chest pain (also pain could be felt in the left shoulder, arm, back, teeth, or jaw), SOB, profuse diaphoresis, palpitation, anxiety, dizziness or syncope, nausea and possibly vomiting  Call000 for help Chewing an aspirin at the onset of symptoms Use of a strong vasodilator (glyceryl trinitrate, GTN) ▪ In an unconscious patient, CPR should be administered Use of thrombolytic drugs to destroy the blood clots that block a coronary artery Angioplasty or coronary artery bypass graft to open up the coronary arteries  Three categories: dilated, hypertrophic and restrictive Dilated cardiomyopathies ▪ A loss of elasticity of the myocardium and an overstretched, flaccid ventricular muscle ▪ A variety of causes ▪ Toxins (e.g. chemotherapy, alcohol), infections, ▪ Metabolic alterations of the tissue (e.g. pregnancy, hyperthyroidism) Hypertrophic cardiomyopathies ▪  Size of the ventricular muscle ▪ Can be an acquired condition (in athletes) ▪ Can be an inherited condition (more problematic) ▪ An autosomal dominant disorder marked by disorganised myocytes and weak connective tissue ▪ The  size of the muscle is asymmetrical  Restrictive cardiomyopathies ▪ A stiff heart muscle, inhibiting both contraction and relaxation ▪ A key cause of restrictive cardiomyopathy is scar tissue formation (e.g. post MI) ▪ Infiltration of the myocardium by materials such as iron, amyloid, and tumours  Any of the valves can be affected, with those on the left side more commonly damaged ▪ Senile stenosis is the consequence of wear and tear on the valve with age (is usually accompanied by calcification) ▪ Vegetations may also develop on the valve, stiffening the valve leaflets ▪ Damage-induced scars can fuse the leaflets Consequence of valve stenosis ▪ Difficulty opening the valve ▪ When a semilunar valve is stenotic → increased ventricular afterload → Hypertrophy of right or left ventricles ▪ When an atrioventricular valve is stenotic → Insufficient preload (filling) for the ventricle ▪ In both cases → Failure to eject adequate stroke volume →  cardiac output → Heart failure  Any of the valves can be affected, with those on the left side more commonly damaged ▪ Aka valve insufficiency or incompetence ▪ Regurgitation occurs when blood leaks backward through the leaflets that don't close correctly Consequence of valve regurgitation ▪ Faulty closure of the valve (leaflets) ▪ When a semilunar valve leaks → Volume overload (excess preload) in the ventricle → Hypertrophy of left or right ventricles → Heart failure ▪ When an atrioventricular valve leaks → Failure to eject adequate stroke volume and cardiac output → Heart failure Rheumatic heart disease can cause both stenosis and regurgitation of valves https://youtu.be/yjwnuNUUdig?si=y7aU3vukoDi1Xonz https://youtu.be/K_klwHDcges?si=yy_VdZiJIZxtUBkf  Two categories ▪ Cyanotic ▪ Not discussed here ▪ Acyanotic ▪ ASD ▪ VSD ▪ PDA ▪ Valve stenosis Both categories ultimately impose a risk of heart failure Septal defects A hole in the septum that divides either the atria or the ventricles (therefore, atrial septal defect (ASD) or a ventricular septal defect(VSD)) ▪ VSD is the most common congenital cardiac anomaly in children Depending on the size of the hole and the amount of blood lost, there might not be any loss of stroke volume and cardiac output As the child ages, a greater and greater proportion of blood will be shunted to the right side, possibly leading to compromised cardiac output and heart failure The hole can be surgically closed, and the condition quickly resolves  Schematic representation of ASD An atrial septal defect can trigger hypertrophy of the right atrium and ventricle due to the volume overload Adapted from L.S. Lily (ed.) (2007), Figure 16.11.  Schematic representation of VSD A ventricular septal defect causes hypertrophy of the right ventricle, left atrium, and ultimately left ventricle due to the volume overload Adapted from L.S. Lily (ed.) (2007), Figure 16.12. Patent ductus arteriosus (PDA) Ductus arteriosus is a blood vessel that connects the aorta and the pulmonary trunk during foetal life Its role in the foetus is to shunt blood away from the lungs and into the systemic circulation Quickly after birth, the ductus arteriosus is closed ▪ If not, this condition in babies is called patent ductus arteriosus, allowing blood from the aorta to be shunted into the pulmonary trunk Surgical closure of the ductus completely resolves the condition and leaves no lasting health concerns  Patent ductus arteriosus Schematic representation of PDA Failure of the ductus to close will trigger hypertrophy of both left atrium and ventricle due, in part, to volume overload coming in from the lungs and from compensatory mechanisms to correct the reduced cardiac output. Adapted from L.S. Lily (ed.) (2007), Figure 16.13. Congenital valve stenosis Congenitally stenotic valves are malformed either because the valve is fused or because it has fewer leaflets than it should have ▪ Aortic valve stenosis (AS) represents about 6% of all CHD, followed by pulmonic valve stenosis Semilunar valve stenosis increases afterload pressure on the respective ventricle as they attempt to open a faulty valve and eject blood ▪ This leads to  cardiac output and ventricular hypertrophy ▪ However, the ejected blood is oxygenated, and therefore, there is no cyanosis Inadequacy of heart pumping so that the heart fails to maintain the circulation of blood Main risk factors (RFs) ▪ IHD ▪ HTN ▪ Valve disorders ▪ Cardiomyopathies ▪ Congenital heart defects ▪ venous insufficiency (e.g. varicose veins) Left heart failure ▪ Systolic HF ▪ Diastolic HF Right heart failure → → Goals Correct the cause, if possible ▪ Pharmacological or surgery Improve cardiac output ▪ Pharmacological Reduce peripheral vascular resistance ▪ Pharmacological, and lifestyle modifications Improve quality of life ▪ All above plus Supplemental O2  A slow and progressive circulation disorder due to narrowing, blockage, or spasms in a blood vessel in the periphery This condition is associated with ▪ Atherosclerosis ▪ Diabetes ▪ Embolism ▪ Vasculitis ▪ Vasospasm ▪ Venous insufficiency ▪ Fibromuscular dysplasia ▪ Entrapment   Perfusion in the peripheral tissues ▪ Leads to ischaemia ▪ Initially, ischaemia only occurs on exertion, when metabolic requirements are elevated in the face of insufficient blood supply ▪ It may worsen over time ▪ Acute arterial occlusion (6Ps) ▪ Ischaemic pain in legs and hands is called claudication ▪ Tissue necrosis is a potential outcome ▪ Claudication at rest is a warning sign https://www.bmj.com/content/bmj/suppl/2018/02/01/bmj.j5842.DC1/morr041877.wi.pdf The goals are maintaining circulation in the periphery and slowing the progression of atherosclerosis Non-pharmacological measures ▪ Cessation of smoking, maintaining an exercise program and ensuring a dependent position for the legs to improve peripheral perfusion Medications ▪ Anticoagulants ▪ Thrombolytics ▪ Vasodilators Surgical management ▪ Endarterectomy (or removal of the intima and occlusive deposits) ▪ A graft or bypass may be needed to restore blood flow  Aka arrhythmia is an abnormal heart rhythm/rate Majority of dysrhythmias are short-lived (