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Esteban Montoya Pathophysiology II January 16, 2023 Alterations in Cardia Function Outline Coronary Heart Disease
- CHD Is characterized by a lack of oxygenated blood being delivered to the cardiac myocytes, and they can’t not produce enough ATP, which results in consequences. A reason for lack of oxygen to the myocytes is caused by CAD (coronary artery disease) , and it is because of atherosclerosis. Sequelae of CHD: Angina pectoris - Pain or pressure in the center of the chest, down by the xiphoid process, may radiate to the back in between the two scapulae. Myocardial infarction – CHD frequently results in the death of heart cells due to lack of O2. Dysrhythmias Heart failure – CHD begets Heart failure/congestive heart failure. Sudden cardiac death
Etiology of CHD: Fats are transported by LDL or HLD: LDL – Low density lipoprotein “bad cholesterol.”
- Apoprotein that gloms onto cholesterol and fats
- Delivers fats and cholesterol to the liver as well, but also deposits it elsewhere such as the endothelial lining of arterial walls. HDL – High density lipoprotein “good cholesterol.”
- Apoprotein that gloms onto cholesterol and fats
- Delivers fat and cholesterol directly to the liver and doesn’t allow what it’s bonded to, to be delivered anywhere else. Atherosclerosis – The building of plague in the wall which narrows the walls of the lumen. Blockages can occur in other areas of the body or branches of the arteries due to atherosclerosis. Examples are: A blockage in the carotid arteries, which feed oxygenated blood to the brain; a positive finding would be carotid bruits. Another is a blockage in the superior mesenteric artery that feeds the small intestines.
Fat underneath friable tissue can also become dislodged and travel downstream and cause an occlusion. Arteriosclerosis (hardening of the arteries/loss of elasticity) can be seen as a subset of atherosclerosis. Various causes such as smoking, drinking, aging, etc. Pathophysiology of Ischemia Ischemia – not enough oxygen to meet metabolic demand of tissues/chronic deprivation. Two big factors involved in oxygen demand: Rate of coronary perfusion – are the lumen of the arteries blocked or wide open? Perfusion can be altered by: Large, “stable” atherosclerotic plaque Acute platelet aggregation and thrombosis Vasospasm – Another word for vasoconstriction. Can result in temporary closure of the lumen, and even if temporary the result is a heart attack. Poor perfusion pressure – heart isn’t contracting nearly hard enough to force blood out at optimal pressure, coronary arteries
experience a dip in perfusion pressure, impacted tissues are inadequately oxygenated. Cardiac workload – how much oxygen does the heart need, at any given time. Clinical Features and Management of Coronary Syndromes Coronary heart disease takes years to develop (slow progression) and is a chronic obstruction issue. Stable angina pectoris – is predictable , angina occurs when doing certain activities, does not occur when not doing those activities. Ischemic cardiomyopathy – not enough oxygen to cardiac myocytes and pathologies develops due to oxygen deprivation. Acute coronary syndrome (ACS) – Many hospitals treat this as an MI (myocardial infarction) (heart attack), but it isn’t the same thing. An MI will happen shortly after ACS sets in, unless there is an intervention. Characterized by unstable angina, which ultimately leads to an MI. The way to distinguish between an MI and ACS is:
Chest pain caused by unstable angina is significantly greater than of that caused by predictable, stable angina, and usually lasts a lot longer. EKG and biomarkers are used for diagnosis Presentation Working diagnosis EKG Cardiac biomarkers Final diagnosis Patient comes in, they’re sweating, and they’ve had severe chest pain that is intermittent and didn’t do anything to trigger it and they’re short of breath. An EKG is done, and an ST elevation is seen. With an ST elevation, there is a hunch that the patient is having a heart attack or has had a heart attack. Labs are done to look for biomarkers. Labs come back positive for biomarkers with an ST elevation, that is called a STEMI (ST elevation MI). Another patient arrives and presents the same way. An EKG is done and there is no ST elevation, patient could still be having or could have had a heart attack. Labs are done to check for biomarkers and come back positive for biomarkers. This is called an NSTEMI (No ST elevation MI)
Worst case scenario is a patient presents with all the symptoms of ACS EKG strip shows no ST elevation And biomarkers come back negative, This does not mean the patient is healthy or out of woods, all that it means is that the patient might have ACS and should be kept in the ER for a while to ensure there isn’t a heart attack on the ride home. Biomarkers When heart cells undergo prolonged ischemia, they undergo apoptosis and dump their contents: Creatine kinase – A positive find indicates that heart cells have died and dumped their contents. Troponin I – a positive find for troponin I that has a spike and gradually decreases indicates that a sarcomere has been destroyed and the wreckage is floating in the circulatory system. Lactase dehydrogenase (LDH) – as a person’s heart cells are dying, they enzyme is used to try and pull off anaerobic respiration and that only works for a while, heart cells eventually die, and you find elevated levels of LDH.
Leaking ions is responsible for the ST change seen on an EKG and ions leaking over time is what’s responsible for dysrhythmias that people experience. If stroke volume decreases, the kidneys detect the reduction in perfusion pressure and trigger the renin-angiotensin aldosterone cascade that releases aldosterone which causes sodium retention and therefore water retention in the nephrons and we build up the volume in circulatory system. When we retain fluids purposely, that increases our preload, increases cardiac output and stroke volume in the intermediate time. Over time, there is increased stress on the left ventricle (could be right, or both) and that triggers hypertrophy of the ventricular wall, which is disastrous and begets heart failure or an MI. Sudden Cardiac Death Death from cardiac causes within 1 hour of symptom onset. External defibrillator done or CPR performed. VFIB (Ventricular fibrillation) is usually the cause for sudden cardiac death. Chronic Ischemic Cardiomyopathy Heart failure develops over time. It’s a progressive ischemia with progressive consequences, long term.
People who develop this usually have a history of a heart attack or angina and is more common in older adults. Endocardial and Valvular Diseases
- Endocardium = endothelial structure - Valvular diseases = pertaining to valves Damage can be brought about in many ways: Congenital malformations Calcification Inflammation scarring – constant triggering and repair brings about scaring which can beget calcification, and tissues are no longer viable. Stenosis: Means a narrowing of the opening where the valve is or that the valve can’t open fully. Regurgitation: Means there is a leaky valve. Not all heart murmurs are caused by leaky valves. A leaky valve indicates we’re not doing isovolumic filling and contraction. Mitral Stenosis
Usually asymptomatic, and for most people doesn’t cause any problems. Aortic Stenosis Comes about usually by age related calcium deposition on the cusp of the aortic valve. If left side can’t push blood through then there is increased pressure, which increases size (hypertrophy) which can beget left sided heart failure. Aortic Regurgitation Due to a leaky aortic valve, as the aortic valve shuts and ventricular contraction happens to open the aortic valve, blood comes back into the left ventricle which causes left ventricular hypertrophy due to increased volume. Diseases of the Endocardium Rheumatic Heart Disease – Follows infection of B – hemolytic streptococci. Antigen-antibody complexes get deposited in the heart, joints, and skin.
Most people don’t need to take antibiotics, but they are taken to prevent from getting others sick and to keep strep from setting up residence in tissues. Mainly occurs in kids. Infective Endocarditis Most common bacteria that cause this are strep and staph infections. Myocardial Diseases Myocarditis Is inflammation of the myocardium. Myocytes undergo apoptosis and then there is necrosis that happens. Causes of myocarditis: Microbial agents Physical agents Immune mediated diseases Most common cause people get it is because of a virus, and it affects the left ventricle but usually causes general dilation in all four chambers of the heart.
Hypertrophic Cardiomyopathy Is often a genetic abnormality. Idiopathic hypertrophic subaortic stenosis: all this means is part of the left ventricle just below aortic valve hypertrophies due to unknown reasons.d Is unpredictable but patients can live many years. Restrictive Cardiomyopathy Usually associated with amyloidosis. Ventricle is impaired due to noncompliance and cardiac output goes to hell and eventually left ventricular heart failure happens. Pericardial Diseases
- Can happen for many reasons, often it happens as a secondary consequence of other issues such as: Systemic infection Trauma to the chest Cancer (neoplasia)
Pericardial Effusion Is an accumulation of fluid in the pericardial sac (sac that surrounds the heart). Suspected fluid is usually: Serous (plasma fluid) Serosanguineous (plasma and blood) Blood Cardiac Tamponade Is a sudden rapid pericardial effusion. What happens is the heart becomes compressed, dramatically drops stroke volume, and reduced cardiac output. Sympathetic NS activates and heart rate goes up. Pericarditis Virtually anything can cause pericarditis Can either be acute or chronic Acute Pericarditis
Congenital Heart Diseases Abnormality of the heart that is present from birth. Could have genetic causes. Congenital means present at birth. just under 1 in every 100 kids has a congenital heart problem and is one of the most common congenital anomalies that there is. Two categories: Shunts: an abnormal pathway Obstructions: blockage of the blood flow, either because of narrowing or no development there. There are a host of cardiac teratogens that can bring about congenital heart anomalies Mom infected with rubella in the first trimester can have disastrous effects on the fetus because of profound proliferation and because of differentiation occurring at that stage. First Category of Congenital Defects
Left to right shunts (Acyanotic Congenital Defects): In time tend to become right to left shunts. Blood goes from left side (oxygenated) of heart to right side (deoxygenated) of heart. Adding extra O2 to the blood going to lungs to pick up O2. Atrial Septal Defect There is a hole in the interatrial septum, the wall that separates the right and left atrium. Oxygenated blood enters the right atrium while in the womb and passes through a hole called the foramen ovale into the left atrium and then goes into left ventricle, then to rest of body. Chemical cascade shuts the foramen ovale and it becomes tissue called fossa ovalis, just below AV node, in the interatrial septum. The defect is the hole didn’t shut. Extra O2 coming back to heart from lungs is coming in at an increased pressure. That blood goes from left atrium through foramen ovale into right atrium. Extra blood in right ventricle goes into right atrium, and it pushes more blood.
