Exercise Prescription for Cardiopulmonary Conditions.pdf

Exercise Prescription for Cardiopulmonary Conditions: Notes Week 1: Cardiovascular System and the role of exercise testing and prescription Refresher - The heart o 4 chambers ▪ Right and left atria (auricles superior) ▪ Right and left v...

Exercise Prescription for Cardiopulmonary Conditions: Notes Week 1: Cardiovascular System and the role of exercise testing and prescription Refresher - The heart o 4 chambers ▪ Right and left atria (auricles superior) ▪ Right and left ventricles o Atrioventricular sulcus ▪ Separates atria and ventricles o interventricular sulcus ▪ Overlies the interventricular septum that divides the right and left ventricle o interatrial septum ▪ Wall that separates atria o Interventricular septum ▪ Muscular wall that separates the ventricles o Pectinate muscles ▪ Interatrial ridges of myocardium in the right atrium and both Auricles o Trabeculae carneae ▪ Internal ridges in both ventricles ▪ Two major circulatory circuits Pulmonary - The Valves o Ensure a one way flow of blood through the heart o Atrioventricular valves control blood flow between the atria and ventricles ▪ Right AV valve has 3 cusps (tricuspid) ▪ Left AV valves has 2 cusps (bicuspid) ▪ Chordae tendinae Connect AV valves to papillary muscles on floor of ventricles o Prevents AV valve from flipping inside out or bulging into the atria when the ventricles contract - The heart wall o Pericardium – double-walled sac that encloses the heart ▪ Allows heart to beat without friction, provides room to expand, yet resists excessive expansion o Parietal pericardium – outer wall of sac ▪ Superficial fibrous layer of connective tissue ▪ Deep, thin serous layer o Visceral pericardium – heart covering ▪ Serous lining of sac turns inward at base of heart to cover the heart surface o Pericardial cavity – space inside the pericardial sac filled with 5-30ml of pericardial fluid o Epicardium – visceral pericardium ▪ Serous membrane covering the heart ▪ Coronary blood vessels travel through this layer o Myocardium ▪ Layer of cardiac muscle proportional to workload Muscle spirals around heart which produces wringing motion  ▪ Fibrous skeleton of the heart: framework of collagenous and elastic fibres ▪ Provides structural support and attachment for cardiac muscle and anchor for valve tissues o Endocardium ▪ Smooth inner lining of heart and blood vessels ▪ Covers the valve surfaces and is continuous with endothelium of blood vessels - Blood flow through the chambers - Coronary circulation o 5% of blood pumped by heart is pumped to the heart itself through the coronary circulation to sustain workload o 250ml blood per min o Left coronary artery LCA branches off ascending aorta o Anterior interventricular branch ▪ Supplies blood to both ventricles and anterior two-thirds of the interventricular septum o Circumflex branch ▪ Passes around left side of heart in coronary sulcus ▪ Gives off left marginal branch and then ends on posterior side of the heart o Right coronary artery RCA branches off the ascending aorta ▪ Supplies right atrium and sinoatrial node (pacemaker) o Right marginal branch ▪ Supplies lateral aspect of right atrium and ventricle o Posterior interventricular branch ▪ Supplies posterior walls of ventricles - Venous drainage o 5-10% drains directly into heart chambers – right atrium and right ventricle o The rest returns to right atrium by the following routes ▪ Great cardiac vein Travels alongside anterior interventricular artery Collects blood from anterior portion of heart Empties into coronary sinus ▪ Middle cardiac vein (posterior interventricular) Found in posterior sulcus Collects blood from posterior portion of heart Drains into coronary sinus ▪ Left marginal vein Empties into coronary sinus ▪ Coronary sinus Large transverse vein in coronary sulcus on posterior side of heart Collects blood and empties into right atrium - Conduction System - Innervation o Sympathetic nerves (raise heart rate) ▪ Sympathetic pathway to the heart originates in the lower cervical to upper thoracic segments of the spinal cord ▪ Continues to adjacent sympathetic chain ganglia ▪ Some pass-through cardiac plexus in mediastinum ▪ Continue as cardiac nerves to the heart ▪ Fibres terminate in SA and AV nodes, in atrial and ventricular myocardium, as well as the aorta, pulmonary trunk, and coronary arteries o Parasympathetic nerves (slows heart rate) ▪ Pathway begins with nuclei of the vagus nerves in the medulla oblongata ▪ Extend to cardiac plexus and continue to the heart by way of the cardiac nerves ▪ Fibers of right vagus nerve lead to the SA node ▪ Fibers of left vagus nerve lead to the AV node  ▪ Little or no vagal stimulation of the myocardium Parasympathetic stimulation reduces the heart rate - Electrical behaviour of the Myocardium - Arteries o Conducting (large or elastic) ▪ Biggest ▪ Aorta, common carotid, subclavian o Distributing (muscular or medium) ▪ Distributes blood to specific organs ▪ Brachial, femoral, renal o Resistance (small) ▪ Arterioles (smallest arteries) ▪ Control amount of blood to various organs  o Metarterioles ▪ Short vessels that link arterioles to capillaries ▪ Muscle cells form a precapillary sphincter about entrance to capillary - Veins o Post capillary venules – smallest vein ▪ Even more porous than capillaries so also exchange fluid with surrounding tissue o Muscular venules – up to 1mm in diameter ▪ One or two layers of smooth muscle in tunica media o Medium veins – up to 10mm in diameter ▪ Thin tunica media and thick tunica externa o Large veins – larger than 10mm in diameter ▪ Some smooth muscle in all 3 tunics - Capillaries o Continuous capillaries – occur in most tissues ▪ Endothelial cells have tight junctions forming a continuous tube with intercellular clefts ▪ Allow passage of solutes such as glucose o Fenestrated capillaries – kidneys, small intestines ▪ Organs that require rapid absorption or filtration o Sinusoids – liver, bone marrow, spleen ▪ Irregular blood-filled spaces with large fenestrations o Capillaries organised into networks called capillary beds Cardiovascular Disease - Describes many conditions affecting heart and blood vessels - Commonly, coronary heart disease, stroke, and heart failure - Major health problem in Australia - Greater impact on males, elderly, indigenous, and people living in remote locations - Hypertension o High blood pressure (hypertension) – major risk factor for chronic conditions including stroke, coronary heart disease, and heart failure - Role of exercise for clients with cardiovascular conditions o Insufficient physical activity ▪ Low levels of physical activity increased risk of chronic conditions such as CVD, T2D, osteoporosis and dementia - CVD and exercise as a viable intervention o Patients with newly diagnosed heart disease who participate in an exercise program report an earlier return to work and improvements in other measures of quality of life, such as more self-confidence, lower stress, and less anxiety (Myers, 2003). o Heart attack patients who participated in a formal exercise program, the death rate is reduced by 20% to 25%. o For patients with existing heart disease, an event can occur an average of once in 62 000 hours→relatively low risk o Risk of a cardiac event is significantly lower among regular exercisers. o Evidence suggests that a sedentary person’s risk is nearly 50 times higher than the risk for a person who exercises about 5 times per week.  - Endothelial dysfunction and CVD - Endothelial dysfunction o Endothelial cells important constituents of blood vessels which play critical role in CV homeostasis by ▪ Regulating blood flow, vascular tone o Imbalance between vasodilators and vasoconstrictors = oxidative stress and reactive oxygen species then endothelial dysfunction o EC maintain a related vascular tone and low levels of oxidative stress by releasing mediators such as nitric oxide o Occurs early in the process of atherogenesis o Contributes to the formation progression and complications of atherosclerotic plaque o Resulting in CV disorders including hypertension, and heart failure ▪ Causes inactivity, aging, and hypertension o Damaged ED ▪ Decreases production and release of NO = oxidative stress ▪ Inflammatory response - Chronic inflammation o Another common underlying mechanism for ED ▪ Endothelium controls vascular inflammation by releasing NO o C-reactive protein CRP – protein present in the acute inflammatory response - Shear Stress o Entire vascular tree is exposed to the risk factors of ED, atherosclerotic lesions usually generate at specific arterial regions ▪ Bifurcations ▪ Branching points o Locally distributed shear stress by pulsatile blood flow is one the modulators of the atherogenic process ▪ Local endothelial shear stress ESS Pathophysiology of Cardiac risk factors - Cardiopulmonary conditions o Hypertension o Atherosclerosis o Myocardial infarction o Ischaemic heart disease o Peripheral arterial disease o Valve diseases o Angina o Chronic heart failure o Revascularisations o Pacemakers and internal defibrillators o Transplant recipients o Asthma o COPD o Cystic Fibrosis - Co-morbidities o Depression o Anxiety o Diabetes  o Arthritis - Cardiac risk factors o Non-modifiable ▪ Family ▪ Gender ▪ Age ▪ Race o Modifiable ▪ Smoking ▪ Hypertension ▪ Dyslipidaemia ▪ Physical inactivity ▪ Obesity ▪ T2d ▪ Diet Week 2: Meeting the Client (A) Learning Outcomes Outline risk factors, complications, and comorbidities in exercise interventions for cardiopulmonary conditions. Describe effects of commonly prescribed medications on exercise responses in cardiopulmonary conditions. Interview Process 1. Steps o General Interview: Collect subjective information. o Assessment and Evaluation: Gather objective measures (anthropometric, BP, CV fitness, strength, mobility). 2. Environment o Minimize interruptions and distractions. o Ensure a quiet, secure setting. o Use understandable language and ask clarifying questions. o Build empathy and trust with appropriate non-verbal communication. 3. Reason for Referral o Clarify and educate the client about their referral reason. o Ensure understanding, especially for conditions requiring lifestyle changes (e.g., CAD). 4. Demographics o Age, sex, and ethnicity influence risk and exercise engagement. o Consider variations in disease onset, treatment outcomes, and access to care. 5. History of Present Illness o Document chief complaint and symptom details. o Include onset, chronicity, symptom types, exacerbating/alleviating factors, interventions, and disease status. o Use OPQRTS (Onset, Provocation, Quality, Region, Severity, Timing, Associated signs/symptoms).  6. Medications and Allergies o Record current medications, dosage, administration, and frequency. o Note any allergies or "no known allergies" (nka). 7. Medical History o Concise list of past medical problems, including dates. o Note conditions influencing exercise prescription (e.g., CHD severity, asthma, COPD). 8. Family and Social History o Heritable disorders in first-degree relatives (cancers, Type II diabetes, familial hypercholesterolemia). o Lifestyle factors: smoking, alcohol, drug use, marital status, occupation, physical activity, nutrition, sleep. 9. Goals (SMARTER) o Specific, Measurable, Achievable, Relevant, Time-bound, Evaluated, and Reviewed. o Focus on behavior changes (smoking, alcohol), nutrition, physical activity, weight management, biomarkers (lipids, BP, glucose), and medications. Physical Examination 1. Informed Consent o Ensure understanding and agreement on test procedures and risks. o Required for ethical and legal compliance. 2. Risk Assessment “Add-Ons” o COPD Assessment Tool (CAT): Evaluates symptoms of pulmonary diseases. o Medical Research Council (MRC) Dyspnoea Score: Rates severity of breathlessness. o Spirometry: Identifies obstructive/restrictive traits. o Visual Inspection: Checks for deformities (e.g., kyphosis, barrel chest). o Auscultation: Listen for lung abnormalities (e.g., wheezing, crackling). 3. Additional Screening Questions o Address night breathlessness, abnormal heart rates, energy changes, swelling, leg pain, color changes, and unexplained bleeding. 4. Blood Pressure and Cholesterol o Conduct BP assessment regardless of client's previous measurements. o Calculate cholesterol hazard ratio using total cholesterol and HDL. 5. Blood Glucose Levels (BGL) o Measure BGL for clients with symptoms (thirst, frequent urination, unexplained weight loss). o Refer to GP if readings are between 7.8mmol/L and 11.0 mmol/L. Week 2: Meeting the Client (B) The document provided is a comprehensive guide on cardiovascular disease (CVD) signs, symptoms, diagnostic procedures, and fitness assessments, with a focus on exercise testing and prescription. It is authored by Charles Sturt University and is protected under copyright law. Key Signs and Symptoms of CVD: Chest pain or discomfort (angina) in various areas, often triggered by exercise or stress. Shortness of breath (SOB) at rest or with exertion. Dizziness or syncope due to reduced brain perfusion. Orthopnea and paroxysmal nocturnal dyspnea (PND) indicating left ventricular dysfunction (LVD). Ankle edema, palpitations, and intermittent claudication.  Known heart murmur, unusual fatigue, or SOB with usual activities. Red Flags: New-onset or changed pattern of SOB or chest pain. Recent syncope or near syncope. Neurologic symptoms suggestive of transient ischemic attack. Severe headache, unexplained tachycardia or bradycardia, and significant blood pressure deviations. Graded Exercise Testing: Used to evaluate chest pain, identify CAD, and assess exercise response for prognosis. Specialist attendance required for diagnostic tests. Tests measure ST-segment depression, functional capacity in METS, and respiratory gas exchange. Also used for pulmonary diseases, pacemaker response, claudication, and disability. Diagnostic Exercise Testing: Aimed at assessing residual myocardial ischemia, ventricular arrhythmias, and prognosis in patients with high disease probability. Contraindications must be considered as per AHA guidelines. Choice of Graded Exercise Test: Treadmill, cycle ergometry, and arm ergometry are options, with considerations for patient condition and test familiarity. Exercise Protocol Design: Customized protocols may be necessary for cardiopulmonary clients. Common protocols include Bruce, Ellestad, Naughton, and Balke-Ware. Tools During Exercise Testing: 12-lead ECG, blood pressure monitoring, pulse oximetry, and scales for perceived exertion, angina, dyspnea, and intermittent claudication are used. Termination of the Test: ACSM guidelines dictate when to stop the exercise test. Post-exercise Period: Monitoring continues for at least 6 minutes post-exercise to observe ST-segment changes and heart rate recovery. Muscular Fitness: Muscular strength, endurance, and power are integral to total health and fitness. Strength-promoting exercise reduces all-cause mortality risk. Testing conditions and methods are standardized for safety and consistency. Flexibility: The ability to move a joint through its complete ROM pain-free is important for ADLs. Various factors affect flexibility, and joint ROM is measured using goniometers and inclinometers. Balance: The ability to maintain a desired position is crucial for falls prevention. Static and dynamic balance tests, such as the Balance Error Test and the Y-balance test, are used for assessment Week 3: Hypertension Hypertension, often called the "silent killer," is a significant risk factor for cardiovascular disease (CVD) with a 90% lifetime risk of developing the condition. It is asymptomatic and can lead to various health complications. The classification of hypertension is based on blood pressure (BP) readings taken over multiple office visits, with an increased risk of CVD for every incremental rise in systolic BP (SBP) or diastolic BP (DBP). The pathophysiology of hypertension is complex, involving multiple systems such as the renal, endocrine, vascular, and central adrenergic systems. Primary hypertension is typically due to increased peripheral resistance, often caused by the contraction of smooth muscle cells in small arterioles, leading to increased intracellular calcium concentration. This can result in structural changes in the arteriolar walls, contributing to an irreversible rise in peripheral resistance. Secondary hypertension can be caused by renal issues, leading to volume expansion or changes in renal secretion of vasoactive materials, or by endocrine abnormalities, particularly of the adrenal glands. The renin-angiotensin system plays a crucial role in BP regulation, with renin converting angiotensinogen to angiotensin I, which is then converted to angiotensin II, a potent vasoconstrictor, by ACE. Angiotensin II also stimulates the release of aldosterone, leading to sodium and water retention and further BP elevation. Co-morbidities associated with untreated hypertension include cardiomyopathy, heart failure, renal disease, myocardial infarction, stroke, and aneurysm. Additionally, hypertension can lead to endothelial dysfunction, hypercoagulability, and autonomic nervous system imbalances, which further exacerbate the risk of cardiovascular events. The lecture also discusses the implications of hypertension on exercise physiology, including the effects of commonly prescribed medications on exercise responses and the importance of considering these effects when applying exercise interventions to individuals with hypertension. It emphasizes the need for proper diagnostic techniques, treatment procedures, and the ability to conduct exercise tests and prescribe exercise as a therapeutic modality for individuals with hypertension. In summary, hypertension is a modifiable risk factor for CVD with a high lifetime prevalence. Its pathophysiology involves multiple systems and can lead to various complications if left untreated. Understanding the implications of hypertension on cardiovascular health and exercise physiology is essential for developing effective treatment and prevention strategies Week 4: Graded exercise testing Non-invasive GXT used for differential diagnosis of adults with suspected IHD < 50 GXT + 12-lead ECG is test of choice to evaluate myocardial ischemia in those with normal resting ECG, and physically able to exert themselves. + expired gas analysis = CPET Physiological responses monitored during standardised incremental work rate exercise  Progressively increased metabolic demand until a sign (S-T segment depression), or symptom limited (angina or fatigue) maximum level of exertion is reached Gas Exchange Independent, graded and inverse association between directly measured or estimated VO2 peak and mortality 13 % reduction in risk for all-cause mortality associated with each 1-MET increase in cardiorespiratory fitness (Grazzi et al. 2014) – increase accuracy with respiratory gas exchange Useful in defining prognosis (and thus help guide the timing for cardiac transplantation) in patients with heart failure Slope of change in VE to change in VCO2 production (Ve-VCO2 slope) during an exercise test = related to prognosis for patients with CHF Others measures from CPET = ventilatory-derived AT, oxygen pulse, oxygen uptake efficiency slope, partial pressure of end tidal CO2, breathing reserve, and respiratory exchange ratio Gas exchange useful to identifying if unexplained dyspnoea has a cardiac or pulmonary aetiology. Factors that influence prognosis of CVD Angina Presence of ST-segment depression evident on the ECG during exercise or in recovery Magnitude of ST depression (1 mm vs. 3 mm, where more ST depression represents greater risk) The number of ECG leads showing significant ST-segment depression Time of onset for ST depression during exercise Time during recovery to resolve ST-segment abnormalities observed during exercise, Functional capacity (FC) as measured by exercise duration or metabolic equivalents of task (METs). GXT Protocols Bruce Protocol Starting at 2.7 km.h and 10% grade) and includes large increments in workload (2 to 3 METs) per stage Suitable for people who Are not frail Do not have an extremely low FC (e.g., no difficulty walking a flight of stairs) - Limitations  Large increments in workload (2 to 3 METs) per stage that can make it difficult to determine a person’s true FC; 3 min stages that for some patients are too fast for walking and too slow for running; A large vertical component - premature leg fatigue 2. Naughton protocol - Suitable for elderly - 1 to 2 min per stage - Testing is terminated when o Record all peak values (HR, ECG, RPE) o 85% submaximal HR - Post monitor period o 6 minutes after testing ST-Segment Depression ST-segment depression = most frequent response during exercise and suggestive of sub- endocardial ischemia Defined as > 1mm of horizontal or downsloping ST-segment depression that occurs 0.08s past the J point = myocardial ischemia Likelihood of CAD is extremely high when Occurrence with angina Early onset, > ST depression, more leads with ST depression, longer duration for ST depression to resolve in recovery J-point depression with an upsloping ST segment > 1.5 mm depressed at 0.08 s past the J point = exercise-induced ischemia slow or gradual upsloping ST depression = increased probability of CAD. S-T Segment Elevation ST-segment or J-point elevation on a resting ECG is often attributable to early repolarization and not necessarily abnormal in healthy people, Should be documented on the GXT report. New ST-segment elevation with exertion (with normal resting ECG)→rare finding May suggest transmural ischemia or a coronary artery spasm. (test termination) When Q waves are present on the resting ECG from a previous infarction, T elevation with exertion may reflect a LV aneurysm or wall motion abnormality ST-elevation can localise ischemic area/ arteries involved T-wave Changes Healthy individuals = T-wave amplitude initially decreases with the onset of exercise then T- wave amplitude increases at maximal exercise. Flattening or inversion of T waves may not be associated with ischemia Common in the presence of LVH Normalization of T-waves also present during ischemic responses associated with coronary spasms Overall, T-wave changes with exertion are not specific to exercise-induced ischemia Week 4 part b: - Atherosclerosis Normal Artery Lumen: Channel for blood flow within the artery Endothelium: Inner, single-cell layer of the artery Vasomotion, regulating hemostasis (anti and pro-thrombotic properties) NO In healthy conditions, protects against the development of atherothombosis Media: contains most of the smooth muscle cells plus elastic connective tissues Smooth muscle cells maintain arterial tone (partial vasoconstriction) Receptors for LDLs, insulin and growth factors Adventita: outermost layer of connecting tissue, fibroblasts and a few smooth muscle cells Highly vascularised and provides media and intima with O2 and nutrients Ischemic heart disease Myocardial Blood Flow, Metabolism and Ischemia Normal contraction and relaxation of cardiac myocytes requires: Adequate amounts of adenosine triphosphate (ATP) Oxygen At rest, coronary blood flow averages 60 to 90 mL · min−1· 100 g−1 of myocardium and may increase five-to sixfold during exercise The myocardium extracts nearly all its oxygen from the capillary blood flow, Coronary blood flow must be closely regulated to the needs of the myocardium Increase in myocardial work = increase oxygen demand and thus coronary blood flow Flow is determined by pressure and peripheral resistance Reduction in blood flow Luminal cross-sectional area must be reduced by 75% or more (significant lesion) to restrict flow under resting conditions Beyond this small decreases (cross-sectional area) result in large reductions in flow. A reduction in the lumen diameter may be caused by several factors Significant atherosclerotic plaque Vasospasm without underlying plaque Vasospasm superimposed over a plaque Thrombus associated with plaque rupture Coronary vasospasm can result from ED, SNS activation and epinephrine Coronary reperfusion and reperfusion injury Reperfusion following ischemia is a double-edged sword and can itself induce severe and also irreversible damage to the myocardium – the reperfusion injury The immediate and full restoration of coronary blood flow results in: Arrhythmias Contractile dysfunction (stunning) Microvascular impairment Irreversible myocardial damage through apoptosis and necrosis. Irreversible reperfusion injury is defined as an injury caused by reperfusion after an ischemic episode and resulting in death and loss of cells that were only reversibly injured and primed for death during the preceding ischemic episode Angina Angina Pectoris Is transient referred cardiac pain resulting from myocardial ischemia Typically located in the substernal region, jaw, neck or arms Feeling of pressure, heaviness, fullness, squeezing, burning, aching or chocking Intensity may vary Can radiate Can experience dyspnoea if due to increased LV end diastolic pressure and increase pulmonary vascular pressure Provoked by exertion, exposure to change in temperature, stress Small number have silent ischemia (no pain) Acute coronary syndromes Acute Coronary Syndromes (unstable angina, acute MI, sudden cardiac death) Unstable angina pectoris, acute myocardial infarction, some sudden cardiac death comprise acute coronary syndromes  Underlying mechanism is atherosclerotic plaque erosion, rupture, or other plaque disruption resulting in a thrombus - vessel occlusion and acute myocardial ischemia. Unstable angina ~ transient vessel occlusion ( 20–40 min Necrosis of cardiac myocytes Developing necrosis spreads from centre to border of occluded vascular territory; and from endocardial layers as a wavefront toward less ischemic areas in the sub-epicardium. Timely reperfusion is critical to stop progression of irreversible damage Distinguishing reversible to irreversible is the disruption of the myocyte membrane Myocyte cannot recover if the membrane disruption occurs and cytoplasmic content spill into the circulation May be preceded by an event or trigger such as physical exertion, stress or anger Evidence of circadian variation: more events in the morning Week 5: Periphery artery disease Risk factors - Smoking - diabetes - Hypertension - Age above 50 Pathophysiology Begins with endothelial damage in arteries in the periphery Process is similar to that outlined in atherosclerosis However, impact now affects the peripheries The abnormal blood flow is predicted on the severity of the stenosis Leg pain symptoms described as cramping, aching, tightening and fatigue Calf claudication: flow-limiting lesions in the femoral and popliteal arteries Buttock pain: flow-limiting lesions in the internal iliac arteries Thigh claudication: flow limiting lesions to the profunda femoral artery Critical limb ischemia Presence of Ischemic rest pain Foot ulcers (nonhealing) Gangrene attributable to objectively proven arterial occlusive disease Typically lesions present at multiple levels of tibial vessels and vessels in the foot Issue is the reduction in perfusion, even at rest Poor prognosis for limb loss and cardiovascular morbidity or mortality Mortality rates: 25% in the first year, with 25 % will require amputation Valvular disorders Valve Disorders/Valvular Heart Disease (VHD) Damage or defect in one of the four heart valves Aortic, mitral, tricuspid or pulmonary Congenital or acquired Risk factors Smoking Gender Age Hypercholesterolemia Hypertension T2DM Valves have an outer layer of endothelial cells, surrounding 3 layers of matrix, all with specialised functions. Matrix has collagens, proteoglycans, elastin Valves open/ close 100,000 day Healthy valves ensure that blood flows with suitable force in the proper direction at the correct time. In valvular heart disease, the valves become too narrow and hardened (stenotic) to open fully, or are unable to close completely (incompetent). Stenotic: forces blood to back up in the adjacent heart chamber Incompetent: allows blood to leak back into the chamber that it has just exited. To compensate for poor pumping action, the heart muscle enlarges and thickens, i.e. LVH. In some cases, blood pooling in the chambers of the heart has a greater tendency to clot, ↑ risk of stroke or pulmonary embolism. Myocardial Infarction Acute MI = necrosis (death) of cardiac myocytes caused by prolonged ischemia due to complete blockage of a vessel Irreversible ischemia (lethal) is disruption of the myocyte membrane  The diagnosis of myocardial infarction is based on the presence of elevated cardiac necrosis biomarkers (cardiac troponin; cTn) plus at least one additional factor Symptoms of ischemia ECG evidence of myocardial ischemia (ST-segment elevation or depression, or new left bundle branch block New pathological Q waves on the ECG Imaging evidence (usually echocardiography) of infarction Diagnosis of MI Symptoms of ischemia ECG evidence of myocardial ischemia (ST segment elevation or depression, or new left bundle branch block) New pathological Q waves on the ECG Imaging evidence (echocardiography) of infarction cTn – biomarker for detection of cardiomyocyte necrosis Highly sensitive to cardiac necrosis MB fraction of creatine kinase (CK-MB) is another biomarker used Classification of MI (pp.227 text) Type 1: Due to pathology of the wall of the coronary artery, commonly plaque rupture; rarely from spontaneous coronary dissection Type 2: Due to increased O2 demand or decreased supply, such as hyperthyroidism, fever, arrhythmias, HT, coronary artery spasm, microvascular spasm, coronary artery embolus, anaemia or hypotension Type 3: Sudden unexpected cardiac death before availability of cardiac biomarker analysis. Type 4a: Associated with percutaneous coronary intervention (PCI). Type 4b: Associated with stent thrombosis (clot formation within a stent). Type 5: Associated with coronary artery bypass graft surgery (CABG) Complications of Acute MI 1. Arrhythmias Supraventricular arrhythmias are common after myocardial infarction. Sinus bradycardia due to excessive vagal tone or ischemia of the sinoatrial node Sinus tachycardia related to pain, fear, heart failure, or excessive sympathetic nervous system activation Premature atrial contractions—provide no prognostic information  Atrial fibrillation—observed in up to 20% of patients, usually transient, more frequent in older patients, associated with increased mortality Ventricular arrhythmias are also common after myocardial infarction. Ventricular fibrillation occurs in approximately 5% of hospitalized patients. β- blockers are effective in decreasing the incidence of this arrhythmia in the peri- infarct period. Ventricular tachycardia is observed in 10% to 40% of hospitalized patients; it is usually transient and benign in the early post infarct period. Accelerated idioventricular rhythm is also observed in 10% to 40% of hospitalized patients. It is not associated with increased mortality. 4. Cardiogenic shock Is the result of inadequate cardiac output with signs of persistent hypotension (systolic blood pressure