Cardiovascular Emergencies PDF

Cardiovascular Emergencies PARA 2024 - Winter 2023 Dan Aitken Cardiovascular Assessments Complete cardiac assessments will be discussed in detail next term (PCT 3) There is no specific questioning that can or cannot rule cardiac ischemia in or out It’s important to gather a complete his...

Cardiovascular Emergencies PARA 2024 - Winter 2023 Dan Aitken Cardiovascular Assessments Complete cardiac assessments will be discussed in detail next term (PCT 3) There is no specific questioning that can or cannot rule cardiac ischemia in or out It’s important to gather a complete history to help us in determining our best working differential diagnosis (DDx) Many cardiac emergencies have “classic” signs and symptoms - but this does not mean that patients with atypical presentations cannot also be suffering from a cardiac event Cardiovascular Assessments A complete history includes: History of presenting illness/symptoms (incident history) Detailed description of signs and systems (OPQRST+) Past medical history (may or may not include family history) Any current investigations/diagnoses/ongoing concerns And much more Terminology Ischemia - decreased blood (and oxygen) supply to a body organ or part, usually due to functional constriction or actual obstruction of a blood vessel Infarction - necrosis or death of tissues due to local ischemia Necrosis - localized tissue death that occurs in grounds of cells or part of a structure or an organ in response to disease or injury Gangrene - death of body tissue due to lack of blood flow or bacterial infection Perfusion - the process or act of pouring over or through, especially the passage of a fluid through a specific organ or area of the body Terminology Thrombus - stationary mass of clotted blood or other formed elements that remains attached to its place of origin along the wall of a blood vessel Embolus - a mass of clotted blood or other formed elements (such as bubbles of air, calcium fragments or fat) that circulates in the blood stream until it becomes lodged in a vessel, obstructing circulation Preload - volume of blood returning to the right atrium of the heart Afterload - pressure/force the left ventricle must obtain to open the aortic semilunar valve and pump blood into systemic circulation Vascular Disorders/Disease Recall that arteries carry oxygenated blood from the heart to all tissues in the body They are also responsible for regulating blood pressure and capillary flow Veins provide a return pathway to the heart and play an important role in providing the preload required to maintain cardiac contraction Many disorders exist in the vasculature that can alter the homeostatic balance of this system Dyslipidemia A condition of imbalance of the lipid components of the blood Triglycerides, phospholipids, and cholesterol Cholesterol and triglycerides combine with water-soluble transport proteins in order to travel through the bloodstream - this transport molecule is called a lipoprotein Lipoproteins are categorized according to their densities (5 classes) For our purposes we will just discuss 2 of these categories: LDL (low-density lipioprotein) and HDL (high-density lipoprotein) Dyslipidemia LDL - is the primary transport molecule for cholesterole liver to target tissues aka - “bad cholesterol” HDL - the primary transport molecule for cholesterol from tissues back to the liver aka - “good cholesterol” Cholesterol - a lipid molecule with many functions including: membrane and hormone synthesis Dyslipidemia Dyslipidemia is characterized by increased triglycerides, increased total blood cholesterol, increased LDL cholesterol and decreased HDL cholesterol Many factors can lead to dyslipidemia (commonly called - “high cholesterol”) Some risk factors for elevated LDL include: Smoking, excessive alcohol consumption, sedentary lifestyle, poor dietary intake, type 2 diabetes, genetic predisposition Many of these risk factors will also decrease HDL levels, worsening the imbalance Atherosclerosis Arteriosclerosis - an abnormal hardening and thickening of the arteries Atherosclerosis - a form of arteriosclerosis characterized by the formation of fibrofatty lesions in the Intima lining of large and medium-sized arteries Etiology and Risk Factors The primary risk factor is dyslipidemia and all of its associated risk factors Males tend to be at higher risk than premenopausal females. Following menopause, this tends to balance out. Atherosclerosis Etiology and Risk Factors Many conditions that cause endothelial damage lead to atherosclerosis (toxins from cigarette smoking, diabetes, hypertension) Significant lifestyle changes (quitting smoking, improved diet, exercise) can drastically decrease ones risk for developing atherosclerosis Pathogenesis Atherosclerosis is, at its core, an inflammatory condition Several triggers exist that create lesions and plaque build-up in the intimal layer of the artery Atherosclerosis Pathogenesis Atherosclerotic plaque consists of smooth muscle cells (SMCs), macrophages/leukocytes, collagen and elastin fibres, platelets, and a large lipid core The development of atherosclerotic plaque occurs as follows: 1) A trigger (smoking, high LDL, etc) causes initial endothelial injury 2) Migration and adhesion of inflammatory cells to the injury site Activated macrophages ingest lipoproteins and become foam cells - removes excess lipids from circulation Atherosclerosis Pathogenesis 3) The foam cells begin to accumulate, which increases the progression of the lesion Proliferation of SMCs and infiltration of ECM in tunica intima Foam cells die and deposit their contents (necrotic debris and lipids) into the vascular wall (contained by the SMC and ECM) 4) Atherosclerotic plaque is contained in the bulging vascular wall (reduction of blood flow) and is prone to rupture (hemorrhage) or thrombotic vessel occlusion Atherosclerosis Atherosclerosis Atherosclerosis Atherosclerosis Atherosclerosis Clinical Manifestations Typically do not become evident for over 20 years of plaque build up Depend on the vessels involved and the extent of vessel obstruction Atherosclerotic plaque exerts its effect through narrowing of the vessel producing ischemia, sudden vessel obstruction (thrombosis, embolism), aneurysm formation (weakened vessel wall) with possible rupture Larger vessels tend to produce aneurysms as a high risk complication and smaller vessels tend to be more prone to vessel occlusion Peripheral Artery Disease aka Peripheral Vascular Disease A disorder of the circulation in the extremities Can produce ischemia, pain, impaired function and, occasionally, infarction and tissue necrosis Caused by atherosclerosis/arteriosclerosis in peripheral arteries Etiology Risk factors are essentially the same as for atherosclerosis Diabetics and smokers are at a significantly elevated risk Peripheral Artery Disease Clinical Manifestations Symptoms don’t start until there is a 50% narrowing of the vessel Pain with walking (commonly in the calf), vague complaints of muscle aches and/or numbness Atrophy of leg muscles and thinning of the skin and subcutaneous tissue Weak or absent peripheral pulses (popliteal/pedal) with signs poor perfusion (pale/mottled while elevated or deep red while dependant, delayed cap refill, cool to touch) Can progress to necrosis, ulceration, gangrene and amputation Raynaud Disease/Phenomenon A functional disorder caused by intense vasospasm of the arteries and arterioles in the fingers and (occasionally) toes Etiology and Pathogenesis Exposure to cold or strong emotions causes vasoconstriction in the fingers (blood shunting) producing temporary, and self limiting, ischemia Cause can be unknown or a direct byproduct of a previous vessel injury (frost bite, prolonged use of heavy/vibrating machinery, etc) Clinical Manifestations Distal pallor/cyanosis, cold sensation/altered sensory perception Following the spasm - intense redness, throbbing, paresthesia Raynaud Disease/Phenomenon Aneurysms An abnormal localized dilation of a blood vessel that can occur in both arteries and veins Aneurysms can be classified according to their cause, location and anatomical features True Aneurysm - bounded by a complete vessel wall and the blood remains within the vascular compartment False Aneurysm - a localized dissection or tear in the inner wall of the artery with formation of an extravascular hematoma (causing vessel enlargement) Aneurysms Berry Aneurysm - a true aneurysm that consists of a small, sperical dilation of the vessel at a bifurcation (usually found in the circle of Willis) Fusiform Aneurysm - a true aneurysm that involves the entire circumference of the vessel with gradual and progressive vessel dilation - these vary in diameter and length Saccular Aneurysm - a true aneurysm that extends over part of the circumference of the vessel (appears “sac-like”) Dissecting Aneurysm - a false aneurysm resulting from a tear in the intimal layer of the vessel that allows blood to enter the vessel wall, dissecting its layers to create a blood filled cavity Aneurysms Aneurysms Weakness that leads to aneurysm formation may be due to congenital defects, trauma, infections or atherosclerosis As the tension/pressure in the vessel increases, so does the size of the aneurysm - eventually may rupture Even an unruptured aneurysm may cause damage by exerting pressure on adjacent structures and interrupting blood flow Aneurysms Etiology Atherosclerosis (and all of its risk factors) is a common cause as is degeneration of the tunica media (unknown cause) Clinical Manifestations Often asymptomatic until vessel rupture Other symptoms (pre-rupture) are dependant upon the vessel location May produce pain, discomfort - severe/significant if ruptured Pulsatile masses may be present in some Aneurysms Rupture A ruptured aneurysm is a significant life threat and must be treated immediately in an operating room Location of aneurysm will dictate the specific symptoms but pain is typically unbearable and rapid blood loss will quickly progress to hypovolemic shock, an altered LOC, and death Observe for signs of shock (increased HR/RR, declining BP, pallor, etc) and prepare for resuscitation Aneurysms Dissecting Aortic Aneurysm An aortic dissection is an acute life threatening condition that involves hemorrhage into the vessel wall with longitudinal tearing that forms a blood- filled channel Can occur anywhere along the length of the aorta but it is most common in the ascending aorta and descending (thoracic) aorta (just distal to the subclavian artery) Aneurysms Dissecting Aortic Aneurysm Etiology and Pathogenesis Any condition that weakens or degenerates the elastic and smooth muscle layers of the aorta (atherosclerosis) Type A - ascending aorta only or both ascending and descending Type B - descending (thoracic) aorta only Aneurysms Dissecting Aortic Aneurysm Clinical Manifestations Abrupt and excruciating pain described as tearing or ripping Ascending Aorta - anterior chest Descending Descending - mid upper back (between scapula) Hypovolemic shock Difference in bilateral blood pressures - poor diagnostic tool!! Varicose Veins Dilated veins of the lower extremities (usually superficial) Often lead to secondary problems of venous insufficiency Prone to rupture with minimal direct trauma - easily managed with direct pressure and often does not require any further medical intervention Deep Vein Thrombosis (DVT) The presence of thrombus, and the accompanying inflammatory response, in the wall of a deep vein - most commonly in the lower extremities Pulmonary embolism (PE) is a significant complication of DVT Etiology and Pathogenesis Virchow’s Triad Stasis of blood (prolonged flights, bed rest, SCI) Increased blood coagulability (clotting deficiencies, oral contraceptive use, hormone therapy, cigarettes) Vessel wall injury (trauma, post surgery, IVs, infection) Deep Vein Thrombosis (DVT) Deep Vein Thrombosis (DVT) Clinical Manifestations Often asymptomatic (usually because the vein isn’t completely occluded) S&S can be related to the inflammatory process - pain, swelling, deep muscle tenderness, fever, general malaise Other findings are dependant on location of the thrombus Most commonly occurs below the knee (calf pain/tenderness, swelling, redness, warm to touch) Hypertension A sustained elevation of arterial blood pressure (typically ≥140mmHg) The primary risk factor for cardiovascular disease Etiology and Pathogenesis Broadly classified based as either primary or secondary hypertension Primary HTN - presence of hypertension without evidence of a specific causative clinical condition Secondary HTN - elevation in blood pressure because of another disease or condition Hypertension Etiology and Pathogenesis - Primary HTN Risk Factors Advancing age, gender (higher incidence of HTN in males, higher incidence of adverse complications in females) Family history/genetic predisposition High sodium diet, dyslipidemia Tobacco use, alcohol consumption Sedentary lifestyle, obesity, insulin resistance Hypertension Clinical Manifestations Symptoms may develop from long-term effects of hypertension on target-organ systems Increased perfusion pressure can damage target organs and increased intravascular pressure can damage endothelial cells (causing inflammation and atherosclerosis) Some organs are more sensitive to altered blood flow than others (kidneys, heart, brain) and are therefore more affected by a change in perfusion pressure Perfusion Pressure - the pressure required to push blood through the vessels in a specific area Hypertension Clinical Manifestations A major risk factor for atherosclerosis (elevated vascular pressure promotes endothelial damage) Predisposes people to coronary artery disease (CAD), heart failure, MIs, strokes and peripheral artery disease (PAD) Increases the workload on the left ventricle by increasing afterload High glomerular pressures decrease filtration and can lead to kidney disease Predisposes people to cognitive impairment, dementia and retinopathy Hypertension Clinical Manifestations Hypertensive Emergency A rare, but potentially fatal, complication of hypertension characterized by a sudden and sustained spike in blood pressure (>180/120mmHg) This acutely worsens target organ damage and must be dealt with promptly Complications can include Ischemia stroke, cardiac ischemia and retinal hemorrhage Orthostatic Hypotension aka Postural Hypotension Abnormal drop in blood pressure (of at least 20mmHg) on assumption of the standing position Changes in blood pressure may or may not be accompanied by clinical symptoms or may be asymptomatic Dizziness, syncope (fainting) Causes are multiple and may include: Normal aging process, hypovolemia, prolonged bed rest/immobility, pharmacologically induced, ANS disorder Disorders of Cardiac Function Layers of the Heart Endocarditis Inflammation of the inner lining of the heart (endocardium) most commonly caused by an infectious agent Recall that the endocardium is continuous the the heart valves and the inner lining of the aorta as it exits the left ventricle Etiology and Pathogenesis A very common cause of endocarditis is illicit IV drug use Usually the heart valves are initially affected with destructive lesions composed of infectious organisms and cellular debris enclosed in a mesh of fibrin strands of clotted blood The lesions can spread from the valves and, in some cases, spread through the different layers of the heart Endocarditis Clinical Manifestations Initial symptoms include fever, chills and other signs of systemic infection (elevated HR, RR, general malaise, SOB, muscle aches/weakness, etc) Complications can include the formation of emboli (may become lodged anywhere in the body and produce a multitude of symptoms) - this includes a coronary artery embolism (MI, cardiac ischemia) Myocarditis or pericarditis can develop should the lesions spread through the different heart layers Congestive heart failure can be a result of valve destruction Myocarditis Inflammation of the myocardium (muscular layer of the heart) A form of primary cardiomyopathy (discussed shortly) Etiology and Pathogenesis Usually caused by a viral infection but may also be bacterial or fungal in origin Occasionally can be caused by hypersensitivity to certain drugs or an autoimmune process May be self limiting and only requiring supportive care, or may become life threatening and require aggressive medical intervention Myocarditis Clinical Manifestations Manifestations vary dependant on causative agent and severity of infection (anywhere from asymptomatic to cardiogenic shock) Signs of infection (fever, chills, malaise, etc) Formation of emboli is possible Inflammatory mediators cause increased coagulability while an irritated myocardium produced a decrease in contractility Signs of heart failure/cardiogenic shock (discussed later) Pericarditis Inflammation of the pericardium Recall that the pericardium is a double layered membrane composed of a fibrous layer and 2 serous layers (visceral and parietal) Between the 2 serous layers of the pericardium is the pericardial space/cavity containing serous fluid (pericardial fluid) that lubricates and protects the heart during movement/contraction Pericarditis promotes an increase in capillary permeability allowing plasma proteins to enter the pericardial fluid This can promote adhesion and scarring between the 2 serous layers Pericarditis Pericarditis Clinical Manifestations Chest pain, pericardial friction rub (auscultated), and ECG changes Chest pain (most common symptom) is often described a abrupt in onset, sharp and located in the precordial area (just superficial to the heart) - may radiate to the neck, back, abdomen or side Pain is typically worse with deep breathing, coughing, swallowing and positional changes Pain is often relieved by sitting upright and a bit forwards - allows for easier venous return and reduced pressure on the pericardium Pericarditis Clinical Manifestations Classic ECG changes associated with pericarditis include widespread ST segment elevation and PR segment depression Pericardial Effusion/Tamponade Pericardial effusion - an accumulation of fluid in the pericardial cavity - usually as a result of an inflammatory or infectious process Pericardial Tamponade - fluid in the pericardial space accumulates to the point of compression on the heart that reduces cardiac output May also be caused by trauma, MI, dissecting aneurysms, or tumours Pericardial Effusion/Tamponade Pathogenesis Effects of the effusion are dependant on the amount and rapidity of accumulating fluid and elasticity of the pericardium Increasing pressure on the heart causes decreased preload, decreased stroke volume (SV) and, therefore, decreased cardiac output (CO) The decrease in preload (due to increased pressure on the heart) causes blood to back up into the venous system - JVD Pericardial Effusion/Tamponade Clinical Manifestations Beck’s Triad - JVD, muffled heart sounds, hypotension Pulsus paradoxus - weakened or absent arterial pulse during inspiration Normally, the decreased intrathoracic pressure during inspiration accelerates venous return (increased right sided filling) As the right atria fills, it bulges into the LV causing a slight decrease in LV filling, SV, and SBP - this process is amplified when there is excessive pressure on the heart from a tamponade ECG changes - nonspecific T-wave changes and low QRS voltage Pericardial Effusion/Tamponade Cardiomyopathies A group of diseases of the myocardium associated with mechanical and/or electrical dysfunction Usually exhibits inappropriate ventricular hypertrophy or dilation Cardiomyopathies may be confined to the heart or part of a generalized systemic disorder that may lead to cardiovascular death or heart failure Primary Cardiomyopathy - heart disorders confined to the myocardium Secondary Cardiomyopathy - myocardial changes that occur with a variety of systemic disorders Coronary Artery Disease (CAD) Impaired coronary blood flow, usually caused by atherosclerosis Can lead to myocardial ischemia, angina, myocardial infarction (MI), cardiac arrhythmias, heart failure, or sudden heart death Major risk factors include: cigarette smoking, HTN, dyslipidemia, diabetes, advancing age, obesity, and sedentary lifestyle Pathogenesis CAD is divided into Acute Coronary Syndrome (ACS) and Chronic Ischemic Heart Disease ACS - unstable angina, MI; Ischemic Heart Disease - stable angina Coronary Artery Disease (CAD) Coronary Arteries Two main coronary arteries arise from the coronary sinus just above the aortic valve The left coronary artery (LCA) divides into the left anterior descending (LAD) and circumflex arteries The right coronary artery (RCA) becomes the posterior descending artery and supplies the posterior heart, septum, SA and AV nodes The larger coronary arteries lie in the surface of the heart (epicardium) while smaller branches penetrate the myocardium Coronary Artery Disease (CAD) Coronary Artery Disease (CAD) Coronary Artery Disease (CAD) Coronary Arteries Anastomoses - a cross-connection between adjacent channels (collateral circulation) Anastomotic channels exist between the smaller branches of coronary arteries - as CAD progresses, these channels will increase in size Coronary Veins Venous system that drains the deoxygenated blood from the myocardium through the coronary sinus into the right atrium Coronary Artery Disease (CAD) Myocardial Oxygen - Supply and Demand An imbalance between supply and demand can lead to myocardial ischemia, MI or sudden cardiac death Myocardial Oxygen Supply Determined by the capillary inflow and the ability of hemoglobin to transport and deliver O2 Ischemia can occur, in absence of decreased coronary flow, due to hypoxia, anemia, or CO poisoning Coronary Artery Disease (CAD) Myocardial Oxygen Demand MVO2 is determined by HR, SV and systolic pressure/myocardial wall stress HR - higher the rate, higher the oxygen demand. Elevated rates also cause a decrease in diastolic filling time SV - increased force of muscle contractions require an increase in oxygen (exercise, inotropes, sympathetic response) LV wall stress - the average tension that individual muscle fibres must generate to shorten (contract) against intraventricular pressure Chronic Ischemic Heart Disease When blood flow through the coronary arteries does not meet the metabolic demands of the heart Most often due to atherosclerosis but may also be caused by vasospasm Main types of chronic ischemic heart disease include: Stable angina, variant (vasospastic) angina, and silent myocardial ischemia Chronic Ischemic Heart Disease Silent Myocardial Ischemia Silent cardiac ischemia occurs in a significant number of patients It is when myocardial ischemia occurs without the presence of cardiac chest pain It can range from mild, non-infarction ischemia to full myocardial infarction Patients may present to emerge with atypical symptoms (fatigue, nausea, malaise, etc) and end up finding elevated serum biomarkers indicating they have had ischemia/infarction Chronic Ischemic Heart Disease Stable Angina Aka angina pectoris - a fixed, partial coronary artery obstruction that produces an imbalance between coronary blood flow and metabolic demands resulting in ischemic chest pain Often the initial manifestation of CAD An increase in baseline MVO2 (physical exertion, exposure to cold, emotional stress) causes cardiac chest pain Symptoms of stable angina typically resolve within minutes of rest (sometimes with the help of nitroglycerin) - should they not resolve within 5-10 minutes the pain is likely more significant (myocardial infarction) Chronic Ischemic Heart Disease Stable Angina Chronic Ischemic Heart Disease Stable Angina Clinical Manifestations Ischemic chest pain Constricting, squeezing, suffocating, pressure, or heaviness Pain is usually consistent and not reproducible (able to worsen) with coughing, inspiration, palpation, or movement Located usually precordial (retrosternal/substernal) or epigastric and may radiate to the left shoulder, jaw or arm (usually left) Chronic Ischemic Heart Disease Stable Angina Chronic Ischemic Heart Disease Stable Angina Nitroglycerin A nitrate medication that causes vasodilation reducing preload and arterial pressure (decreased workload on the heart) Thus, a reduction in MVO2 (myocardial oxygen demand) and, hopefully, eliminates the chest pain Mechanism of Action - within the body, nitro converts to nitric oxide (NO) which relaxes the smooth muscle in blood vessels It is important to note that nitro does not eliminate obstruction, it merely reduces MVO2 and (hopefully) Chronic Ischemic Heart Disease Vasospastic (Variant) Angina aka Prinzmetal Angina - cardiac ischemia caused by coronary vasospasm Can be brought on by minimal exercise or spontaneously while at rest May be self limiting or may lead to cardiac dysrhythmias and even death Exact cause is unknown but may be associated with: hyperactive sympathetic nervous system, altered NO production, cocaine (and other amphetamine) use Acute Coronary Syndrome (ACS) Includes unstable angina, non-ST-segment elevation myocardial infarction (NSTEMI), and ST-segment elevation myocardial infarction (STEMI) Indicates an acute and severe obstruction in coronary blood flow that requires immediate medical intervention to prevent death or permanent cardiac damage ACS is typically associated with ECG changes and serum biomarkers Acute Coronary Syndrome (ACS) ECG Changes Complete interpretation of 12-lead ECGs will occur next semester ECG changes that may occur with ACS include: T-wave inversion, ST-segment elevation, and development of an abnormal Q-wave ECG changes may not be present at onset of symptoms and will progress/change as infarction/ischemia continue ST-segment and T-wave represent ventricular repolarization - ischemic tissue has a shortened repolarization period and reduction in resting membrane potential Acute Coronary Syndrome (ACS) ECG Changes Acute Coronary Syndrome (ACS) Serum Biomarkers (aka Cardiac Enzymes) ACS labs should be drawn promptly upon arrival to the ED but ECG changes indicative of cardiac ischemia, and clinical presentation should prompt the start of treatment (labs can take time to return results and delay treatment) Presence of serum biomarkers may take hours to show up in blood work Elevated cardiac troponin and creatine kinase levels indicate myocardial damage (aka “CK and tropes”) As myocardial cells become necrotic, they release their intracellular contents into the blood stream Acute Coronary Syndrome (ACS) Serum Biomarkers (aka Cardiac Enzymes) Troponin - a regulatory protein found in muscle cells that aids in the contraction of the actin-myosin filaments Cardiac muscle tissue has specific cardiac troponins that can be differentiated from skeletal muscle cells Creatine Kinase - intracellular enzyme found in muscle cells responsible for converting creatine phosphate into ATP Acute Coronary Syndrome (ACS) Unstable Angina Angina becomes classified as unstable when the pain occurs while at rest and does not subside promptly without intervention What often occurs in UA, is the fibrous cap of an atherosclerotic lesion either ruptures or thins significantly exposing the lipid core which promotes platelet aggregation and inflammatory infiltration Platelet aggregation can cause thrombus formation with can further obstruct the artery Without resolution, UA can result in ischemia significant enough to cause infarction Acute Coronary Syndrome (ACS) Unstable Angina Acute Coronary Syndrome (ACS) Unstable Angina The fibrous cap can become worn down, thinned or ruptured by ongoing hypertension (high pressures putting more force on the lesion as blood flows past it) Many patients with atherosclerosis, dyslipidemia or chronic ischemic heart disease take a daily low dose aspirin (ASA) to reduce platelet aggregation The most important thing a patient can do when diagnosed with any of these conditions is to make lifestyle changes Patients with UA may exhibit some minor ECG changes but will not present with serum biomarkers in their lab results Acute Coronary Syndrome (ACS) NSTEMI Non-ST-segment Elevation Myocardial Infarction Myocardial Infarction - Cardiac muscle death Associated with symptoms of cardiac ischemia and the presence of serum biomarkers and the absence of ST-segment elevation Patients with NSTEMI may display some ST-segment depression and/or T-wave inversion NSTEMI MAY PROGRESS TO A STEMI IF LEFT UNTREATED Acute Coronary Syndrome (ACS) NSTEMI As with unstable angina, an atherosclerotic lesion may develop a thrombus should the fibrous cap rupture or thin enough to promote platelet aggregation Should the thrombus grow enough, it may obstruct coronary circulation enough to cause distal infarction Continued pressures on the thrombus may also cause it to become dislodged and eventually stop and completely obstruct a smaller vessel Acute Coronary Syndrome (ACS) UA vs NSTEMI UA - ischemic chest pain, may be resolved/improved with nitro, may present with minor ECG changes (t-wave inversion, ST depression), no elevation in serum biomarkers NSTEMI - ischemic chest pain, may be resolved/improved with nitro, may present with minor ECG changes (t-wave inversion, ST depression), presents with elevation in serum biomarkers Acute Coronary Syndrome (ACS) STEMI An acute STEMI is characterized by ischemic death of myocardial tissue The area of infarction is determined by the coronary artery that is affected and by its distribution of blood flow (anastomosis/collateral circulation) STEMI occurs with a complete obstruction of a coronary artery due to a thrombus/embolus Anaerobic metabolism results which, as we know, is not sustainable Decrease in contractile function occurs within 60 seconds of onset and irreversible damage within 20-40 minutes (“time is Acute Coronary Syndrome (ACS) STEMI Acute Coronary Syndrome (ACS) STEMI A STEMI is a true medical emergency that can rapidly lead to death It is common for STEMI patients to deteriorate into a lethal cardiac arrhythmia called ventricular fibrillation (VF) - discussed shortly For this reason, we apply defibrillator pads to STEMI patients ASAP so that critical intervention (defibrillation) is not delayed Nitro can be administered in an attempt to reduce MVO2 but it will not do anything to change/reverse infarction - typically does not improve STEMI pain ASA - inhibits platelet aggregation and will prevent the thrombus from getting worse, but it will not decrease the already formed thrombus Acute Coronary Syndrome (ACS) STEMI - Right Sided MI It is important to note that a STEMI that affects the right side of the heart can cause death of the pacemaker cells (SA node) These patients may present with bradycardia and hypotension Since nitro relaxes smooth muscle to reduce MVO2, any administration of nitro could drastically alter the hearts already limited ability to provide adequate CO for systemic tissue perfusion Diagnosis of right sided MIs is performed with a modified 12-lead (or 15-lead) ECG - to be discussed in detail next term Acute Coronary Syndrome (ACS) Clinical Manifestations Classic presentation of ACS is: Ischemic chest pain Constricting, squeezing, suffocating, pressure, or heaviness Pain is usually consistent and not reproducible (able to worsen) with coughing, inspiration, palpation, or movement Located usually precordial (retrosternal/substernal) or epigastric and may radiate to the left shoulder, jaw or arm (usually left) Acute Coronary Syndrome (ACS) Clinical Manifestations Other associated symptoms of ACS may include: Shortness of breath GI complaints (nausea, vomiting) Epigastric discomfort (may be mistaken for indigestion) Fatigue, weakness Anxiety, tachycardia, feeling of impending doom Skin - pale, cool, diaphoretic Acute Coronary Syndrome (ACS) Clinical Manifestations Female patients often have atypical presentations of cardiac ischemia (may be absent of chest pain) whereas males tend to have more classic presentations This should not be diagnostic, it should just serve as a reminder to treat all patients with an open mind and not to tunnel vision or exclude differential diagnoses Detailed and thorough assessments and questions are of paramount importance on all patient complaints Heart Failure A complex syndrome resulting from any functional or structural disorder of the heart that results in low cardiac output and/or pulmonary congestion Heart failure can result from any heart condition that reduces the pumping ability of the heart CAD, HTN, cardiomyopathies and valvular heart disease Heart failure is usually a progressive disease but may be the result of an acute problem (STEMI) Heart failure can be classified as either right sided or left sided but long term failure typically involves both Heart Failure Heart Failure Right-Sided Heart Failure When the right ventricle fails there is a reduction in the deoxygenated blood moving into the pulmonary circulation and ultimately a decrease in left ventricular cardiac output If blood isn’t pumping into the pulmonary circulation, it backs up into the systemic venous system This backup causes an increase in right ventricular and right atrial end diastolic pressure as well as systemic venous pressure A common side effect of right sided heart failure is peripheral edema (commonly seen in the distal lower extremities) Heart Failure Right-Sided Heart Failure Further venous congestion causes systemic organ problems Blood backs into the hepatic vein causing hepatomegaly, portal hypertension and all of its side effects Severe right failure can cause JVD in patients presenting sitting or standing Causes of right failure include anything that impedes blood flow through the lungs (left heart failure and pulmonary hypertension are the most common causes) Valve disorders, right MI, cardiomyopathies Heart Failure Right-Sided Heart Failure Pulmonary Hypertension - HTN within the pulmonary circulation (arterial) Commonly occurs in patients with chronic pulmonary disease (COPD), severe pneumonia, pulmonary embolism (PE) or aortic or mitral valve stenosis - also caused by left sided heart failure Pulmonary vessels constrict in the presence of hypoxemia and hypercapnea (opposite to the response in systemic circulation) This is thought to occur as a compensatory mechanism to promote gas exchange (divert the blood away from non- ventilating alveoli) Cor Pulmonale - right heart failure resulting from pulmonary Heart Failure Heart Failure Heart Failure Left-Sided Heart Failure Impairment of the left ventricle decreases systemic cardiac output and causes a backup (congestion) of blood into the left atrium and pulmonary circulation The backup of blood in the pulmonary circulation causes a rise in pulmonary venous pressure When the pressure in the pulmonary capillaries exceeds the capillary osmotic pressure, intravascular fluid shifts into the interstitium of the lungs and ultimately the alveoli This fluid is called pulmonary edema Left heart failure is commonly referred to as Congestive Heart Heart Failure Left-Sided Heart Failure Pulmonary edema commonly occurs at night when patients are lying supine and gravitational forces are no longer at play (peripheral edema can return to circulation and make its way into the lungs) - common for patients with diagnosed heart failure to sleep in a recliner or propped up with many pillows Common causes of left ventricular failure are hypertension (progressive), acute MI (acute failure), and valve disorders As pulmonary pressure rises, left sided heart failure often progresses to right sided heart failure Heart Failure Heart Failure Compensatory Mechanism Many compensatory mechanisms exist to help maintain an adequate CO as heart failure progresses Unfortunately, like any other compensatory mechanism, these cannot work forever, and may also contribute to the worsening of the disease Sympathetic response (increased HR, SV, vasoconstriction) Frank-Starling - since SV is usually decreased, in order to maintain CO the heart must require an increase in preload - the kidneys reabsorb sodium in an effort to increase fluid volume RAAS - reduction in renal blood flow triggers this system Heart Failure Compensatory Mechanism ANP - increased ANP secretion due to low circulating fluid volume promotes water retention Myocardial Hypertrophy - enlargement of the ventricles by myocytes and non-myocytes can lead to fibrosis and remodelling of the heart tissue It is an attempt at compensation that typically leads to worsened cardiac function The remodelling and fibrosis replaces normal conduction cells which often leads to cardiac arrhythmias Heart Failure Compensatory Mechanism Heart Failure Acute Heart Failure As previously discussed heart failure may be a gradual and progressive process or an acute and emergent onset Symptoms of both mechanisms may often become severe and require medical intervention Usually the emergent symptoms are a result of increased pulmonary edema causing shortness of breath Rapid development of pulmonary edema due to acute heart failure is called: Acute Cardiogenic Pulmonary Edema (ACPE) and presents a significant life threat due to a lack of gas exchange - sometimes referred as “flash edema” Heart Failure Clinical Manifestations Exertional SOB Orthopnea (SOB while lying supine) Paroxysmal nocturnal dyspnea (sudden SOB during sleep) Bilateral crackles on auscultation (coughing pink frothy sputum indicates significant congestion) Wheezes (bronchospasm caused by irritation of the bronchi due to pulmonary edema - cardiac asthma) Heart Failure Clinical Manifestations Fluid retention and edema (pitting edema in the distal extremities - usually ankles) May also present as diffuse weight gain, ascites, hydrothorax (pleural effusion) Nocturia - increase in urination at night While patient is supine, the excess edema recirculates and makes its way to the kidneys where it gets excreted in urine Weakness, fatigue, mental confusion Shock Shock (aka circulatory failure) is an acute failure of the circulatory system to supply peripheral tissues and organs with an adequate blood supply, resulting in cellular hypoxia Causes include: Altered cardiac function (Cardiogenic) Decreased fluid/blood volume (Hypovolemic) Vasodilation with maldistribution of blood flow (Distributive) Obstruction of blood through the circulatory system (Obstructive) Shock Cardiogenic Shock - occurs when the heart fails to pump blood sufficiently to meet the body’s demands Decreased CO, hypotension, hypoperfusion, tissue hypoxia Common causes include: Acute MI, sustained arrhythmias, CHF, end-stage CAD or cardiomyopathy Electrophysiology Review Sinoatrial (SA) Node - pacemaker, 60-100bpm, P-wave Internodal Pathways - predetermined pathways between SA and AV Atrioventricular (AV) Node - delays impulse conduction, 40- 60bpm isoelectric line following P-wave Bachmann’s Bundle - impulse connection between the R and L atria Bundle of His - conducts impulse from AV to purkinjes (R and L bundles) Purkinje Fibres - conducts impulse from bundle branches to Electrophysiology Review Electrophysiology Review Action Potential - represents the sequential change in electrical potential that occurs across a cell membrane following excitation - causes the heart to contract Movement of + and - ions across a selectively permeable membrane - K+, Na+, Ca2+ Phase 4 - resting membrane potential/diastole Phase 0 - rapid depolarization of the ventricles (QRS complex) Phase 1 - early repolarization Phase 2 - plateau phase (ST segment) Phase 3 - rapid repolarization (T-wave) Electrophysiology Review Electrophysiology Review Electrophysiology Review Refractory Periods Absolute Refractory Period - no external stimulus can initiate another action potential Relative Refractory Period - larger than normal stimulus can initiate another action potential Supernormal Excitatory Period - weak stimulus can initiate another action potential (the origin for many arrhythmias) Electrophysiology Review Cardiovascular Trauma Myocardial Contusion Bruising to the heart that may occur with deceleration forces that cause the heart to collide with the sternum or spinal column Characterized by local tissues contusion, hemorrhage, edema and myocardial damage Direct or indirect damage (edema) to coronary arteries may cause disruption in myocardial blood flow - ischemia Disruption/damage to conductive cells may produce cardiac arrhythmias Damage to the left ventricle may cause fluid backup into the lungs (left-sided heart failure) Cardiovascular Trauma Myocardial Rupture When one of the walls of the heart is ruptured or penetrated due to blunt or penetrating trauma Almost always fatal Can produce: pericardial tamponade, arrhythmias, hypovolemic shock, heart failure, etc. Cardiovascular Trauma Commotio Cordis If the patient receives significant blunt force trauma to the chest during ventricular repolarization (specifically the upstroke of the T- wave) it may cause sudden cardiac arrest, presenting with ventricular fibrillation (VF) This typically occurs during the relative refractory period or supernormal excitatory period These patients typically respond well to prompt defibrillation A rare condition, usually occurs as a sports injury