Cardiovascular Alteration, Week 1-4 PDF

Week # 1: Cardiovascular Alteration Disorders of the Pericardium 1. Acute pericarditis- inflammation of the pericardium (sack around the heart that gets swollen and irritated). Acute inflammation of the pericardium Clinical manifestations: fever, myalgias, and malaise...

Week # 1: Cardiovascular Alteration Disorders of the Pericardium 1. Acute pericarditis- inflammation of the pericardium (sack around the heart that gets swollen and irritated). Acute inflammation of the pericardium Clinical manifestations: fever, myalgias, and malaise, followed by the sudden onset of severe chest pain Treatment: rest, salicylates, and nonsteroidal anti-inflammatory drugs; combined nonsteroidal and colchicine (make sure the swelling does not come back) 2. Constrictive (restrictive) pericarditis ○ Fibrous scarring with occasional calcification of the pericardium causes the visceral and parietal pericardial layers to adhere. - The scar forms on the pericardium. ○ The scar tissue makes the pericardium become thick and rigid, which makes the heart hard to pump blood. ○ Clinical manifestations: exercise intolerance, dyspnea on exertion, fatigue, and anorexia ○ Treatment: dietary sodium restriction and diuretics to improve cardiac output ○ Anti-inflammatory drugs ○ If these treatments are not successful, then surgical excision is performed. 3. Pericardial effusion Accumulation of fluid in the pericardial cavity- life-threatening. Assessment findings: murmur, chest pain Tamponade Treatment: pericardiocentesis, insert needle to extract fluid, fluid restriction Disorders of the Myocardium: 1. Cardiomyopathies - diseases that affect the heart muscle called the Myocardium, making it harder for the heart to pump blood properly. Effects of neurohumoral responses to ischemic heart disease or hypertension on the heart muscle cause remodeling Many cases of cardiomyopathy are idiopathic  2. Dilated cardiomyopathy - heart muscle becomes weak and stretches out which makes it harder to pump blood. Impaired systolic function ( heart ability to squeeze) which is not very strong, leading to increases in intracardiac volume, ventricular dilation, and systolic heart failure Causes: ischemic heart disease; valvular disease; diabetes; alcohol; drug toxicity; renal failure; hyperthyroidism, diabetes, deficiencies of niacin, vitamin D, and selenium; infection Clinical manifestations: dyspnea, fatigue, pedal edema Treatment: reduce blood volume, increase contractility, reverse underlying disorder 3. Hypertrophic cardiomyopathy Hypertrophic obstructive cardiomyopathy Hypertensive or valvular, hypertrophic cardiomyopathy 4. Hypertrophic obstructive cardiomyopathy Common inherited heart defect of a thick septal wall- the heart muscle gets too thick. ○ septal and left side Clinical manifestations: angina, syncope, palpitations, symptoms of MI, symptoms of left heart failure Treatment: ○ Beta-blockers or ACE inhibitors ○ Surgical resection of the hypertrophied myocardium ○ Septal ablation ○ Prophylactic placement of implantable cardioverter-defibrillators in high-risk individuals 5. Hypertensive or valvular hypertrophic cardiomyopathy Hypertrophy of the myocytes: attempts to compensate for increased myocardial workload- the myocytes become bigger and thicker Clinical manifestations: asymptomatic or may complain of angina, syncope, dyspnea on exertion, and palpitations Hypertrophic Obstructive Cardiomyopathy (HOCM): Cause: HOCM is typically genetic, meaning it runs in families. It happens when the heart muscle, especially in the lower chambers (the ventricles), becomes abnormally thick without any other underlying condition like high blood pressure or valve problems.  Obstruction: In HOCM, the thickened muscle blocks (or obstructs) blood flow as it leaves the heart. This obstruction can make it much harder for the heart to pump blood out to the body. Symptoms: Because of this obstruction, people with HOCM often experience symptoms like: ○ Chest pain (angina) ○ Shortness of breath (dyspnea) ○ Dizziness or fainting (syncope) ○ Palpitations or irregular heartbeats Hypertensive or Valvular Hypertrophic Cardiomyopathy: Cause: This type of cardiomyopathy happens as a result of long-term high blood pressure (hypertension) or problems with the heart valves. It’s the heart’s way of trying to cope with the extra workload caused by these conditions. No Obstruction: Unlike HOCM, there’s no obstruction to blood flow. The heart muscle thickens in response to the increased workload but doesn’t block the flow of blood out of the heart. Symptoms: People with hypertensive or valvular hypertrophic cardiomyopathy may have similar symptoms, such as: ○ Chest pain ○ Shortness of breath during physical activity ○ Dizziness or fainting ○ Palpitations However, they might also be asymptomatic for a long time, especially if the condition is mild. Treatment focus: In HOCM, the goal is to reduce the obstruction, while in hypertensive/valvular hypertrophy, treatment focuses on controlling blood pressure or addressing valve problems. 6. Restrictive cardiomyopathy (amyloid)- builds up in the heart Myocardium becomes rigid and noncompliant, impeding ventricular filling and raising filling pressures during diastole. ○ Cause backflow Clinical manifestations: right heart failure occurs with systemic venous congestion- swelling of the legs and ankles, shortness of breath. Treatment: correct the underlying cause Disorders of the Endocardium: Valvular Heart Disease 1. Valvular dysfunction ○ Stimulates chamber dilation (due to pressure) and/or myocardial hypertrophy  i. Causes the heart chambers to stretch (dilate) ○ Manifestations of cardiac valve disease vary ○ Depends on the valve involved, form of dysfunction, and severity and rate of onset of dysfunction ○ Treatment: Careful fluid management, Valvular repair or valve replacement with a prosthetic valve, followed by long-term anticoagulation therapy and life-long antibiotic prophylaxis before invasive procedures Valvular Heart Disease - affects the heart valves, which are responsible for keeping blood flowing in the right direction through the heart’s chambers. Normal valves maintain the normal direction of If they do not close properly, they can allow blood flow through the heart’s chambers backflow (regurgitation) - when the blood flows back, the heart has to work harder to pump it forward again. If the valve does not fully open or is narrowed (stenosed), then the raised resistance impedes blood movement on its normal route, and extra propulsive force must be applied by the myocardium - The myocardium has to work harder, using extra force to push blood through the narrow opening. It can weaken the heart overtime. Abnormalities of valvular structure and/or Acquired ( Develops later in Life)valvular function can either be congenital or acquired disease is by far the most common and is most prevalent in the elderly- often caused by conditions like high blood pressure, infection or age related degeneration of the valves. Congenital (present at birth):valvular defects arise from disrupted heart development, about 50 percent of which involve the valves - some people are born with valve defects due to abnormal heart development. Valves exposed to high blood flow and pressures Makes them particularly susceptible to other risk factors that promote valvular damage Summary: Heart valves control the flow of blood through the heart, but if they don’t open or close properly, they can cause serious problems. Valvular heart disease can be either congenital (present at birth) or acquired (develops later in life, often due to aging or high blood pressure). The valves that face the most stress are particularly prone to damage, and this can lead to issues like regurgitation (backflow) or stenosis (narrowing). Disorders of the Endocardium: Valvular Heart Disease Either congenital or acquired The acquired forms are more common in adults and result from ○ Inflammatory, ischemic, traumatic, degenerative, or infectious alterations of valvular structure and function Worldwide, the most common cause of acquired valvular dysfunction is degeneration or inflammation of the endocardium secondary to rheumatic heart disease Structural alterations of heart valves are caused by remodeling changes in the valvular extracellular matrix and lead to stenosis, incompetence, or both Previously undiagnosed, mild valvular heart disease is present in approximately 1/2 of individuals ≥ 65 years of age The prevalence of undiagnosed moderate or severe valvular heart disease may be as high as 6.4% Risk Factors Age Gender Tobacco use Hypercholesterolemia Rheumatic heart disease HTN Type 2 diabetes Pathophysiology The constant stress of facing high flow and pressure over thirty to forty million cardiac contractions a year is not without its consequences. Each contraction pushes blood through the valves, which can create a lot of stress on them. ○ Most common valvular disorder is calcification that comes with “wear-and-tear” and aging ○ Calcification is when calcium builds on the heart valves over time. Presence of other factors such as hyperlipidemia (high levels of fats in the blood) , hypertension, and inflammation accelerate this process and promote the deposition of a form of calcium phosphate ○ Aortic and mitral valves are more prone to calcification due to the pressure they face ○ Most common pattern of calcification in aortic valve is mounded masses within cusps of the valve that eventually fuse and stop the valve from opening fully ○ Calcification in the mitral valve tends to start in the fibrous annulus, which does not impact valvular function to the same extent, but in exceptional cases can cause  regurgitation or stenosis, or even arrhythmias as calcium deposits impinge on the atrioventricular conduction system. Valvular stenosis -Narrowing or constriction of a heart valve which reduces blood flow through the valve and increases the workload on the heart. Valve orifice is constricted and narrowed Aortic- Valve becomes narrowed or obstructed. Mitral- Valve between the left atrium and left ventricle becomes narrowed. Valvular regurgitation The valve fails to shut completely Is also called insufficiency or incompetence Aortic Mitral Tricuspid Characteristic heart sounds, cardiac murmurs, and systemic complaints: assist in determining which valve is abnormal Mitral valve prolapse syndrome Aortic stenosis Orifice of the aortic semilunar valve narrows, causing diminished blood flow from the left ventricle into the aorta Clinical manifestations: angina, syncope, and dyspnea Treatment: ○ Most require valve repair or replacement with a prosthetic valve, followed by long-term anticoagulation therapy ○ Transcatheter aortic valve implantation Pathophysiology of Aortic Stenosis 1) Critical Aortic stenosis a) This refers to the severe narrowing of the aortic valve, which restricts blood flow from the left ventricle ( LV) into the aorta. 2) Increased Resistance to LV systolic Ejection a) Due to the narrowing of the aortic valve, the left ventricle has to work harder to eject blood through the valve, leading to increased resistance during systole( the contraction phase of the heartbeat). 3) LV hypertrophy a) The left ventricle undergoes hypertrophy ( thickening of the heart muscle). This is the heart's way of compensating for the increased workload. 4) Myocardial Remodeling ( fibrosis) a) Over time the hypertrophied left ventricle begins to remodel. This process includes fibrosis ( formation of the scar tissue) in the heart muscle, which reduces its flexibility and efficiency. 5) Gradual decrease in LV contractility a) As fibrosis progresses, the left ventricle's ability to contract weakens, resulting in decreased contractility. This reduces the heart's ability to pump blood effectively 6) Outcomes of LV Dysfunction Increased LV Pressure: As the left ventricle struggles to pump blood, the pressure inside the LV increases. This leads to an increase in pressures in the left atrium and pulmonary veins, eventually causing pulmonary edema(fluid buildup in the lungs).  Symptoms include dyspnea (shortness of breath), orthopnea (difficulty breathing when lying down), and cough. Decreased Cardiac Output: The decreased ability of the left ventricle to pump blood leads to a reduction in overall cardiac output (the amount of blood the heart pumps per minute). This results in decreased perfusion (reduced blood flow) to both the systemic circulation (the body) and the coronary arteries (which supply blood to the heart muscle). 7. Consequences of Decreased Perfusion Tissue Ischemia: ○ Decreased perfusion to tissues causes ischemia (inadequate oxygen supply to tissues), leading to symptoms such as: Angina (chest pain due to reduced blood flow to the heart). Syncope (fainting episodes caused by decreased blood flow to the brain). Oliguria (reduced urine output, indicating poor kidney perfusion). Stroke (due to poor blood flow or embolism) Mitral stenosis- narrowing of the mitral valve to impaired blood flow from the left atrium to the left ventricle. Impairment of blood flow from the left atrium to the left ventricle Snapping sound ( known as an opening snap) upon auscultation Most common cause: acute rheumatic fever ( lead to long term valve damage ) Clinical manifestation: opening snap Treatment: surgical repair; may require valve replacement Pathophysiology of Mitral Stenosis Disorders of the Endocardium: Valvular Heart Disease Aortic regurgitation ○ Inability of the aortic valve leaflets to close properly during diastole - allowing blood flow back into the left ventricle. ○ Clinical manifestations: widened pulse pressure as a result of increased stroke volume and diastolic backflow ○ Treatment: valve replacement may be delayed for many years with the use of vasodilators and inotropic agents Mitral regurgitation ○ Most common causes: mitral valve prolapse, rheumatic heart disease, infective endocarditis, MI, connective tissue disease, dilated cardiomyopathy  ○ Permits backflow of blood from the left ventricle into the left atrium ○ Treatment: surgical repair or valve replacement Tricuspid regurgitation ○ Leads to volume overload in the right atrium and ventricle, increased systemic venous blood pressure, and right heart failure Mitral valve prolapse syndrome ○ Anterior and posterior cusps of the mitral valve billow upward (prolapse) into the left atrium during systole ○ Clinical manifestations: asymptomatic ○ Treatment: none needed or beta-blockers Use Your Clinical Judgement! A client has a diagnosis of valvular regurgitation. What pathophysiologic process is the client experiencing? The valves: A. Are constricted and narrowed, impeding the forward flow of blood (STENOSIS) B. Fail to close completely, permitting the backflow of blood to continue C. Have an inherited defect, such as thickening of the septal wall (CARDIOMYOPATHY) D. Cause acute pericarditis and filling of the pericardial sac (PERICARDIAL EFFUSION) Cardiovascular Alterations in Children Congenital Heart Disease Leading cause of death (except for prematurity) in the first year of life Cause is known in only 10% of defects Prenatal, environmental, and genetic risk factors ○ Maternal: rubella, lupus, insulin-dependent diabetes, alcoholism, illicit drug use, age (> 40 years) phenylketonuria (PKU), and hypercalcemia ○ Chromosomal aberrations Classification of Congenital Heart Disease Based on blood flow ○ Lesions increasing pulmonary blood flow ○ Defects that shunt from high-pressure left side to low-pressure right side with pulmonary congestion; acyanotic Lesions decreasing pulmonary blood flow ○ Generally complex with right-to-left shunt and cyanosis Obstructive lesions  ○ Right- or left-sided outflow tract obstructions that curtail or prohibit blood flow out of the heart; no shunting Mixing lesions Desaturated blood and saturated blood mix in the chambers or great arteries of the heart’ Lesions increasing pulmonary blood flow: These defects cause extra blood to flow to the lungs because blood leaks from the high-pressure left side of the heart to the low-pressure right side. This can make the lungs congested, but it doesn’t cause the skin to turn blue (acyanotic). 2. Lesions decreasing pulmonary blood flow: These are more complicated problems where blood flows from the right side of the heart to the left, and less blood gets to the lungs. This can cause a blue tint to the skin because the blood doesn’t get enough oxygen from the lungs (cyanosis). 3. Obstructive lesions: These defects block blood flow as it tries to leave the heart, either on the right side or the left side. There’s no mixing of blood between the heart’s sides, but blood has a hard time getting out of the heart to go to the body or lungs. 4. Mixing lesions: These defects allow oxygen-rich blood (saturated) and oxygen-poor blood (desaturated) to mix inside the heart or in the big blood vessels leaving the heart. This can cause the blood going to the body to have less oxygen than it should. In simple terms, these are different ways heart defects can affect the flow of blood, whether it’s making too much blood go to the lungs, blocking blood flow, or mixing blood with and without oxygen Acyanotic Heart Defects Shunting of blood flow from the left heart into the right heart is called a left-to-right shunt. ○ Left-to-right shunt increases volume in the right side of the heart. ○ Results in increased blood flow into the pulmonary circulation.  ○ Because blood continues to flow through the lungs before passing into systemic circulation, there is no decrease in tissue oxygenation or cyanosis. Cyanotic heart defects Cause shunting of blood from the right side of the heart directly into the left side of the heart (right-to-left shunt) Right-to-left shunt decreases blood flow through the pulmonary system Causes less-than-normal oxygen delivery to tissues, resulting in cyanosis Most congenital heart defects are named to describe underlying defects (valvular abnormalities, abnormal openings in the septa, malformation or abnormal placement of great vessels) *USE THIS PICTURE TO STUDY Shunting of Blood in Congenital Heart Disease A. Normal B. No septal wall, shunt present, blood is mixing (affects oxygenation) C. Tetralogy (4 defects) Defects With Increased Pulmonary Blood Flow Patent Ductus Arteriosus (PDA) Failure of the ductus arteriosus to close ○ Normally closes within the first few hours of birth.  ○ Before birth, PDA allows blood to shunt from the pulmonary artery to the aorta. Clinical manifestation ○ Continuous, machinery-type murmur ○ Bounding pulses, active precordium, thrill upon palpation, and signs and symptoms of pulmonary overcirculation. Treatment ○ Surgical closure involving ligation by incision, catheter, or video-assisted thoracoscopy Atrial Septal Defect Abnormal communication between atria Blood shunted from left to right Clinical manifestations: Often asymptomatic; diagnosed by murmur Three major types of defect ○ Ostium primum ○ Ostium secundum ○ Sinus venosus Treatment: Surgical closure before school age results in better health Ventricular Septal Defect Abnormal communication between ventricles ○ Shunting from high-pressure left side to low-pressure right side Clinical manifestations: Depends on age of child, size of defect, level of PVR ○ Heart failure ○ Poor weight gain ○ Murmur and systolic thrill Treatment ○ Minimal treatment to surgical repair Use Your Clinical Judgement! In a child with a ventricular septal defect, blood flow is shunted from the: A. left ventricle to the right ventricle B. right ventricle to the left ventricle C. aorta to the pulmonary artery D. left atria to the right atria Atrioventricular Canal Defect  Results from nonfusion of the endocardial cushions Abnormalities demonstrated in the atrial and ventricular septa and AV valves Complete, partial, and transitional AVC defects Clinical manifestations: Presents with a murmur, heart failure, respiratory tract infections Treatment: Complete repair between 3 and 6 months of life Obstructive Defects Coarctation of the Aorta Narrowing of the lumen of aorta that impedes blood flow ○ 8% to 10% of defects Is almost always found in the juxta ductal position But can occur anywhere between origin of aortic arch and bifurcation of aorta in lower abdomen Clinical manifestations: Newborns usually exhibit HF ○ Once the ductus closes, rapid deterioration occurs from hypotension, acidosis, and shock Clinical manifestations: ○ Older children ○ Hypertension in the upper extremities ○ Decreased or absent pulses in the lower extremities ○ Cool mottled skin ○ Leg cramps during exercise Treatment: ○ Prostaglandin administration ○ Mechanical ventilation ○ Inotropic support ○ Maintain cardiac output ○ Surgery Intervention: Bring babies knees to chest Use Your Clinical Judgment! A nurse is assessing a child with coarctation of the aorta. What will the nurse find? A) Squatting when short of breath B) Hyper cyanotic spells C) High blood pressure in the upper extremities with decreased pulses in feet D) Syncopal episodes with chest pain Aortic Stenosis Narrowing of the aortic outflow tract (10% of defects) Caused by malformation or fusion of the cusps  Causes an increased workload on the left ventricle Clinical manifestations ○ Often asymptomatic ○ Signs of exercise intolerance in preadolescence ○ Syncopal episodes, epigastric pain, and exertional chest pain in more severe forms ○ Murmur Treatment ○ Commissurotomy; aortic valvotomy; Ross procedure Pulmonic Stenosis Narrowing of pulmonary outflow tract Abnormal thickening of valve leaflets Narrowing of valve Pulmonary atresia ○ Severe form Clinical manifestations ○ Often asymptomatic ○ Exertional dyspnea, murmur, fatigue, thrill, cyanosis, HF Treatment ○ Mild Not treated, closely observed ○ Severe Balloon angioplasty; pulmonary valvotomy Defects With Decreased Pulmonary Blood Flow Tetralogy of Fallot Syndrome represented by four defects ○ Large ventricular septal defect ○ Overriding aorta straddles the ventricular septal defect ○ Pulmonary stenosis ○ Right ventricle hypertrophy Cyanosis, hypoxia, and clubbing, feeding difficulty, dyspnea, restlessness, squatting Hypercyanotic spell or a “tet spell” that generally occurs with crying and exertion Most cases corrected surgically in early infancy before 1 year of age; Blalock-Taussig shunt, transcatheter pulmonary valve replacement, patch Tricuspid Atresia Imperforate tricuspid valve No communication between the right atrium and the right ventricle Additional defects ○ Septal defect ○ Hypoplastic or absent right ventricle ○ Enlarged mitral valve and left ventricle ○ Pulmonic stenosis Mixing Defects Transposition of the Great Arteries Aorta arises from the right ventricle and the pulmonary artery arises from the left ventricle Results in two separate, parallel circuits ○ Unoxygenated blood continuously circulates through the systemic circulation ○ Oxygenated blood continuously circulates through the pulmonary circulation Extrauterine survival requires communication between the two circuits Clinical manifestations: Cyanosis may be mild shortly after birth and worsen during the first day Treatment: Surgery to switch the arteries Total Anomalous Pulmonary Venous Connection Pulmonary veins connect to the right side of the heart, directly or indirectly, through one or more systemic veins that drain into the right atrium Non Obstructive vs. obstructive Clinical manifestation ○ Cyanosis Treatment ○ Obstructed lesions are repaired at the time of diagnosis  ○ Unobstructed lesions are generally repaired during infancy ○ Surgery: Anastomosis of the common pulmonary vein to the left atrium; closure of the atrial septal defect Truncus Arteriosus ​Is failure of embryonic artery to divide into pulmonary artery and aorta Trunk straddles an always present ventricular septal defect Types I through IV ○ I: Most common; main pulmonary artery arises from truncus ○ II: Pulmonary arteries arise from posterior aspect of truncus ○ III: Pulmonary arteries arise from lateral aspect of truncus ○ IV: Pseudotruncus; is a severe form of tetralogy of Fallot with bronchial arteries arising from descending aorta to supply lungs Clinical manifestations: ○ Mild-to-moderate cyanosis that worsens with activity ○ Murmur Treatment: ○ Modified Rastelli procedure involving VSD patch closure to divert the blood flow from the left ventricle outflow tract into the truncus ○ Correct pulmonary arteries Hypoplastic Left Heart Syndrome Abnormal development of left-sided cardiac structures Obstructs blood flow from the left ventricular outflow tract Left ventricle, aorta, and aortic arch are underdeveloped; mitral atresia or stenosis is observed Clinical manifestations ○ As ductus closes, systemic perfusion is decreased, resulting in hypoxemia, acidosis, and shock ○ Loud and single-second heart sound Treatment ○ Prostaglandin administration ○ Correction of acidosis ○ Inotropic support for adequate cardiac output ○ Ventilatory manipulation ○ Surgery ○ Cardiac transplantation Week # 2: ECG Interpretations The Five Phases of the Cardiac Cycle Conduction System of the Heart Electrocardiogram (ECG) and Cardiac Electrical Activity Electrocardiography ○ Serial 12-lead ECGs establish the presence of myocardial ischemia and infarction or conduction defects and dysrhythmias ○ Holter monitoring Baseline = isoelectric Anatomy of an ECG Basic ECG interpretation 1. ECG rate (6 second strip method, big box method, small box method) - You have to count the number of small squares between the R waves. You can also count the number of big squares depending on the formula. Small square method = 1500 Divide by the number of squares in a straight line between the R waves. Start with the R count the number of small squares between them. Large square METHOD 300 divided by how many big squares in between the R waves. RR intervals – are they regular? 2. Is there a P wave for every QRS complex? Is there a QRS complex for every P wave? 3. Do the P waves come at consistent intervals or “march out”? The QRS complexes? 4. Is the QRS complex wide or narrow? It should be three small squares = 0.12 seconds which is narrow, if it's more than 3 small squares it is more than 0.12 seconds. Putting it all together Normal Sinus Rhythm The normal rhythm of heart is sinus rhythm Recognized on ECG by regular P-waves, at a rate between 60 and 100 beats per minute (bpm), with every P-wave followed by a QRS complex and every QRS complex preceded by a P-wave Depolarization and repolarization of the atria and ventricles show as 3 distinct waves/deflections (P, QRS, T) on ECG Composite Chart of Heart Function Acute Coronary Syndromes (ACS) Types of Myocardial Ischemia and Infarction Degree of occlusion caused by plaque and oxygen demand of myocardium determine degree of ischemia that can develop Arterial occlusion tends not to be a significant factor until the lumen is occluded by about in70 percent- the heart starts struggling to get enough oxygen ○ Inside of your blood vessels there is a plaque ( a mix of fat and other stuff) can build up over time. Vascular occlusion may also be masked by formation of anastomoses Rupture of plaque and formation of a thrombus can drastically and quickly reduce lumen and blood flow ○ Causing a blood clot ( thrombus ) to form. The clot makes it harder for the blood to flow. Degree and duration of ischemia determine type of acute coronary syndrome (ACS) that occurs and the clinical impact Mild or brief ischemia can lead to angina ( chest pain) But when ischemia is prolonged then MI becomes more likely( heart attack) ○ Significant changes in ECG and release of cardiac enzymes are seen ○ The doctor checks to see if it's in the blood to know if the heart attack is happening. Types of Myocardial Ischemia and Infarction 1) Inside of your vessels there is stuff called plaque that can build up. This make is harder for the blood to pass through ( ischemia ). 2) You might not notice anything until 70% is blocked. 3) Anastomosis is when the heart finds a way to get blood around the blockages using tiny blood vessels called anastomosis. 4) Rapture plaque causes a clot to form, blocking more blood.  5) Which accuses angina but if its severe then a heart attack can occur. 6) ECG is done and cardiac enzymes Unstable Angina, Non- STEMI and STEMI Unstable Angina (UA) Form of acute coronary syndrome Transient episodes of thrombotic vessel occlusion and vasoconstriction at site of plaque damage Sign of impending infarction! EMERGENCY!  Serious heart condition where the blood flow to the heart is temporarily blocked or reduced due to a blood clot and the narrowing if blood vessels ( vasoconstriction) where the plaque is built up. Diagnostics: ECG Affected area can be identified on 12-lead ECG UA: partial blockages that are serious but have not yet caused permanent damage Non-STEMI: Partial heart attack STEMI: heart attack where the blood flow is completely blocked affecting the entire thickness of the heart wall ECG changes depend on Duration of ischemic event (acute vs evolving) Extent (partial/subendocardial vs full wall thickness/transmural) Location Ischemic / injured / infarcted tissue does not function like normal myocardial tissue! UA ECG Presentation UA is first step in progressive spectrum of ischemia-related myocardial injury Now is grouped under classification of Non-STEMI( only partial but its still serious ) ○ The ECG most commonly shows ST segment depression and T wave inversion ○ ST - the flat line between heartbeats goes down) ○ T- the part of the heartbeat wave that usually goes up, goes down instead. Types of MI and ECG Presentations 1. Subendocardial Infarction If thrombus ( blood clot) disintegrates before complete distal tissue necrosis has occurred ○ Infarction will involve only the myocardium directly beneath endocardium Partial wall thickness damage Present with ST segment depression and T wave inversion without ST elevation on ECG ○ Non ST-Segment Elevation MI (Non-STEMI 2. Transmural Infarction If thrombus lodges permanently in vessel, infarction will extend through myocardium all the way from endocardium to epicardium  ○ Full wall thickness damage ○ Presents with ST segment elevation on ECG ○ ST-Segment Elevation MI (STEMI) Clients with STEMI at highest risk for serious complications Should receive definitive intervention without delay! Types of MI and ECG Presentations Non-STEMI: ST segment depression and T-wave inversion indicative of partial wall thickness (subendocardial) damage STEMI: ST segment elevation indicative of full myocardial wall thickness (transmural) damage Arrhythmias/ Dysrhythmias Are disturbances of the heart rhythm Ranges from an occasional “missed” beat or rapid beats to severe disturbances that affect the pumping ability of the heart Can be caused by an abnormal rate of impulse generation or an abnormal impulse conduction Quick reference guide for arrhythmias Atrial Fibrillation Most common cardiac arrhythmia Caused by rapidly firing potentials in atrial myocardium ○ Aberrant depolarizations often result of myocardial remodeling ○ Causes include HTN, valvular and ischemic heart disease, genetics Rapid depolarizations result in very fast atrial rate 400 to 600 bpm ○ Because atrial rate is so fast, ECG shows very rapid, irregular atrial deflections of varying shapes and sizes called “fibrillatory waves” ○ Action potentials produced are low amplitude, so P-waves will not be seen Atrial Fibrillation: ECG Fibrillatory waves indicated by arrows Atrial Fibrillation: Summary No visible P-Waves Irregularly irregular QRS complexes High ventricular rate Atrial fibrillatory waves Atrial Flutter Atria contracts very rapidly – usually 300 times a minute! ○ Recognized by characteristic ‘sawtooth’ pattern Not all atrial impulses conduct to ventricles (e.g., 1 in 4 impulses) ○ Results in ventricular rate less than atrial rate e.g., approx. 70 bpm (e.g., 280 bpm / 4 = 70 bpm) Important NOT to assume on basis of normal heart rate that this must be sinus rhythm Atrial flutter of new onset often associates. with HR of 150 bpm when 1 in 2 atrial impulses conducted to ventricles ○ A useful tip is to suspect atrial flutter in anyone with resting HR of 150 bpm (ventricular rhythm: 300 bpm/2=150bpm) ○ Once atrial flutter is suspected, flutter waves can often be identified Atrial Fibrillation: ECG - Fibrillatory waves indicated by arrows. Atrial Flutter: Summary - Atrial flutter is a type of abnormal heart rhythm ( arrhythmia ). - The atria ( upper chambers of the heart ) beat very fast in a regular pattern. - The heart's electrical activity shows a distinct “ sawtooth” pattern on an ECG due to the rapid, consistent atrial contractions. - The ventricular response ( how the lower heart chambers react) can vary meaning the ventricles may not beat as fast or as regularly as the atria. Premature Atrial Contractions Premature Atrial Contractions: ECG Premature P-wave indicated by arrow Premature Atrial Contractions: Summary Extra P-wave with abnormal morphology Compensatory pause leading to atrial bigeminy (complexes appear to be in pairs) Premature Ventricular Contractions Premature Ventricular Contractions: ECG Indicated by arrow Premature Ventricular Contraction: Summary Out of step with normal R-R interval Wider complex Followed by compensatory pause Ventricular Tachycardia Can be monomorphic or polymorphic QRS complexes in monomorphic ventricular tachycardia Have same shape and are symmetrical because they start in same place in myocardium Polymorphic ventricular tachycardia Has variable QRS shape because depolarizations are instigated at multiple points Ventricular Tachycardia: ECG At 190 BPM What is the nursing implication? Would you call a code blue? Ventricular rate >100 bpm QRS complex not associated with P-wave Wide QRS complex morphology Ventricular Fibrillation Ventricular Fibrillation: ECG No recognizable P-waves or QRS complexes Ventricular Fibrillation: Summary  Chaotic, irregular, and varying intervals No P-waves, QRS complexes, or T-waves High rate Heart Block: Atrioventricular (AV) Block Three categories - First-degree heart block - Results from slow action potential conduction through AV node Second-degree heart block - Not all atrial impulses are conducted to the ventricles - Second-degree heart block is sub-divided - Wenckebach (Mobitz I) - Mobitz II Third-degree heart block - Commonly known as complete heart block - No atrial impulses conduct to the ventricles First-Degree Heart Block First-Degree Heart Block: ECG - P-R interval >0.20 seconds - P-R interval = 6 small boxes = 0.24 seconds = first-degree block Second-Degree Heart Block Also has changes in P-R interval ○ But starts to show failure as some P-waves not followed by a QRS complex Depolarization intermittently fails to reach ventricles Pattern of missed ventricular depolarizations, or blocked P-waves, is often very regular and described as a ratio of P-waves to QRS complex Way in which P-R interval changes in relation to blocked P-waves produces subclassifications of second-degree blocks, Mobitz I and II Wenckebach (Mobitz I) Wenckebach (Mobitz I): ECG P-R interval (shown with blue bars) progressively lengthens until a P-wave is missed (indicated by arrows) ○ Then goes back to its original length and starts increasing again Mobitz II Mobitz II has blocked P-waves as well, but P-R interval remains unchanged There is a widening of the QRS complexes that are generated Rarer and more serious condition ○ Usually involves problems with conduction system below AV node, most commonly in the bundle branches  Usually associated with progressive disease of heart’s conduction system ○ Normally leads to implantation of a permanent pacemaker Mobitz II: ECG Blocked P-waves indicated by arrows. Third-Degree Heart Block Complete heart block ○ No atrial impulses conducted to ventricles ○ To be compatible with life, AV node or ventricles must generate their own impulses No P-waves have associated QRS complexes ○ P-waves and QRS complexes are completely unrelated to each other ○ Termed “AV dissociation” Because of damage affecting AV node ○ Ischemia or disease (i.e. Lyme disease) Most worrying consequence is intermittent ventricular standstill ○ May cause dizziness or, if prolonged, loss of consciousness Depending on client’s presentation ○ Pacemaker may be implanted Complete Heart Block: ECG Three hallmarks: Atrial rate is faster than ventricular rate i.e. 80 bpm and 35 bpm respectively Ventricular rate is slow and regular No relationship between atrial and ventricular impulses ○ Atria contract completely independently of ventricles P-waves and QRS complexes indicated with arrows Heart Block: Summary First-degree Prolonged P-R interval (>0.20 seconds) Results from slow action potential conduction through AV node But all impulses get through! Second-degree Prolonged P-R interval (>0.20 seconds) Intermittently blocked P-waves Variable P-R interval (Mobitz I) or stable P-R interval (Mobitz II) Third-degree Complete heart block No atrial impulses conducted to ventricles  AV node or ventricles must generate their own impulses for survival Amiodarone Mechanisms of Action Blocks potassium + sodium ion channels, beta-adrenergic and calcium channel (latter decreases heart rate + resistance Indications Ventricular tachycardia, atrial dysrhythmias, PVC, atrial fibrillation/flutter Desired effects Normal heart rhythm, stable cardiac activity, increased VF threshold Adverse effects Pulmonary fibrosis, bradycardia, hypotension, QT prolongation, blue-grey skin, nausea, vomiting, photosensitivity, rashes, fatigue, thyroid disorders, liver toxicity, drug interactions Week 3 - Traumatic Brain Injury CEREBRAL HEMODYNAMICS & INCREASED INTRACRANIAL PRESSURE (ICP) Cerebral Hemodynamics Alterations in Cerebral Hemodynamics Increased ICP Normal is 1-15 mmHg or 5−15 mmHg Caused by ○ Edema- ○ Excessive cerebrospinal fluid- decreases first as a mechanism ○ Hemorrhage- increase blood to the area Occurs when one or more of the contents of the cranial vault—brain tissue, CSF, and blood—increases in volume Because cranial vault itself is a rigid, fixed compartment Stages of Increased ICP Stage 1 - no interventions, just monitor Stage 2 - start to have symptoms like confused but still somewhat stable Stage 3 - pressure is rising brain can herniate Stage 4 - ICP is worsening and potential loss of reflexes Manifestations of Increased ICP Therapeutic Management Goals for Individuals With Altered Cerebral Hemodynamics Use Your Clinical Judgment! A nurse recalls that increased intracranial pressure can occur because of: A) loss of cerebrospinal fluid B) increased cerebral activity- increase brain function C) Loss of cerebral function- patients that have demntia D) cerebral edema TRAUMATIC BRAIN INJURY (TBI) What is a TBI? Types of TBI Open (penetrating) trauma ○ Injury breaks the dura and exposes the cranial contents to the environment ○ Causes primarily focal injuries ○ Break in the skull Closed (blunt) trauma ○ Head strikes a hard surface, or a rapidly moving object strikes the head ○ Dura remains intact; brain tissues are not exposed to the environment  ○ Causes focal (local) or diffuse (general) brain injuries ○ More common than open trauma injuries ○ There is no penetration the brain will be intact if the skull is not fractured but just the brain experiencing trauma First…Some Terms! Classifications of Brain Injuries: Primary Brain Injuries Classifications of Brain Injuries: Secondary Brain Injuries Indirect result of primary brain injury, including trauma and stroke syndromes Contributing factors = systemic and cerebral processes Brain damage develops hours to days later  Brain hypoperfusion, ischemia Includes a cascade of cellular and molecular brain events and systemic responses Systemic processes Intracerebral processes Cellular processes Secondary Brain Injuries: Management Pathophysiology of Brain Injury PRIMARY BRAIN INJURY FOCAL BRAIN INJURY - Focal Brain Injury: Coup-Contrecoup Injury Coup injury ○ Injury at site of impact Contrecoup injury ○ Injury from brain rebounding and hitting opposite side of skull ○ Think of motorcycle accidents. ○ The brain rebounds Focal Brain Injury: Contusions Force of impact typically produces contusions Contusions ○ Blood leaks from an injured vessel (bruising of the brain) Manifestations: loss of consciousness (usually less than 5 minutes) Treatment: - control of intracranial pressure (ICP); possibly surgery The smaller the area of impact, the greater the severity of injury  Contusions can cause ○ Epidural (extradural) hematoma ○ Bleeding between the dura mater and the skull ○ Usually arterial and with a skull fracture Subdural hematoma ○ Blood between the dura mater and brain ○ Usually venous Intracerebral hematoma ○ Bleeding within the brain Focal Brain Injury: Epidural Hematoma Most commonly caused by motor vehicle accidents but also occasionally by falls and sporting accidents Temporal fossa is most common site ○ Caused by injury to middle meningeal artery or vein Clinical manifestations ○ LOC at the time of injury, followed by a lucid period that lasts from a few hours to a few days, and increasingly severe headaches, vomiting, drowsiness, confusion, seizure, and hemiparesis Treatment ○ Medical emergency! ○ Surgical evacuation of hematoma Focal Brain Injury: Subdural Hematoma Acute ○ Develops within hours ○ Is often located at the top of the skull ○ Expanding clots directly compress the brain Clinical manifestations ○ Begins with headache, drowsiness, restlessness or agitation, slowed cognition, and confusion Treatment ○ Burr hole to remove clot  Subacute ○ Develops after 48 hours to 2 weeks Chronic ○ Develops over weeks to months ○ Subdural space gradually fills with blood. Clinical manifestations ○ Approximately 80% complain of chronic headaches and have tenderness at the site of injury. Treatment ○ Craniotomy to evacuate the gelatinous blood ○ Percutaneous drainage Focal Brain Injury: Intracerebral Hematoma Hematoma acts as an expanding mass ○ Increased ICP and compression of brain tissues with resultant edema and ischemia Delayed: appears 3–10 days after injury Clinical manifestations ○ Decreasing level of consciousness Treatment ○ Reducing ICP; allowing the hematoma to reabsorb slowly ○ Surgery Use Your Clinical Judgment! An unconscious person is admitted to the hospital after a motorcycle accident. The client experienced a brief loss of consciousness at the scene followed by an awake, lucid period of 1 hour. The nurse suspects this client has a(n): A) subdural hematoma - DOES NOT HAPPEN IMMEDIATELY B) open penetrating trauma C) temporal extradural hematoma D) mild concussion- Doesn't always lead to loss of consciousness PRIMARY BRAIN INJURY DIFFUSE BRAIN INJURY Diffuse Brain Injury Diffuse Brain Injury: DAI AKA traumatic axonal injury or multifocal axonal injury ○ Involves widespread areas of brain ○ Occurs with all severities of brain injury Mechanical effects of high levels of acceleration and deceleration injury  ○ Whiplash, or rotational forces cause shearing and stretch of delicate axonal fibers and white matter tracts that project to or from cerebral cortex ○ Severity correlates with how much shearing force was applied If enough axons are harmed, ability of nerve cells to communicate with each other may be lost or greatly impaired ○ May have behavioral, cognitive, physical changes ○ Severe disabilities DAI generally not visible on CT imaging ○ But, may be seen as diffuse hemorrhages in areas where axons and small blood vessels are torn Axonal damage seen at postmortem with electron microscope DAI may induce long-term neurodegenerative processes ○ Changes may continue for years after injury Development of chronic traumatic encephalopathy (CTE) and Alzheimer disease–like pathologic changes Diffuse Brain Injury: Axial or Rotational Injury Diffuse Brain Injury: Subarachnoid Hemorrhage When vessel tears, blood is pumped into subarachnoid space ○ Escaped blood coats nerve roots, clogs arachnoid granulations impairing CSF reabsorption, and obstructs foramina (passages) within ventricular system impairing CSF circulation ○ Blood also produces inflammatory responses! Vasospasm with microthrombosis causes decreased cerebral perfusion with extension of ischemic injury ○ Delayed cerebral ischemia occurs in 3 to 14 days after hemorrhage in approximately 50% of cases and is significant cause of morbidity and mortality  Clinical manifestations ○ Leaking vessels Episodic headache, transient changes in mental status or LOC, N or V, focal neurologic defects including visual or speech disturbances Ruptured vessel ○ Sudden throbbing, “explosive” headache associated with N/V, visual disturbances, motor deficits, loss of consciousness Other findings ○ Meningeal irritation and inflammation, causing neck stiffness (nuchal rigidity), photophobia, blurred vision, irritability, restlessness, and low-grade fever ○ Positive Kernig sign and Brudzinski sign Hunt and Hess classification scale commonly used based on manifestations Diffuse Brain Injury: Concussion  Mildest form of TBI ○ Occurs when head injury causes sudden change in mental status Loss of consciousness lasting