PAT 401 Week 1-4 Cardiovascular Alterations PDF

PAT 401 Week 1: Cardiovascular Alterations TEST 1: KNOW THESE: Diff ecg interpretations, heart defects, pericardial effusion, complications and cardiac tamponade, (to drugs, know cause), anatomy of heart, pericarditis constrictive restrictive, MI, drugs, amniodarone, d...

PAT 401 Week 1: Cardiovascular Alterations TEST 1: KNOW THESE: Diff ecg interpretations, heart defects, pericardial effusion, complications and cardiac tamponade, (to drugs, know cause), anatomy of heart, pericarditis constrictive restrictive, MI, drugs, amniodarone, diff stenosis, congenital defects conditions more common in Down syndrome, cardiac drugs into abcds, furosemide, anti platelet anticoagulant, assessment and management priority assessment in cardiac pt, arterial & ductus arteriorsis, aortic regurgitation ecgs, subdural hematomas, Subarachnoid hemorrhages, icp understand this, compensatory measures, CSF, Venous blood, arterial blood know the hierarchy, typically know s/s at 20mmhg, GCS, coup,contrecoup,contusion vs concussion, diffuse focal injury, shutof of respiratory system when transfer of respiration what does it mean for someone to be brain dead, Acute Pericarditis Acute inflammation of pericardium Etiology - mostly idiopathic (autoimmune) or by viral infection Other causes MI, trauma, neoplasm, surgery, uremia, bacterial infection (TB), connective tissue disease or radiation therapy Pericardial membranes become inflammed and roughned Pericardial effusion may develop, can be serous, purulent or fibronous Symptoms - sudden onset severe chest pain (worsens with respiratory movements or recumbent position), fever, myalgias (muscle ache and pain), malaise, dysphagia Physical examination - low onset fever, sinus tachycardia, friction rub scratchy grady sound may be heard on auscultation (roughned pericardial membranes rubbing against each other) Diagnosis 2/4 needed - 1. Chest pain, 2. Pericardial rub, 3. ECG changes, 4. New or worsening pericardial effusion Treatment - rest, salicylates, NSAID: combined nonsteriodials and colchicine (prevents fibrosis) Constrictive Pericarditis - Chronic Fibrous scarring w/ occasional calcification of the pericardium causes the visceral and parietal layers to adhere obliterating the pericardial cavity Pericardium is thickened and encase heart in rigid shell CP compresses the heart impairing ventricular relaxation during diastole, reduces ventricular filling, reduces cardiac output onset of CP is gradual clinical manifestations develop slowly Clinical manifestations→ exercise intolerance, dyspnea on exertion, fatigue, anorexia Pain is also due to difficulty of expansion of heart ⅔ of indivdiuals present with heart failure Clinical assessment → edema, juglar vein distention, hepatic congestion Restricted ventricular filling may cause pericardial knock (lub knock), early diastolic sound White blood cells go up (inflammation marker), CRP increase, ESR increase Increase in cardiac markers tronopium Treatment → dietary sodium restriction, diuretics, antiinflammatory drugs, Unsuccessful treatment → surgical excision of restrictive pericaridum (pericardiectomy) Pericardial Effusion Accumulation of fluid in pericardial cavity, can occur in all forms of pericarditis Most are idiopathic (20%) , other causes neoplasm and infection Fluid maybe transudate - pass through a membrane or squeeze through tissue- such as serous effusion that develops with left heart failure Fluid is usually exudate - leaks out of blood vessels into tissues Fluid exudate indicates pericardial inflammation seen in acute pericarditis If fluid is serosanginoues - underlying cause likely TB, neoplasm, uremia or radiation Chyles leaks from thoracic duct, it may enter the pericardium leading to cholesterol pericarditis PE may create sufficient pressure to cause cardiac compression which is a serious condition known as tamonade If effusion develops gradually the pericaridm can stretch to accommodate large quantities of fluid without compressing the heart Fluid accumulates rapidly even small amount 50ml→ can cause serious tamponade Danger is pressure exreted by pericardial fluid will equal diastolic pressure and interfere with right atrial filling during diastole ○ Causes increased venous pressure ○ systemic venous confestion  ○ signs and symptoms of right heart failure (distentiosn of jugular veins, edema, hepatomegaly) ○ Decreased atrialfilling leads to decreased ventricular filling, decrease stroke volume and reduce cardiac output Symptoms of tamponade - dyspnea, tachycardia, jugular venous distention, cardiomegaly, pulsus paradoxus Pulsus paradoxus - arterial blood pressure during expiration exceeds arterial pressure during inspiration by more than 10mmHg Clinical finding reflects impairment of diastolic filling of the left ventricle plus reduction of blood volume within all four cardiac chambers Clinical manifestions of PE - ○ distant/muffled heart sounds, crackles ○ poorly palpable apical pulse ○ dyspnea on exertion ○ sharp pain in supine ○ dull chest pain in high fowlers (put pt in this position to reduce pain) ○ pitting edema ○ increased juglar venous pressure Chest x-ray, may have water bottle configuration of the cardiac silhouette Echocardiogram can detect effusion as small as 20mL, most accurate reliable method of diagnosis, CT or MRI used too Treatment → pericardiocentesis (aspiration of excesisve pericardial fluid) Disorders of the Myocardium: The Cardiomyopathies Cardio=heart, myo=muscle, pathy=disease Cardiomyopathies diverse group of diseases that affect myocardium Disease of heart muscle myocardium which inhibits effective pumping Less cardiac output = less O2 to the body Most are result of remodeling caused by effect of neurohumoral repsonses to ischemic heart disease or hypertension on heart muscles Cause is usually idiopathic Categorized as dialeted hypertrophic or restrictive based on tissues characteristics, genomics and hemodynamic effects Indivdiual may display characteristic of more than one type Pre load - stretching and filling - diastole Afterload - pressure to pump against - systole Dilated Cardiomyopathy Impaired systolic function leading to increases in intracardiac volume, ventricular dilation, heart failure with reduced ejection fraction Simplified Explanation: Distended muscle walls, the heart chambers are stretched far out, becoming thin, loosening the valves so they dont close all the way Weaker contraction not effective pump or systolic squeeze for BP, leads to bump failure or systolic heart failure blood doesnt go forward and backs up into the lungs and or body Blood backing up = Less blood being pumped out to body= less cardiac output-= less oxygen Can be associated wiht inherited disorders Causes→ ○ schemic heart disease ○ valvular disease ○ Diabetes ○ renal failure ○ alcohol or drug toxicity ○ Hyperthyroidism ○ Diabetes ○ deficiencies of naicin and vitamin D selenium infection Clinical Manifestations→ dyspnea, fatigue, pedal edema Examination→ displaced apical pulse, S3 gallop, peripheral edema, jugular venous distention, pulmonary congestion Diagnosis → confirmed by x-ray and echocardiogram Treatment→ ○ reducing blood volume ○ increasing contractility ○ reversing underlying disorder Hypertrophic Cardiomyopathy Refers to 2 major categories both are very different in etiology, pathophysiology, clinical presentation Big thick trophy like heart septum  Limits heart from filling 1. Hypertrophic obstructive cardiomyopathy a. Most common inherited heart defect associated with left ventricular hypertrophy b. characterized by thickening of the septal wall → causes outflow obstruction to the left ventricle outflow tract c. Obstruction of left ventricular outflow can occur when HR is increased and intravascular volume is decreased d. Simplified explanation: i. The thickened septum suddenly blocks all the oxygenated blood going out to body and happens when there's sudden straining such as exercise ii. Causes more bulging out of the heart muscles and obstructs aortic valve blocked oxygenated blood out the body e. Clinical manifestations→ asysmptoic usually no s/s, until strain i. Angina ii. Syncope (fainting) iii. Palpitations iv. Symptoms of MI v. Left heart failure vi. Sudden death f. Examination→ extra heart sounds, murmurs g. Diagnosis → echocardiography and MRI h. Treatment: i. Beta blockers - slow heart rate ii. ACE inhibitors - reverse hypertrophic changes iii. Surgical resection of hypertrophied myocardium iv. Prophylactic placement of an implantable cardioverter-defibrillator in high risk individuals - significantly decreases risk of arrhythmia related sudden death 2. Hypertensive or Valvular Hypertrophic Cardiomyopathy a. Occurs due to increased resistance to ventricular ejection b. Commonly seen in hypertension or in valvular stenosis (usually aortic) c. Hypertrophy of myocytes attempts to compensate for increased myocardial workload d. Clinical Manifestations i. Asymptomatic ii. Angina iii. Syncope  iv. Dyspnea on exertion v. Palpitations e. Examinations → extra heart sounds, murmurs f. Diagnosis → echocardiography, cardiac catheterization Restrictive Cardiomyopathy Characterized by ○ restrictive filling ○ reduced diastolic volume of either or both ventricles with normal or near normal systolic function ○ Wall thickness Can occur idiopathically or as cardiac manifestation of systemic diseases Myocardium becomes rigid and nonmpliant, impeding ventricular filling and raising filling pressures during diastole Simplified Explanation: Heart muscle is stiff and hard, ventricles dont stretch, blood can't get in = no refilling Clinical and hemodynamics picture mimics constrictive pericarditis Clinical Manifestations ○ Right heart failure with systemic venous congestion ○ Cardiomegaly, dysrhytmias are common Treatment → correct underlying cause, may require placement of ventricular assist devices Type of Cardiomyopathy Chart Pathophysiology Dilated HYPERtrophic Restrictive Associated Ischemic heart Untreated htn, Infiltrative disease conditions disease, alcoholism, inherited defect of pregnancy, infection, muscle growth and nutrtional deficiency, development exposure to toxins Alterations of Volume increased Volume decreased, Volume normal to chamber volume particularly in left decreased ventricle  Alterations of Compliance Compliance Compliance chamber compliance increased decreased decreased, particularly in left particularly in left ventricle ventricle Alterations of Contractility Contractility normal None myocardial decreased in left contractility ventricle Dysrhytmias Sinoatrial Atrial and ventricular tachydysrhythmias tachycardia, atrial dysrhythmias and ventricular dysrhythmias Eventual Left Heart failure Left Heart failure Right Heart failure Cardiovascular event Disorders of the Endocardium: Valvular Heart Disease Disorders of endocardium damage heart valves which are made of endocardial tissue Endocardial damage can be congenital or acquired Structural alterations of heart valves result from remodeling changes in the valvular extracellular matrix → leads to stenosis, regurgitation or both All 4 heart valves may be affected - mitral and aortic valves, tricuspid and pulmonic valves Normal valves maintain normal direction of blood flow through hearts chambers Abnormalities of valvular structure and or function can either be congenital or acquired Acquired → most common and most prevalent in elderly Acquired forms results from inflammatory, ischemic, traumatic, degenerative or infectious alterations of valvular structure and function Most common cause of acquired valvular dysfunction is degeneration or inflammation of the endocardium secondary to rheumatic heart disease congenital valvular defects → arise from disrupted heart development about 50% involves the valves Valves exposed to high blood flow and pressures - makes them particularly susceptible to other risk factors that promote valvular damage Risk Factors of Valvular Heart Disease Age Gender high in males  Tobacco use Hypercholesterolemia Rheumatic heart disease HTN Type 2 diabetes Pathophysiology Most common valvular disorderis calcification that comes with “wear and tear” and aging Presence of other factors such as hyperlipidemia, htn 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 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 fully opening 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 arrhythmias as calcium deposits impinge on atrioventrivular conduction system Valvular dysfunction Stimulates chamber dilation and or myocardial hypertrophy Both are compensatory mechanisms intended to increase the pumping capability of the heart Myocardial contractility is diminished, the ejection fraction is reduced, diastolic pressure increases and affected heart chamber fails from overload Manifestations of cardiac valve disease vary Depends on valve involved form of dysfunction and severity and rate of onset dysfunction Treatment→ careful fluid management, valvular repair or replacement with prosthetic valve, long term anticoagulation therapy and life long antibiotic prophylaxis before invasive procedures Valvular Stenosis: Valve is constricted and narrowed aortic or mitral Aortic Stenosis: Orifice of the aortic semilunar valve narrows causing diminished blood flow from left ventricle into aorta  Outflow obstruction increases pressure within the left ventricle as it tries to eject blood through the narrowed opening Left ventricular hypertrophy develops to compensate for increased workload Hypertrophy increase myocardial oxygen demand that the coronary arteries may not be able to supply Ischemia may cause attacks of angina AS develops gradually Clinical manifestations: due to decreased cardiac output ○ Angina ○ Syncope ○ Dyspnea ○ Heart failure Examination: Decreased stroke volume, reduced systolic pressure , narrowed pulse pressure ○ Slow HR, faint pulse Treatment: ○ Valve repair or replacement with prosthetic valve, followed with long term anticoagulation therapy ○ Transcather aortic valve implantation Mitral Stenosis: Impairment of blood flow from the left atrium to the left ventricle Most common cause: rheumatic heart disease Autoimmune activation of lymphocytes and macrophages leads to inflammatory damage and scarring of valve leaflets Scarring causes leaflets to become fibrous, fused and chordae becomes shortened Impedance of blood flow results in incomplete emptying of the left atrium and elevated atrial pressure as chamber tries to force blood through the stenotic valve Continued increases in left atrial volume and pressure cause chamber dilation and hypertrophy and eventually result in pulmonary hypertension Outcomes of untreated → pulmonary hypertension and right ventricular failure Clinical manifestations: depend of size of orifice ○ Symptoms of decrease cardiac output occur especially during exertion ○ Blood flow through stenoic valves rumbling decresecendo diastolic murmur heard ○ Mitral valve forced open during diastole makes sharp noise - opening snap ○ JVD, peripheral edema right heart failure also can occur  Treatment: ○ Surgical repair may require valve replacement Aortic Regurgitation Inability of aortic valve leaflets to close properly during ventricular diastole resulting from abnormalities of leaflets or aortic root Primary caused by congenital biscuspid valave disease or degeneration Secondary caused by htn, rheumatic heart disease, bacterial endocarditis, trauam, atherloscelrosis or idiopathic Hemodynamic reperucssions depend on size of leak Systole- blood is ejected from left ventrivle into aorta Diastole - blood flows back into left ventricle through leaking valve Volume overload occurs in ventricle - gets blood from left atrium and aorta during diastole End diastole volume of left ventricle increase, myocardial fibers stretch to accommodate extra fluid Compensatory dilation permits left ventricle to increase stroke volume and maintain cardiac output Ventricular hypertrophy occurs as adaptation to the increase volume and increased afterload created by high stroke volume and resultant systolic htn Eventually both stop compensating for aortic incompetence and heart failure happens Clinical manifestations: ○ Widened pulse pressure from increased stroke volume and diastolic backflow ○ Bounding peripheral pulse Treatments: ○ Valve replacement may be delayed for many years with use of vasodilators and inotropic agents Mitral Regurgitation Cause of 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 during ventricular systole Loud murmur is heard Volume of backflow reentering the left atrium increases leads to atrial dilation and fibrillation  Left atrial enlarges, valves stretch and become deformed = more backflow Increased volume in left atrium increases the colume that enters the ventricle = left ventricle dilated, hypertrophied to maintain cardiac output Left ventricle function becomes impaired to failure Right heart failure and pulmonary hypertension occur Clinical manifestations: caused by heart failure Treatment: ○ Surgical repair or valve replacement Tricuspid Regurgitation More common than tricuspid stenosis Associated with dilation and failure of the right ventricle secondary to pulmonary htn Rheumatic heart disease and infective endocarditis are less common causes Incompetence leads to volume overload in right atrium and ventricle, increased systemic venous blood pressure and right heart failure Pulmonic valve dysfunction can have same consequences as tricuspid valve dysfunction Mitral Valve Prolapse Syndrome Anterior and posterior cusps of mitral valve billow upwards (prolapse) into the left atrium during systole To maintain competency the mitral valve has to be supported by what is called mitral valve complex, any dysfunction of those elements can lead to prolapse of the valve Common cause = myxomatous degeneration if the leaflets in which the cusps are redundant, thickened and scalloped Clinical manifestations= asymptomatic Treatment = none or beta blockers Congenital Heart Disease Leading cause of death except for prematurity in first year of life Cause is known in only 10% of defects or cases Factors that Risk fetus of developing CHD are prenatal, environmental and genetic factors Maternall factors→ rubella, insulin dependent diabetes, alcoholism, illicit drug use, age (over 40), phenylketonuria (PKU) and hypercalcemia Chromosal aberrations Etiology of most CHD unknown Classification of CHD Based on blood flow pattern 1. Lesions increasing pulmonary blood flow a. Defects that shunt from high pressure left side to low pressure right side with pulmonary congestion - acyanotic 2. Lesions decreasing pulmonary blood flow a. Generally complex with right to left shunt and cyanosis - cyanotic 3. Obstructive lesions a. Right or left sided outflow tract obstructions that curtail or prohibit blood flow out of the heart - no shunting b. Right sided lesions = lead to hypoxia and cyanosis c. Left sided lesions = lead to HF 4. Mixing lesions a. Desaturated blood and saturated blood mix in the chambers or great arteries of the heart Classification: Acyanotic Heart Defects Shunting of blood flow from left to right Increases volume in right side of heart Increased blood flow into the pulmonary circulation Because blood continues to flow into systemic circulation there is no decrease in tissue oxyegenation or cyanosis Causes JVD, edema, heptameghaly, murmurs, crackles Classification: Cyanotic Heart Defects Shunting of blood flow right to left directlly into left side of heart Decrease blood flow through pulmonary system Causes less than normal oxygen delivery to tissues = cyanosis Increased Pulmonary Blood Flow Defects 1. Patent Ductus Arteriosus (PDA) - Acyanotic →PA Failure of the ductus arteriosus to close Normally closes within first few hours of birth Before birth PDA allows blood to shunt from pulmonary artery to aorta After birth when placenta is removed, lungs expanded the PDA will start to constrict (closes) Blood is going from left to right, increases pulmonary blood flow, increased pulmonary venous return to LA and LV and increased workload on left side This increases right ventricular pressure Clinical manifestations: ○ Continuous machinery type murmur ○ Boudning pulses ○ Active precordium ○ A thrill on palpation ○ s/s of pulmonary overcirculation ○ Small PDA = asymptomatic Treatment: ○ Surgical closure involving ligation by incision, catheter or video thorascopic therapy 2. Atrial Sepetal Defect Abnormal communication between atria Blood from left to right Three major types of defects: ○ 1. Ostium Primum defect An opening in the low septum may be associated with AV valve abnormalities especially mitral insufficiency ○ 2. Ostium Secundum defect Opening in center of septum the most common atrial defect ○ 3. Sinus Venosus defect Opening high up in the atrial septum near superior vena cava and RA junction Right atrial and ventricular enlargement develops Clinical manifestations: Mostly asymptomatic - diagnosis by auscultation of murmur Treatment: surgical closure before school age, after school age leads to →pulmonary htn, right ventricular hypertrophy, HF, atrial dysrhtymias, embolic events 3. Ventricular Sepetal Defect Abnormal communication between ventricles High pressure left side to low pressure right side When PVR is decreased after 1-2 week of life moderate sized - large VSD allow large amounts of shunting left to right Blood flows directly out the RV and into PA rather than staying in RV cavity PA, LA, and LV all enlarge, LV hypertrophy occurs to pump the additional volume Clinical manifestations: depends on age of child, size of defect, level of PVR ○ Newborns with small VSD= asymptomatic ○ Once PVR drops = murmur occurs ○ Large VSD= HF and poor weight gain Treatment: VSD close usually first year of life, minimal treatment to surgical repair 4. Atrioventricular Canal Defect Results from nonfusions of the endocardial cushions Causes abnormalities demonstrated in the atrial and ventricular septa and AV valves Three types: ○ 1. Complete AVC (CAVC) Consist of an inlet VSD, a primum ASD and defects in mitral + tricuspid valve Reflect the hemodynamics of ASD and VSD resulting biatrial and biventricular enlargement  ○ 2. Partial AVC (PAVC) Primumm type ASD and cleft in septal or anterior leaflet of mitral valve Mimics hemodynamics of secundum ASD ○ 3. Transitional AVC (TAVC) Involve partial fusion of the endocardial cushions = varibale AV valve abnormalities Left to right shunting occurs through the septal defects resulting in increased pulmonary blood flow and HF Clinical Manifestation: murmur, HF, respiratory tract infections Treatment: surgical complete repair between 3-6 months after birth to avoid pulmonary vascular changes Obstructive Defects Are conditions in which anatomic stenosis narrowing in either the right or left outflow tract obstructs blood flow and results in a pressure load on the affect ventricle 1. Coarctation of the Aorta Narrowing of the lumen of aorta that impedes blood flow 8% to 10% of defects Almost always juxtaductal position Can also occur anywhere between origin of aortic arch and bifurcation of the aorta in the lower abdomen About 50%-80% of individuals with COA have biscuspid aortic valve and may have associated VSD Can develop because of abnormal contractile ductal tissue that constricts at time of ductal closure In postductal COA, RV cannot pump enough blood through the ductus to descedning aorta because of pressure caused by narrow aorta Clinical Manifestations: ○ Newborns present with HF symptoms Once ductus closes, they will deteriorate rapidly from development of hypotension, acidiosis and shock ○ Older children Hypertension in upper extremities Decreased or absent pulses in lower extremities  Cool mottled skin Leg cramps during exercise Systolic ejection murmur Treatment: ○ Prostaglandin administration ○ Mechanical ventilation ○ Inotropic support ○ Maintain cardiac output ○ Surgery 2. Aortic Stenosis owing of the aortic outflow tract, 10% of defects Caused by malformation or fusion of the cusps Most common type of AS tends to be progressive and rare cases lead to sudden death from MI or low cardiac output Obstructions to blood flow out of the aorta, increased workload on LV, leads to LV hypertrophy, LV failure can develop, increased LA pressure and back up in the system, leading to pulmonary vascular congestion and pulmonary arterial hypertension Clinical manifestations: ○ Often asymptomatic ○ Signs if exercise intolerance may not appear until preadolsecne ○ Syncopal episodes, epigastric pain, extertional chest pain in severe forms ○ Murmur systolic ejection Treatment: ○ Commisurotomy ○ Aortic valvotomy ○ Ross procedure 3. Pulmonary Stenosis Narrowing of pulmonary outflow tract Abnomal thickening of the valve leaflets or narrowing of the arterial or ventricular side of the valve Pulmonary atresia is the severe form of PS, involves complete fusion of the commissures and narrowing of the main PA allowing no lblood flow out of the RV to the PA Pulmonary blood flow to lungs is now dependent on a PDA or extra blood vessels that arise from the aorta and connect to the pulmonary arteries with decompression of RV through ASD PS accounts for 8-12% of CHD  Clinical Manifestations: ○ Often asymptomatic ○ Murmur ○ Extertional dyspnea and fatiagbility ○ Fatigue ○ Thrill may be palpated ○ Cyanosis ○ HF Treatment: ○ Mild PA→ not treated, observed closely ○ Severe PA→ addressed immediately, balloon angioplasty, pulmonary valvotomy Decreased Pulmonary Blood Flow Defects Decreasing pulmonary blood flow involve obstruction from blood flow and septal communications RV outflow tract obstruction, right-sided pressures exceed left sided pressures - right to left shunting Children wil have hypoxemia and cyanosis 1. Tetralogy of Fallot Syndrome represented by four defects ○ 1. Large ventricular spetal defect ○ 2. Overriding aorta that straddles the VSD, ○ 3. Pulmonary stenosis ○ 4. RV hypertrophy Pulmonary stenosis decreases blood flow to the lungs and consequently the amount of oxygenate blood that returns to left heart Blood shunt from right to left through VSD, deoxygenanted blood mixes with ocygenated blood returning from lungs Result is low O2 sat (hypoxemia) Body attempts to comensate for chronic hypoxemia by producing more red blood cells Clinical manifestations: ○ If ductus closes cyanosis will happen ○ Hypoxia ○ Clubbing ○ Feeding difficulty ○ Dyspnea ○ Restlessness  ○ Squatting ○ Hypercyanotic spell or tet spell generally occurs with crying or exertion Treatment: ○ Correct surgically in early infancy before 1 year of age, placement of a shunt called Blalock-taussig shunt ○ transcatheter pulmonary valve replacement ○ Patch placement 2. Tricuspid Atresia Is imperforate tricuspid valve No communication between the right atrium and right ventricle Is a combo of defects - septal defect, hypoplastoc or absent right ventricle, enlarged mitral valve and left ventricle, pulmonic stenosis Maybe associated with transposition of great vessels Clinical manifestations: ○ Central cyanosis ○ Growth failure ○ Exertional dyspnea, tachypnea, hypoxemia ○ Long term effects - of hypoxemia - polycythemia and clubbing ○ Hepatomegaly Treatment: ○ Prostaglandin administration ○ Blalock-Taussing shunt placement ○ Rashkind procedures - balloon atrial septostomy ○ PA band placement ○ Closure of septal defects Mixing Defects Dependence on mixing of pulmonary and systemic circulations for survival during the postnatal period Mixing results in desaturated systemic blood flow and cyanosis Pulmonary congestion occurs because of preferential pulmonary blood flow because PVR is lower than SVR 1. Transposition of the Great Arteries Aorta arises from the right ventricle and the pulmonary artery rises from the left ventricle Results in two separate parallel circuits  ○ Unoxygenated blood continously circulates through systemic system ○ Oxyegnated blood continosuly circulates through the pulmonary circulation Extrauterine life require communication between the two circuits therefore this condition is not compatible with life Clinical Manifestations: ○ Cyanosis may be mild shortly after birth and worsen during first day ○ Hypoxemia cause metabolic acidosis ○ Tachycardia ○ Tachypnea Treatment: ○ Surgery to switch the arteries 2. Total Anomalous Pulmonary Venous Connection Pulmonary veins abnormally connect to the right side of the heart either directly or through one or more systemic veins that drain into the right atrium Can be obstructive or nonobstructive Hemodynamics of nonobstructive group involves the right atrium receiving oxyegnated blood that would normally flow into left atrium hemodynamics of osbtructive causes pulmonary venous hypertension because resistance cause by obstruction resulting in an elevation in pulmonary vascular and RV pressure Pulmonary edema occurs Clinical manifestations: ○ cyanosis caused by the mixing of the de and oxygenated blood ○ Obstructed TAPVC causes cyanosis and rapid deterioration needing immediate surgical correction or death occurs Treatment: ○ Obstructed lesions are repaired at the time of diagnosis ○ Unobstructed lesions are generally repaired during infancy ○ Surgery: anastomisis of the common pulmonary vein to the left atrium: closure of atrial septal defect 3. Truncus Arteriosus Failure of embryonic artery to divide into pulmonary artery and aorta Results in single vessel arising from both ventricles, providing blood flow to the pulmonary and systemic circulations Trunk straddles the VSD thats always present and has a single valve with 3 or 4 leaflets, may result in stenosis, regurgitation or both Four types:  ○ 1. Type I → most common- pulmonary artery arising from the truncus ○ 2. Type II → less common- pulmonary arteries arise form posterior aspect of truncus ○ 3. Type III → least common - Pulmonary arteries arise from lateral aspect of truncus ○ 4. Type IV → Pseudotruncus - severe form of tertalogy of fallot with bronchial arteries arising from descending aorta to supply lungs Clinical manifestations: ○ Mild to moderate cyanosis that worsens with activity ○ Harsh systolic Murmur Treatment: ○ Modified rastelli procedure involving VSD patch closure to divert the blood flow from the left ventrivle outflow tract into truncus ○ Correct pulmonary arteries 4. Hypoplastic Left Heart Syndrome Abnormal development of left sides cardiac structures Obstructs blood flow from left ventrivular outflow tract Underdevelopment of the left ventricle, aorta and aortic arch as well mitral atresia or stenosis Infants must have well functioning RV and presence of a PDA and atrial septal communication to survive High pressures cased by LV outflow tract obstruction saturated blood enters the LA and mixes with desaturated blood in the RA through an atrial septal communication Clincial manifestations: ○ As ductus closes, systemic perfusion is decreased resulting in hypoxemia, acidosis and shock ○ No heart murmur detected and second heart sound is lound and single because of aortic atresia Treatment: ○ Prostaglandin administration ○ Correction of acidosis ○ Inotropic support for adequate cardiac output ○ Ventilatory manipulation ○ Surgery ○ Cardiac transplantation Pharmacotherapy Overall Cardiovascular Pharmacological Goals 1. Treat symptoms 2. Decrease heart workload and oxygen demands 3. Improve oxygenation 4. Improve cardiac function 5. Reduce pain Drugs Prednisone Classification→ Synthetic Glucocorticoids Indications for use → anti-inflammatory, percarditis Mechanism of action → decreased vasodilation and permeability of capillaries as well as decreased leukoytes migration to sites of inflammation Desired effects → prevent inflammation, reduce risk of bronchospasm in patients with asthma or certain cancers, immunosuppressive at higher dose Adverse effects → cushing syndrome (long term), fluid retention NSAIDs Inhibit cyclooxygenase An enzyme responsible for formation of prostaglandins When cycloyxgenase is inhibited inflammation and pain are reduced USE: relieve mild to moderate pain, especially for pain associated with inflammation DESIRED EFFECTS: antipyretic, anti-inflammatory, analgesic Arachidonic Acid Pathway Arachidonic acid is relased from cell membrane phospholipids using phospholipase Its converted by enzymes within two different pathways 1. Leukotriene pathway → lipoxygenase enzyme (LOX) → leukotrienes → smooth muscle contraction, constricts pulmonary aorwyas (bronchoconstiriction), vasoconstriction, vascular permeability 2. Cyclooxygenase pathway → cyclooxyegnase enzymes (COX 1 and COX 2)--> can be expressed under normal conditions homeostasis or in response to triggering event ie injury → maintain organ function, protect gastric mucosa, mediate pain and inflammation, vasodilation/vasoconstriction, bronchoconstriction, platelet function Ibuprofen Classification→ NSAID Indications for use → relieve mild to moderate pain, fever and inflammation Mechanism of action → inhibition of prostaglandin sysnthesis Desired effects → reduction of pain, temp and inflammation Adverse effects → nausea, heart burn, epigastric pain, dizziness, GI ulceration with occult or gross bleeding Acetaminophen Classification→ Non opioid analgesic Indications for use → treat fever, relief of mild to moderate pain Mechanism of action → inhibits synthesis of prostaglandins in CNS, direct action at level of hypothalamus and causes dilation of peripheral blood vessels, enabling sweating and dissipation of heart Desired effects → reduces fever and pain Adverse effects → very rare at therapeutic doses - inhibits warfarin metabolism, causing warfarin to accumulate to toxic levels, high doses or long term use may result in elevated warfarin levels and bleeding, acute toxicity - nausea vomiting chills abdominal discomfort Diuretics Hydrochlorothiazide Classification→ thiazide diuretic Indications for use → HF, HTN, edema Mechanism of action → reduces Na and Cl reabsorption by inhibiting Na/Cl symporter, reducing water reabsorption in nephron distal convoluted tubule Desired effects → promotes diuresis → decreases preload, decreases BP Adverse effects → hypotension, orthostatic hypotension, dizziness, H/A, electrolyte imbalances, hypokalemia (dysrhtymias), hyponatremia, hypercalcemia Furosemide Classification→ loop diuretic Indications for use → treat acute edema associated with liver cirrhosis, CKD, HF, pericaridal effusion, HTN Mechanism of action → blocks Na, K, Cl symporter in ascending limp of loop of Henle- increase urinary secretion of the Na, K, Cl, hydrogen ions / region of nephron that normally filters buld of sodium causes +++ diuresis Desired effects → removes large amounts of fluid in short time, decreases preolaod and BP Adverse effects→ hypovolemia (orthostatic hypotension, syncope), electrolyte imbalances, tachycardia, dysrhtmias, N/V, hypkalemia and metabolic alkalosis Spironolactone Classification→ mineralocorticoid receptor antagonists Indications for use → severe stages of HF, liver disease (aldersterone not metabolized) Mechanism of action → blocks aldorestone receptors (distal convoluted tubles and collecting ducts), blocks Na reabsorption Desired effects → Na and H2O excretion is increase, decreases cardiac preload, decreases morbidity and mortality rates in severe HF when added to standard therapy Adverse effects → hyperkalemia (K+ sparing diuretic, Na is lost K is retained), muscles weakness, ventricular tachycardia, fibrillation Lisinopril - caution with concurrent use of K+ sparing diuretics Classification→ ACE inhibitor Indications for use →HF, HTN Mechanism of action → inhibits angiotensin converting enzyme (ACE), angiotensiin cannot be converted to angiotensin II Desired effects → enhanced excretion of Na and h2O (decreases blood volume), decreases BP (afterload) and increases CO, dilation of veins returning blood to heart, decreases preload and reduces peripheral edema Adverse effects → hyperkalemia, hypotension, H/A, dizziness, cough Propranolol Classification→ non selective beta-adrenergic blockers Indications for use →HTN, angina, prevent MI  Mechanism of action → affects beta 1 recpetors in heart and beta 2 receptors in pulmonary and vascular smooth muscle Desired effects → reduces HR, slows conduction velocity, lowers BP, very effective for tachycardia caused by excessive sympathetic stimulation Adverse effects → bradycardia, hypotension, fatigue Contraindications→ clients with asthma - can cause bronchospasms DONT SUDDENLY STOP THIS DRUG Warfarin Classification→ anticoagulant Indications for use →prophylaxis of thromboembolic events (DVT, PE, AF), arterial thromboembolism (prevention of CVA/MI), valvular dysfunction (long term anticogulation) Mechanism of action → inhibits action of vitamin K, without adequate vitamin K, synthesis of clotting factors II, VII, IX, X is diminished, decreases production of clotting factors including thrombin Desired effects → prevents intravascular clots/ thrombosis Adverse effects → abnormal bleeding Recall→ anticoagulant activity of warfarin take several days to reach its max effect, this iswhy heparin and warfarin therapy are overlapped Dietary Requirements: Warfarin maintennace dose can fluctuate significantly Depends on amount of vitamin K in diet Do not need to avoid but need to be consistent with diet of leafy greens veggies once warfarin maintenance dose established Ex→ kale, swiss chard, spinach, collard greens Food high in vitamin K may lower warfarin ability to prevent clots Monitor PT/INR regularly - measures how long it takes blood to clot Antidote for Warfarin Therapy: VITAMIN K Reverses anticoagulant activity of warfarin Vitamin k is essential for synthesis of blood coagualtion Indications for use → whenPT/INR indicates blood taking too long to clot Mechanism of action → vitamin k ovverides mechanism by which warfarin inhibits production of vitamin K dependent clotting factors Desired effects → effective blood clotting  Adverse effects → vitamin K is relatively nontoxic and causes minimal adverse effects, may have hypersensitivity reactions Week 2: ECG Interpretations 5 Phases of the Cardiac Cycle 1. Atrial systole Atria contracts, pushing blood through the open tricuspid and mitral valves into ventricles Semilunar valves are closed 2. Beginning of ventricular systole Ventricles contract, increasing pressure within the ventricles The tricuspid and mitral valves close causing first heart sound S1 3. Period of rising pressure Semilunar valves open when pressure in the ventricle exceeds that in arteries Blood spurts into the aorta and pulmonary arteries 4. Beginning of ventricular diastole Pressure in the relaxing ventricles drops below that in arteries Semilunar valves snap shut causing second heart sound 5. Period of falling pressure Blood flows from veins into relaxed atria Tricuspid and mitral valavesd open when pressure in the ventricles falls below that in the atria Conduction System of the Heart Electrical impulses normally arise in the sinoatrial (SA) node the usual pacemaker of the heart SA node located at junction of right atrium and superior vena cava, above triscupid valve SA node 1mm beneath visceral pericardium therefore vulnerable to injury and disease → especially pericardial inflammation SA node hevaily innervated by both sympathetic and parasympathetic nerve fibers Resting adult SA node generates 60 to 100 action potentials per min depending on age and physical condition Each action potential travels rapidly from cell to cell through the atrial myocardium onwards to atrioventricular node (AV node)--> both atria to contract, begins sytole AV node conducts action potentials to ventricles From AV node conducting fibers converge to form the bundle of his (atrioventricular bundle) within the posterior border of the interventricular septum Bundle of his then gives rise to the right and left bundle branches Left anterior bundle branch (LABB) passes left anterior papillary muscle and the base of the left ventricle and crosses the aortic outflow tract Left posterior bundle branch spreads diffusely through posterior inferior left ventricular wall Terminal branches of the RBB and LBB are the Purkinje Fibers (PF) RBB , LBB activate septum  Rapid spread of the impulse to ventricular apexes is accomplished from extensive network of PF Last to be activated are basal and posterior portion of the ventricles Normal Electrocardiogram P wave = atrial depolarization PR interval = measure of time from onset of atrial activation to onset of ventricular activation, normal 0.12-0.20 sec QRS complex= sum of all ventricular muscle cell depolarization, normally 0.06-0.10 sec T wave= The repolarization of the ventricles following contraction ST interval= entire ventricular myocardium is depolarized QT interval= electrical systoleof ventricles, lasts 0.4 sec, varies inversely with HR Electrocardiogram (ECG) and Cardiac Electrical Activity Electrocardiography, 12-lead ECGs gives information about HR and rhythm Serial 12 lead establishes the presences of myocardial ischemia, infarction, conduction defects, dysrhythmias Holter monitoring Anatomy of ECG Basic ECG Interpretation 1. ECG rate (6 second strip method, big box method, small method) a. Count number of QRS complexes in a 6 second strip x 10 2. RR intervals - are they regular? 3. Is there a P wave for every QRS complex, Is there a QRS complex for every P wave? a. The ratio of P waves to QRS complexes should be 1:1 in a normal rhythm 4. Do the P waves come at consistent intervals or march out? The QRS complexes? a. March out means they all occur at consistent, regular intervals 5. Is QRS complex wide or narrow? a. Normal QRS complex is 0.12 secs or less, which is referred to as a narrow complex b. Wide QRS is considered anything above 0.12 secs P wave is the first thing tells you is a sinus rhythm Normal Sinus Rhythm Normal heart rhythm is sinus rhythm Recognized on ECG by regular P waves Rate between 60-100 bpm With every P wave followed by a QRS complex preceded by P-wave  Depolarization and repolarization of the atria and ventricles show as a 3 distinct waves/deflections (P, QRS, T) on ECG Acute Coronary Syndromes (ACS) Unstable angina NSTEMI STEMI Types of Myocardial Ischemia and Infarction Degree of occlusion caused by plague and oxygen demand of myocaridum determine degree of ischemia that can develop Arterial occlusion tends not to be a significant factor until the lumen is occuled by about 70 percent Vascular occlusion may also be masked by formation of anastomes Rupture of plaque and formation of a thrombus can drastically and quickly reduce lumen and blood flow Degree and duration of ischemia determine type of ACS that occurs and the clinical impact Mild or brief ischemia can lead to angina When ischemia is prolonged then MI becomes more likely Significant chnages in ECG and release of cardiac enzymes are seen 1. Sudden coronary obstruction caused by thrombus formation over ruptured atherosclerotic unstable plaque → ACS results 2. Plaque progression, disruption and subsequent clot formation 3. ACS → Unstable angina or MI (STEMI and Non-STEMI)  4. Common complications→ arrythmias/dysrhythmias, heart failure, pericarditis, aneurysm, rupture of wall or septae of infarcted ventricle, systemic arterial thromboembolism, pulmonary thromboembolisim, sudden cardiac death A = unstable angina w/ zone of ischemia, dotted area = the ischemia, if ischemia prolongs than the inside cells will die first cuz it’s farthest from blood vessel B= MI, tissue death happening its partial and not full C= no blood and oxygen entering, complete blockage Unstable Angina (UA) Form of ACS Transient episodes of thrombotic vessel occlusion and vasoconstriction at site of plaque damage Sign if impending infarction = EMERGENCY UA is first step in progressive spectrum of ischemia related myocardial injury Now grouped under classification of Non-STEMI ECG Presentation: ○ Commonly shows ST segment depression and T wave inversion Diagnostics : ECG Affected area can be identified on 12-lead ECG ○ UA ○ Non-STEMI ○ STEMI ECG changes depend on ○ Duration of ischemic event (acute vs evolving) ○ Extent → partial/subendocardial vs full wall thikness/transmural  ○ Location Types of MI and ECG Presentations 1. Subendocardial Infarction a. If thrombus disintegrates before complete distal tissue necrosis has occurred b. Infarction will involve only the myocardium directly beneath endocardium i. Partial wall thickness damage c. Present with ST segment depression and T wave inversion without ST elevation on ECG i. Non ST-Segment Elevation MI (Non- STEMI) 2. Transmural Infarction a. If thrombus lodges permanently in vessel, infarction will extend through myocardium all the way from endocardium to epicardium i. Full thickness damage ii. Presents with ST segment elevation on ECG iii. ST-Segment Elevation MI (STEMI) Clients with STEMI at highest risk for serious complications Needs definitive intervention without delay Non- STEMI: ST- segment depression and Twave inversion indicative of partial wall thickness (subendocardial) damage ○ Depression of ST segment has to be 3 small squares or more below baseline STEMI: ST- segment elevation indicative of full myocardial wall thickness (transmural) damage ○ Elevation had to be 4 small squares or more up Arrhythmias/Dysrhythmias 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 Atrial Fibrillation Most common cardiac arrhythmia Caused by rapidly firing potentials in atrial myocardium ○ Aberrant depolarizations often result of myocardial remodeling Causes HTN, valvular and ischemic heart disease (mitral valve, coronary artery disease, MI or pericarditis), genetics, lung conditions (COPD) 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 Fibrillatory waves are indicated by arrows Quivering of atria → blood in atria is being pooled leading to formation of blood clots, can travel to brain causing stroke Afib pts are given blood thinners Pts usually on a pacemaker since there is no full contraction of the heart SUMMARY: No visible P-WAVES - atria is quivering Irregularly irregular QRS complexes High ventricular rate → frequent pr wave leads to frequent ventricular rate Atrial fibrillatory waves Atrial Flutter Atria contracts very rapidly - usually 300 times a minute Recognized by SAWTOOTH pattern  There are abnormal P-waves, presentation is regular Causes: heart valve problems (tricuspid or mitral valve), MI, heart surgery, overactive thyroid Not all atrial impulses conduct to ventricles (1 in 4 impulses) ○ Ventricular rate less than atrial rate approx 70bpm (280bpm/4=70bpm) ○ Important NOT to assume basis of normal heart rate that this must be sinus rhythm New onset is often associated with with HR of 150bpm when 1 in 2 atrial impulses conducted to ventricles ○ Useful tip is to suspect atrial flutter i anyone with resting HR of 150bpm (ventricular rhythm→ 300bpm/2=150 bpm) ○ Once atrial flutter is suspected, flutter waves can often be identified SUMMARY: SAWTOOTH atrial pattern Regular atrial activity Variable ventricular response Premature Atrial Contractions Generated by a depolarization instigated outside of SA node Produces premature P-wave Premature P-wave is a different shape from normal P-wave of sinus node origin Early P-wave is usally followed by QRS complex, after which there is a short pause before the next sinus beat appears In this case, premature P-wave is superimposed on the t-wave of previous beat Premature atrial contractions are considered benign and rarely need treatment SUMMARY: Extra P-wave with abnormal morphology - P-wave appears earlier than normal Compensatory pause leading to atrial bigeminy (complexes appear to be in pairs) Premature Ventricular Contractions Originates in ventricles Occurs when a focus in the ventricle generates an action potentialbefore the pacemaker cells in SA node depolarize ○ Results in ventricular beat not preceded by a premature P-wave and QRS is broad and bizarre A compensatory pause follows the premature ventricular contarction as the unscheduled depolarization puts the ventricular myocardium into refractory state ○ Forces to skip a beat Common and often occur in healthy individuals More common in people with heart disease SUMMARY: Out of step with normal R-R Wider complex Followed by compensatory pause Ventricular Tachycardia Originates in ventricles and is recognized on ECG by a regular rhythm ○ broad and bizarre QRS complex ○ not preceded by P-waves ○ No T-waves or PR interval Electrical conduction system is sending abnormal electrical signical causes ventricles to contract rapidly Fast rhythm between 120-250bpm With disorganized contractility and reduced filling time, vtach can lead to hemodynamic instability and severe hypotension Problem with output and filling heart Potentially lifethreatning arrhythmia Needs to be identified, dealt with quickly - EMERGENCY Can progress to ventricular fibrillation Most common in pt with significant structural heart disease Usually unconscious because they are dead Can be monomorphic or polymorphic ○ QRS complexes in monomorphic vtach Have same shape and are symmetrical because they start in samee place in myocardium Looks the same throughout ○ Polymorphic ventricular tachycardia Has variable QRS shape because depolarizations are instigated at multiple points Rhythm does NOT look the same throughout *HR is high, at 90bpm, no p-wave, wide waves SUMMARY: Ventricular rate>100 bpm QRS complex not associated with P-wave Wide QRS complex morphology Nursing Implications → CALL CODE BLUE, need crash cart and debrillator, CPR or epinephrine Ventricular Fibrilliation Occurs when ventricular rate exceeds 400 bpm Disorganzied and uncoordinated contraction of myocardium causes cardiac output to fall to catastrophic levels ○ Rates of survival for out of hospital vfib are low Electrical conduction system is sending abnormal electrical signical causes ventricles to QUIVER rapidly Coronary artery disease and resultant myocardial ischemia or tissue scarring are most common causes ○ Tissue damage allows formation of reentry patterns that cause chaotic ventricular depolarization ○ These re-enrty patterns break up into multiple smaller wavelets that accuse high frequency activation of the myocytes ECG shows → NO RECOGNIZABLE P-WAVES OR QRS COMPLEXES Nursing Implications → CALL CODE BLUE, need crash cart and debrillator, CPR or epinephrine, give amiodorone SUMMARY: Chaotic, irregular and varying intervals No P-waves, QRS complexes but wide or T-waves High rate Deadly rhythm can die in minutes No cardiac output, leads to flat line pt is dead Heart Block: Atrioventricular (AV) Block Three categories 1. FIRST degree heart block ○ Results from slow action potential conduction through AV node 2. SECOND degree ○ Not all atrial impulses are conducted to the ventricles ○ Subdivided into Wenckebach (Mobitz I) and Mobitz II 3. THIRD degree ○ Known as complete heart block ○ No atrial impulses conduct to the ventricles First Degree Heart Block: Mostly asymptomatic, does not require any treatment ○ Long term monitoring for worsening conduction is advisable Results from slow action potential conduction through AV node SIMPLE TERMS – electrical signals are moving slowly through the AV node that's why the PR interval is LONG ○ Slowing can be due to changes in vagal tone or structural changes associated with damage or disease affecting conductive tissue of atria, AV node (most common), bundle of HIS or bundle branches and Purkinje system  Defined by prolong PR interval ○ Takes longer for action potential to reach ventricles so P and R appear further apart → EXCEEDS 0.20 secs (5 small boxes) Each P-wave is accompanied by QRS complex - all impulses get through Image below PR interval = 6 small boxes= 0.24 second = first degree block Only difference between normal sinus rhythm and first degree heart block is the PROLONGED PR INTERVAL Second Degree Heart Block: Has changes in PR interval Starts to show failure as some P-waves not followed by QRS complex  ○ Depolarization intermittently fails to reach ventricles Pattern of missed ventricular depolarization or blocked P-waves, is often very regular and described as ratio of P-waves to QRS complex Way in which PR interval changes in relation to blocked P-waves produces subclassifications of second-degree blocks, Mobitx I and II Wenkeback (Mobitz I) 1. PR interval increases beat to beat until → P-wave is not followed by QRS, results in a pause 2. After pause PR interval returns to normal, them starts increasing again in successive beats 3. PR is longest before dropped QRS complex and shortest immediately after → sequence typically repeats 4. Often a benign finding and may be due to hgh vagal tone → But maybe associated with symptoms of possible cardiac origin PR interval progressively lengthens until is missed (shown in arrows), than goes back to its original length and starts increasing again Treatment: No symptoms - continue to monitor Stop meds that slow AV conduction system→ calcium channel blockers, beta blockers, digoxin  Assess PT for MI Presenting with low cardiac output symptoms → CALL CODE BLUE Mobitz II Has blocked P waves as well but PR interval stays constant during the rhythm remains unchanged Widening of QRS complexes that are generated Rarer and more serious condition Usually involves problems with conduction system below AV node, most commonly in bundle branches Associated with progressive disease of hearts conduction system ○ Can lead to implantation of permanent pacemaker Blocked P-waves indicated by arrows Considered worse than type 1, ventricular rate is slower, lowering cardiac output, symptoms more likely to be present Treatment: Assess pt for symptoms of low cardiac output Temporary pacing given  Permanent pacemaker 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 (BOTH DOING THERE OWN THING) ○ Termed AV DISSOCIATION Cause due to damage affecting AV node ○ Ischemia or disease (Lyme disease) Most worrying consquence is intermittent ventricular standstill ○ May cause dizziness or is prolonged loss of consciousness Depending on clients presentation ○ Pacemaker maybe implanted Three hallmarks: ○ 1. Atrial rate is faster than ventricular rate - 80bpm and 35 bpm respectively - more P-waves and few QRS complexes thats why atrial is faster and ventricular is slower ○ 2. Ventricular rate is slow and regular ○ 3. No relationship b/w atrial and ventricular impulses - atria contract completely independently of ventricles P-waves and QRS complexes indicated with arrows  Symptoms will likely to be present Low cardiac output- low BP, weak pulse, mental status changes, pale clammy skin → EMERGENCY ACTIVATE CODE BLUE Treatment: Permanent pacemaker SUMMARY Heart Blocks: 1. First degree a. Prolonged PR interval (>0.20 secs) b. Results from slow action potential conduction through AV node c. All impulses get through 2. Second degree a. Prolonged PR interval >0.20 secs b. Intermittently blocked P-waves c. Variable PR interval (Mobitz I) or stable PR interval (Mobitz II) 3. Third degree a. Complete heart block b. No atrial impulses conducted to ventricles c. AV node or ventricle must generate their own impulses for survival Medications: Amiodarone Classification→ anti-arrhythmic Indications** for use →Vtach, atrial dysrhytmias, PVC, Afib and Aflutter - treats these ventricular arrhythmias Mechanism of action → blocks potassium and sodium ion channels, beta-adrenergic and calcium channel (latter decreases HR and resistance) ○ Blocks potassium channels on the heart → makes heart take longer to reset (repolarization), this slows down HR and breaks electrical circuit that causes arrhythmia Desired effects → normal heart rhythm, stable cardiac activity, increase VF threshold Adverse effects → ○ Pulmonary fibrosis**(scarring of the lungs, makes it difficult to breathe) ○ Bradycardia, ○ hypotension ○ QT prolongation → causes T wave indicates repolarization and amiodarone blocks potassium channels, so heart takes longer to repolarize causing QT interval prolongation ○ blue grey skin, N/V, photosensitivity, rashes, fatigue, ○ thyroid disorders → hyperthyroidism- high iodine content in amiodarone accuses reduced thyroid function ○ liver toxicity ○ drug interaction  NOTE: dont give if they are addicted to alcohol or have thyroid conditions Can be ordered to bring down HR even if BP is normal **Potassium channel blocker, need potassium to leave for depolarization. Delaying conduction of heart chambers Need to understand why potassium channels are needed to target which types of arrhythmias Week 3: Brain Injury Hemodynamics→ how blood flows through your blood vessels Cerebral Hemodynamic Cerebral blood flow (CBF) to brain Normally maintained at a rate that matches local metabolic needs of the brain CBF to gray matter is about 3-4 times greater than that to white matter because of increased metabolic activity **Cerebral perfusion pressure (CPP) → 70 - 90 mmHfg Pressure required to perfuse cells of brain Pressure that pushes blood to brain hence influences cerebral blood flow CBF Cerebral blood volume (CBV) Amount of blood in intracranial vault at a given time Cerebral blood oxygenation (CBO) Measured by oxygen saturation in internal jugular vein Alterations in Cerebral Hemodynamics Features of cerebral hemodynamic injury ○ Alterations in cerebral blood flow, intracranial pressure and oxygen delivery Goal of hemodynamics ○ To balance intracranial pressure with internal jugular vein oxygen saturation Alterations in cerebral hemodynamics ○ Increased ICP ○ Cerebral Edema Increased ICP Normal is 1-15mmHG or 5-15 mmHg Caused by:  ○ Edema ○ Excessive cerebrospinal fluid (CSF) ○ Hemorrhage 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 SIMPLE TERMS→ The 3 structures that can alter ICP - BRAIN, CSF and BLOOD Medical Emergency Stages of Increased ICP Stage 1 - Vasoconstriction (compression of the vessels to deliver less volume)and external compression → trying to compress size of everything to fit in brain Stage 2 - Compromised neuronal oxygenation; systemic arterial vasonconstriction occurs → signs of ischemia Stage 3 - Brain hypoxia and hypercapnia; autoregulation lost → Hypercapnia - accumulation of CO2 cause vessels are compressed, less oxygen is being delivered to brain → Autoregulation - natural regulation when O2 and CO2 levels change, brain can't change vessel diameter cause of ICP Stage 4 - Brain herniates; several herniation syndromes Manifestations of Increased ICP Vital sign is last to be affect **important for test  Therapeutic Management Goals for Indivdiuals with Altered Cerebral Hemodynamics Central Perfusion Pressure → >70mmHg Intracranial Pressure →