Cardiology Part 2 Week 12 Lecture Notes PDF

Summary

This document provides lecture notes on various cardiovascular topics, including details on abdominal aortic aneurysm (AAA), carotid artery disease (CAD), and congenital heart diseases. It discusses risk factors, clinical presentations, diagnoses, and management approaches for each condition.

Full Transcript

Week 12 -- Cardiology Part 2 Lecture Notes **[Abdominal Aortic Aneurysm (AAA)]** - Abdominal Aortic Aneurysm - AAA is abd aortic dilation of 3 cm or greater - Abd aortic dilation is a normal part of aging of about 2 cm - 2 types of aneurysm (true vs false) - True: Inv...

Week 12 -- Cardiology Part 2 Lecture Notes **[Abdominal Aortic Aneurysm (AAA)]** - Abdominal Aortic Aneurysm - AAA is abd aortic dilation of 3 cm or greater - Abd aortic dilation is a normal part of aging of about 2 cm - 2 types of aneurysm (true vs false) - True: Involves all three vessel wall layers, AAA most common true aneurysm - False: (pseudoaneurysm) occurs when intimal and medial layers are disrupted usually due to trauma and or infection - Risk factors for AAA - Atherosclerosis - Cerebrovascular disease - First degree relative with AAA - Hx of other vascular aneurysms - HTN - HLD - Obesity - Old age - Tobacco Use - Clinical presentation and physical exam findings for AAA - Classic triad of ruptured AAA -- hypotension, pulsatile abd pain, abd/back pain - MEDICAL EMERGENCY - Physical exam is only moderately sensitive - Most common finding is pulsatile mass above umbilicus - Abd auscultation may reveal bruit - Dx usually incidental based on imaging studies - Screening for AAA - US has high sensitivity and specificity - Cost affective and no harms associated with US - Screening recommendations - One time screening is recommended for - Men age 65-75 who have smoked - Men age 65-75 who are non smokers but have first degree relative who have required repair of AAA or died from AAA - AAA = usually silent disease process so screening can be beneficial to cath them early - If you have found an aneurysm you will need surveillance q 6 months to 3 years depending on size - If you are caring for a patient and find an aneurysm, recc refer to vascular surgeon to manage - Things impacting AAA rupture - Size \> 6.0 cm - Rapid expansion (\>0.5 cm/year) - Female gender - Smokers - COPD - Family hx of AAA - Asymmetric AAA - Clinical management of AAA - Smoking cessation - Associated w/ 0.35 mm/year growth of aneurysm - Treatment of risk factors (HTN, HLD, DM) - Increase exercise - Several medications have been studies but no pharmacologic therapies aimed at limiting AAA expansion and rupture have been proven - Surgical management of AAA - Elective surgical repair - Goal is to prevent rupture - High risk surgery - 5.5 cm is size threshold for repair in average patient - Women 4.5-5 - Have higher risk of rupture at smaller sizes of aneurysm - Repair can be open or endovascular (75% of surgeries) **[Carotid Artery Disease (CAD) ]** Definition -- Atherosclerotic narrowing of the internal carotid arteries 60-99%\... most often occurring at a bifurcation 2 carotid arteries (internal and external) - Internal feeds brain - External brings blood to structures outside the skull including face CAD can be associated w/ symptoms depending on ipsilateral stenosis or bilateral stenosis (increased risk for ischemic stroke originating in the carotid artery) Risk factors - Modifiable - HTN - Smoking - HLD - DM - Elevated homocysteine levels - Obesity - Nutrition - Physical inactivity - CKD - Non-Modifiable - Age - Gender - Race - Ethnic background Carotid Artery Disease -- Physical Exam - Complete cardiac and neurological evaluation - Palpation of all bilateral peripheral pulses - Auscultation for bruits - Carotid artery bruit = marker for generalized atherosclerosis produced by turbulent blood flow - Does not rule out possibility of carotid artery disease because you can't hear a bruit - Neuro exam - Mental status - CN with fundoscopic evaluation - Assessment for amaurosis fugax - Motor and sensory function Carotid Artery Disease -- Diagnostics - Catheter based angiography (gold standard) for diagnosis of the degree and characteristics of plaque formation in carotid artery stenosis - US - Primary diagnostic tool due to cost and high specificity/sensitivity - MRI - CT angiography Carotid Artery Disease -- Management - Medical therapy - Aggressive management of risk factors (the non-modifiable as discussed) - Statin therapy and antiplatelet therapy - Carotid revascularization - Endarterectomy - Recc for pt w/ high grade lesions (\>75%) and life expectancy of at least 5 years - Usually performed in conjunction w/ medical therapies - Management = done in conjunction w/ subspecialty (neurology and gen surg) - Pt education for lifestyle management **[Congenital Heart Disease -- PEDIATRICS ]** - Pathophysiology - Alteration in the development of or failure of embryonic heart to progress beyond an early developmental stage - Alteration usually in 2^nd^-8^th^ week of gestation - Most cases have no identifiable cause - 2%-4% caused by teratogens, maternal conditions, or environmental influences - Drugs or teratogens include Lithium, retinoic acid, antiepileptics, ibuprofen, naproxen, ACEI, TCA, tobacco, EOTH, cocaine - Environmental -- pesticides, air pollution - Maternal conditions: DM, connective tissue disorders, rubella, febrile illness (influenza) - Can be genetic cause - Can occur with other anomalies (trisomy disorders) - Initial evaluation of congenital heart disease - Congenital defects can be divided into two major groups - Presence of or absence of cyanosis - Further divided according to whether the chest radiograph shows evidence of pulmonary vascular markings - Increased - Normal - Decreased - EKG - Can be used to determine if right/left/or biventricular hypertrophy exists - Physical exam -- further used to narrow ddx - Character of heart sounds - Presence and character of any murmurs - Types of congenital heart diseases (discussing 5) - Atrial septal defect (ASD) - Ventricular septal defect (VSD) - Patent ductus arteriosus (PDA) - Coarctation of Aorta - Tetralogy of Fallot (TOF) KNOW THIS IMAGE -- MEMORIZE = EXAM QUESTIONS R/2 IT 1\. **[ASD (atrial septal defect)]** - Defect (hole) in the atrial septum - LEFT-RIGHT shunting disease - Extra blood shunts from high pressure left size (oxygenated) to low pressure right side (deoxygenated) which results in increased pulmonary blood flow - Most common involves mid-septum in the area of foramen ovale - Children are usually asymptomatic and may fatigue easily, be somewhat thin, or have hx of frequent respiratory infections - Physical exam - Murmur may not be noted until age 2-3 - Split S1 - Dx studies - Cxray (cardiac enlargement)\ Echocardiogram = identify the area of the defect - Management (Pediatrics) - Small defects in infancy may close spontaneously - Larger defects require intervention after child is 1 year old - Done in cardiac cath lab with closure device - Long term outcomes are good after ASD closure - Small risk of atrial arrythmias in teen years/early adulthood - If left untreated ASD can results in RV enlargement, fibrosis or failure or pulmonary HTN - Adults - 2^nd^ most common congenital lesion in adults - May be asymptomatic until adulthood -- typically symptomatic by age 40 - Potential complications of undetected lesion - Reversible pulmonary HTN - Right ventricular failure - Progressive tricuspid valve regurgitation - Atrial arrythmias - Paradoxical embolization - Cerebral abscess **[2. VSD (Ventricular septal defect)]** - Patho - Hole or defect in ventricular septal region - Accounts for 20-30% of all congenital heart defects - 2^nd^ most common congenital heart lesion in kids and 5% of individuals with VSD have chromosomal defect (13, 18, or 21) - Congenital bicuspid valve is the most common congenital heart lesion - Murmur may not be heard initially but when more blood is shunted across VSD causes a loud murmur -- also may develop s/s of CHF - Direction and severity of the shunt is determined by functional size and ratio of pulmonary to systemic vascular resistance - Larger VSDS generally cause left to right shunts with left ventricular volume overload - If uncorrected pulmonary HTN can develop - If this becomes severe enough, right ventricular pressure can reach systemic levels - Causing reversal of shunt - Results in hypoxemia and cyanosis - Leading to right ventricular hypertrophy and R atrial enlargement - 78% of small defects undergo spontaneous closure within the first two years of life - Physical exam - Small VSD - Harsh high-pitched murmur at left lower sternal boarder - All other findings normal - Large VSD - Low pitched holosystolic murmur over the left lower sternal boarder - Diastole rumble at apex - Thrill along the left sternal boarder - Signs of progressing CHF after first week of life - S3 or S4 if CHF is present - Adults - Isolated small restrictive VSD with small left to right shunt - Generally asymptomatic into adulthood - May develop aortic regurgitation - Low risk of endocarditis - Moderate to large VSDs are typically symptomatic in childhood - Dyspnea and fatigue may result from either: - Left ventricular overload - Significant aortic regurgitation - Pulmonary HTN - Double chambered R ventricle - Develops because of hypertrophy of a barren muscle bundle in the region of the VSD flow - Diagnostics - EKG - Small and isolated VSD will have normal EKGS - Chest Xray - Small uncomplicated VSD = normal films - Large VSD = Cardiomegaly (prominent left ventricular contour) - Echo - Most important clinical test for dx 3\. **[PDA (Patent Ductus Arteriosus) ]** - Occurs when the ductus arteriosus from fetal circulation between the main pulmonary artery in the aorta -- fails to close completely in the postnatal period - Normal functional closure of the ductus arteriosus occurs in the first 12-72 hours after birth with permanent sealing in 2-3 weeks, ductus arteriosus may remain patent in some infants and leave a connection between the aorta and pulmonary artery - As pulmonary vascular resistance falls, aortic blood is shunted into pulmonary artery and recirculated through the lungs - 2:1 female predominance - Also seen in infants born at high altitude more commonly - Most important risk factor is prematurity - Small PDA - May go undetected without identifiable symptoms - Most commonly identified during cardiac exam -- characteristic continuous flow murmur - Presentation - Moderate PDA - Exercise intolerance - Left to right shunt increases volume load on the left atrium and ventricle - Causes ventricular dilation and dysfunction - Larger PDA - Initially causes left ventricular volume overload - Over time pulmonary artery pressure is increased - Flow reverses from right to left shunt as pulmonary pressures exceed systemic - Cyanotic heart disease develops - Age - Infant - Large PDA present w/ symptoms of heart failure - Failure to thrive, poor feeding, resp distress - Older child - May present w/ SOB or easily fatigued - Adult - Uncorrected large PDA may present with - Short systolic ejection murmur - Evidence of cyanotic heart disease includes cyanosis and clubbing - Diagnostics - EKG - Chest Xray - ECHO 4\. **[Cortication of Aorta ]** - Defined as the narrowing of the aorta that can obstruct blood flow leading to increased risk for blood pressure - Leading to left ventricular hypertrophy - Can be in combination with congenital heart defects such as bicuspid aortic valve, ventricular septal, or patent ductus arteriosus - Symptoms - Poor feeding, difficulty breathing, failure to thrive in infant - Older children -- hypertension, headaches, leg cramps or exercise intolerance - Diagnostics - Made with ECHO - May need MRI, or CT angiography to assess narrowing - Need lifelong monitoring regardless of surgical intervention w/ CATH **[5. Tetralogy of Fallot (TOF)]** - Combination of 4 anatomic cardiac defects resulting in right ventricular outflow tract obstruction - Pulmonary valve stenosis - VSD - Aorta that overrides ventricular septum - Right ventricular hypertrophy - Accounts for 7-10% of congenital heart disease cases - Physiologic consequences and clinical presentation are largely dependent on the degree of R ventricular outflow obstruction - Clinical Presentation - Most kids are symptomatic and cyanotic - May appear comfortable and in no distress at rest which progresses to spells that include cyanosis with agitation - R. Ventricular impulse may be palpated - Murmur may be auscultated - Typically, crescendo, decrescendo w/ harsh systolic ejection quality - Best appreciated along left mid to upper sternal boarder - Diagnostics - Chest xray -- may show a boot shaped heart with decreased pulmonary markings - EKG - R ventricular hypertrophy - Echo - Shows extent of pulmonary obstruction - Pulse oximetry - Decrease over time OVERVIEW -congenital heart disease treatment - Pt w/ suspected congenital heart disease warrant a referral to cardiology and or cardiovascular surgery for dx and management - Tx plans are variable, depending upon the type and severity of the lesion - Surgical repair is often indicated.

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