Cardiology Part 2 Week 12 Lecture Notes PDF

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.