Cm - cardiopulm Exam 1 lectures 1-12

Cm - cardiopulm Exam 1 lectures 1-12
There are 70 title slides Some of the pearls did not match the lecture number/title I adjusted things, so hopefully everyone can follow it clearly Cm - cardiopulm Exam 1 lectures 1-12

Lecture 1: imaging of cardiac pulmonary systems
Most common PE test Low radiation risk tests Lecture 1: imaging of cardiac pulmonary systems

1. Most common PE test

CTA (CT Angiography) See lecture 1, slide 9
You’ll need a magnifying glass to see it on that ppt

2. Low risk radiation tests

MRI No exposure to radiation According to Dr. Google / FDA,
“MRI does not use ionizing radiation (high-energy radiation that can potentially cause damage to DNA, like the x-rays used CT scans). There are no known harmful side-effects associated with temporary exposure to the strong magnetic field used by MRI scanners.”

Echocardiography Fast, bed side, no radiation exposure, immediate results, less costly NOTE: this is from lecture 2, slide 32

Lecture 2: Noninvasive Cardiac Testing
When to use each (INDICATION) and data obtained (RESULT) Exercise stress Nuclear stress Stress echo 24 hr Holter Lecture 2: Noninvasive Cardiac Testing

2. Nuclear stress test (PMI)
3. Stress Echo 1. Exercise stress test

1. Exercise stress test / GXT (graded exercise test)

Indication Low risk (stable) angina pectoris (i.e. angina pectoris induced by exercise) The goal is to increase workload incrementally to induce ischemia or until a predetermined workload is reached-peak HR = 220-age. Result (+) test = ST segment depression greater than or equal to 1mm signifying a positive test result If angina develops during exercise, there is a correlation b/w myocardial ischemia and CAD Severity of CAD depends on: Increased ST downslope Greater ST depression ST depression at low workload (i.e. early in the test)

2. Nuclear stress test / Myocardial Perfusion Imaging ( MPI)

Definition Indication
Inject cardiac specific radioactive tracer (Technetium-labeled agents, such as sestambi or tetrofosmin) to visualize blood flow to the heart. Indication CAD and angina patients whose baseline EKG abnormality (i.e. LVH (LVH with strain), LBBB) would interfere with interpretation of ST segment changes during an exercise stress Compare rest vs. stress images

Result Detect perfusion defects of cardiac blood flow
(+) test is reversible ischemia 2 types of perfusion defects: Reversible defect – when exercise/cardiac stress is discontinued, the isotope reperfuses areas that were underperfused/ischemic during exercise due to ischemia Fixed defect - regions of the heart that are irreversibly damaged (scar/MI) do not demonstrate resolution of the defect on resting image

SA=Short axis HLA=Horizontal long axis VLA=Vertical long axis
Perfusion deficits are obvious SA view – normal (rest vs. stress) VA view – Rest = okay Stress = no perfusion

3. Stress echo

Definition Purpose – Indication – Result –
Perform a ECHO while the heart is undergoing exercise, pharmacologically induced or active chest pain Purpose – Visualize wall motion abnormalities Indication – CAD, stable/exercise induced angina Result – (+) stress echo = stress induced decrease (hypokineses) in regional wall motion correlating with the involved coronary artery: Left anterior descending (LAD) anterior, septal and apical Left circumflex (LCx)- posterior and basal Right coronary artery (RCA)- inferior and basal

Stress Echocardiography
Dobutamine Stress Echo Exercise Stress Echo

Rest – normal ventricular contractions
Stress – LV needs more blood, ischemic area is reduced contraction

4. 24-hour holter

Indication Result Patient with brief or transient events
Continuous monitoring Result Records cardiac dysrhythmias and conduction disturbances over and extended period ( hours) Detect electrical abnormalities

Lecture 3: Hypertension guidelines Emergencies, Urgency
Diagnosing primary aldosteronism Drug that are bad for the kidneys Blood pressure control for AAA Diagnosing renal artery stenosis Lecture 3: Hypertension guidelines Emergencies, Urgency

1. Diagnosing primary aldosteronism

Screening for Hyperaldo: Aldosterone - plasma renin ratio
Hyperaldosteronism Adrenal glands secrete abnormally high levels of aldosterone Aldosterone stimulates the kidney: 1) retention of sodium and 2) excretion of potassium: Hypernatremia – high [Na+] Hypokalemia – low [K+] … lost in urine Elevated [Na+] draws water in Elevated volume Elevated BP Reduces renin release  Low renin Aldosterone : PRA > 25 : 1

Physiologic and Pathophysiologic Effects of Aldosterone on the Kidney and Heart in Relation to Dietary Salt Levels. Hyperaldosteronism Extra secretion of aldosterone from adrenal glands Goes to kidney Retention of Na and H20  HYPERNATREMIA Excretion of K  HYPOKALEMIA Hold fluids Elevated volume Elevated BP If body sense high volume/BP, it reduces renin release  Low renin Dluhy RG, Williams GH. N Engl J Med 2004;351:8-10.

2. Drug that are bad for the kidneys
I pulled this from Dr. Ochs, Lecture 6, Slides 34-35 I pulled this from Dr. Ochs, Block 4, Lecture 6, Slides 34-35

Nitroprusside: Pharmacokinetics
Complex of iron, cyanide groups and a nitroso moiety Metabolized by rapid uptake into red blood cells with liberation of cyanide Cyanide is metabolized to thiocyanate  distributed in extracellular fluid and slowly eliminated by the kidney With prolonged administration, thiocyanate may accumulate, especially in the face of renal insufficiency Thiocyanate toxicity: Manifestations include abdominal pain, weakness, tinnitus, vomiting, tremor, agitation, disorientation, progressing to lethargy, seizures and coma in severe cases.

Nitroprusside: Indication and Toxicity
Hypertensive emergency Administered via IV infusion Unstable; decomposes when exposed to light Onset within 30 seconds, peak within 2 minutes, cessation 3 minutes after discontinuation Toxicity Thiocyanate accumulation Weakness Disorientation Psychosis Muscle spasms Convulsions Make it there in on the spot, brown bag because it decomposes when exposed to light

3. Blood pressure control for AAA

On physical exam, auscultate for bruits in carotid, abdominal and femoral aa
Control renal HTN b/c AAA might  renal artery stenosis  renal HTN Refer to vascular surgeon

4. Diagnosing renal artery stenosis

Renovascular HTN Diagnosis is made by renal artery ultrasound (also called renal artery duplex) Renal artery stenosis - elderly Fibromuscular dysplasia – younger; females  elevated BP Kidney US; if 1 kidney is small, one is large with elevated BP, think renal artery stenosis Tx Stent Medical management

Lecture 4: Diagnosis and Management of Lipid Disorders
Greatest risk for CV events Diseases which can cause of high LDL, triglycerides and low HDL Goals for LDL cholesterol Primary treatment medication Lecture 4: Diagnosis and Management of Lipid Disorders

1. Greatest risk for CV events

2. Diseases which can cause of high LDL, triglycerides and low HDL

LDL HDL VLDL Triglycerides + - Obesity/Type II Diabetes Hypothyroidism
Nephrotic Syndrome Liver Disorder Alcohol Estrogens Cushing’s disease Cushing’s – looks like obesity and T2DM

2a. High LDL Familial hypercholestermia (FH) Obesity T2DM
Heterozygous vs. homozygous Obesity T2DM Hypothyroidism Cushing’s disease Syndrome X Insulin Resistance Syndrome Dysmetabolic Syndrome

2b. High TG Familial hypercholestermia (FH) Obesity T2DM
Heterozygous vs. homozygous Obesity T2DM Hypothyroidism Cushing’s disease Syndrome X Insulin Resistance Syndrome Dysmetabolic Syndrome

2c. Low HDL Hypoalphalipoproteinemia Alcohol Estrogens
Tangier’s disease Hypoalphalipoproteinemia Syndrome X Insulin Resistance Syndrome Dysmetabolic Syndrome

3. Goals for LDL cholesterol

Three Categories of Risk that Modify LDL-Cholesterol Goals
Risk Category CHD and CHD risk equivalents Multiple (2+) risk factors Zero to one risk factor LDL Goal (mg/dL) <100 <130 <160 FUTURE RESEARCH

ATP III Lipid and Lipoprotein Classification
LDL Cholesterol (mg/dL) <100 Optimal 100–129 Near optimal 130–159 Borderline high 160–189 High 190 Very high FUTURE RESEARCH

4. Primary treatment medication

Lipid Lowering Agents Cholesterol Absorption inhibitors- ezetimbe (Zetia) Interferes with transport across the intestinal brush border Fibrates-gemfibrozil (Lopid) lowers VLDL and triglycerides Bile sequestration- cholestyramine lowers LDL, but may raise triglycerides Nicotinic acid- Niacin raises HDL and lowers LDL and triglycerides Statins- HMG-CoA reductase inhibitors (Pravachol, Lipitor, Crestor, Zocor) lower LDL, raise HDL and lower triglycerides Ezetimbe- increased risk of liver disease and cancer-on-going studies to determine this association.

Lecture 5 and 6: Congenital Heart Defects I and II
Most common simple congenital defect Treatment for hypercyanotic spells Syndromes and heart defects Drugs linked to Ebstein anomaly Right to left shunts in kids Cyanotic heart defects – progressive errors Mechanism of murmur in VSD Heart defects with superior axis deviation EKGs Downs and VSD types EKG findings and VSD types Lecture 5 and 6: Congenital Heart Defects I and II

1. Most common simple congenital defect

Ventricular Septal Defect (VSD)
20-25% of CHD Most common defect seen Four major types of VSDs include: Perimembranous Muscular Inlet Supracristal/subarterial. Perimembranous defects may be associated with aortic valve insufficiency or subarterial stenosis. Small asymptomatic. Large CHF growth restriction and FTT Indomethacin is a prostaglandin synthesis inhibitor – Used for infants only. PULES PRESSURE = DIFFERENCE BETWEEN SYSTOLIC AND DIASTOLIC. VSD – like as fire hydrant opened

2. Syndromes and heart defects

Bonus: Genetics with CHD
Turner Syndrome Coarctation Aortic Ectasia Noonan Syndrome Dysplastic Pulmonary Valve Branch Pulmonary Stenosis Williams Syndrome Supravalvar Aortic Stenosis Coronary Ostial Stenosis Down Syndrome VSD Complete AV Canal Tetralogy of Fallot Noonan syndrome = “male’s turner syndrome” Down’s: Most common simple defect in Down’s syndrome  VSD Most common complex defect in Down’s sybdrome AV canal (partial, transitional, incomplete) Maybe Tetralogy of Fallot What is the most common cyanotic defect know to mankind? Tetralology of Fallot Most common complex heart defect seen in Down’s - Tetralolgy Aortic overriding Pulmonary valve atresia Causing RV hypertrophy Truncus ateriosus – failure of separation of heart tube into pulm and aorta Transposition of great vessels – no spiraling LV  pulm and RV  aorta Williams’ – irritable infants, wonderful as adults, triangle face

3. Right to left shunts in kids

The 5 T’s, P, H, E Tetralogy of Fallot Transposition of the Great Aa
Truncus Arteriosus, persistent Tricuspid Atresia Total anomalous pulmonary venous return Pulmonary atresia Hypoplastic left heart sydnrome Ebstein’s anomaly

4. Mechanism of murmur in VSD

Ventricular Septal Defect
Exam Classic holosystolic murmur covering first heart sound The larger the defect the larger the shunt/volume load Right venticular enlargement leads to broad RV impulse Possible lateral and upward displacement of LV impulse Studies Saturations normal unless associated RVOT/increased PVR EKG – RVE, possible right axis deviation CXR – possible cardiomegaly, possible increased pulmonary vasculature ECHO – confirms anatomy and function Pulmonary overcirculation

5. Downs and VSD types

Bonus: Genetics with CHD
Down Syndrome VSD Complete AV Canal Tetralogy of Fallot Noonan syndrome = “male’s turner syndrome” Down’s: Most common simple defect in Down’s syndrome  VSD Most common complex defect in Down’s sybdrome AV canal (partial, transitional, incomplete) Maybe Tetralogy of Fallot What is the most common cyanotic defect know to mankind? Tetralology of Fallot Most common complex heart defect seen in Down’s - Tetralolgy Aortic overriding Pulmonary valve atresia Causing RV hypertrophy Truncus ateriosus – failure of separation of heart tube into pulm and aorta Transposition of great vessels – no spiraling LV  pulm and RV  aorta Williams’ – irritable infants, wonderful as adults, triangle face

Down’s and VSD types What is the most common simple defect in Down’s syndrome? VSD What is the most common complex defect in Down’s syndrome AV canal (partial, transitional, incomplete) What is the most common cyanotic defect know to mankind? Tetralology of Fallot Most common complex heart defect seen in Down’s

6. EKG findings and VSD types

Ventricular Septal Defect
Exam Classic holosystolic murmur covering first heart sound The larger the defect the larger the shunt/volume load Right venticular enlargement leads to broad RV impulse Possible lateral and upward displacement of LV impulse Studies Saturations normal unless associated RVOT/increased PVR EKG – RVE, possible right axis deviation CXR – possible cardiomegaly, possible increased pulmonary vasculature ECHO – confirms anatomy and function Pulmonary overcirculation

Tricuspid Atresia EKG: Chest Xray: Treatment: Embryology:
Failure of Tricupsid Valve to Form Needs associated ASD VSD presence/size determines RV size/Pulmonary Valve development Key Exam: Variable cyanosis Plus Variable Single S2 most common due to diminished /absent pulmonary valve (P2) vs A2/P2 atop each other if TGA also present HSM of VSD vs SEM of PS EKG: Superior Axis Deviation, RAE, LVH Chest Xray: Heart Size usually normal with bilaterally decreased PBF Enlarged heart with prominent PBF would suggest large VSD Treatment: Decreased PBF => PGE1, Oxygen Palliative Shunt/Fontan Series Right Atrial Enlargement

Transposition of Great Arteries 2nd most common CCHD after TOF
Embryology: Failure of great vessel rotation after septation Need PDA/PFO-ASD to survive May have associated VSD Key Exam: Cyanosis Plus Happy tachypneic Single S2 due to A2/P2 in AP relationship paO2 on 100% oxygen often in 40s EKG Usually normal as neonate RVH usually develops Chest Xray: A degree of ventrcular enlargement with narrow upper mediastinum in most classic presentation has been described as egg on a shoestring Variable Treatment: Oxygen / PGE1 Rashkind balloon septostomy Good anatomy/coronaries – arterial switch Subpulmonic stenosis – atrial switch Subpulmonic stenosis / VSD – Rastelli

Tetralogy of Fallot 8% CHD, most common CCHD beyond 1 week of age
Embryology: Incomplete ventricular septation allowing aorta to shift ‘into’ RVOT leading to pulmonary valve/artery/RVOT hypoplasia and RV body hypertrophy Key Exam: Variable cyanosis Plus Increased RV Impulse Possible thrill at MLSB to ULSB Coarse early systolic ejection murmur at ULSB EKG: Right axis deviation, RVH Chest Xray: Normal to boot shape due to absent PA segment prominence Treatment: Treatment of Tet Spell +/- Beta blockade Pallative shunt vs primary repair Pulmonary AVM (intrapulmonary Rl shunt)  cyanotic Do not exchange CO2 for O2 Carries deoxy blood back to the LA

7. Treatment for hypercyanotic spells

Hypercyanotic Spell MECHANISM Infundibular RVOT obstruction Lower SVR
Increased right to left shunt Severe hypoxia Irritability, uncontrolled crying, hyperpnea/tachypnea, fainting TREATMENT Calm the child Knee to chest position Oxygen Subcutaneous morphine +/- IV access Phenylephrine drip General anesthesia Shunt/repair Infundibular blockage Pass out and recover OR die Calm the child down; let mom calm the child down Tubes in chest Milk legs to increase venous return Open the outflow track Increase SVR?? Not really Morphine (not in office, EMS or ER)  calm down Drops hypercapnic drive Vasodilation IV access Phenylephrine drip  vasoconstriction

8. Drugs linked to Ebstein anomaly

Bonus: Linking Maternal Drugs with CHD
Lithium  Ebsteins anomaly SSRIs – Conotruncal defects Dilantin – VSD, DTGA Alcohol - VSD Cocaine – fetal myocardial injury

Ebstein’s Anomaly +/- CCHD
Mild – can leave, MATERNAL DRUG EXPOSURE of LITHIUM (Psych drugs) LV vs RV Autopsy or OR, Can atrialize the RV No anterograde Q Mild – can leave, MATERNAL DRUG EXPOSURE of LITHIUM (Psych drugs) Risk factors – Keep mom healthy with Lithium, deal with the cardiac exposure Might have to ask mom not to get pregnant

Ebstein’s Anomaly: Key Points
Embryology: Failure of the septal leaflet of the tricuspid valve to detach from endocardial surface thus atrializing a portion of the right ventricle Key Exam: Cyanosis depends on severity of anomaly Depends on elevated RA pressures and right to left atrial shunt Inadequate pulmonary blood flow will also contribute to cyanosis Harsh holosystolic murmur on exam EKG: RAE Superior axis deviation CXR: Mild to severe cardiomegaly Normal to decreased PBF Echo: Confirms tethered TV septal leaflet, degree of tricuspid regurgitation, right atrial enlargement, and atrial level shunt

9. Cyanotic heart defects – progressive errors

The Failures of Cyanotic CHD
Truncus Arteriosus Failure to septate Transposition of the Great Arteries Failure to rotate Tetralogy of Fallot (VS) Tri Atresia (TV) HLHS (MV) Failure to form Total Anomalous Pulmonary Venous Return Failure to Fuse Septate/separate

10. Heart defects with superior axis deviation EKGs

Tricuspid atresia Pulmonary atresia/IVS Ebstein’s anomaly

Key Points: Tricuspid Atresia
EKG: Superior Axis Deviation, RAE, LVH Chest Xray: Heart Size usually normal with bilaterally decreased PBF Enlarged heart with prominent PBF would suggest large VSD Treatment: Decreased PBF => PGE1, Oxygen Palliative Shunt/Fontan Series Right Atrial Enlargement

Key Points: Pulmonary Atresia/IVS 10th most common neonatal CHD, 23rd most common CHD
EKG: Superior axis deviation with diminished RV forces Right axis deviation with RVH would suggest severe tricuspid regurgitation with enlarged right heart Chest Xray: Small heart with diminished pulmonary blood flow in most Enlarged heart with diminished pulmonary blood flow with severe TR/RVE Treatment: PGE1, oxygen Palliative Shunt vs Balloon Valvuloplasty MUST ADDRESS SINUSOIDS – recent patient listed for transplantation

Ebstein’s Anomaly EKG: CXR: Echo: RAE Superior axis deviation
Mild to severe cardiomegaly Normal to decreased PBF Echo: Confirms tethered TV septal leaflet, degree of tricuspid regurgitation, right atrial enlargement, and atrial level shunt

Clicker Questions Right atrium Right ventricle Left atrium
Which fetal chamber has the highest oxygen saturation? Which infant chamber has the highest oxygen saturation? Right atrium Right ventricle Left atrium Left ventricle Right atrium Right ventricle Left atrium Left ventricle B C

Clicker Question The most common cyanotic heart disease is
A. Tricuspid atresia B. Truncus arteriosus C. Tetralogy of Fallot D. Transposition of the Great Vessels C – TOF = most common after 1 week D – TGA = 2nd most common Most common simple defect in Down’s syndrome  VSD Most common complex defect in Down’s sybdrome AV canal (partial, transitional, incomplete) Maybe Tetralogy of Fallot What is the most common cyanotic defect know to mankind? Tetralology of Fallot Most common complex heart defect seen in Down’s - Tetralolgy Aortic overriding Pulmonary valve atresia Causing RV hypertrophy Truncus ateriosus – failure of separation of heart tube into pulm and aorta Transposition of great vessels – no spiraling LV  pulm and RV  aorta

Clicker Question Cyanotic CHD is often associated with EKG axis deviation form norm due to relative increased or diminished forces on one side of the heart or displacement of the conduction system. Which is correct? A. Tetralogy of Fallot – Right axis deviation B. Ebstein’s anomaly – Right axis deviation C. Tricuspid atresia – Right axis deviation D. Complete AV Canal – Right axis deviation A B, C = Superior axis deviation problems

Clicker Question The most common form of total anomalous pulmonary venous return to present in neonatal distress is: A. Supradiaphragmatic B. Infradiaphragmatic C. Intracardiac D. Mixed B

Lecture 7: Adult Congenital Heart Disease
Distinguish between ostium primum and secundum ASD on exam/EKG – provide treatment Best treatment for severe congenital aortic valve stenosis, Tetrology of Fallot, Eisenmengers Lecture 7: Adult Congenital Heart Disease

1. Distinguish between ostium primum and secundum ASD on exam/EKG
1. Distinguish between ostium primum and secundum ASD on exam/EKG. Provide treatment.

1. Atrial Septal Defect Represent 10 to 17% of CHD.
Sinus Venosus (10% of ASD) are located in the Superior Septum and may be associated with anomalous pulmonary venous drainage into the superior vena cava or right atrium. 4. Coronary sinus (rare) unroofed Represent 10 to 17% of CHD. Incidence is 1/1500 live births 4 types: Ostium Secundum Defect (60% of ASD and 6-10% of all ACHD). Location is central and more superior. Ostium Primum (20% of ASD). Location is inferior and involves the atrioventricular junction (cushion defect… if the superior and inferior endocardial cushion do not migrate  ostium primum ASD) Usually has a cleft mitral valve and mitral regurgitation. Rarely assoc. with large Ventriculoseptal defect and single AV valve (i.e. Down’s Syndrome) Secundum is central, while primum is lower down, at same level as mitral and tricuspid valves, so one or both valves may be defective, with associated MR or TR. Sinus Venosus defects involve the junction of the SVC (usually) or IVC (less commonly) with the RA and are hard to visualize on echo. A high SV defect is usually associated with an anomalous right upper pulmonary vein.

Atrial Septal Defect The majority of ASDs are recognized & repaired in childhood. Mild forms may present in adolescence or adulthood Immigrants who have not had the surgical opportunity may present in adulthood With age, more severe symptoms develop including: Congestive Heart Failure Atrial Fibrillation Emboli - Stroke AFib and CHF may occur in pts. in their 40s or 50s—i.e., unexpectedly young. ASD  CVA Periosteal embolism R  L shunt (via PFO or VSD)  strokes

ASD: Diagnostics Examination reveals pulmonary flow murmur and fixed splitting of the second heart sound EKG with a Secundum defect shows rightward axis and a RBBB, Priumum defect, left axis deviation with a RBBB Transthoracic echo and transesophageal echo are the tests of choice. Cardiac catheterization is rarely used anymore. Secundum defect usually has RBBB and R axis deviation on EKG. Primum defect has L axis deviation. CXR shows signs of RV volume overload, with RV enlargement and prominent PA and pulmonary plethora.

Atrial Septal Defect Criteria for closing ASD's
ASD's that cause significant shunting of volume to the right heart should be closed, measured by shunt fraction Qp/Qs by either echo or cardiac catheterization with a shunt run. Qp/Qs greater than 1.5 should prompt closure. More important than Qp/Qs is RV and RA enlargement. ASD's should be closed regardless of symptoms if there is right sided volume overload. Can be closed percutaneously or surgically Supravalvular AS may occur as part of Williams’ syndrome.

2. Best treatment for severe congenital aortic valve stenosis, Tetrology of Fallot, Eisenmengers

2a. Best Tx for severe congenital aortic valve stenosis

Subaortic Stenosis Usually diagnosed in adulthood
Discrete fibrous ridge encircling the left ventricular outflow tract between the mitral annulus and the basal inter-ventricular septum. May have mild symptoms up to exertional syncope. Systolic outflow murmur but no click. Develop Left Ventricular Hypertophy (LVH) and post-stenotic aortic dilation. Within the LV outflow tract can form Gradings across valve – is it the valve or area below valve Echo can distinguish Same issues results as aortic stenosis Can be comorbid with aortic stensosis Tx Must treat the valve Infants – air balloon valvuloplasty Adults – aoritc valve replacement Tx, must treat the valve Infants – air balloon valvuloplasty Adults – aoritc valve replacement

If severe congenital aortic valve stenosis is involved with coarctation of the aorta

Coarctation Repair Surgical correction – Patch aortoplasty
Removing the dysfunctional segment Performing EITHER: End to end anastomosis OR Subclavian flap or bypass tube grafting of segment End-to-end anastomosis often not possible after age 8 and rarely after age Stent treatment an alternative Rx with effective results but increases chance of repeat intervention later. Edmunds’ Cardiac Surgery in the Adult, Ch 47

2b. Best Tx for Tetrology of Fallot

Tetralogy: Initial Surgical Treatment Usually Done as Infant
INITIAL = begin as a temporary shunt between systemic and pulmonary circulation Blalock-Taussig (subclavian > PA) Waterston (Asc Ao > R PA) Potts (Desc Ao > L PA) LATER = Complete Repair takedown of prior shunt patch VSD resection of subpulmonic obstruction transannular patch around pulmonary valve annulus (usually leads to severe pulmonary insufficiency) Temporary shunt = “ Palliatiation “

2c. Best Tx for Eisenmengers

Eisenmenger: Treatment
If polycythemia exists  phlebotomy Oxygen Diuretics for CHF Definitive - Heart Lung transplant Avoid non-urgent aggressive testing as many patients die during cardiovascular procedures Polycythemia - abnormally increased concentration of hemoglobin in the blood

Eisenmenger’s Syndrome
In LR shunts (i.e. ASD or VSD), unrestricted pulmonary blood flow may lead to pulmonary vascular occlusive disease (PVOD); Eisenmenger syndrome represents a very specific form of extreme pulmonary arterial hypertension (PAH) seen with congenital heart disease. Unlike patients with idiopathic PAH, in Eisenmenger syndrome the clinical and cardiac status is often slow in development. Initial L  R shunting Changes to RL shunting due to increased PVR, and the patient develops cyanosis. COMPLICATIONS Coagulopathy/platelet consumption, Brain abcess, Cerebral microemboli, hemoptysis, and right heart failure.

Hiremath’s 2013 Exam Questions
The answers are in the notes section.

Tetralogy of Fallot is:
VSD, overriding aorta, pulmonary stenosis and RV hypertrophy ASD, mitral stenosis, LA enlargement, and Wolf-Parkinson-White Syndrome Tricuspid malformation ,WPW, ASD, and atrialization of RV Bicuspid aortic valve, coartation of the aortia valve, sysmteic HTN and LV hypertrophy A

Of the following, the most common adult congenital heart defect is:
ASD Bicuspid aortic valve VSD Ebstein’s anomaly Supravalvular AS B

An ASD should be closed if:
Only the patient has symptoms of SOB LV is enlarged Qp/Qs ratio is greater than 1.5 ASD’s don’t need to be closed since their course is benign There is volume overload of the right heart with enlargement of RA and RV E

A patient presents with a history of systolic murmur and decreased femoral pulses with no risk factors for CAD. Your Dx is: Peripheral vascular disease (PVD) and hypertrophic cardiomyopathy Pulmonary valve stenosis and coarctation of the aorta Hypertrophic cardiomyopathy and coarctation of the aorta Bicuspid aorta valve and coarctation of the aorta D Systolic murmur Decreased femoral pulses = coarctation of aorta

Eisenmenger’s syndrome is caused by:
Decreased red cell mass and desaturation with exercise Left to right shunting at the atrial level and right to left shunting at the ventricular level Right to left shunting due to fixed pulmonary HTN Right to left shunting due to pulmonary valve stenosis C

Lecture 8: Acute Coronary Syndromes
Plaque rupture pathogenesis Normal EKG findings in V2-3 Treatment options for LBBB Right ventricular infarction treatment options and differences Posterior MI pathology / EKG findings Lecture 8: Acute Coronary Syndromes

1. Plaque rupture pathogenesis

Plaque composition = fibrous cap + lipid core
Large plaques do not necessarily cause stenosis and anginal symptoms (before the infarct occurs) Plaque composition = fibrous cap + lipid core Vulnerable plaques – not necessarily a large plaque. Thinner fibrous cap – like a volcano, susceptible to blow Thicker lipid core Stable plaques – may be large Thicker fibrous cap – takes a lot more energy to break this thick cap Thinner lipid core

The vulnerable plaques – not necessarily a large plaque.
Large plaques do not necessarily cause stenosis and anginal symptoms (before the infarct occurs) The vulnerable plaques – not necessarily a large plaque. The composition – how much of a fibrous cap Thick (won’t rupture) Thin (dangerous volcanoes that are about to blow) How big is the lipid core? Small amount won’t rupture Large amount will rupture How many macrophage cells are present in the plaque?? Focal inflammation plays a role The more inflammatory cells – the more likely to rupture CRP – Sed Rate – WBC’s – increase the chance of infarction in next 3-6 months

2. Normal EKG findings in V2-3

Where do you measure the ST Segment? At the J-point or 0.04 sec later?
Guidelines say measure the ST elevation at the J-Point 1mm is the cut-off to meet STEMI criteria; Must be in 2 contiguous leads except for V2 and V3 In V2 and V3 - Women 1.5 mm - STEMI <40 yr old men 2.5 mm - STEMI >40 yr old men 2.0 mm - STEMI

3. Treatment options for LBBB

When should we activate the cath lab in the presence of a LBBB?
Don’t worry if it’s new or old If hemodynamically unstable or in acute heart failure (acute cardiogenic pulmonary edema, not just mild failure) – go to cath lab or get lytics If the patient is stable – if you have concordant ST elevation or ST depression – STEMI equivalent, only need one lead (not 2 contiguous) – go to cath lab First two Sgarbossa criteria - if only 1 lead measures > 1mm to cath lab or lytics QRS upwards ST elevation 1mm QRS downwards (V1, V2, V3) ST depression 1 mm

LBBB diagnosis of AMI – Sgarbossa criteria

4. Right ventricular infarction treatment options and differences

Therapeutic Hypothermia Cath lab
Thrombolytics Unfractionated heparin Chewable ASA immediately Therapeutic Hypothermia Cath lab

Post Cardiac Arrest After A STEMI OR STEMI After Arrest
Therapeutic Hypothermia GET THEM ON ICE and GET THEM TO THE CATH LAB Best evidence is code after V-Fib Both Class I Interventions Cooling cath into femoral aa Ice into axilla or groin

Unfractionated Heparin (not Lovenox or Enoxaparin) on way to cath lab.
ASA immediately…CHEWABLE New or presumed new LBBB with chest pain Prior recommendation to cath lab; treat as STEMI equivalent. New guidelines (2013) – removed new onset LBBB from the guidelines. No longer a criteria to give lytics or go to the cath lab. LBBB - Left Bundle Branch Block - New, old, control – no differences in treatment if given lytics or cath labs

Right Ventricular MI

Clues to RV Infarction on the 12-Lead ECG
ST Depression in lead V2 AND ST elevation in lead V1 OR Isoelectric ST segments in leads V1 + V3 ST elevation in lead III >> ST elevation in lead II

5. Posterior MI pathology / EKG findings

Posterior Myocardial Infarction
ECG changes Posterior MI is usually associated with inferior MI due to RCA or circumflex occlusion: RCA occlusion – in a right dominant heart LCX occlusion – in a left dominant heart Increased M&M compared to isolated IMI Mirror image of septal MI in leads V1-V2 Large R waves (instead of Qs) STD (instead of STE) on V123 Upright T-Waves (instead of inversions)

Isolated PMI Big R waves Upright T waves ST depression V123

Acute Myocardial Infarction
Who gets acute reperfusion therapy for presumed STEMI? Concerning symptoms AND ECG 1mm STE in 2 contiguous leads OR Posterior STEMI OR Presumed new LBBB OR LBBB with Sgarbossa criteria OR [Pacemaker with Sgarbossa criteria]

PLMI – Posterior Leads (V3-V6)
STE V5-6; place leads V3-6 posteriorly confirms a posterior MI Posterior MI – should see STE in V3-6 ST depression V2, V3 Big R wavesPut V5 and V6 with St elevation in posterior leads…confirms a posterior MI - STE in V3456

Acute Myocardial Infarction /Ischemia
ECG changes ST depression – ischemia or infarction High morbidity and mortality if untreated T-wave inversions – ischemia Lower specificity and morbidity ST elevation – injury pattern Q-Waves – infarcted tissue Develop within hours “Significant” Q-Waves at least one box wide and one box deep

Lecture 9: Chronic management of coronary artery disease
CABG indications Papillary muscle rupture Lecture 9: Chronic management of coronary artery disease

1. CABG indications

CABG Preferable Procedure … Indications … see lecture 10, slide 35
Left main stenosis >50% (PCI an option) 3 vessel CAD with EF <45% 2 vessel CAD with proximal LAD involvement (PCI an option), especially in diabetics At least one vessel totally occluded such that complete revascularization not achievable by PCI or unlikely to adequately relieve symptoms. Patient has no comorbidity that would significantly reduce expected surgical survival Decreased LV EF

2. Papillary muscle rupture pathogenesis

PAPILLARY MUSCLE RUPTURE
Lecture 9, slide 46 May be partial or total A complication of inferior MI, usually due to occlusion of RCA (supplies PM pap muscle) May involve anterolateral pap muscle Causes acute MR and LV failure May involve an RV pap muscle and cause severe TR and RV failure May occur with small infarcts since is due to localized ischemia to pap m. itself Severity of MR depends on extent of pap m ruptured and extent of tear Complete transection of muscle = sudden, massive MR + pulmonary edema/death Rupture of head or tip of muscle = less massive MR due to flail leaflet and prolapse Mitral regurg and LV failure Backflow into LA and pulmonary system Leads to pulmonary edema Tricuspid regug

SURGERY Listen to the patient Wide open regurg Listen for the murmur DO a FULL EXAM every day

PAPILLARY MUSCLE RUPTURE/ACUTE MR
PE: Murmur of MR is usually holosystolic, at apex, and no palpable thrill. But may be inaudible. Also signs of acute CHF. Not a VSD – will have a thrill, will have shunt and step-up Echo: Flail mitral leaflet and significant MR. LV is hyperdynamic. Cath: MR is seen on ventriculography and coronaries are visualized for CABG. Right heart cath shows no oxygen step-up in RV or PA. Treatment: Hemodynamic deterioration occurs rapidly. Acute stabilization with diuretics and mechanical support (IABP or Impella). Rapid mobilization for prompt surgical MV repair or replacement and CABG.

Lecture 10: Cardiac Catheterization
Indications for treatment based off of angiography findings (observe, CABG, stenting) Compare radial vs. femoral artery cath sites Drug eluting vs. bare stents Papillary muscle rupture pathogenesis Lecture 10: Cardiac Catheterization

1. Indications for treatment based off of angiography findings (observe, CABG, stenting)

Diagnosing Coronary Disease
ETT (for patients with normal EKG and ability to walk 2 flights of stairs) ETT with nuclear imaging or echo Pharmocologic testing with nuclear (adenosine or regadenoson), dobutamine stress echo Coronary calcium score Coronary CT angiography (good negative predicative value, not good with calcified arteries, or previous stents) Direct coronary angiography Remember that nuclear stress testing can miss balanced multi-vessel disease! CTA Contrast into veins Track into coronary arteries and veins Less invasive than heart cath Good NPV (negative predictive value) PPV (positive preditive value) not as high Poor images with calcified aa ETT – exercise treadmill testing Good for those with normal EKG, nor prior caths Ability to walk Can you walk up 2 flights of stairs, therefore can walk on treadmill LBBB infarction, cannot track the patient on the EKG stress test (cannot monitor the STE) Perfusion scans help localize stenosis Whichever artery we stent is helping with functional flow BEFORE YOU STENT IT Pharm stress test Adenosine – coronary artery VASODILATOR Dobutamine Do with patients who are exercise intolerant Coronary calcium score = CT non-contrast Is there calcium in coronary aa? Males >40 Females > 50; calcium is DIRECTLY related to stenosis 0 = normal, 400 = stenosis

Cardiac Catheterization Technique
Local anesthetic Arterial puncture and sheath insertion (Seldinger technique) Pressure Measurement Left ventriculography Selective coronary angiography Additional angiography (aortic, renal, peripheral)

Left Heart Cath Indications
Acute Myocardial Infarction “Code STEMI” Other acute coronary syndromes Stable angina Unacceptable symptoms despite adequate Rx High risk stress test – Possible LM or 3V CAD Preop assessment for patient undergoing valve replacement or major vascular surgery Silent myocardial ischemia Status post cardiac arrest Assessment of possible ischemic cardiomyopathy “Need to know” Get STEMI patient to cath lab within 90 minutes

Rt & Lt Heart Cath Indications
Evaluation of valvular heart disease Stenosis or insufficiency of any valve Cardiac output determination Cardiomyopathies – Hypertrophic, restrictive Cardiac tamponade, pericardial constriction Congenital heart disease Ischemic heart disease associated with significant LV dysfunction

PCI Indications Clinical indications Angiographic indications
Acute coronary syndrome ST-segment elevation myocardial infarction (Code STEMI) Non–ST-segment elevation myocardial infarction Unstable angina Stable angina pectoris – unacceptable symptoms despite adequate medical therapy Recurrent angina post CABG or Stenting with objective evidence of ischemia Angiographic indications Single, multi-vessel, multi-lesion CAD Stenosis greater than 70% or FFR < 0.8 LMCA stenosis if CABG is a poor option Avoid ocular-stenotic reflex Does angiogram… looks bad Your eye sees stenosis worse than it is Do not fix aa that are not ischemic Fractional flow reserve Place doppler flow wire through stenosis Measure FFR ( Transducer at tip of wire past stenosis Get mean distal pressure Divide by mean distal pressure in guide catheter Checks mean aorta pressure Ratio should be 1:1 Should be no drop-off Stenosis reduces the ratio < 1.0 Fractional flow reserve = 0.8 Lesion is ischemic If normal at baseline, add adenosine Vasodilator = provocative challenge via IV If FFR falls to 0.7, this means ISCHEMIA…put a stent in this one

CABG Preferable Procedure … Indications
Left main stenosis >50% (PCI an option) 3 vessel CAD with EF <45% 2 vessel CAD with proximal LAD involvement (PCI an option), especially in diabetics At least one vessel totally occluded such that complete revascularization not achievable by PCI or unlikely to adequately relieve symptoms. Patient has no comorbidity that would significantly reduce expected surgical survival Decreased LV EF

2. Compare radial vs. femoral artery cath sites

Left Heart Cath Approaches
Femoral Axillary Brachial Cutdown – Sones Percutaneous Radial Trans-septal Direct apical puncture Radial a caths are becoming more common

Rt and Lt Heart Cath - Femoral vs Brachial/Radial Approach

Arterial Access - femoral
Seldinger Technique Local anesthesia for percutaneous approach 3-4 cm inf. to inguinal ligament 0.5cm. Incision over vessel and “tunnel” made with hemostat 18ga. Needle inserted Teflon-coated guide wire passed through needle and needle removed. Sheath advanced over guide wire and dilator and wire removed. Catheter advanced through sheath Sizes from 4-9f, various lengths Seldinger Technique Remove sheath faster, decreases bleeding risk Smaller cath wire, decreases bleeding risk

Radial Approach to Cath
Relatively recent adoption in US – frequent in rest of world Advantages: Pts. with PVD, markedly obese Fewer bleeding complications – can be done without reversing warfarin (mechanical valves) Shorter hospital stays – outpatient Cath and PCI Reduced discomfort, immediate ambulation Improved post-procedural quality of life Decreased risk of neurovascular complications Limitations: Steeper learning curve Smaller size occasional limits interventional device options (5f, 6f only, except in very big patients) Make sure ulnar collateral flow is okay, the risk of radial artery obstruction

Radial Artery Approach
Need a good radial artery pulse Radial artery occlusion in 3% - normal Allen’s test is essential Can use ulnar artery Requires anticoagulation after sheath insertion Verapamil is administered to prevent radial artery spasm Allen’s Test: When blocking both radial and ulnar aa and then you release the ulnar a Look for blanching of palm with brisk refill When blocking both radial and ulnar aa and then you release the ulnar a Look for blanching of palm with brisk refill

3. Drug eluting vs. bare stents

Percutaneous Coronary Intervention (PCI)
History Dotter and Judkins in transluminal angioplasty for peripheral arteries Gruentzig, first balloon angioplasty in a peripheral artery , Zurich, Switzerland Gruentzig and Myler and the cardiac surgeon Hanna, 1977 – first intraoperative balloon angioplasty Gruentzig, Sept first PCI case - Switzerland >5 million cases yearly worldwide PCI performed more frequently than CABG Bare metal stents (BMS) replace POBA Drug eluting stents (DES) pretty much replace BMS Current re-stenosis < 5% 30 yrs ago, re-stenosis ~30-50% Small aa and long stenosis = higher re-steosis rates Larage aa and short stenosis = very low re-stenosis rates

Coronary Stents Metal scaffold – no recoil Bare metal stents
Endothelialization in 4-6 weeks Restenosis in 20-25% of cases Drug Eluting stents Sirolimus, Tacrolimus, Everolimus, Zotarolimus Special polymers, thinner struts Endothelialization in 5-6 months Restenosis in 4-5% Late stent thrombosis in 0.6% - more frequent than BMS

Lecture 10: Hiremath’s 2013 Exam Questions
Name the heart dominance in most adults: Right dominant circulation What is the best current accepted therapy for acute MI PTCA and Stent What determines long term re-stenosis? Lesion length and reference diameter How is CAD best diagnosed? No single best test What is the benefit over radial artery cath vs. femoral artery cath? Lower complication rates Patient can walk right out and leave PTCA - Percutaneous transluminal coronary angioplasty (PTCA) is a minimally invasive procedure to open up blocked coronary arteries, allowing blood to circulate unobstructed to the heart muscle.

Lecture 11: Vasculitis Refer to Pathology Lecture
I put colored copies of my personal study guide in the library cubby (top box, 2nd column from the left) Lecture 11: Vasculitis

Lecture 12: chronic management of CAD
NYHA classifications Distinguish angina types / atypical chest pain / MI / Prinzmetals angina Coronary vasospasm treatment Lecture 12: chronic management of CAD

1. NYHA classifications

NYHA Classifications Class I No limitation of activity. Ordinary activity does not cause undue fatigue, palpitation, dyspnea, or anginal pain. Class II Slight limitations of physical activity. Patient is comfortable at rest. Ordinary activity results in fatigue, palpitation, dyspnea, or anginal pain. (walking up stairs rapidly, exertion after meals, cold weather) Class III Marked limitation of physical activity. Patient is comfortable at rest, but less than ordinary activity causes fatigue, palpitation, dyspnea, or anginal pain. (walking on level ground 1-2 blocks, stairs at normal pace). Anginal equivalents.* Class IV Inability to carry out physical activity without symptoms. Fatigue, palpation, dyspnea, or anginal pain at rest. Increased symptoms or discomfort with even minor physical activity. *Anginal equivalents: sweating, exertional dyspnea, excessive fatigue, fainting are common in women and elderly; women commonly report atypical symptoms

2. Distinguish angina types / atypical chest pain / MI / Prinzmetals angina

2a. Stable angina

Stable Angina Pectoris
See lecture 12, slide 7 Stable pattern, induced by physical exertion, exposure to cold, eating, emotional stress, Lasts 5-10 min, Relieved by rest or nitroglycerin Baseline often normal or nonspecific ST-T changes Signs of previous MI, ST-segment depression during angina, ≥70% Luminal narrowing of one or more coronary arteries from atherosclerosis Aspirin, Sublingual nitroglycerin , Anti-ischemic medications Stable angina occurs predictably and reproducibly at a certain level of exercise and is relieved with rest or nitroglycerin

2b. Unstable angina

Unstable Angina See lecture 12, slide 8
Increase in anginal frequency, severity, or duration Angina of new onset or now occurring at low level of activity or at rest. May be less responsive to sublingual nitroglycerin. Same as stable angina, although changes during discomfort may be more pronounced; occasional ST-segment elevation during discomfort. Plaque rupture with platelet and fibrin thrombus, causing worsening coronary obstruction. Aspirin, Anti-ischemic medications, Heparin or LMWH Glycoprotein IIb/IIIa inhibitors, Statins

2c. Prinzmetals angina

Prinzmetal's or variant angina
See lecture 12, slide 9 Angina without provocation, typically occurring at rest Transient ST-segment elevation during pain Often with associated AV block or ventricular arrhythmias Coronary artery spasm Calcium channel blockers, Nitrates

2d. Atypical chest pain I’m not sure… pretty vague term

2e. MI You know… You know…

3. Coronary vasospasm treatment

Prinzmetal's or variant angina
See lecture 12, slide 9 Angina without provocation, typically occurring at rest Transient ST-segment elevation during pain Often with associated AV block or ventricular arrhythmias Coronary artery spasm Tx with Calcium channel blockers Nitrates

Cm - cardiopulm Exam 1 lectures 1-12

Similar presentations

Presentation on theme: "Cm - cardiopulm Exam 1 lectures 1-12"— Presentation transcript:

Similar presentations

About project

Feedback

Log in

Auth with social network:

Cm - cardiopulm Exam 1 lectures 1-12

Similar presentations

Presentation on theme: "Cm - cardiopulm Exam 1 lectures 1-12"— Presentation transcript:

Similar presentations

About project

Feedback