Cardio Stuff Flashcards
(107 cards)
1
Q
When does the heart start to develop in embryos?
A
4 weeks
- first functional organ*
2
Q
What does a defect in Dynein (as seen in kartagener syndrome) do to the developing heart?
A
Dextrocardia (inverses the heart)
3
Q
Patent foramen ovale
A
Caused by a failure of septum primum and septum secundum to fuse after birth
- this is usually in response to increased LA pressure and decreased RA pressure when born, forming the atrial septum
Most are asymptomatic but can lead to paradoxical venous emboli entering arterial supply.
4
Q
What is the most common congenital cardiac anomaly?
A
Ventricular septal defects
5
Q
What does the truncus arteriosus and bulbous cordis correlate to in the adult heart respectively?
A
Ascending aorta and pulmonary trunk = TA
Outflow tracts of left/right ventricles = BC
6
Q
What are the three shunts important to Embryo circulation
A
1) ductus venosus
- blood entering fetal bypasses hepatic portal system and enters directly in IVC.
2) foramen ovale
- highly oxygenated blood bypasses lungs and moves straight from RA -> LA
3) ductus arteriosus
- deoxygenated blood moves from pulmonary artery -> aorta via this duct (since lungs dont work yet)
- aorta -> placenta to pick up oxygen
7
Q
What medication is given to close a patent ductus arteriosus (PDA)?
A
Indomethacin
- best NSAID at blocking synthesis of PGE series specifically
high levels of PGE is responsible for PDAs
8
Q
What prostaglandins cause a PDA if in high doses?
A
E1/2
9
Q
How does the fetal circulation change into adult circulation at birth?
A
Once the baby comes out and takes first breath:
- inflates lungs
- decreases pulmonary resistance
- increases LA pressure and decreases RA pressure (This closes foramen ovale)*
- increases oxygen saturation
- decreases prostaglandins due to maternal seperation (this causes the ductus arteriosus to shrivel and turn into ligamentum arteriosum)
10
Q
Ortner syndrome
A
A syndrome caused by enlargement of the left atrium, causing impingement onto the esophagus and left recurrent laryngeal nerve
- causes spontaneous dysphagia, hoarseness/muteness, pain in the throat
11
Q
What are the 3 layers of pericardium? What is the pericardium innervated by?
A
1) fibrous pericardium
2) parietal serous pericardium
* between 2/3 is where pericardial effusion occurs*
3) visceral serous pericardium
All 3 are innervated via phrenic nerve
12
Q
What are the parts of the coronary artery circuit
A
Left anterior descending artery (LAD)
- anterior 2/3 of IV septum
- anterior 2/3 LV
- LV papillary muscles
Posterior Descending artery (PDA)
- AV node
- posterior 1/3 of IV septum
- posterior 2/3 of RV/LV
- RV papillary muscles
Right coronary artery (RCA)
- SA node
- anterior 2/3 of RV
- right atrium
Left circumflex artery (LCX)
- posterior 1/3 LV
- Anterior 1/3 LV
- left atrium
Acute marginal artery
- anterior 1/3 of RV
- posterior 1/3 RV
coronary blood flow is primarily done in diastole
13
Q
Cardiac output equation
A
CO = (Stroke volume) x (Heart rate)
Stroke volume: Increases - increasing contractility - increases preload - decreases afterload Decreases - everything opposite
14
Q
What factors cause an increase in myocardial oxygen demand?
A
Increases contractility
Increases afterload
Increases heart rate
Increases diameter of the ventricle/ wall tension
15
Q
What do each heart sounds correlate to?
A
S1 = mitral/tricuspid valve closure
- loudest at mitral area
S2 = aortic/pulmonary valve closure
- loudest at left upper sternal border
S3 = rapid ventricular refill
- early diastole (after S2)
- loudest at apex in Left lateral decubitus
- can be abnormal (Mitral regurgitation/Atrial regurgitation/ Heart failure)
- can be normal (children and athletes)
S4 = “atrial kick” due to increased atrial pressure
- late diastole (before S1)
- loudest at apex in left lateral decubitus
- always abnormal (LV hypertrophy)
16
Q
What are specific maneuvers used when determining heart murmurs and what effects do they have
A
1) Standing valsalva = decreases preload
- less blood rushing through heart)
- increases MVP/HOCM
- decreases all other murmurs
2) Passive leg raise (increases preload) and squatting (increases afterload and preload)
- more blood rushing through the heart
- increases all other murmurs
- decreases HOCM and MVP (moves the anomaly out of the way so it sounds normal)
3) handgrip (increase afterload)
- more pressure needed to push out blood on left side of heart
- increases left-sided murmurs (AR/MR/MVP/MS) EXCEPT AS
- decreases right-sided murmurs (TR/TS/PS/PR), HOCM and AS
* AS decreases because pressure gradient across value decreases since LV pressure is close to matching systemic pressure*
4) inspiration (increases preload to right heart, decreased preload to left heart)
- increases right-sided murmurs (TS/TR/PS/PR)
- increases left-sided murmurs (MS/MVP/AS/AR/MR/HOCM)
17
Q
What are the two congenital long QT syndromes?
A
1) Romano-ward syndrome
- autosomal dominant
- causes NO deafness
- only causes prolonged QT segment
2) jervell and Lange-neilsen syndrome
- autosomal recessive
- causes deafness and prolonged QT segment
both cause loss-o-function in K+ ion channels of cardiac tissues, which predisposes to MIs and sudden cardiac death
18
Q
Brugada syndrome
A
Autosomal dominant disorder which causes a pseudo-RBBB w/ ST elevations
looks kind of like a heart attack
High in Asian populations
Increases risks spontaneous torsades de points and ventricular tachycardia.
- need implantable ICD
19
Q
Wolff-Parkinson white (WPW) syndrome
A
- most common type of ventricular pre-excitation syndrome*
- caused by accessory conduction pathway from the atria-> ventricle (called bundle of Kent)
- this bundle of Kent allows an impulse to bypass the rate-limiting AV node = ventricles slowly begin to depolarize quicker causing a “delta wave” w/ widened QRS.
Increases chances of supraventricular tachycardia and ventricular tachycardia
20
Q
What is physiological splitting of the S2 sound?
A
Increases in RV ejection time due to a drop in intrathoracic pressure from inspiration
- ONLY HEARD ON INSPIRATION
Also delays closure of the pulmonic value
Completely normal and okay
21
Q
What is wide splitting of the S2 sound a sign of?
A
Delayed RV emptying into pulmonary system
- RBBB
- pulmonic stenosis
- etc.
HEARD ONLY ON INSPIRATION
Is exaggerated physiological splitting of S2
22
Q
What is a fixed splitting of S2 a sign of?
A
Atrial septal defects (usually a left -> right shunt)
- causes increased volume through the pulmonic valve = increases pulmonic valve closure time
is heard in both inspiration and expiration at the same intensity
23
Q
Paradoxical splitting of the S2 sound is a sign of what?
A
Delayed aortic valve closure causing the semilunar valve to close before the aortic valve
- AS
- LBBB
CAN ONLY HEAR SPLIT ON EXPIRATION
- is not present on inspiration
24
Q
What is the standard conduction pathway in a normal heart?
A
SA node -> atria -> AV node -> bundle of his -> bundle branches -> purkinje fibers -> ventricles
- LBB divides into anterior and posterior fascicles, right only has 1*
25
Where is the SA node and AV node located
Between the RA and IVC = SA node
Posterior-inferior intraatrial septum = AV node
26
What is the order of speed of conduction through each part of the pathway (from fastest -> slowest)
Bundle of his = purkinje fibers > atria > ventricles > AV node
*SA generates the signal so conduction *
27
What does the presence of a U-wave usually indicated on a ECG?
Hypokalemia
28
How do you treat torsades de pointes?
Magnesium sulfate injections (IV)
29
Why does AAAs usually occur below the renal arteries (L2 segment)?
This area of the AAA lacks vasa vasorum, which makes the tunica media more susceptible to ischemia and therefore weakening of the vessels
30
What is the #1 highest risk factor for AAA aneurysms and dissections?
CAD/atherosclerosis
31
At what diameter is an AAA likely to rupture and needs immediate attention?
> 5cm
32
What are the common risk factors for TAAs?
HTN
Bicuspid aortic valve
Marfan/ehlos Danlos syndromes (connective tissue disorders)
Tertiary syphilis
- causes vasculitis in the vasa vasorum of the TA which can cause ischemia
33
Difference between Stanford type A/B dissections
Stanford type A:
- hits ascending aorta @ sinotubular junction
- treatment = surgery always (almost always ruptures)
- often heads into the carotid artery or coronary arteries which causes strokes and MIs respectively
Stanford type B:
- hits the left subclavian artery and descending aorta
- treatment = surgery or BBs/CBBs (depending on severity)
34
Where is the most common site of traumatic aortic ruptures?
The aortic isthmus
- located just after the left subclavian artery attachment
- this is because it is tethered by the ligamentous arteriosum which easily breaks due to trauma
35
What are the three most common cyanotic congenital heart defects that are caused by outflow tract abnormalities
Persistent truncus arteriosus
Transposition of the great vessels
Tetralogy of Fallot
36
Persistent truncus arteriosus
Cyanotic congenital defect that is caused by failure of neural crest cells to travel to the bulbus cordis which prevents it to spiral and form both he aorta/pulmonary artery
Results in both pulmonary artery and aorta to receive deoxygenated blood
37
Transposition of the great vessels
No spiraling of the aorticopulmonary system occurs (bulbus cordis and truncus arteriosus)
Causes aorta -> right ventricle and pulmonary artery -> left ventricle
- oxygenated blood stays in the lung system where as deoxygenated blood stays in the systemic system.
*requires a patent ductus arteriosus to stay open in order to keep infant alive for surgery*
38
Tetralogy of Fallot
4 main defects in 1:
1) pulmonary stenosis
2) RV hypertrophy
3) VSD
4) over ridding aorta over VSD
Symptoms appear at different parts of life based on degree of pulmonary stenosis
- the cyanosis especially is directly proportional to degree of pulmonary stenosis
- this is why some patients are cyanotic right out of the womb, whereas others takes months to show cyanosis
*very heavily tied to degeroge syndrome (22q11)
39
What is eisenmenger syndrome?
Can be seen in any congenital heart defect that is untreated, but specifically tetralogy of Fallot gets it the most.
Caused when pressure in the right side of the heart gets so high that it exceeds LV pressure so deoxygenated blood moves into LV
- under normal conditions, LV->RV
- also shows pulmonary HTN and RV hypertrophy
Causes late cyanosis, clubbing and Polycythemia
40
What is a “tet spell”
A spasm of the infundibular septum seen in tetralogy of Fallot patients.
Some actions (feeding, eating, crying etc.) cause cyanotic spells in infants with tetralogy of Fallot since the spasm increases pulmonary stenosis for a moment = cyanosis
*squatting down decreases the cyanosis and helps decrease the time frame of tet spell since squatting increases afterload*
41
Total anomalous pulmonary venous return (TAPVR)
A cyanotic congenital condition where pulmonary veins fuse somewhere along the right side of the heart instead of the left atrium while developing.
This induces a closed oxygenated circuit with the pulmonary system = cyanosis
*requires an ASD to be present in order to survive and always shows pulmonary HTN*
42
Tricuspid atresia
Malformation got he tricuspid valve during development causing either a fused shut tricuspid valve or no valve at all to be formed.
Incompatible with life (100% kill rate) UNLESS an ASD and a VSD are present as well.
- even in the best case scenario, still shows cyanosis due to RV atrophy.
43
What kinds of heart murmurs are present in cyanotic congenital heart defects?
Tetralogy of Fallot
- has a VSD
- holosystolic heart murmur at left lower sternal border
TAPVR
- has a ASD
- systolic ejection murmur at Left upper sternal border
Transposition of great vessels and PDA
- both have a PDA
- continuous machine like murmur between scapula/infraclavicular
Tricuspid atresia
- has both a VSD and ASD
- both holosystolic and systolic ejection click murmurs
44
What is an ebstein anomaly?
Idiopathic displacement of the tricuspid valve leaflets into the RV
Associated with tricuspid regurgitation, accessory conduction pathways and right sided HF.
- also prenatal lithium exposure
45
What is the pathophysiology behind patent ductus arteriosus?
Stable PGE synthesis and low oxygen tension allows the patent ductus arteriosus to stay open
Normally would close at birth due to increased oxygen tension and disabling of PGE synthesis
46
Pathophysiology of coarctation of the aorta
Aortic narrowing near the insertion of the ductus arteriosus
- the physiology behind closing the PDA now occurs at the aorta
- infantile form = before the ductus arteriosus insertion
- adult form = after the ductus arteriosus insertion
Associated with
- bicuspid aortic valve
- Turner syndrome
- cyanotic congenital heart defects
Symptoms:
* over time enlarges intercostal arteries and erodes ribs appearance is notched ribs on XRay*
- infantile form only = differential cyanosis
- both forms = brachial-femoral delay BP
Increases odds of:
- cerebral hemorrhages
- aortic ruptures
- endocarditis
- heart failure
47
What is Libman-Sacks endocarditis?
Endocarditis caused by systemic lupus erythematous
- also can be via any other autoimmune disorder that forms antigen-antibody complexes
antigen-antibody complexes bind and form vegetations on heart valves.
- called verrucous vegetations or “verrucae”
48
Rank the valves in order of most likely to be affected by endocarditis
Mitral valve
Aortic valve
Tricuspid valve
Pulmonary valve
49
What are the HÁČEK group of bacteria?
The following species and are normal flora in the mouth and throat
- Haemophilus
- Aggregatibacter
- Cardiobacterium
- Eikenella
- Kingella
Can be causes of native valve endocarditis
50
What are the different types of ANCA proteins
P-ANCA = autoantibodies against neutrophil myeloperoxidase
- microscopic polyangitis (MPA)
- Chung-Strauss (eosinophilic granulomatosis w/ polyangitis (GPA))
C-ANCA = autoantibodies against neutrophil proteinase-3
- Wegners (Granulomatosis w/ polyangitis (GPA))
51
What is granulomatosis w/ polyangitis (GPA) often confused with?
Goodpasture syndrome
- difference is there are NO UPPER RESPIRATORY TRACT SYMPTOMS in good pasture
- there is in GPA though
52
How to differentiate GPA from MPA?
MPA presents with NO NASOPHAYNGEAL SYMPTOMS (upper respiratory tract)
53
What is the pathergy test?
A test used for Behcets syndrome diagnosis
Insert a blunt needle into the skin and look for papule/pustule or ulceration at the site of insertion within 24-48 hrs
- (+) = has behcets
54
What are the infectious vasculitis?
1) Rocky Mountain spotted fever
- rickettsia rickettsii
- petechiae rash on hands/soles which spreads to trunk
2) Neisseria meningitidis infections
- meningitis w/ petechiae/purpura
- possible after house-friderichsen syndrome (infarction of adrenal glands)
3) syphilis
- spirochete treponema pallidum
- petechiae/skin chancre on genitals
- aortic anyeusms/ regurgitation
55
What are the most common secondary causes for all 3 catagories of cardiomyopathies?
Amyloidosis
Hemochromatosis
Sarcoidosis
Radiation/chemotherapy treatment
56
What is loffler endocarditis?
Restrictive infiltrative cardiomyopathy where eosinophilia causes eosinophils to infiltrate the cardiac tissue and causes fibrosis overtime
Diagnosed via diagnosing restrictive cardiomyopathy first and adding high eosinophil count and cardiac biopsy showing eosinophils in cardiac tissue
57
What are the specific heart sounds for each category of cardiomyopathy?
Dilated and restrictive = S3 heart sound
Hypertrophic = S4 heart sound at apex of heart
58
What medications are contraindicated in HOCM?
Dihysropyridine CBBs
Nitroglycerin
ACE inhibitors
Digitalis (positive inotropic agents)
59
Type 1 hyperlipidemia (hyperchylomicronemia)
Autosomal recessive genetic disorder that causes a deficiency in lipoprotein lipase (LPL) and apoplipoprotein C2
Symptoms:
- puritic xanthomas along the back and buttocks (Eruptive)
- acute pancreatitis
- hepatosplenomegaly
- creamy layer present on a fasting serum sample*
* DOES NOT PRODUCE ATHEROSCLEROSIS*
60
Type 2 hyperlipidemia (Familial Hypercholesterolemia)
Autosomal dominant disorder that results in an elevation of only LDL (type A) or both LDL and VLDL (type B).
- both are caused by a defect or absence of Apo-B100 protein receptors on hepatocytes
- defect or absence of Apo-B100 receptors causes hepatocytes to produce LDL de novo, increasing hypercholesterolemia
Symptoms:
- CAD/ MIs very early in life (starting at 20 yers old)
- Achilles tendon xanthomas
- corneal Arcus
*INCREASES DEVELOPING ATHEROSCLEROSIS*
61
Type 3 hyperlipidemia (familial dysbetalipoproteinemia)
Autosomal recessive disorder that results in a defective/absent apolipoprotein-E (ApoE)
- prevents uptake of VLDL from chylomicrons which leads to elevated VLDL and chylomicrons
Symptoms:
- similar to type 2 except the xanthomas are seen on the palm/hand tendons and skin
*INCREASES CHANCES OF ATHEROSCLEROSIS*
62
Type 4 hyperlipidemia (familial hypertriglyceridemia)
Idiopathic disorder where the liver generates VLDL levels at high rates
- lipoprotein activity is decreased as well, so the VLDL and chylomicrons is not broken down
- also leads to triglyceride levels
symptoms:
- similar to type 2
*VERY HIGH RISK OF EARLY ATHEROSCLEROSIS AND ACUTE PANCREATITIS*
63
Secondary causes of hyperlipidemia
Diabetes
Nephrotic syndrome
Hypothyroidism
Oral contraceptives,BBs and thiazides diuretics at high doses
64
Abetalipoproteinemia
Most common cause of hyperlipidemia
Autosomal recessive defects that leads to a deficiency in Microsomal triglyceride transfer protein (MTPs) and both ApoB-48 and ApoB-100
Leads to low levels of VLDL, LDL, chylomicrons, triglycerides, cholesterol total.
Symptoms:
- malabsorption of fat (steatorrhea, failure to thrive)
- fat soluble vitamin deficiency symptoms
- intestinal biopsy shows excess fats in cells
Treatment:
- decrease fat diet and vitamin E/A/D/K supplements
65
What is the cut off for hypertension?
130/80 that is persistent over a period of time
66
What is the cut off for both hypertensive emergency and urgency?
180/120
Urgency = no end organ failure/damage symptoms
Emergency = presence of end organ failure/damage symptoms
67
What is the most common cause of constrictive pericarditis?
Idiopathic reasons of coxsackie B virus infections = low income
TB = high income
68
What is kussmaul sign?
During inspiration jugular venous pressure rises instead of falls
Seen in constrictive pericarditis,
69
What is the becks triad
Three clinical signs associated with pericardial tamponade
1) JVD
2) Hypotension
3) distant hear sounds on auscultation
70
How to separate cardiac tamponade from tension pneumothorax?
Cardiac tamponade
- silent heart sounds
- symmetric chest wall expansion
Tension PNX:
- normal heart sounds
- asymmetric chest wall expansion
71
What are the three parts of virchows triad?
Stasis blood flow
Hyper-coagulability state
Endothelial injury
* three states that increase chances of DVTs/ clots to form*
72
What is May-Thurner syndrome
A syndrome which results in the left iliac vein being compressed between right Iliac artery and the lumbar vertebrae
- very high chance to develop DVTs
Symptoms:
- similar to DVTs/PEs
Treatment: requires stent placement, normal anticoagulation therapy isn’t enough.
73
Coronary steal syndrome
Mass coronary vessel dilation via administration of vasodilators.
- this is the syndrome that occurs during a pharmacological stress test for angina
Shows mass st depressions on ECGs
#1 used vasodilator is dipyridamole
74
What is acute coronary syndrome
Syndromes that are caused by disturbance to atherosclerotic plaques in the coronary arteries
Includes:
1) unstable angina
2) NSTEMI
3) STEMI
75
What are the 3 populations of people who can present without angina during acute coronary syndrome?
Females
elderly >65yrs
Diabetic patients
*instead they show with dyspnea, fatigue, dizziness*
76
What are the three key cardiac bio markers of cardiac cell death?
Troponin I and T
- elevated 2-4 hrs after infarction
- peaks 48 hrs
- stays elevated for 7-10 days
- *most useful for diagnosing acute infarction*
- * specific to heart
CK-MB
- elevated 2-4 hrs after infarction
- peaks 24 hrs
- stays elevated for 48 hrs
- *most useful for diagnosing reinfarction*
- *not specific to heart
77
Which leads show ST elevations in an anteroseptal MI?
V1/V2
The Left anterior descending artery (LAD) is the site of occlusion
78
Which leads show ST elevations in an anteroapical MI?
V3/V4
*the left anterior descending artery (LAD) is occluded*
79
Which leads show ST elevations in an anterolateral MI?
V5/V6
*the left anterior descending artery (LAD) and/or the left circumflex artery (LCX) are occluded*
80
Which leads show ST elevations in an lateral MI?
1 and AVL
*The left circumflex artery (LCX) is occluded*
81
Which leads show ST elevations in an inferior MI?
2/3/AVF
*The right coronary artery (RCA) is occluded*
** also often presents with epigastric abdominal pain instead of chest pain **
82
Which leads show ST depressions in an posterior MI?
V1/V2/V3
* the posterior descending artery (PDA) is occluded*
** also will show peaked r-waves **
83
What is the most common cause of sudden cardiac death?
>35 yrs old = ventricular arrhythmias (V. FIB)
<35 yrs old = HOCM
84
What is the time cutoff for reversible reperfusion therapy to work on an infarction?
30 minutes
85
Reperfusion injury
Is not fully known but is believed to be caused by a to quick influx of calcium in damaged cardiac myocytes, causing them to strongly contract and rupture/ cant relax and under go necrosis
- also oxygen returning might expose damaged cardiac myocytes to ROS species further enhancing damage
Must not rush the reperfusion in order to slow this down as best as possible.
86
How many readings on how many visits are required to diagnose someone with HTN?
2 separate readings on separate visits at minimum
- HTN diagnosis requires persistent HTN to be present
- also eliminates “white coat HTN” as a possibility
87
What is conn syndrome?
Primary hyperaldosteronism and is a cause of 2nd HTN
Caused by hyperplasia or tumors in the adrenal glands that release too much aldosterone and results in low renin levels.
Signs:
- aldosterone: renin ratio is high ( >35)
- hypokalemia
- metabolic acidosis
Symptoms:
- muscle spasms/weaknesses
- low back/flank pain
- paresthesia/tingling
- excessive urination
- stroke/MIs
88
What is Cushing syndrome?
A 2nd cause of HTN
Due to a tumor in the adrenal glands or pituitary gland or over medicated on corticosteroids (prednisone, etc.)
Causes increased cortisol levels in blood and increased ACTH levels
Signs:
- hyperglycemia
- high BP
- high ACTH
- high cortisol
Symptoms:
- hyperplasia of supraclavicular fat pads (“buffalo hump”)
- “moon facies”
- truckload obesity
- abdominal striae present
- increased hair in women
- headaches/malaise
89
What is the most common cause of isolated systolic HTN?
Aging of the aorta
90
What is Cushing triad?
A cause of 2nd HTN
Caused by increased ICP which triggers the CNS to increase arterial pressure to overcome the increased ICP.
- is often the 1st sign of acute increased ICP
Symptoms: Classic triad
- bradycardia
- HTN with a very wide pulse pressure
- chyne-stokes breathing pattern
91
How can you tell HTN retinopathy on a fundus exam?
Dot/flame-shaped hemorrhages throughout retina
Arteriovenous nicking throughout retina
Silver/copper wiring appearance of arteries (light up due to being occluded) throughout retina
92
What HTN drugs should be used in patients with HTN and heart failure?
ACEIs
ARBs
Aldosterone antagonists
BBs (NOT in decompensated HF)
93
What what HTN drugs to use with patients with HTN and diabetes?
ACEIs (especially)
ARBs (especially)
Thaiazide diuretics
Dihydropyridine
BBs (watch for hypoglycemia)
94
What HTN drugs to use with patients with HTN and asthma?
ARBs
Thazide diuretics
Dihydropyridine
Cardioselective BB (can only target B2)
*no ACE since it almost always causes coughing*
95
What HTN drugs should be used in patients with HTN and pregnancy
Hydralazine
Methyldopa
Labetalol
Nifedipine
*”Hypertensive Moms Love Nifedipine”*
96
Describe the embryology physiology behind atria Seperation in neonates
1) septum primum begins to form as a long out pouch of membranous tissue from the top of the single atria
2) septum primum moves down towards endocardial cushion until a could centimeters from closure (the hole left is called Ostium primum)
3) septum primum then fuses with endocardial cushion and closes the ostium primum. At the same time, a hole appears spontaneously in the septum primum called the osteum Secundum.
4) a second out pouch of membranous tissue just lateral to the septum primum forms called the septum secundum and grows to cover the osteum Secundum, but not enough to form a seal, so blood can shunt from the right -> left normally in neonate form
5) at birth, during the first neonate breath, the septum Secundum slams shut on the osteum secondum and fuses with the septum primum to form the atrial septum.
4) septum Secundum grows to c
97
What is a cryptogenic stroke?
A stroke caused by paradoxical emobil in a patient with a ASD/patient foramen ovale.
Emboli starts in venous system, and crosses into arterial system instead of pulmonary system via the ASD/ PFO.
98
In what congenital heart defects can differential cyanosis be seen?
Infantile form of Coarctation of the aorta
Patent ductus arteriosus
99
What is the ankle brachial index test (ABI)?
A diagnostic test used to determine PAD diagnosis
Take ankle systolic BP measurement and brachial systolic BP measurement
normal ankle BP/brachial BP ratio = 1.0
Positive PAD ankle BP/brachial BP ratio = <0.9
100
What is cilostazol?
A phosphodiesterase inhibitor that is used as 1st line therapy for PAD.
Dilated arteries and acts as an anti-platelet. Usually taken with asprin co-comittently
101
What are non-atherosclerotic causes of Peripheral artery disease (PAD)?
Thromboangitis Obliterans (Burgers syndrome)
Popliteal artery aneurysms
Atrial fibrillation
102
What are differential diagnosis of Peripheral artery disease?
1) DVT
- shows leg swelling. Erythema and pain which is not usually seen in PAD
2) lumbar spinal stenosis
- shows NORMAL peripheral pulses and ankle-brachial index tests, not seen in PAD
- also shows back pain is relieved with flexion of the back and worsens with extension of the back (neither is seen in PAD)
103
What is the general pathology behind an AV heart block?
The delayed signal between the AV note and bundle of His that allows for the ventricle to fill before contraction is delayed too much
104
What type of MI is most heavily associated with type 3 heart block formation?
Inferior MI
- occluded the Right coronary artery (RCA)
*RCA has a small branch that supplies the AV node*
105
Myxoma
Most common primary cardiac tumor in adults
- is made up of connective tissues and gelatinous material made up of glycosaminoglycans
*90% are found in the atria with 70% of the 90% being in the left atrium*
Are “ball valve” tumors in that they obstruct the mitral valve
- associated with multiple episodes of syncope
*Can show “tumor plop” murmur as an early diastolic murmur sometimes*
Fever and weight loss are also symptoms since the tumor promotes IL-6 production
Diagnosis = TEE imaging
106
Cardiac rhabdomyoma
Most common primary cardiac tumor in children
- benign hyperplastic growth of cardiac muscle
* Very heavily associated with tuberous sclerosis*
- will show adenoma sebaceous lesions throughout the skin
107
Are most cardiac tumors primary or secondary?
Secondary via metastasis
