Cardio Stuff Flashcards
When does the heart start to develop in embryos?
4 weeks
- first functional organ*
What does a defect in Dynein (as seen in kartagener syndrome) do to the developing heart?
Dextrocardia (inverses the heart)
Patent foramen ovale
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.
What is the most common congenital cardiac anomaly?
Ventricular septal defects
What does the truncus arteriosus and bulbous cordis correlate to in the adult heart respectively?
Ascending aorta and pulmonary trunk = TA
Outflow tracts of left/right ventricles = BC
What are the three shunts important to Embryo circulation
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
What medication is given to close a patent ductus arteriosus (PDA)?
Indomethacin
- best NSAID at blocking synthesis of PGE series specifically
high levels of PGE is responsible for PDAs
What prostaglandins cause a PDA if in high doses?
E1/2
How does the fetal circulation change into adult circulation at birth?
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)
Ortner syndrome
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
What are the 3 layers of pericardium? What is the pericardium innervated by?
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
What are the parts of the coronary artery circuit
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
Cardiac output equation
CO = (Stroke volume) x (Heart rate)
Stroke volume: Increases - increasing contractility - increases preload - decreases afterload Decreases - everything opposite
What factors cause an increase in myocardial oxygen demand?
Increases contractility
Increases afterload
Increases heart rate
Increases diameter of the ventricle/ wall tension
What do each heart sounds correlate to?
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)
What are specific maneuvers used when determining heart murmurs and what effects do they have
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)
What are the two congenital long QT syndromes?
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
Brugada syndrome
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
Wolff-Parkinson white (WPW) syndrome
- 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
What is physiological splitting of the S2 sound?
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
What is wide splitting of the S2 sound a sign of?
Delayed RV emptying into pulmonary system
- RBBB
- pulmonic stenosis
- etc.
HEARD ONLY ON INSPIRATION
Is exaggerated physiological splitting of S2
What is a fixed splitting of S2 a sign of?
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
Paradoxical splitting of the S2 sound is a sign of what?
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
What is the standard conduction pathway in a normal heart?
SA node -> atria -> AV node -> bundle of his -> bundle branches -> purkinje fibers -> ventricles
- LBB divides into anterior and posterior fascicles, right only has 1*
Where is the SA node and AV node located
Between the RA and IVC = SA node
Posterior-inferior intraatrial septum = AV node
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 *
What does the presence of a U-wave usually indicated on a ECG?
Hypokalemia
How do you treat torsades de pointes?
Magnesium sulfate injections (IV)
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
What is the #1 highest risk factor for AAA aneurysms and dissections?
CAD/atherosclerosis
At what diameter is an AAA likely to rupture and needs immediate attention?
> 5cm
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
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)
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
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
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
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
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)
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
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
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
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.
