March 20 - Cardiology Flashcards
Blunt aortic injury
Most common cause is MVA - sudden deceleration.
Injury most commonly occurs to aortic isthmus which is lethered by the ligamentum arteriosum, making it realtively fixed and immobile. Located between aortic arch and descending aorta
Most ant and post chambers of heart
RV most anterior and is most likely damaged by blunt trauma. LA is most posterior and can compress the esophagus or recurrent laryngeal nerve resulting in dysphasia and hoarseness
Coronary circulation
Aorta gives rise to R coronary and L main coronary.
R coronary supplies right side of heart and in 90% gives off PDA which supplies the inferior wall and inferior septum
L main coronary gives rise to LAD and L circumflex. LAD supplies anterior wall, ant septum, and apex. LCX supplies lateral wall. In 10%, PDA comes off of LCX
Mitral valve prolapse pathophys
Caused by stretching of chordae teninae and billowing of valves. Can lead to tear and sudden HF in a young woman
Locations of SA, AV nodes and bundle of his
SA node: right atrial wall
AV node: intra-atrial septum
Bundle of his: intra-ventricular septum
Paradoxical embolism: pathophys
Stroke from venous thromboembolism. Most common causes are ASD and PFO.
In ASD there is an open defect in the atrial wall due to absence of septum primum or secundum during development. Characteristic S2 split
PFO caused by fusion between primum and secundum not occuring after birth. Usually stays functionally closed because LA pressure exceeds RA pressure, but can get transient increases in RA pressure that produce transient R to L shunt and allow for paradoxical embolism to form
Beta1 receptors
Found in cardiac tissue and renal JG cells
Beta blocker selectivity
B1 selective: atenolol, esmolol, betaxolol, metoprolol (A through M)
B1 and B2: nadolol, pindolol, propranolol, timolol (N through Z)
Alpha and beta: carvedilol and labetaolol
S gallolyticus
Nonenterococcal group D strep. Causes subacute endocarditis. Associated with colon cancer in 25% of cases
Barorecptor physiology
Two baroreceptors
1) carotid sinus: uses glossopharyngeal to communicated with brain
2) aortic arch: uses vagus nerve to communicate
Increase BP results in increased stretch on baroreceptors and increased firing to brain. Brian responds via sympathetic and parasymathetic systems to alter HR and constrict and dilate vessels. Fast response (compared with slower venous response)
Venous pressure tracing
A wave: RA contraction (rise in pressure)
C wave: tricuspid valve closure
X descent: atrial relaxation
V wave: venous filling, opening of tricuspid valve
Y descent: emptying of atrium
Changes in venous pressure tracing: large a wave, canon a wave, absent a wave, giant v wave
Large a wave: tricuspid stenosis; atria have to contract harder
Canon a wave: AV dissociation, such as complete heart block; atria contract against closed tricuspid resulting in really high pressure
Absent a wave: afib, just see v wave after v wave
Giant v wave: tricuspid regurg
Liver angiosarcoma
CD31+ (PECAM1)
Associated with aresenic and PVC exposure
Nitroglycerin
Venodilator that acts by decreasing preload and decreasing cardiac demand. Large veins are most susceptible
At large doses, can also affect arterioles, causing flushing and headache
Mitral stenosis murmur
Opening snap caused by abrupt tensing of valve leaflets after S2. Timing correlates with severity of stenosis: increased severity results in increase LA pressure and valve opens more forcefully, decreasing A2 to opening snap interval.
Diastolic rumble intensity does not correlate well with stenosis severity
Lateral shift of PMI
Indicates an enlarged heart
Carcinoid heart disease
Fibrous deposits on tricuspid and pulmonic valves resulting in stenosis and regurg. Lungs inactivate serotonin so left side unaffected
Changes in murmurs with inspiration
Increases venous return to right side increasing intensity of R murmurs
Decreases venous return to left side, decreasing intensity of L murmurs
Maneuvers that alter preload and effect on murmurs
Increase preload: leg raise, squatting
Decrease preload: valsalva (increases intrathoracic pressure and compresses veins), standing (blood falls toward feet, away from heart)
Most murmurs increase when preload increased with exception of hypertrophic cardiomyopathy and mitral valve prolapse
Maneuvers that alter afterload and effect on murmurs
Increase afterload: hand grip
Decrease afterload: amyl nitrate
Increased afterload increases backward flow murmurs, decreases forward flow murmurs
Drug effects: additive, synergistic, and permissive
Additive: combined effect of two drugs equal to sum of their individual effects
Synergistic: each drug has an effect individually but when used together, effect is greater than their sum
Permissive: drug not effective alone but increases efect of a second drug, allowing it to have max effect
Cardiac cath placement
Ideally in common femoral artery below the inguinal ligament as placement above the ligament can cause retroperitoneal hemorrhage
Class III antiarrhythmic: names
amiodarone, sotalol, dafetilide
Adenosine
Activates K+ channels, increasing K+ conductance and causing membrane potential to stay negative longer, decrasing sinus rate and increasing AV node conduction delay. Used to diagnose supraventricular tachyarrhythmias
Non-bacterial thrombotic endocarditis
Bland thrombus without inflammation or valve damage. Related to hypercoagulability, often from malignancy
Trousseau syndrome
Migratory thrombophlebitis due to hypercoag of malignancy, Vessel inflammation due to clot appears as nodule under the skin
SA node location
Located in right atrium near SVC opening
Dopamine
Low dose: stimualtes D1 receptors on renal vasculature and tubules, increasing RPF and GFR
Medium dose: stimulates beta1 receptors, increasing cardiac contractility and systolic BP
High dose: stimulates alpha1 receptors, resulting in systemic vasocnostrction, increasing afterload and decreasaing CO
Effects of epinephrine vs phenylephrine
Epinephrine: alpha and beta
- increases systolic BP
- increases HR
- decreases diastolic BP
Phenylephrine: alpha only
- increases systolic BP
- decreases HR
- increases diastolic BP
Normal aging in heart
- decreased LV cavity size
- sigmoid shaped septum
- dilated aortic root
- enlarged LA
- lipofuscin
Retinal artery occlusion: presentation and cause
Presentation: sudden, painless, monocular vision loss
Cause: usually an embolism that passes from internal carotid to ophthalmic a to retinal a
Ergonovine
Used to diagnose coronary vasospasm of variant angina. Causes constriction of vascular smooth muscle by agonizing alpha and serotonin receptors. In those with variant angina, low doses stimulate symptoms
Fibrous cap of atherosclerosis
Laid down by vascular smooth muscle cells. Fibroblasts don’t play significant role in atherosclerosis
Dystophic calcification of aged heart valves
Due to chronic hemodynamic stress that results in cell necrosis, allowing for Ca++ to deposit
Great saphenous vein
Used for coronary bypass. Courses from medial foot up medial leg and thigh before diving deep inferolateral to pubic tubercle to join femoral vein. Surgical access via medial leg or in femoral triangle
Pathogenesis of infective endocarditis with strep
- Disruption of normal endocardium
- Focal adherence of fibrin and platelets creating a sterile nidus
- Bacteremia allows bug to colonize the nidus
Buerger’s disease pathology
Segmental vasculitis that extends into contiguous veins and nerves
Pathogenesis of tetralogy of fallot
Abnormal neural crest migration restuls in deviation of the infundivular septum during development resulting in malaigned VSD and overriding aorta
Pathogenesis of transposition of great vessels
Failure of the infundibular septum, formed from neural crest, to spiral
Pathogenesis of persistent truncus arteriosus
Infundibular septum, which forms from neural crest to divide aorta and pulmonary artery, only partially forms
Endocardial cushion defect
Associated with Down syndrome. Can cause both ASD and VSD
Coronary steal phenomemon
Seen when adenosine or dipyridamole (selective coronary vasodilators) are given to patients with CAD.
In CAD, collaterals are already maximally dilated to maintain flow to ischemic regions. The drugs vasodilate other coronary vessels, increasing flow to non-ischemic regions by “stealing” blood from collaterals that can’t further dilate. Results in worsened ischemia
Abdominal aortic aneurysm pathogenesis
Usually below the renal arteries. Transmural inflammation of the aortic wall results in degradation of elastin and collagen and weakening and expsnion of the wall, forming an aneurysm
Thoracic aortic aneurysm of syphilis pathogenesis
Vasa vasorum endarteritis (only in thoracic aorta because no vasa vasorum in the abdominal aorta)
Relationship between flow, resistance, and radius of vessel
Flow proportional to r^4
Resistance proportional to 1/r^4
Flow proportional to 1/R
Compensation in severe aortic regurgitation
In chronic, severe aortic regurg, the regurg flow increases LVEDV (preload) causing eccentric hypertrophy. This increases SV to maintain CO.
LVH: eccentric vs concentric
Eccenctric hypertrophy is increase in chamber size and decrease in wall thickness. Seen in volume overload (aortic or mitral regurg, MI, dilated cardiomyopathy)
Concentric hypertrophy is decrease in chamer size and increase in wall thickness. Seen in pressure overload (chronic HTN, aortic stenosis)
Diastolic heart failure vs systolic heart failure
Diastolic: normal LV ejection fraction and normal EDV with increased LV filling pressure. Caused by decreased LV compliance/increased wall stiffness.
Systolic: decreased LV ejection fraction with increased LVEDV and increased LVEDP
Most vulnerable vessels to atherosclerosis
Abdominal aorta and coronaries
Phentolamine
alpha antagonist
Used as an antidote to extravsation and ischemic necrosis during infusion
Cardiac tamponade: presentation, pathophys, treatment
Presentation: Typically follows severe trauma such as stab wound. Pulsus paradoxus, JVD, muffled heart sounds, hypotension
Pathophys: Blood accumulates in pericardial space and compresses heart chambers. Decreased LV size results in decreased SV and thus decreased CO and hypotension. Decreased RA size results in JVD.
Treatment: pericardiocentesis
IA antiarrhythmics
Disopyramide, quinidine, procainamid
Inhibit phase 0 depolarization, prolonging action potential
IB antiarrhythmics
Lidocaine, tocainide, mexiletine
Weak inhibition of phase 0, shortens action potential
IC antiarrhythmics
Moricizine, flecainide, propafenone
Strong inhibition of phase 0, no effect on AP duration
Thiazide: lesser known metabolic side effects
Hyperglycemia, hypercholesterolemia, hyperuricemia
Plaque stability
Determiens likelihood of rupture. Depends on strength of fibrous cap. Ongoing inflammation weakens plaque and predisposes to MI bcause activated macrophages secrete MMPs that degrade collagen
Severity of mitral regurg
Determined by presence of S3 gallop. Gallop indicates severe LV overload due to large volume of regurgitant flow
Fick principle
Calculate CO based on O2 consumption
CO=O2 consumption/arteriovenous O2 difference
Maintenance of CO when blood is lost
Constriction of veins, increasing preload, is most important mechanism
Formula for MAP
2/3 DBP + 1/3 SBP
Cardiac response to exercise
Initial response is to increase contractility, later increase HR. Coronaries dilate to increase O2 delivery to heart. SBP increases, DBP often decreases. SVR decreases due to dilation of skeletal muscles. EF increases and ESV decreases
Formula for blood flow/pressure
Delta P = CO x TPR = Q x R
Compliance
How easily a system can be stretched. High compliance =low resistance. Compliance = deltaV/delta P
Sign and symptom of aortic regurg
Widened pulse pressure results in involuntary head bobbing. Palpitations occur due to forceful contractions ejecting large stroke volumes
Paroxysmal supraventricular tachycardia
Due to reentrant impulses. Vagal maneuvers can be used to terminate as they increase AV node refractory period. PResents with sudden onset palpitations and tachycardia
Digoxin in afib
Enhances vagal tone leading to inhibition of AV node contraction although atria continue beating rapidly but ventricular response is controlled so that there is adequate diastolic filling time
Eisenmenger syndrome pathophys
L to R shunt results in increased flow through pulmonary vessels. This causes pulmonary vascular remodeling leading to PAH and shunt reversal
