March 20 - Cardiology Flashcards Preview

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Flashcards in March 20 - Cardiology Deck (67):

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



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



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



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


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



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

1. Disruption of normal endocardium
2. Focal adherence of fibrin and platelets creating a sterile nidus
3. 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



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



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