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Designated study period: daily cards > March 20 - Cardiology > Flashcards

March 20 - Cardiology Flashcards

1
Q

Blunt aortic injury

A

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

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2
Q

Most ant and post chambers of heart

A

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

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3
Q

Coronary circulation

A

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

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4
Q

Mitral valve prolapse pathophys

A

Caused by stretching of chordae teninae and billowing of valves. Can lead to tear and sudden HF in a young woman

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5
Q

Locations of SA, AV nodes and bundle of his

A

SA node: right atrial wall
AV node: intra-atrial septum
Bundle of his: intra-ventricular septum

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6
Q

Paradoxical embolism: pathophys

A

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

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7
Q

Beta1 receptors

A

Found in cardiac tissue and renal JG cells

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8
Q

Beta blocker selectivity

A

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

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9
Q

S gallolyticus

A

Nonenterococcal group D strep. Causes subacute endocarditis. Associated with colon cancer in 25% of cases

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10
Q

Barorecptor physiology

A

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)

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11
Q

Venous pressure tracing

A

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

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12
Q

Changes in venous pressure tracing: large a wave, canon a wave, absent a wave, giant v wave

A

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

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13
Q

Liver angiosarcoma

A

CD31+ (PECAM1)

Associated with aresenic and PVC exposure

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14
Q

Nitroglycerin

A

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

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15
Q

Mitral stenosis murmur

A

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

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16
Q

Lateral shift of PMI

A

Indicates an enlarged heart

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17
Q

Carcinoid heart disease

A

Fibrous deposits on tricuspid and pulmonic valves resulting in stenosis and regurg. Lungs inactivate serotonin so left side unaffected

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18
Q

Changes in murmurs with inspiration

A

Increases venous return to right side increasing intensity of R murmurs

Decreases venous return to left side, decreasing intensity of L murmurs

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19
Q

Maneuvers that alter preload and effect on murmurs

A

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

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20
Q

Maneuvers that alter afterload and effect on murmurs

A

Increase afterload: hand grip
Decrease afterload: amyl nitrate

Increased afterload increases backward flow murmurs, decreases forward flow murmurs

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21
Q

Drug effects: additive, synergistic, and permissive

A

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

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22
Q

Cardiac cath placement

A

Ideally in common femoral artery below the inguinal ligament as placement above the ligament can cause retroperitoneal hemorrhage

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23
Q

Class III antiarrhythmic: names

A

amiodarone, sotalol, dafetilide

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24
Q

Adenosine

A

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

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25
Q

Non-bacterial thrombotic endocarditis

A

Bland thrombus without inflammation or valve damage. Related to hypercoagulability, often from malignancy

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26
Q

Trousseau syndrome

A

Migratory thrombophlebitis due to hypercoag of malignancy, Vessel inflammation due to clot appears as nodule under the skin

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27
Q

SA node location

A

Located in right atrium near SVC opening

28
Q

Dopamine

A

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

29
Q

Effects of epinephrine vs phenylephrine

A

Epinephrine: alpha and beta

  • increases systolic BP
  • increases HR
  • decreases diastolic BP

Phenylephrine: alpha only

  • increases systolic BP
  • decreases HR
  • increases diastolic BP
30
Q

Normal aging in heart

A
  • decreased LV cavity size
  • sigmoid shaped septum
  • dilated aortic root
  • enlarged LA
  • lipofuscin
31
Q

Retinal artery occlusion: presentation and cause

A

Presentation: sudden, painless, monocular vision loss

Cause: usually an embolism that passes from internal carotid to ophthalmic a to retinal a

32
Q

Ergonovine

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

33
Q

Fibrous cap of atherosclerosis

A

Laid down by vascular smooth muscle cells. Fibroblasts don’t play significant role in atherosclerosis

34
Q

Dystophic calcification of aged heart valves

A

Due to chronic hemodynamic stress that results in cell necrosis, allowing for Ca++ to deposit

35
Q

Great saphenous vein

A

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

36
Q

Pathogenesis of infective endocarditis with strep

A
  1. Disruption of normal endocardium
  2. Focal adherence of fibrin and platelets creating a sterile nidus
  3. Bacteremia allows bug to colonize the nidus
37
Q

Buerger’s disease pathology

A

Segmental vasculitis that extends into contiguous veins and nerves

38
Q

Pathogenesis of tetralogy of fallot

A

Abnormal neural crest migration restuls in deviation of the infundivular septum during development resulting in malaigned VSD and overriding aorta

39
Q

Pathogenesis of transposition of great vessels

A

Failure of the infundibular septum, formed from neural crest, to spiral

40
Q

Pathogenesis of persistent truncus arteriosus

A

Infundibular septum, which forms from neural crest to divide aorta and pulmonary artery, only partially forms

41
Q

Endocardial cushion defect

A

Associated with Down syndrome. Can cause both ASD and VSD

42
Q

Coronary steal phenomemon

A

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

43
Q

Abdominal aortic aneurysm pathogenesis

A

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

44
Q

Thoracic aortic aneurysm of syphilis pathogenesis

A

Vasa vasorum endarteritis (only in thoracic aorta because no vasa vasorum in the abdominal aorta)

45
Q

Relationship between flow, resistance, and radius of vessel

A

Flow proportional to r^4
Resistance proportional to 1/r^4
Flow proportional to 1/R

46
Q

Compensation in severe aortic regurgitation

A

In chronic, severe aortic regurg, the regurg flow increases LVEDV (preload) causing eccentric hypertrophy. This increases SV to maintain CO.

47
Q

LVH: eccentric vs concentric

A

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)

48
Q

Diastolic heart failure vs systolic heart failure

A

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

49
Q

Most vulnerable vessels to atherosclerosis

A

Abdominal aorta and coronaries

50
Q

Phentolamine

A

alpha antagonist

Used as an antidote to extravsation and ischemic necrosis during infusion

51
Q

Cardiac tamponade: presentation, pathophys, treatment

A

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

52
Q

IA antiarrhythmics

A

Disopyramide, quinidine, procainamid

Inhibit phase 0 depolarization, prolonging action potential

53
Q

IB antiarrhythmics

A

Lidocaine, tocainide, mexiletine

Weak inhibition of phase 0, shortens action potential

54
Q

IC antiarrhythmics

A

Moricizine, flecainide, propafenone

Strong inhibition of phase 0, no effect on AP duration

55
Q

Thiazide: lesser known metabolic side effects

A

Hyperglycemia, hypercholesterolemia, hyperuricemia

56
Q

Plaque stability

A

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

57
Q

Severity of mitral regurg

A

Determined by presence of S3 gallop. Gallop indicates severe LV overload due to large volume of regurgitant flow

58
Q

Fick principle

A

Calculate CO based on O2 consumption

CO=O2 consumption/arteriovenous O2 difference

59
Q

Maintenance of CO when blood is lost

A

Constriction of veins, increasing preload, is most important mechanism

60
Q

Formula for MAP

A

2/3 DBP + 1/3 SBP

61
Q

Cardiac response to exercise

A

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

62
Q

Formula for blood flow/pressure

A

Delta P = CO x TPR = Q x R

63
Q

Compliance

A

How easily a system can be stretched. High compliance =low resistance. Compliance = deltaV/delta P

64
Q

Sign and symptom of aortic regurg

A

Widened pulse pressure results in involuntary head bobbing. Palpitations occur due to forceful contractions ejecting large stroke volumes

65
Q

Paroxysmal supraventricular tachycardia

A

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

66
Q

Digoxin in afib

A

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

67
Q

Eisenmenger syndrome pathophys

A

L to R shunt results in increased flow through pulmonary vessels. This causes pulmonary vascular remodeling leading to PAH and shunt reversal

Designated study period: daily cards (32 decks)

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