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

March 20 - Cardiology Flashcards

(67 cards)

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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
Non-bacterial thrombotic endocarditis
Bland thrombus without inflammation or valve damage. Related to hypercoagulability, often from malignancy
26
Trousseau syndrome
Migratory thrombophlebitis due to hypercoag of malignancy, Vessel inflammation due to clot appears as nodule under the skin
27
SA node location
Located in right atrium near SVC opening
28
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
29
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
30
Normal aging in heart
- decreased LV cavity size - sigmoid shaped septum - dilated aortic root - enlarged LA - lipofuscin
31
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
32
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
33
Fibrous cap of atherosclerosis
Laid down by vascular smooth muscle cells. Fibroblasts don't play significant role in atherosclerosis
34
Dystophic calcification of aged heart valves
Due to chronic hemodynamic stress that results in cell necrosis, allowing for Ca++ to deposit
35
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
36
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
37
Buerger's disease pathology
Segmental vasculitis that extends into contiguous veins and nerves
38
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
39
Pathogenesis of transposition of great vessels
Failure of the infundibular septum, formed from neural crest, to spiral
40
Pathogenesis of persistent truncus arteriosus
Infundibular septum, which forms from neural crest to divide aorta and pulmonary artery, only partially forms
41
Endocardial cushion defect
Associated with Down syndrome. Can cause both ASD and VSD
42
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
43
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
44
Thoracic aortic aneurysm of syphilis pathogenesis
Vasa vasorum endarteritis (only in thoracic aorta because no vasa vasorum in the abdominal aorta)
45
Relationship between flow, resistance, and radius of vessel
Flow proportional to r^4 Resistance proportional to 1/r^4 Flow proportional to 1/R
46
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.
47
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)
48
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
49
Most vulnerable vessels to atherosclerosis
Abdominal aorta and coronaries
50
Phentolamine
alpha antagonist | Used as an antidote to extravsation and ischemic necrosis during infusion
51
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
52
IA antiarrhythmics
Disopyramide, quinidine, procainamid | Inhibit phase 0 depolarization, prolonging action potential
53
IB antiarrhythmics
Lidocaine, tocainide, mexiletine | Weak inhibition of phase 0, shortens action potential
54
IC antiarrhythmics
Moricizine, flecainide, propafenone | Strong inhibition of phase 0, no effect on AP duration
55
Thiazide: lesser known metabolic side effects
Hyperglycemia, hypercholesterolemia, hyperuricemia
56
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
57
Severity of mitral regurg
Determined by presence of S3 gallop. Gallop indicates severe LV overload due to large volume of regurgitant flow
58
Fick principle
Calculate CO based on O2 consumption CO=O2 consumption/arteriovenous O2 difference
59
Maintenance of CO when blood is lost
Constriction of veins, increasing preload, is most important mechanism
60
Formula for MAP
2/3 DBP + 1/3 SBP
61
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
62
Formula for blood flow/pressure
Delta P = CO x TPR = Q x R
63
Compliance
How easily a system can be stretched. High compliance =low resistance. Compliance = deltaV/delta P
64
Sign and symptom of aortic regurg
Widened pulse pressure results in involuntary head bobbing. Palpitations occur due to forceful contractions ejecting large stroke volumes
65
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
66
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
67
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

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