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HD 1 > Cardiology > Flashcards

Cardiology Flashcards

0
Q

location of heart apex

A

used to palpate precordium to find apical impulse.

= in 4th or 5th intercostal spaces, along mid-clavicular line (in supine patient)

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1
Q

Jugular venous pressure

A

horizontal distance from sternal angle (aorta) to height of jugular distention (in neck).
Normal = 8 cm
Above normal –> CHF, tamponade, …

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2
Q

apical impulse

A 
gentle pressure ("tap") felt at apex of heart, 
= 1st 1/3 of systole
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3
Q

diastolic murmur

A

low sound heard with bell,

= from mitral stenosis

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4
Q

sounds heard with bell of stethoscope

A

LOW sounds

  • Rumble = diastolic murmur/mitral stenosis
  • gallop = S3 and S4
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5
Q

sounds heard with diaphragm of stethoscope

A

HIGH pitched sounds,

  • S1 and S2 (normal)
  • ejection/mid-systolic clicks
  • aortic regurgitation murmur
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6
Q

S1 heart sound

A

= mitral and tricuspid valves closing (AV valves),
normal. before carotid pulse. loudest at apex.
* changes w/ leaflet mobility & rate of L ventricular rise
Abnormal: short P-R interval, mitral stenosis

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7
Q

S2 heart sound

A

= semilunar valves closing (aortic and pulmonic)
normal. loudest at base. after carotid pulse.
* physiologic splitting: w/ exhale A closes before P closes
Abnormal:
- wide split w/ exhale: RBB block or pulm. valve stenosis
- wide, fixed split: atrial septal defect
- paradoxical/reverse splitting: LBBB, left ventricular failure, or hypertensive cardiovascular disease

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8
Q

Gallop heart sounds

A

abnormal. = S3 and S4,
S3 = rapid LV filling (LA P < LV P), after S2.
S4 = vigorous LA contraction, before S1, @ max. LA pressure.
* sign of heart failure.

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9
Q

C-reactive protein

A

non-specific serum marker of inflammation,
*hsCRP assay (high sensitivity) to ID risk of atherosclerosis
BUT CRP does not CAUSE IHD
** also high CRP if: lupus, rheumatiod arthritis **
(so not useful atherosclerosis test in these patients)

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10
Q

current biomarkers for MI

A

1. Troponins (I or T):

rise 2-3 hrs after, peak 24 hrs, stay for 10-14 days 2. creatine kinase (CK-MB).  Also (older): Myoglobin, White cell count, AST
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11
Q

Forward heart failure

A

inability of the heart to pump blood forward sufficiently to meet metabolic demands of the body

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12
Q

Backward heart failure

A

inability of the heart to pump sufficient blood to body to meet metabolic demands EXCEPT when cardiac filling pressures are abnormally high.

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13
Q

preload

A

ventricular wall tension at the end of diastole.
= end diastolic Pressure
– if high => increased CO

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14
Q

afterload

A

degree of pressure to overcome during systole.
= wall stress during systole [= (P x r)/(2 x thickness)]
–> measure as systolic pressure

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15
Q

systolic Heart Failure

A

impaired ventricular contractility

  • -> increased afterload
    1. normal filling (but enlarged ventricles),
    2. decreased % blood pumped out
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16
Q

diastolic heart failure

A

impaired ventricular filling;

  1. stiff ventricles –> reduced filling (less volume in)
  2. ~same % pumped out, but since total volume = less, still less blood out to body
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17
Q

concentric hypertropy

A

add muscle fibers in parallel, so get thick walls.
can be from:
- Aortic stenosis (HTN)
- pulmonary stenosis (pulm. HTN)

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18
Q

eccentric hypertrophy

A

add myocyte fibers in series, so dilate chambers (walls not thicker),
from: aortic insufficiency, mitral regurgitation, pulmonic insufficiency, tricuspid regurgitation, shunts

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19
Q

calcific aortic stenosis pathogenesis

A

increased LDL combines with inflammatory cells, and interacts w/ myocytes –> causes smooth muscle cell proliferation and ossification of cardiac tissue (by osteopontin).

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20
Q

aortic stenosis clinical picture

A

Sx: syncope, angina, dyspnea
Test findings:
- echo: reduced valve opening, dilated chambers, calcified valve
- ECG: ???
Tx: diuretics, inotropes, vasodilators;
* need surgery to replace valve if have Sx!

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21
Q

3 possible causes of aortic stenosis

A
  1. bicuspid stenosis
  2. calcific stenosis
  3. rheumatic stenosis
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22
Q

3 main types of lesions in congenital heart defects

A
  1. Left to right shunt - increased BF to lungs
  2. Right to Left shunt
  3. Obstruction(s)
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23
Q

Left to right shunt (a congenital heart defect)

A

shunt of oxygenated blood into pulmonary flow, => increase pulmonary BF
ie: ventricular septal defect, atrial septal defect, patent ductus arteriosus
Long-term: pulmonary HTN (w/ sm m hypertrophy) –> SWITCH to Right-Left Shunt (BAD!)

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24
Q

Eisenmenger Syndrome

A

Central cyanosis, exercise and risk of sudden death

bc de-oxygenated blood is being pumped into systemic circulation (w/ congenital R-L shunt)

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25
Q

Long term complications of Cyanotic Heart Disease

A
  • Failure to thrive (low O2 perfusion to body)
  • Polycytemia (too many RBCs)
  • Digital clubbing (chronic hypoxemia)
  • Cerebral hypoxemia (poor neuro f(x))
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26
Q

Right to Left Shunt (congenital defects)

- Problem - Causes

A 
Problem: mix deoxygenated blood in LV, pump to systemic circ.,
--> hypoxemia, cyanotic heart disease
Causes = "terrible T's"
- Transposition of the Great Vessels
- Tetralogy of Fallot
- Truncus Arteriosus
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27
Q

Common causes of Congenital Heart Obstruction

A
  • Aortic atresia
  • Aortic coarctation
  • Pulmonary stenosis
    • often occur w/ shunt (structural “defect”) which allows for circulation & survival! (ie: VSD, ASD, patent ductus)
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28
Q

Ductus Arteriosus (normal)

A

in the fetus, connects RV/Pulm. artery to aorta
–> shunts blood into systemic circulation bc all blood is oxygenated by mom (enters via placenta), so no need to go to lungs

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29
Q

Closure of ductus arteriosus

A

stimulated by decrease in prostaglandin levels.
–> when placenta cut (placenta secretes prostaglandins)
–> when take NSAIDs
*may be dangerous if need the shunt to provide blood to body!
=> prevent closure by giving exogenous prostaglandins

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30
Q

Ductus-dependent Lesions (congenital)

A

(when ductus shunt provides most or all oxygenated blood for body)

  • neonatal emergency, MUST give prostaglandin E until fixed!
  • transposition w/ intact septa
  • aortic atresia
  • interrupted aortic arch
  • hypoplastic left heart
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31
Q

Ventricular Septal Defect (congenital)

A

L to R shunt, (bc LV has higher P)

  • Large –> heart failure @ birth; => failure to thrive bc can’t meet metabolic need (from high work of breathing).
  • Small –> holosytolic murmur w/ mid-diastolic rumble only after 2-6 wks bc pulm. vascular resistance changes; LA & LV hypertrophy; heart failure @ 3 mo.
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32
Q

Atrial Septal Defect

A

L to R shunt btwn atria, w/ diastolic flow murmur & fixed wide splitting of S2, classic RSR’ on ECG.

  • may be asymptomatic in adults,
  • secundum: incomplete closure of foramen ovale (gap persists)
  • primum
  • sinus venosus defect
  • flow determined by ventricular compliance
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33
Q 
Atrioventricular canal
(aka atrioventricular septal defect)
A

failure of endocardial cushions to fuse.
Complete = 3 problems:
- atrial septal defect
- ventricular septal defect/membranous ventricular septum
- AV valve abnormalities
** 50% of Down syndrome (trisomy 21) pts have AV canal**

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34
Q

“Conotruncal” abnormalities

A

= defects in arterial outflow tracts; cause cyanotic heart disease.

  • transposition of great arteries
  • truncus arteriosus
    • strong connection w/ Del 22q11 syndrome**
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35
Q

transposition of the great arteries

A

defect where connections to aorta & pulmonary artery = switched
(R ventricle to aorta, L ventricle to pulmonary artery)
* NEED shunt to survive!
- 40% stable VSD,
- 60% UNstable patent foramen ovale OR ductus arteriosus)
Tx: arterial switch surgery

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36
Q

Truncus Arteriosus

A

(aka: common arterial trunk)
failure of aorta and pulmonary artery to separate;
* often underlying VSD or other anomaly
–> cyanosis & high pulmonary blood flow

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37
Q

Del 22q11 syndrome

A

abnormal migration of neural crest cells to neck & upper thorax;
can cause conotruncal defects:
- transposition of great vessels
- tetralogy of Fallot
- Interrupted aortic arch
Also: thymic hypoplasia/aplasia, parathyroid defects

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38
Q

Tetralogy of Fallot

4 main features

A

most common cyanotic congenital heart defect
problems bc displaced “infundibular” (outflow) septum;
4 features:
1. pulmonary outflow tract stenosis
2. overriding aorta
3. Ventricular septal defect (VSD)
4. R ventricular hypertrophy

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39
Q

Tetralogy of Fallot symptoms

A
  • cyanotic episodes (“Tet spells,” bc of RV outflow tract spasms)
  • R to L shunt in 1st 6 months if “classic” (moderate/severe)
  • systolic ejection murmur
  • 2/3 pts also have valvar pulmonary stenosis, fewer pts: pulmonary atresia, NO associated CHF
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40
Q

Aortic Coarctation

A

= narrowing of the aorta, near ductus arteriosus;
=> infant heart failure, & BP higher in upper extremities than lower extremities
Often w/: bicuspid aortic valve, VSD (ventricular septal defect), other lesions
** some association w/ Turner’s Syndrome (monosomy X, aka 45X)

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41
Q

incidence of congenital heart disease

in live births

A

8/1000! (fairly common)

– most common = VSD

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42
Q

heart response to increasing metabolic demands

A
  • near maximal O2 extraction from coronary vessels at rest!

- -> MUST increase coronary blood flow to increase oxygen supply to heart.

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43
Q

3 factors influencing blood flow to heart

A
  1. basal viscous resistance (blood quality)
  2. autoregulatory resistance (resistance vessels dilate)
  3. compressive resistance (increase R w/ activity, highest in systole)
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44
Q

Effect of systole on heart tissue perfusion

A

In Systole: endocardium gets disproportionately LOW perfusion
(in diastole, all layers ~equal perfusion)

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45
Q

endogenous triggers for coronary vasodilation

A

Metabolic: hypoxia, high pH, high PaCO2, high adenosine
Neurologic: a-adrenergic and beta-adrenergic innervation
Endothelial factors (NO, adenosine indirectly)

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46
Q

Coronary stenosis (physiology, consequences)

A

coronary vessels become thickened –> increase resistance,
—> vessels dilate to compensate (even at rest).
=> worse w/ exercise (get ischemia) bc vessels are already @ max dilation.
* no significant Sx until 70%+ lumen narrowing!

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47
Q

2 main treatment strategies for ischemic heart disease

A
  1. Limit heart’s oxygen demand (beta blockers)
  2. Increase dilation capacity (nitrates, angioplasty/re-vascularization)
    * Re-vascularization treats Sxs, but does NOT change mortality rate.
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48
Q

4 determinants of O2 demand

A
  1. Wall tension
  2. heart rate
  3. contractility
  4. basal cost
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49
Q

equation for calculating wall tension

A

wall tension = P*d/h

= (systolic LV pressure x LV chamber diameter)/wall thickness

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50
Q

path to angina

A
  1. ischemia
  2. ATP loss
  3. impaired relaxation (requires O2)
  4. systolic dysfunction
  5. ST depression
  6. angina
51
Q

locating ischemic tissue w/ ECG

A
  • ST Depression if: ischemic tissue is behind healthy tissue
    (electrode on other side of healthy tissue from ischemia)
  • ST Elevation if: ischemic tissue = closest to the electrode
52
Q

Utility of exercise stress testing

A
  • Diagnosis of angina/ischemic heart disease
  • evaluating Prognosis of diagnosed CAD
  • Monitor efficacy of treatment
  • Screen for CAD/heart disease
53
Q

mechanism of action of nitrates (for angina/ischemic heart disease)

A
  1. coronary vasodilation (& coronary collaterals)

2. dilate systemic veins (–> decrease LV size = decrease wall tension)

54
Q

Classical Angina Pectoris

A

(= stress-induced endocardial ischemia, stops w/ rest bc return to fully compensated O2 perfusion)
Sx: diffuse visceral chest discomfort/pressure, 1-10 min., w/ stress & esp. in AM or after meals
Dx: exercise stress test (also: rales, S4, mitral regurg, tachycardia)
Tx: nitroglycerine & beta-blockers; + stop smoking, ASA…

55
Q

physical exam findings for angina & why

A
  • S4: stiff L ventricle
  • Mitral Regurgitation: papillary m. dysfunction
  • Rales: pulmonary congestion
  • Tachycardia (perfusion compensation)
56
Q

variant angina (“prinzmetal”)

A

angina @ rest, = ischemia due to coronary artery spasm;
Dx: ST elevation
Tx: nitroglycerine, beta-blockers, ASA

57
Q

common causes of myocardial infarction

A

atherosclerosis, aortic dissection, vasculitis, congenital anomaly, embolism, trauma, increased blood viscosity…

58
Q

main pathogenic recipe for MI

A
  1. endothelial injury
  2. platelet activation & clotting cascade
  3. failure of anti-thrombotic mechanisms
59
Q

steps involved in endothelial injury for MI

A

= Plaque rupture caused by stressors (infection, surgery, emotional/physical stress, hormones…) => decrease vessel diameter.

  1. macrophages/foam cells: degrade collagen of fibrous cap & make TF (pro-coagulant)
  2. T cells: increase macrophage synth, decrease collagen synth, & induce sm. m. cell apoptosis!
60
Q

Steps of platelet activation for MI

A

When blood is turbulent and endothelial collagen is exposed:

  1. platelets stick to endothelial integrins –> change formation
  2. secrete alpha granules
  3. aggregate (w/ more platelets)
61
Q

steps in coagulation cascade (causing MI)

A
  1. TF from macrophages/foam cells triggers activation of thrombin and fibrinogen.
  2. PAI (plasminogen activator inhibitor) stops plasmin from degrading clot.
62
Q

major reason for anti-thrombotic mech failure in MIs

A

Endothelial dysfunction –> less prostacyclin, EDRF, & NO

==> less vasodilation and platelet inhibition.

63
Q

pathological findings of MI & their molecular causes

A
  1. intracellular edema: low ATP production –> increased intracellular Ca2+ and extracellular K+
  2. chromatin clumping: lactic acidosis (low pH)
  3. PMN infiltration of tissue (= acute inflammatory response)
64
Q

time intervals to tissue damage

A

20 minutes of ischemia: IRReversible damage
18 hrs - 4 days: coagulative –> total necrosis
2-3 weeks: fibrosis
* 3-6 weeks: healing

65
Q

partial vs. complete occlusion from coronary thrombosis

A
  • Partial: NSTEMI, w/ ST depression & T wave inversion
    (= subendocardial MI), OR Unstable angina
  • Complete: STEMI / Q wave MI = transmural (all layers affected)
66
Q

stunned myocardium

A

injured but not necrotic myocardial tissue that remains dysfunctional after blood flow is restored; recovers over time.

Mech: Ca2+ overload from mitochondia, ROS accumulation, or disrupted excitation coupling.

67
Q

Hibernating myocardium

A

hypocontractile myocardium due to chronic hypOperfusion (not MI); ~immediately reversed when restore full blood flow.
ie: from severely (& chronically) atherosclerotic coronary artery

68
Q

Ventricular remodeling

A

changes in shape & thickness of the L ventricle due to MI
–> expand & hypercontract either infarcted or opposite wall.
==> decreased systolic f(x) & high risk of LV aneurysm!

69
Q

TIMI score

A 
used to quantify risk of MI (points if yes for each question)
Patient Hx: 
1. age > 65;	 2. 3+ CAD risk factors;
3. prior coronary stenosis > 50%, 
4. 2+ anginal events in past 24 hrs
5. took ASA in last 7 days
Test results:
6. ST shift on ECG;      7. + biomarkers (troponin, Ck-MB, etc.)
70
Q

treatments for MI

A

1: Re-perfusion (surgical angioplasty > thrombolytics)

  1. anti-platelet Tx (ASA, P2Y12 inhibitors, GP2b3a inhibitors)
  2. anti-thrombolytic Tx: (heparin, Xa inhibitors)
  3. cardioprotective (beta blockers, ACE Is/ARBs, nitrates)
71
Q

Common complications of MI

A
  1. Decreased contractility –> LV aneurysm, CHF
  2. Electrical instability –> Arrhythmias
  3. Tissue necrosis –> papillary m rupture, ventricular-septal rupture, myocardial rupture
72
Q

Cardiogenic shock

A

systemic hypoperfusion due to low CO; (w/ multi-vessel CAD)
Sx: systemic hypOtension, acidosis, cool extremities
Tx: use permanent balloon pump to hold coronary vessel open during diastole (so won’t collapse)

73
Q

cause of Recurrent Ischemia/Infarction after MI

A

= due to damage/injury of tissue from using balloon pump for re-perfusion.

74
Q

Arrhythmias due to electrical failure

A

(= ventricular)

  • PVCs - V-fib.
  • ventricular tachycardia
  • accelerated idioventricular rhythm
75
Q

Consequences of tissue necrosis (from MI)

A
  1. Papillary muscle rupture
  2. Ventricular Septal rupture
  3. Myocardial rupture
76
Q

Arrhythmias due to pump failure

A
  • sinus tachycardia
  • A-fib or Atrial flutter
  • paroxysmal supraventricular tachycardia
77
Q

Arrhythmias due to damaged conduction

A

(aka: increased parasympathetic tone)
- sinus bradycardia
- junctional escape rhythm
- atrioventricular block
* * these ppl need catheterization IMMEDIATELY & pacemakers**

78
Q

Common causes of heart failure

A

MI/CAD, HTN, valve disease, congenital heart disease, cardiomyopathies.

79
Q

Factors influencing Cardiac Output

A
  1. Heart Rate
  2. Stroke Volume
    - preload, afterload, & contractility
80
Q

Use of beta blockers for Heart Failure

A

YES: bc interrupts compensatory neurohormonal cycle (prevent pulm. edema & peripheral hypOperfusion)
BUT: careful not to use too much –> causes Na+ retention & myocyte hypertrophy/death (=> ischemia, arrhythmias)

81
Q

Compensatory endogenous responses to Heart Failure

A
  • increase Renin-Ang-Aldosterone system (increase blood volume)
  • increase sympathetic signaling (increase HR, vasoconstrict)
  • ventricular hypertrophy
82
Q

Pathologic changes w/ Heart Failure

A
  1. decrease contractility (bc chronic volume overload)
  2. increase afterload –> systolic dysf(x)
  3. impair LV filling & relaxation –> diastolic dysf(x)
83
Q

problems associated w/ systolic dysfunction from Heart Failure

A

Systolic dysf(x):

  • decrease contractility –> MI/ischemia, mitral/aortic regurg., dilated cardiomyopathy
  • increase afterload –> aortic stenosis, HTN
84
Q

problems associated w/ diastolic dysfunction from Heart Failure

A

= impaired LV filling & relaxation;

–> LV hypertrophy, trannsient ischemia, hypertrophic OR restrictive cardiomyopathies.

85
Q

NYHA classification of Heart Failure

A

Class I: no physical limitations
Class II: Sx (dyspnea, fatigue) w/ moderate activity
Class III: Sx w/ normal daily activities (minimal exertion)
Class IV: symptoms present @ rest

86
Q

Normal hemodynamic values (from catheterization)

A 
R atrium: 0-6 mmHg
R ventricle: 15-30/0-6
Pulmonary a: 15-30/6-12
L atrium: 6-12
L ventricle: 100-140/6-12 
Aorta: 100-140/60-80
87
Q

Phases of hemodynamic changes in heart failure

A
  1. warm & dry = normal perfusion, no edema
  2. warm & wet = edema/congestion from bc increase preload to maintain CO
  3. cold & wet = edema, no longer able to compensate for perfusion (cold extremities)
  4. cold & dry = end-stage. low perfusion (cold extremities) and loss of volume & CO (no edema)
88
Q

Common exam signs for congestion

A

orthopnea, edema, rales, systolic murmur & S3

89
Q

Common signs of poor perfusion

A

(= from low CO)

sleepy, cool extremities, pulsus alternans, hypotension when on ACE Inhibitor

90
Q

Goals of treatment for Heart Failure

A
  1. Identify and treat cause of heart failure
  2. manage symptoms (congestion & limit neurohormonal response)
  3. increase long term survival (*not possible for diastolic dysfunction)
91
Q

Recommended drug treatment for Congestive Heart Failure

A

1: ACE inhibitor & beta blocker

  • not b-blocker if volume overload*
    2nd line: ARB (if can’t tolerate ACE I)
    3rd: Nitrates & Hydralazine combo (if can’t tolerate 1st 2 options, OR esp. if african-american)
92
Q

Contraindications for ACE inhibitors in CHF

A
  • = 1st line therapy, but can’t use if:
  • pregnant
  • renal stenosis
  • asthma
  • DM (only if unable to ID drops in glucemia)
93
Q

Dilated Cardiomyopathy (DCM)

A

enlarged L ventricular chamber, may also have enlarged L atrium;
usually in ages 20-60, = #1 reason for heart transplant.

94
Q

Symptoms and tests for diagnosing Dilated cardiomyopathy

A

Sx: CHF, arrhythmias, sudden death; may be asymptomatic.
Dx: cardiac catheterization, ECG, echocardiogram, CMP (blood), thyroid & drug screens, genetic testing.

95
Q

causes of Dilated Cardiomyopathy (4 types)

A
  1. familial/genetic (sarcomere proteins)
  2. inflammatory (viral, sarcoidosis, peripartum, CT disorders)
  3. toxic (EtOH, chemotherapy - ie: adriamycin)
  4. neuromuscular
96
Q

Treatment for dilated cardiomyopathy

A
  1. alter diet - fluid and Na+ restriction
  2. ACE inhibitor & beta-blockers (if symptomatic)
    • may also use ARBs or diuretics
  3. anti-coagulants (if experience thromboembolic events)
97
Q

Hypertrophic cardiomyopathy

A

disease of the heart muscle –> enlarged intraventricular septum and/or L ventricular hypertrophy (not from CHF).
Sx: dyspnea, angina, syncope.
* most common age: ~20s

98
Q

exam findings for diagnosing Hypertrophic cardiomyopathy

A

S4 w/ systolic murmur.

* murmur: LOUDer w/ valsalva (when increase preload)

99
Q

treatment for hypertrophic cardiomyopathy

A

If…

  • No/mild Sx: no drugs
  • CHF: beta blockers, +/- diuretics (decrease afterload)
  • A-fib: cardioversion, rate control, & anti-coagulation
    • NO sports participation (= contraindicated for disease!)
100
Q

Restrictive Cardiomyopathy

A

rare disease of heart muscle => rigid ventricles & atria may be larger than ventricles.
Caused by infiltrates into muscle fibers OR muscle tissue fibrosis.
=> Normal contraction, but poor filling.

101
Q

Symptoms of restrictive cardiomyopathy

A

R heart failure, ascites, edema;

*must be distinguished from constrictive pericarditis!

102
Q

Causes of Restrictive Cardiomyopathy

A

Infiltrates (4): amyloidosis, sarcoidosis, hemochromatosis, glycogen storage disease.
Fibrosis (3): metastatic tumors, hypereosinophilic syndrome, radiation therapy.

103
Q

incidence of congenital heart disease in live births (in USA)

A

8/1000 (fairly common)

104
Q

congenital heart diseases that may NOT cause cyanosis

A
  • VSD
  • PDA
  • ASD
105
Q

treatment for Restrictive Pericarditis

A
  • Poor prognosis, but:
    1. treat underlying disease
    2. diuretics
106
Q

True Anuerysm

A

bulging of vessel wall involving all 3 vessel wall layers,
> 50% increase in diameter.
2 types: fusiform (symmetrical) or saccular (localized)

107
Q

causes of aneurysm in ascending aorta

A

due to cystic medial necrosis, from:

  • bicuspid aortic valve
  • HTN
  • Connective tissue disease (Marfans, Ehlers-Danlos)
108
Q

False Aneurysm

A

Bulging of vessel wall only lined by adventitial layer

  • -> high risk of rupture!
    causes: infection, trauma
109
Q

classes of aortic dissection (2)

A 
A = occurring before/up to aortic arch
B = occurring AFTER (distal to) the aortic arch
110
Q

treatment for aortic dissection

A

1: reduce BP & ejection force to limit progression of dissection

    • type A: surgical treatment (early = best)
    • type B: Percutaneous catheter repair
      • –> surgery ONLY if major branch occlusion or imminent rupture
111
Q

path of fetal blood circulation

A

placenta –> ductus venosus –> IVC;
R atrium –> foramen ovale –> L atrium (… -> aorta, body…)
*R ventricle –> pulmonary artery –> ductus arteriosus –> aorta
(to body, umbilical arteries –> back to mom)

112
Q

clinical appearance of Left-sided obstruction lesions (congenital defect)

A

cause anterograde conduction problems –> poor/no systemic perfusion!
* appear mottled & gray (like newborn strep) BUT have NO/weak femoral pulse!

113
Q

Key observation to Dx ductal-dependent coarctation of the aorta

A

systolic BP in legs LOWER than in arms (when supine)

[should be same or higher if healthy]

114
Q

transposition of great vessels vs. Tetralogy of Fallot

A

Transposition: cyanotic RIGHT AWAY at birth, no murmur usually,
“Big blue, happy tachypnic newborn,” w/ cardiomegaly.
Tetralogy: cyanotic 1 month AFTER birth,

115
Q

atherosclerosis

A

thickening of the inner layer of the aorta and muscular arteries w/ fatty deposits and fibrous tissue

116
Q

normal function of endothelium (4)

A
  • barrier to large molecs
  • modulate sm. muscle action
  • resist leukocyte adhesion
  • antithrombotic mechanisms
117
Q

steps of atherosclerosis formation (5)

A
  1. endothelial dysfunction (from oxidative & shear stress)
  2. lipid accumulation
  3. recruit leukocytes
  4. form foam cells
  5. deposit extracellular plaque
118
Q

layer of vessel wall which produces inflammatory molecs

A

Smooth muscle cells in media

* sm. muscle cell proliferation/hyperplasia in atherosclerosis

119
Q

characteristics of activated endothelium

A

(activated by irritants)

  • leaky - decreased NO & prostaglandin production
  • produce cell surface adhesion molecs
  • release inflammatory cytokines
120
Q

Causes of acute limb ischemia

A
  • Embolic (A-fib, MI, cardiomyopathy)
  • paradoxical embolism (if patent foramen w/ bearing down)
  • thrombosis in situ (atherosclerosis or trauma)
  • atheroembolism
121
Q

atheroembolism

A

crystals from plaque break off and obstruct SMALL vessles,
ie: after cardiac catheterization
“Blue toe syndrome”

122
Q

Reynauld’s Phenomenon

A

digital artery vasospasm induced by cold or vibration
- triphasic: 1. blanch, 2. cyanosis (blue), 3. “rubor” (red & sting)
may be primary or secondary
Tx: Ca channel blockers, alpha adrenergic antagonists

123
Q

types of primary vasculitis

A
  • Takayasu’s arteritis (“pulseless disease,” -> in carotid or limb pulses)
  • Giant cell arteritis (in temporal or opthalmic arteries)
  • Buerger’s disease (in male smokers, Tx: stop smoking!)
124
Q

modifiable risk factors for HTN

A

smoking, dyslipidemia, diabetes, obesity/sedentary lifestyle

125
Q

2 growth patterns for atherosclerosis

A
  1. stable plaque – steady rate, w/ fibrous cap.
  2. vulnerable plaque – growth spurts, w/ high risk of rupture (not well attached to wall)
    • rupture may be asymptomatic,
    • plaque hemorrhage will cause more growth

HD 1 (9 decks)

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