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Step 1 > cardio (from HD1) > Flashcards

cardio (from HD1) Flashcards

1
Q

diastolic murmur

A

low sound heard with bell, = from mitral stenosis

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2
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 riseAbnormal: short P-R interval, mitral stenosis

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3
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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4
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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5
Q

preload

A

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

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6
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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7
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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8
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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9
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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10
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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11
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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12
Q

3 possible causes of aortic stenosis

A
  1. bicuspid stenosis
  2. calcific stenosis
  3. rheumatic stenosis
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13
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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14
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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15
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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16
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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17
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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18
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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19
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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20
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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21
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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22
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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23
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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24
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 (45 XO)

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25
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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26
Q

path to angina

A
  1. ischemia
  2. ATP loss
  3. impaired relaxation (requires O2)
  4. systolic dysfunction
  5. ST depression
  6. angina
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27
Q

variant angina (“prinzmetal”)

A

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

28
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)
29
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

30
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)
31
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.

32
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

33
Q

Arrhythmias due to damaged conduction

A

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

34
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
35
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)
36
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)
37
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
38
Q

exam findings for diagnosing Hypertrophic cardiomyopathy

A

S4 w/ systolic murmur. * murmur: LOUDer w/ valsalva (when increase preload)

39
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.

40
Q

Causes of Restrictive Cardiomyopathy

A

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

41
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)

42
Q

causes of aneurysm in ascending aorta

A

due to cystic medial necrosis, from:

  • bicuspid aortic valve
  • HTN
  • Connective tissue disease (Marfans, Ehlers-Danlos)
43
Q

False Aneurysm

A

Bulging of vessel wall only lined by adventitial layer–> high risk of rupture!
causes: infection, trauma

44
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]

45
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,

46
Q

Leads showing INFERIOR MI

A

ST-elevation: II, III, aVFreciprocal: aVL

47
Q

Leads showing LATERAL MI

A

St elevation: I, aVL (also V5, V6)reciprocal: II, III, aVF

48
Q

leads showing SEPTAL MI

A

ST elevation: V1, V2

49
Q

leads showing ANTERIOR MI

A

ST elevation: V4, V5* often w/ V-fib (common complication)

50
Q

leads showing POSTERIOR MI

A

reciprocal change (ST depression): V1-V4* “carousel” shaped pattern

51
Q

possible causes of S2 splitting

A
  • Variable splitting, w/ inspiration: physiologic, RBBB, pulmonary stenosis
  • Fixed wide splitting: atrial septal defect
  • Variable reversed splitting (“paradoxical”): LBBB, LV failure, HTN
52
Q

midsystolic click indicates

A

systolic mitral valve prolapse,

* later w/ increased LV volume.

53
Q

causes of S3 & S4

A 
S3 = early rapid filling
S4 = vigorous atrial contraction
54
Q

cause of opening snap

A

rheumatic mitral stenosis.

55
Q

innocent flow murmur

A

twangy, crescendo-decrescendo systolic murmur; from high flow through normal valves.

56
Q

P wave > 2.5 in lead II

A

Right atrial enlargement

57
Q

prolonged P wave on ECG (> 1 mm, negative @ end)

A

Left atrial enlargement, P wave changes = in lead I, changes = early and negative

58
Q

typical ABG results for pneumonia

A

Low V/Q –> hypoxemia due to focal shunt. * may have increased PaCO2 if severe lung damage.

59
Q

obstructive disease PFT

A

FEV1/FVC < LLN = obstructive disease
* high RV & often high TLC (bc air trapping)!
= slow emptying (bc decreased elastic recoil)
ie: asthma, COPD, upper airway obstruction

60
Q

PFT for restrictive disease

A

TLC < 80% predicted w/ symmetrically low RV (not if just poor effort)
(also often low FVC and high FEV1/FVC).
ie: interstitial lung disease, pulmonary fibrosis

61
Q

Variable Extrathoracic Upper airway obstruction

A

when tracheal P < atmospheric P w/ Inspiration (only, not expiration) –> trachea narrows. ==> reduced INspiratory limb (bottom) on Flow volume loop
ie: laryngeal tumor

62
Q

Obstructive vs. Restrictive Flow Volume Loops

A

Obstructive: scooped out expiratory limb, otherwise normal shape
Restrictive: small, squished loop (shorter & earlier on horizontal axis)

63
Q

Variable Intrathoracic Upper Airway obstruction

A

when pleural P > tracheal P => trachea narrows. ==> reduced EXpiratory limb (top) on Flow Volume Loop

64
Q

Fixed Upper Airway obstruction

A

BOTH INspiratory & EXpiratory limbs reduced on flow volume loop(could be intrathoracic or extrathoracic)

65
Q

measuring RV (residual volume) of lung

A
  • cannot measure directly bc RV = volume left after maximal expiration!
    ==> RV = FRC - ERV(ERV = expiratory reserve volume)

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