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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
equation for calculating wall tension
wall tension = P*d/h= (systolic LV pressure x LV chamber diameter)/wall thickness
26
path to angina
1. ischemia 2. ATP loss 3. impaired relaxation (requires O2) 4. systolic dysfunction 5. ST depression 6. angina
27
variant angina ("prinzmetal")
angina @ rest, = ischemia due to coronary artery spasm; Dx: ST elevation Tx: nitroglycerine, beta-blockers, ASA
28
pathological findings of MI & their molecular causes
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
time intervals to tissue damage
20 minutes of ischemia: IRReversible damage 18 hrs - 4 days: coagulative --> total necrosis 2-3 weeks: fibrosis * 3-6 weeks: healing
30
partial vs. complete occlusion from coronary thrombosis
- Partial: NSTEMI, w/ ST depression & T wave inversion (= subendocardial MI), OR Unstable angina - Complete: STEMI / Q wave MI = transmural (all layers affected)
31
stunned myocardium
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
Hibernating myocardium
hypocontractile myocardium due to chronic hypOperfusion (not MI); ~immediately reversed when restore full blood flow. ie: from severely (& chronically) atherosclerotic coronary artery
33
Arrhythmias due to damaged conduction
(aka: increased parasympathetic tone) - sinus bradycardia - junctional escape rhythm - atrioventricular block * * these ppl need catheterization IMMEDIATELY & pacemakers**
34
Normal hemodynamic values (from catheterization)
``` 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
Recommended drug treatment for Congestive Heart Failure
#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
Contraindications for ACE inhibitors in CHF
* = 1st line therapy, but can't use if: - pregnant - renal stenosis - asthma - DM (only if unable to ID drops in glucemia)
37
causes of Dilated Cardiomyopathy (4 types)
1. familial/genetic (sarcomere proteins) 2. inflammatory (viral, sarcoidosis, peripartum, CT disorders) 3. toxic (EtOH, chemotherapy - ie: adriamycin) 4. neuromuscular
38
exam findings for diagnosing Hypertrophic cardiomyopathy
S4 w/ systolic murmur. * murmur: LOUDer w/ valsalva (when increase preload)
39
Restrictive Cardiomyopathy
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
Causes of Restrictive Cardiomyopathy
Infiltrates (4): amyloidosis, sarcoidosis, hemochromatosis, glycogen storage disease. Fibrosis (3): metastatic tumors, hypereosinophilic syndrome, radiation therapy.
41
True Anuerysm
bulging of vessel wall involving all 3 vessel wall layers, > 50% increase in diameter. 2 types: fusiform (symmetrical) or saccular (localized)
42
causes of aneurysm in ascending aorta
due to cystic medial necrosis, from: - bicuspid aortic valve - HTN - Connective tissue disease (Marfans, Ehlers-Danlos)
43
False Aneurysm
Bulging of vessel wall only lined by adventitial layer--> high risk of rupture! causes: infection, trauma
44
Key observation to Dx ductal-dependent coarctation of the aorta
systolic BP in legs LOWER than in arms (when supine)[should be same or higher if healthy]
45
transposition of great vessels vs. Tetralogy of Fallot
Transposition: cyanotic RIGHT AWAY at birth, no murmur usually, "Big blue, happy tachypnic newborn," w/ cardiomegaly. Tetralogy: cyanotic 1 month AFTER birth,
46
Leads showing INFERIOR MI
ST-elevation: II, III, aVFreciprocal: aVL
47
Leads showing LATERAL MI
St elevation: I, aVL (also V5, V6)reciprocal: II, III, aVF
48
leads showing SEPTAL MI
ST elevation: V1, V2
49
leads showing ANTERIOR MI
ST elevation: V4, V5* often w/ V-fib (common complication)
50
leads showing POSTERIOR MI
reciprocal change (ST depression): V1-V4* "carousel" shaped pattern
51
possible causes of S2 splitting
- Variable splitting, w/ inspiration: physiologic, RBBB, pulmonary stenosis - Fixed wide splitting: atrial septal defect - Variable reversed splitting ("paradoxical"): LBBB, LV failure, HTN
52
midsystolic click indicates
systolic mitral valve prolapse, | * later w/ increased LV volume.
53
causes of S3 & S4
``` S3 = early rapid filling S4 = vigorous atrial contraction ```
54
cause of opening snap
rheumatic mitral stenosis.
55
innocent flow murmur
twangy, crescendo-decrescendo systolic murmur; from high flow through normal valves.
56
P wave > 2.5 in lead II
Right atrial enlargement
57
prolonged P wave on ECG (> 1 mm, negative @ end)
Left atrial enlargement, P wave changes = in lead I, changes = early and negative
58
typical ABG results for pneumonia
Low V/Q --> hypoxemia due to focal shunt. * may have increased PaCO2 if severe lung damage.
59
obstructive disease PFT
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
PFT for restrictive disease
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
Variable Extrathoracic Upper airway obstruction
when tracheal P < atmospheric P w/ Inspiration (only, not expiration) --> trachea narrows. ==> reduced INspiratory limb (bottom) on Flow volume loop ie: laryngeal tumor
62
Obstructive vs. Restrictive Flow Volume Loops
Obstructive: scooped out expiratory limb, otherwise normal shape Restrictive: small, squished loop (shorter & earlier on horizontal axis)
63
Variable Intrathoracic Upper Airway obstruction
when pleural P > tracheal P => trachea narrows. ==> reduced EXpiratory limb (top) on Flow Volume Loop
64
Fixed Upper Airway obstruction
BOTH INspiratory & EXpiratory limbs reduced on flow volume loop(could be intrathoracic or extrathoracic)
65
measuring RV (residual volume) of lung
* cannot measure directly bc RV = volume left after maximal expiration! ==> RV = FRC - ERV(ERV = expiratory reserve volume)

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