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Flashcards in cardio (from HD1) Deck (65):
1

diastolic murmur

low sound heard with bell, = from mitral stenosis

2

S1 heart sound

= 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

3

Forward heart failure

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

4

Backward heart failure

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

5

preload

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

6

afterload

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

7

systolic Heart Failure

impaired ventricular contractility--> increased afterload
1. normal filling (but enlarged ventricles),
2. decreased % blood pumped out

8

diastolic heart failure

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

9

concentric hypertropy

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

10

eccentric hypertrophy

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

11

calcific aortic stenosis pathogenesis

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

12

3 possible causes of aortic stenosis

1. bicuspid stenosis
2. calcific stenosis
3. rheumatic stenosis

13

Left to right shunt (a congenital heart defect)

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!)

14

Right to Left Shunt (congenital defects)- Problem - Causes

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

15

Ductus Arteriosus (normal)

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

16

Ductus-dependent Lesions (congenital)

(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

17

Ventricular Septal Defect (congenital)

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.

18

Atrial Septal Defect

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

19

Atrioventricular canal (aka atrioventricular septal defect)

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**

20

"Conotruncal" abnormalities

= defects in arterial outflow tracts; cause cyanotic heart disease.
- transposition of great arteries
- truncus arteriosus
** strong connection w/ Del 22q11 syndrome**

21

transposition of the great arteries

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

22

Del 22q11 syndrome

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

23

Tetralogy of Fallot (4 main features)

*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

24

Aortic Coarctation

= 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)

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)