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Block 2 Week 3 > MI & CHF Applications & Principles > Flashcards

MI & CHF Applications & Principles Flashcards

1
Q

what is myocardial ischemia?

A

an abnormality where nutrients and O2 supply don’t meet metabolic demands (MVO2)

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2
Q

What is a myocardial infarction?

A
  • an area of cell death due to prolonged ischemia
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3
Q

What are the 3 zones of a myocardial infarction ?

A

a) zone infarction: where the cells are dead due to complete loss of O2 and nutrients
b) zone of injury: surrounds area of infarction, functional impaired but can recover if blood flow quickly restored
c) zone of ischemia: blood flow is inadequate for normal function but enough to avoid irreversible injury, cell function reversibly repaired

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4
Q

What are the 6 signs of ischemia and infarction?

A

1) angina pectoris
2) dyspnea
3) diaphoresis
4) Nausea
5) Signs of dying heart muscle cells
6) EKG changes

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5
Q

What is angina pectoris?

A
  • a gradual onset of pressure & discomfort, never localized pain
  • referred pain from area of ischemia, cells release vasodilator metabolites but flow is blocked so no blood reaches dying cells
  • they activate SNS&PNS afferents that travel through spine and activate somatic pain receptors so angina perceived as visceral pain
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6
Q

What is dyspnea? diaphoresis?

A
  • dyspnea= uncomfortable awareness of breathing effort (shortness of breathe)
  • diaphoresis= cold sweats
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7
Q

What are the signs of dying heart muscle cells?

A

a) release of troponin-I, creatine kinase, myoglobin in the blood
b) ventricle dysfunction due to wall thickness (prolonged depolarization)

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8
Q

What happens to cells in the ischemic region?

A
  • cells have inadequate O2 delivery so have inadequate ATP synthesis
  • can’t fuel SERCA, Ca remains in cytosol longer promoting prolonged contraction
  • muscles remain in partial contraction= rigor or VENTRICLE STIFFENING
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9
Q

What causes the stiffening of the ventricle in the ischemic region?

A

1) slow and incomplete relaxation
2) Dissipaton of Na and K gradients due to insufficient ATP to fuel the pump. Now 3Na/Ca pump not working so more Ca in the cytoplasms
3) reduced contractile force due to acidotic env & inability to fully relax so can’t fully contract

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10
Q

What are the 7 metabolic consequences to ischemia (7)?

A

1) ATP generation interrupted
2) creatine phosphate stores consumed, [ATP] drops
3) metabolism converts to anerobic glycolysis, lactic acid and H+ accumulate as glycogen consumed
4) cytosol acidifies, myocytes loose contractility
5) impaired rate of relaxation (No ATP= cross bridges can’t release)
6) leak of K+ from the cell…Em depolarized (partially)
7) sustained contraction, rigor

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11
Q

Why does the ischemia result in depolarization?

A
  • the resting Em is partially depolarized
  • due to not enough ATP to fuel ATPase, K leaks to outside and not enough blood flow to wash it away, so equal K and now gradient equal can’t loose any more K so can’t repolarize the cell
  • now have an area of constant depolarization, causes rigor & slow conduction
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12
Q

What causes low conduction velocity?

A

-rate of depolarization
-size of depolarization
both decreased in ischemia

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13
Q

What happens to conduction through the ischemic zone?

A
  • the conduction velocity is reduced due to slow movement through the ischemic zone (slow depolarization)
  • some cells unable to conduct AP since are in permanent inactive state due to partial depolarization (decreased depolarization)
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14
Q

What are the consequences that result form fucked up conduction through ischemic region?

A

a) speed and path of excitation through the heart is altered (conduction velocity drops)
b) delayed conduction promotes re-entry (arrhythmia)
c) currents of injury

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15
Q

When is EKG trace truly isoleectic?

A

-in a healthy heart
a) systole (QT interval); when entire heart is depolarized (-) so no vector
B) diastole (TQ interval) where entire heart is repolarized so all (+) and no vector
look at lead 2, where positive pole is at left foot

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16
Q

What happens to EKG in transmural ischemia (as result of MI)?

A
  • ST segment elevation
  • diastole: the area of ischemia will not re-polarize, creates a current of injury w/ vector pointing from the (-) depolarized area up toward the re-polarized (+) area
  • this current points away from lead 2, so causes the once isoelectric TQ interval to now be below isoelectric
  • causes ST to look elevated
  • systole: entire heart depoalrized so have true isoelectric line
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17
Q

What does ST segment elevation signal?

A

-a transmural ischemia or SUPPLY ischemia

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18
Q

Supply ischemia vs demand ischemia?

A
  • supply: complete occlusion and ischemia even at rest

- demand: only ischemic when active due to incomplete occlusion

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19
Q

What is non-transmural ischemia? Where is it usually located

A
  • demand ischemia/ischemia during exertion
  • occurs most in the endocardium since it is subjected to a greater extravascular compression & further away from the blood supply (coronary arteries in epicardium)
20
Q

What happens to EKG in non-transmural ischemia?

A
  • Diastole: the endocardium remains partially depolarized (-) and the injury current vector points down towards the positive pole of lead 2 causes an above isoelectric TQ interval which shows as a depressed ST segment
  • in systole everything is depolarized (-) so true isoelectric
21
Q

Why do you get a reduced coronary perfusion pressure in ischemia?

A
  • ventricle in diastole can’t relax/expand well (reduced capacitance )
  • stiff ventricle reduces contractility so releasing a lower CO
  • the left ventricle diastolic bp is very low due to low capacitance & contractility , so low CPP
22
Q

How control supply? demand?

A
  • supply= blood flow, blood O2 content/saturation

- demand= work (P xV); HR, contractility, Wall Tension

23
Q

How decrease preload (volume work)? how increase it?

A

-decrease pre-load: organic nitrates (nitroglycerin),
diuretics (much slower)
-increase: intravenous infusions to increase the flow volume

24
Q

How decrease Afterload (pressure work)? how increase it?

A
  • decrease: vasodilator drugs (angiotensinogen, ACE)

- increase: vasoconstrictor drugs

25
Q

How do you manage angina and MI?

A

a) anti-ischemic therapy (MONA)
b) anti-coagulant therapy
c) anti-platley therapy
d) cardiac catheterization

26
Q

congestive heart failure

A
  • this is a secondary disease due to some initial damage of the heart
  • see a depressed starling curve
  • heart unable to pump enough blood to meet metabolic demands of the body, so adequate CO can only be reached by an elevated LV filling (pre-load)
  • must operate at higher pressure to satisfy baroreceptors & keep out of shock
27
Q

What is CHF characterized by?

A
  • fatigue
  • exercise intolerance
  • rapid resting HR (tachycardia)
  • pale, clammy skin
  • weak, thready pule due to low SV and perfusion
28
Q

What are the signs/symptoms of volume overload?

A
  • dyspnea (SOB)
  • rales (edema in lungs)
  • JVD due to high atrial pressure
  • edema in body
29
Q

orthopenia

A
  • dyspnea worked when supine (lying down)

- have to sleep with 1, 2, or 3 pillows so sleeping upright

30
Q

What is nocturia?

A
  • frequent need to urinate at night
  • since are laying down so less gravity effects and can better perfuse thorax, kidneys etc
  • now kidneys saying too much blood so try to release it all since had released none all day
31
Q

Kidneys compensatory action in CHF?

A

a) shitty CO results in hypotension which activate barroreflex which results in SNS acitvation (vasoconstriction) and RAA activation
b) shitty LV also causes poor renal perfusion which activates RAA
c) now have increased blood vol and CVP, are no longer at risk for hypotensive shock, but now blood volume so large at risk for pulm edema

32
Q

Consequences of kidneys compensatory actions in CHF?

A
  • if the RAA & SNS response too severe, then at risk for pulmonary edema which often leads to right heart failure
  • *left heart failure leads to right heart failure**
33
Q

Why is RAA elevated in CHF? And how prevent the negative side effects?

A
  • AT-II & aldosterone contribute to fluid retention & high filling pressures in CHF
  • to decrease pulmonary edema risks and pre-laod pressure use ACE inhibitors that prevent AT-I–> AT-II and prevent huge fluid accumulation
34
Q

What is captopril?

A

-ACE inhibitor

35
Q

What is losartan?

A

-AT-II inhibitor

36
Q

Why do we get edema in CHF? What are the 4 types of edema?

A
  • CHF leads to fluid volume overload which leads to systemic venous hypertension which leads to fluid transudation (edema)
    1) pedal edema
    2) dependent pitted edema
    3) JVD
    4) cardiac ascites
37
Q

what is cardiac ascites ?

A
  • a form of edema due to CHF fluid overload
  • hypertension causes right heart failure that leads to hepatic (liver) venous hypertension & congestion
  • transudate from liver accumulates in perineal cavity, and get several liters dissented from the abdomen
  • is VERY rare, only in SEVERE CHF
38
Q

What are the 2 forms of CHF?

A
  • systolic dysfunction: dilated cardiomyopathy, impaired ventricular contractility, LVEF reduced
  • diastolic dysfunction: impaired ventricular compliance/filling, LVEF is normal
39
Q

How does CHF ventricular remodeling occur?

A

1) first insult sends patient into CHF
2) early CHF heart compensates for high tension by hypertrophy (Law of LaPlacE), decrease tension
3) neurohumoral factors (SNS NE , AT-2) promote wall remodeling by acting on each myocardial cell, functioning myocytes replaced w/ fibrotic scar tissue (very thin), wall dilates to give systolic dysfunction

40
Q

CHF chest x-ray

A

a) prominent (distended) pulmonary vasculature w/ cephalization
b) Kerley B Lines
c) heart very very large when heart reached dilated cardiomyopathy stage

41
Q

cephalization

A
  • ## rising up, see near lungs is a sign of/due to pulmonary hypertension
42
Q

Kerley B Lines

A
  • fuzzy lines, a sign of pulmonary edema

- all fluid din lower aspect of lungs= transudate into interstitial space

43
Q

S3 and S4 in heart failure?

A

b) S4 atrial contraction (kick) into a stiff (ischemic) o hypertrophied ventricle, S4-S1-S2, often in early CHF
b) S3 hear due to rush of blood entering an already overfilled ventricle causing it to vibrate & release sound waves, indicated dilated ventricle, S1-S2-S3

44
Q

How does inotropic drugs effect the CHF frank-starling curve?

A
  • CHF lowers the starling curve down and to the right*
  • will simply raise the CHF curve up, so increases SV/CO without decreasing EDV (preload), is not ideal only used for severe situation
  • stay at risk for pulmonary edema
45
Q

How do vasodilator drugs effect the CHF frank-starling curve?

A
  • CHF lowers the starling curve down and to the right*
  • they increase the CHF curve up and to the left, so are the best to use
  • they increase SV/CO while and decrease SVR which decreases he Afterload pressure and preload pressure
46
Q

How do diuretics drugs effect the CHF frank-starling curve?

A
  • CHF lowers the starling curve down and to the right*
  • diurteics allows you to move down (to the left) of the new starling curve
  • so you loose blood volume which means less preload pressure, so leave pulmonary edema risk range BUT don’t improve CO/SV so now at major risk for shock

Block 2 Week 3 (6 decks)

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