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556 - Physiology & Pathophysiology II > Exam 2 - Heart Disease & Cardiac Failure > Flashcards

Exam 2 - Heart Disease & Cardiac Failure Flashcards

1
Q

Effect of lowered cardiac function on cardiac function curve

A
  • Drops curve
  • VR > CO at that RAP
  • RAP goes up until new equilibrium reached
  • Curve shift happens first and fast
  • Over time…new equilibrium reached
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2
Q

Coronary Heart Disease

A
  • Most common cause of death in Western culture
  • 35% of 65+yo die from CHD
  • Most common is ischemic heart disease
    - coronary occlusion
    - fib of heart
    - weakening of cardiac function
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3
Q

Coronary blood supply

A
  • Major vessels on surface of heart
  • Only innermost portion of endocardium is perfused by blood in the chambers
    - Branches are what supply the heart
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4
Q

Left Coronary

A
  • Supplies anterior / left part of LV (most of it)
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5
Q

Right Coronary

A
  • supplies most of RV and posterior part of LV

- in 80-90% of people

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6
Q

How does coronary flow return to heart

A
  • 75% via Coronary sinus
    • most of the flow from LV
    • also true for cardioplegia (except bi-caval)
    • which is why retrograde doesn’t protect heart as well
  • Most flow from RV via anterior cardiac vein directly to RA
  • Very small portion return via thebesian veins into all chambers
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7
Q

Coronary blood supply

A
  • Major vessels on surface (epicardial coronary arteries)
  • Branches come off at 90 degree angles down to subendocardium
  • LARGE subendo plexus allows more flow during diastole
    - big plexus to help overcome increased resistance during systole
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8
Q

Normal resting flow

A
  • 70 ml/min/100 grams
  • 225 mls/min antegrade
  • 4-5% of CO
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9
Q

When does coronary flow happen

A
  • Diastole
  • Resistance in systole too high to flow well
    • Flow=dP/R
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10
Q

What determines target flow on pump

A
  • Delivery pressures

- Flow is what it is at delivery pressure

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11
Q

What determines how much flow the heart gets

A
  • Metabolic activity
  • Changes in HR / strength of contraction / afterload
    • controlled by O2 levels in tissue
    • controlled by release of vasoactive substances
      - Adenosine (if high [adenosine]…heart is bad…too low O2)
      - Adenosine phosphate compounds
      - K / H / CO2 / NO / prostaglandins
  • 70-75% of O2 given to cardiac tissue is used by cardiac tissue
    - Venous sat is therefore 25-30%….mixed sat is 70-75%
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12
Q

Besides metabolic activity….what affects cardiac flow

A
  • Autonomic tone (Ach and NE)
    Direct: Ach dilates coronary arteries
    Alpha receptors constrict epicardial vessels
    - involved with vasospastic myocardial ischemia
    Beta receptors dilate intramuscular vessels
    Indirect: Bigger effect than direct
    Increase symp tone -> increase HR/contractility -> increase myocardial metabolism -> increase flow
  • Changes in metabolic activity overrides all this…metabolism changes determine all flow changes
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13
Q

Aerobic metabolic conditions

A
  • 70% of energy from fatty acids
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14
Q

Anaerobic metabolic conditions

A
  • heart cannot function under this….not enough energy

- Glycolysis consumes glucose which produces lactic acid

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15
Q

Most energy produced is used for…

A
  • Making ATP
  • 95%
  • Mostly for isovolumetric contraction
  • Breakdown of ATP to ADP releases energy (most common path)
    • ADP -> AMP -> Adenosine
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16
Q

Cell membrane in heart permeable to….

A
  • Adenosine
  • Intracellular [ ] goes down during ischemia
  • loss of intracellular adenosine base big player in cell death following ischemia to heart
  • Adenosine replaced at 2% per hour
  • Half Adenosine base lost in 30 minutes into ischemia
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17
Q

Two death time tables for Ischemic heart disease

A
  • Sudden: Acute Coronary occlusion / Vfib / Ventricle rupture
  • Slow: CHF
  • Most caused by reduced flow due to atherosclerosis
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18
Q

Risk factors for Atheroslcerosis

A
  • Genetics
  • Obesity
  • Sedentary lifestyle
  • High BP
  • High Cholesterol
  • Diabetes
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19
Q

Atheroslcerosis

A
  • Like an immune response rxn
  • deposition beneath endo cells but no actually in blood lumen
  • plaque formation bulges into vessel lumen
  • flow distal to bulge affected (turbulent and low flow)
  • plaque can burst through into blood - stimulates clots
    - don’t have to break through to get clot formation
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20
Q

Acute Coronary Occlusion causes

A
  • Clot formation (thrombus)
    • interaction w/ blood clot factors and plaque surface
    • clot can form and break off…block downstream… embolus
  • Coronary spasm of smith muscle
    • rough surface of plaque irritates smooth muscle
    • causes excess vascular wall contraction
  • Both stop blood flow….bigger the vessel…bigger the problem
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21
Q

Where is collateral circulation

A
  • none between big arteries
  • many bridges in arteries in 20-250 micron range
  • Sudden occlusion
    - bridges provide <50% flow
    - 24-48 hrs after block…collateral flow up…more bridges
    - 1 month… flow may be normal or close
  • Slow occlusion
    - patient may never get symptoms
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22
Q

MI

A
  • tissue death….once dead…it is dead
  • CAN have ischemia w/o infarction
  • cells distal to occlusion may die depending on extent of ischemia
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23
Q

Myocardial O2 requirements

A
  • needs 1.3 mls O2 / 100g of tissue to live (not actively)
  • Normal is 8 mls O2 / 100g tissue
  • Resting heart can survive if flow drops to 15-30% of normal
24
Q

MI effects

A
  • cells die when energy reserve depleted
  • tissues turn brown/blue since no saturated blood
  • vessels/membranes break down -> causes edema
  • cell death in 1-2 HOURS
25
Q

Physiologic changes of MI

A
  • Subendocardial muscle higher risk for MI than epi
    • due to higher R and less blood flow
  • not able to conduct normal/any electrical activity
  • not able to contract or provide SV
  • MI tissue loses mass / gets thinner / potential for aneurysm
26
Q

Death from acute coronary occlusion

A
  • Decreased CO
  • Block blood in pulmonary circ -> pulm edema
  • Heart fib
  • Heart rupture
27
Q

Decreased CO

A
  • dead tissue doesn’t help w/ contraction
  • tissue may bulge out -> force not only going toward contraction -> less EF
  • No adequate SV if 40%+ of ventricular mass infarcted
    • coronary shock / cardiogenic shock / cardiac shock
    • 70% of cardiac shock will die unless outside intervention
28
Q

Blocking of blood in pulmonary circulation

A
  • SV of LV drops -> more volume in pulm vessels
  • more pressure build up -> more fluid into 3rd space in pulm
  • Drop in SV means less renal flow -> Kidneys hold water
    (Only if CO not high enough to keep renal flow normal)
  • Immediate problem….but several days for symptoms to occur
  • Once pulmonary edema begins…death within hours
29
Q

Fib of ventricles

A
  • More common in big MI
  • Can occur in small MI or chronic coronary insufficiency
  • biggest risk in 10 min after MI / 1-3 hrs after MI
  • drop in K from ischemic cells / increase of extra cellular K
    • makes cells more sensitive to depolarize
  • injury current created (diff in potential from injured to healthy cells)
  • MI drops CO/BP -> up symp -> up irritability of cardiac cells
  • Infarcted tissue dilates and causes circus movement
    • non-unified contraction of heart
30
Q

Rupture of infarcted area

A
  • several days after MI….tissue gets thinner
  • risk of systolic stretch increases as area of infarction increases
  • if thin enough…can rupture
    • pericardium fills w/ fluid…heart cannot fill up…down CO
      (Example of input failure)
31
Q

Recovery of MI

A
  • Ischemic area size determines if death
  • cells in non-functional area die/recover in 3 weeks
  • dead cells replaced by fibrous tissue…makes heart stiff
    • less risk for aneurysm but poor contractility
  • Normal area of heart will hypertrophy to compensate
  • Important to decrease workload of patient
32
Q

Coronary steal

A
  • If workload too high after MI / during recovery
  • take flow away from ischemic areas
  • as work goes up…dilation…but not down in affected MI area
33
Q

Can heart fully recover from MI

A
  • May or may not
  • Need to generate enough CO and get rid of original ischemia
  • usually some form of hypoeffective as remains on cardiac curve
  • Level of activity depends on shift in cardiac function curve
34
Q

Heart reserve

A
  • 300-400%

- Can generate CO higher than needed

35
Q

NY classification

A

I - Cardiac disease but no symptoms
II - Mild symptoms (mild SOB, angina, slightly limitation)
III - Marked limitation even during normal activity
- comfortable only at rest
IV - Sever limitations / symptoms at rest / mostly bed bound

36
Q

Canadian Angina Grading Scale

A

1 - Angina only with strenuous exertion
2- Angina w/ moderate exertion
3 - Angina w/ mild exertion
4 - Angina at rest

37
Q

Angina Pectoris

A
  • Occurs when myocardial tissue is Ischemic
  • Does not mean you get MI
  • May be result of build up of waste -> stimulate nerve endings
    • Lactic acid / histamine / Kinins / Proteolytic enzymes
  • Felt in neck / face / L arm -> nerves that feel pain arise from same spot in spinal cord
38
Q

Treatment

A
  • decrease area of ischemia
  • Coronary vasodilators: Nitroglycerin
  • Systemic vasodilators (both given with inotropic agents)
  • Beta blockers: block sympathetic stim (long term solution)
  • blood flow back to Ischemic area (treat right away)
    • Thrombolytic agents
    • Balloon angio
    • stents
    • CABG
39
Q

Cardiac shock

A
  • Cardiac failure taken to the end stage
40
Q

Cardiac failure

A
  • any condition that decreases ability of heart to pump enough to meet needs of body
  • Decreased contractility
  • Damaged valves
  • Pericardial disease
  • Vitamin B deficiency (Beriberi)
  • Primary heart muscle disease
41
Q

Two factors that determine how one responds to drop in cardiac function

A
  • How bad the insult is
    - how much does the cardiac shift down
    - how much reserve is left
  • If enough cardiac function left for kidneys to maintain normal intake/output balance (CBV)
42
Q

Cardiac reserve

A
  • Max % that CO can go up above normal
  • Normal: from 5 to 13 - 260%
    Increasing RAP by 4
  • Hypereffective: from 5 to 25 - 500%
    Symp tone
  • Hypereffective + hypertrophy: 5 to 30 - 600%
  • Hypoeffective: any condition that lowers the reserve
43
Q

When symptoms of heart failure show

A
  • Hypoeffective heart can be to different degrees
  • at rest patient may be fine (enough CO)
  • depending on reserve…activity may induce symptoms if not enough CO can be reached based on metabolic need
    • Why we have NY classification system
    • SOB / muscle fatigue (ischemia) / big HR increase (symp)
44
Q

How can cardiac reserve be tested

A
  • via stress

- physical OR chemical

45
Q

Kidneys able to maintain normal function if

A
  • Normal MAP and CO

- If not…kidneys keep holding onto salt/water

46
Q

Acute moderate failure step 1

A
  • Cardiac function curve shifts down
  • No change in VR curve (no immediate CBV or Res change)
  • New equilibrium point reached
    • drop in CO but increase in RAP
  • Conditions last FEW SECONDS
47
Q

Acute moderate failure step 2

A
  • In seconds, ANS kicks in
    • Baroreceptors / Chemoreceptors / CNS Ischemic
  • Cardiac curve shifts up: up in HR/contractility
  • VR shifts up: constriction increases mean systemic fill pressure
  • New equilibrium up and right
  • CO up / RAP up again
  • Patient may feel ok / minor angina
48
Q

Acute moderate failure step 3

A
  • chronic stage….takes several days
  • After step 2…CO still lower…Kidneys hold salt/water
  • Urine output stops when CO drops 50-60% of normal
  • Increase in CBV / mean systemic filling pressure
  • Cardiac function curve shifts up: damaged tissue heals
  • VR curve shifts right: mean filling pressure up / more CBV
  • Slope of VR up: veins stretched by increase in CBV
  • Final equilibrium point based on extent of recovery…
    - more recovery…more reserve…able to be more active
49
Q

What if failure is not moderate…but severe

A
  • Not be able to compensate with ANS / Kidneys
  • CO not high enough for proper renal function
  • Continued holding of water/salt is bad for patient
  • Angiotensin II / Aldosterone will stay elevated
  • Minimum CO never met…VR keeps shifting right
  • RAP keeps increasing….never reaching minimum CO
  • Patient into cardiogenic shock
  • Graph shows multiple cardiac function curves after each compensation step
50
Q

Pharmacological treatment

A
  • Increase Cardiac function
    • Ionotropics: Digitalis/Dopamine/Dobutamine
      - Increase contractility but also O2 consumption
    • Increase BP: vasoconstrictor / Nitro
      - Maintain coronary flow and reduce amount of injury
    • Ionotropic/dilator combo
      - up cardiac performance but drop res. to drop O2 demand
  • Increase urine output
    • Diruetics: to get rid of that overload and rip RAP
  • Decrease salt/water intake
51
Q

Treat original causes

A
  • Flow back to ischemic heart
    - drugs that break clots
    - balloon angio
    - stents / CABG
  • Repair/replace damaged valve
  • Replace heart
52
Q

Edema due to failure

A
  • L failure / R normal = up volume in pulm circulation
  • increase in mean pulmonary filling pressure
  • increase mean pulmonary cap pressure
  • Once mean pulm cap pressure = pulm oncotic…
    Volume gets into interstitial and alveoli…
  • Patient drowns in 20-30 min.
53
Q

Capillary hydrostatic

A
  • pushes fluid out of caps
54
Q

Pulmonary oncotic

A
  • pulls fluid into caps from 3rd space

- normal is 28 mmHg

55
Q

What if R side failure…Normal L side

A
  • causes peripheral edema
  • does not happen immediately
  • begins during compensatory stage of failure
    • when increase in CBV / mean systemic fill pressure
  • driven by: decrease in glomerular filter rate
    Activation of renin-angiotensin system (more volume)
    More aldosterone
    Increase sympathetic tone
    - afferent arterioles constrict
    - more reabsorption
    - more renin / ADH release
56
Q

Lethal pulmonary edema

A
  • fluid leaks into 3rd space
  • O2 transfer goes down
  • less O2 for heart….drop in cardiac function
  • less O2 dilates periphery… increases VR
  • More VR adds more volume to pulm circ -> more pressure
  • Lethal cycle
57
Q

How to treat pulmonary edema

A
  • Get left heart to start working

- LVAD?

556 - Physiology & Pathophysiology II (8 decks)

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