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
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
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
4
Q
Left Coronary
A
- Supplies anterior / left part of LV (most of it)
5
Q
Right Coronary
A
- supplies most of RV and posterior part of LV
- in 80-90% of people
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
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
8
Q
Normal resting flow
A
- 70 ml/min/100 grams
- 225 mls/min antegrade
- 4-5% of CO
9
Q
When does coronary flow happen
A
- Diastole
- Resistance in systole too high to flow well
- Flow=dP/R
10
Q
What determines target flow on pump
A
- Delivery pressures
- Flow is what it is at delivery pressure
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%
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
13
Q
Aerobic metabolic conditions
A
- 70% of energy from fatty acids
14
Q
Anaerobic metabolic conditions
A
- heart cannot function under this….not enough energy
- Glycolysis consumes glucose which produces lactic acid
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
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
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
18
Q
Risk factors for Atheroslcerosis
A
- Genetics
- Obesity
- Sedentary lifestyle
- High BP
- High Cholesterol
- Diabetes
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
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
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
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
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)
- pericardium fills w/ fluid…heart cannot fill up…down CO
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
- Ionotropics: Digitalis/Dopamine/Dobutamine
- 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?
