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test 2 Flashcards

(48 cards)

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1
Q

Significance of coronary heart disease

A

 35% of people 65 years and older die from coronary heart disease

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2
Q

Most common form is ischemic heart disease

A

 Acute coronary occlusion
 Fibrillation of heart
 Progressive weakening of cardiac function

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3
Q

what provides the nutrients to the myocardial tissues

A

-branches from the major blood vessels

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4
Q

what portion of the heart receives nutrition
directly from blood in chambers (1/10
mm)

A

-inner most portion of

endocardium

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5
Q

Left coronary supplies

A
  • anterior & left lateral part of LV
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6
Q

Right coronary supplies

A

most RV and posterior part of LV (80-90% of population)

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7
Q

75% of total coronary flow

returns to circulation via

A
  • coronary sinus

- most flow from LV

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8
Q

Most of the flow from RV returns to circulation via

A

-anterior cardiac veins directly to RA

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9
Q

Very small portion of flow returns to all cardiac chambers via

A

-thebesian veins

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10
Q

Coronary blood supply in the cardiac muscle

A

 Major vessels on surface of heart (epicardial coronary arteries)
 Branches come off at 90 degrees then dive all way to subendocardium
 “Large” subendocardial plexus allow increased flow during diastole

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11
Q

Subendocardial arterial plexus helps with what

A

-help overcome the large resistance so you can still get flow during systole

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12
Q

Normal coronary flow, resting human

A

 70 ml/min/100 grams
 225 mls/min
 4 to 5% of cardiac output
-resistance is very high in systole resulting in little flow even though pressure is very high

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13
Q

Coronary blood flow directly related to

A

-changes in cardiac metabolic activity
-Mediated by changes in tissue oxygen concentration and tissue release
of various vasoactive substances

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14
Q

increase in concentrations of adenosine means

A
  • we are not creating enough O2

- energy is being released at each level

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15
Q

normal venous sat in coronary sinus

A

-25-30%

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16
Q

only way to increase O2 in myocardial tissue

A

-increase coronary blood flow

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17
Q

Coronary blood flow directly and indirectly related to

A

-autonomic tone

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18
Q

direct effect of autonomic tone on coronary blood flow

A

 Direct effects created by interaction with acetylcholine and /or norepinephrine
 Acetylcholine has direct dilatory effect on coronary arteries
 Sympathetic alpha receptors: epicardial vessels (at the surface) –> constriction (vasospastic myocardial ischemia)
 Sympathetic beta receptors: intramuscular vessels (deep) –> dilation
 Changes in metabolic activity will usually over ride contradictory direct effects

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19
Q

indirect effect of autonomic tone on coronary blood flow

A

 Indirect effects created by changes in cardiac activity
 Have greatest affect on changes in coronary blood flow
 Increased sympathetic tone –> increased HR & contractility –> increased myocardial metabolism –> increased coronary blood flow due to increased metabolic activity

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20
Q

Aerobic conditions for metabolism

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A

-70% of energy comes from fatty acids

21
Q

during ischemia, the intracellular concentration of adenosine

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A
  • goes down
  • because cell membrane is permeable to adenosine
  • 1/2 adenosine will be lost in 30 mins
  • can replace adenosine 2% per hour
  • major contributor to cell death
22
Q

Most ischemic heart disease caused by

Study These Flashcards
A

reduced coronary blood flow due to atherosclerosis

23
Q

Atherosclerosis common contributors

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A 
 Genetics
 Obesity
 Sedentary lifestyle
 High blood pressure
 High cholesterol
24
Q

Atherosclerosis basic mechanism

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A

 Deposition of cholesterol beneath endothelial cells of arterial blood vessels
 Deposits invaded by fibrous tissue and calcium deposition
 Plaque formation that bulges into vessel lumen
 Blood flow distal to plaque will be affected (turbulent)
 Plaque may burst through endothelial cells so foreign surface of plaque in direct contact with the blood (clot formation)

25
Acute coronary occlusion caused by (2)
 Clot formation (thrombus) -Clot could form then break away, then completely block one or more vessels down stream (coronary embolus)  Coronary spasm of smooth muscle surrounding blood vessel
26
Collateral circulation
-normally not present in the large vessels but many in the smaller arteries
27
Collateral circulation during sudden occlusion
 Bridges able to provide <50% of flow needed via dilation of arteries  24 to 48 hours after occlusion, collateral flow begins to increase as new bridges created  Within 1 month flow may return to normal or very close to normal
28
Collateral circulation during slow occlusion
 Patient may never experience symptoms of cardiac dysfunction
29
Myocardial infarction
 Ischemic cells distal to the occlusion may die depending on the extent of the ischemia
30
Myocardial oxygen requirement
 Cardiac muscle needs 1.3 mls of oxygen per 100 grams of tissue  Under normal conditions 8 mls of oxygen per 100 grams is provided  Resting heart can still survive if coronary blood flow drops to 15% to 30% of normal
31
what happens during myocardial infarction
 When energy reserve within cells depleted, cells begin to die  Since blood within the area of the infarct has been desaturated, tissue turns bluish-brown color  Structure of blood vessels in the area breaks down allowing fluid to move into the interstitial spaces  Cell membranes begin to break down allowing intracellular fluid to move into the cells causing cellular edema  Cell death will occur within 1 to 2 hours (no blood flow)
32
what part of the heart muscle is at greater risk for infarction
 Subendocardial muscle at greater risk for infarction than epicardial muscles due to forces acting on epicardial blood vessels (higher resistance)
33
physiological changes of the infarcted tissue
 Not able to conduct normal electrical impulse so may actually generate abnormal impulses  Not able to contract or contribute to stroke volume  Infarcted tissue will begin to lose mass over time and become thinner (aneurysm)
34
most common causes of Death from acute coronary occlusion
 Decreased cardiac output  Damming of blood in pulmonary circulation and the pulmonary edema that results  Fibrillation of heart  Rupture of heart
35
Decreased cardiac output reason for cause of death
 Nonfunctional tissue does not contribute to contraction  Tissue may bulge outward during ventricular contraction (systolic stretch) so overall force of contraction is divided between the generation of stroke volume and movement / bulging of infarcted tissue (decrease in ejection fraction)  Heart not able to generate adequate stroke volume when 40% or more of ventricular mass is infarcted  70% of patients who go into cardiac shock will die unless there is outside intervention
36
Damming of blood reason for cause of death
 As stroke volume of LV decreases, more volume will accumulate in pulmonary blood vessels  Decreased stroke volume means less renal blood flow so kidneys begin to hold onto water  Usually does create an immediate problem but it takes several days for symptoms to occur  Once pulmonary edema begins to form, patient will die within hours
37
fibrillation of ventricles reason for cause of death
 Most common with larger infarctions, but can occur in patients with small infarctions or with chronic coronary insufficiency  Times of greatest risk: -during first 10 minutes after infarction -1-3 hours following infarction
38
Factors that add to potential for fibrillation
 Rapid depletion of potassium from ischemic cells and subsequent increase of extracellular potassium makes cells irritable (leaking out of K+)  Cells in infarcted area not able to completely repolarize so they remain at a different membrane potential from normal cells which can setup potential “injury current” from infarcted cells (potential difference)  Usually see decrease in cardiac output and blood pressure following myocardial infarction which leads to extensive sympathetic stimulation which will increase irritability of all cardiac cells  Infarcted tissue may dilate causing increased pathway length and vary abnormal pathway conduction which enhances potential for development of “circus-movment”
39
rupture of infarcted area reason for cause of death
 Several days following infarction, tissue of infarcted area begins to degenerate and will become thinner  Potential for systolic stretch increases as the area of the infarction increases  If area becomes thin enough, it can rupture during ventricular contraction (pericardium fills)
40
Recovery of ischemic area
 Size of ischemic area will determine if tissue will die  During recovery, the area of dead fibers will grow as cells within the non-functional area die -Cells in original non-functional area will either recover or die within 3 weeks  Fibroblast growth is stimulated within the area of dead cells so eventually dead cells replaced by fibrous tissue which will decrease in size over time  Normal areas of heart will hypertrophy to compensate for lost myocardial tissue
41
Recovery causes heart work to do what
-decrease myocardial workload of the patient  As myocardial work increases coronary arteries will undergo extensive dilation – but the extensive amount of dilation does not extend down to the level of the collateral vessels (coronary steal= epicardial layer gets high flow while deep tissue gets low flow)
42
Outcome of the heart from recovery
 Heart may or may not return to full functional capability (hypoeffective)  Heart has reserve of 300 to 400%  Level of activity the patient can maintain will depend on the overall shift of the cardiac function curve
43
Cardiac disease, but no symptoms and no limitation in ordinary physical activity, e.g. no shortness of breath when walking, climbing stairs, etc. (NY class)
I
44
Mild symptoms (mild shortness of breath and/or angina) and slight limitation during ordinary activity (NY)
II
45
Marked limitation in activity due to symptoms, even during less-than ordinary activity, e.g. walking short distances (20–100 m). Comfortable only at rest. NY
III
46
Severe limitations. Experiences symptoms even while at rest. Mostly bedbound patients NY
IV
47
Angina Pectoris
-Occurs when myocardial tissue becomes ischemic  May be result of build up of metabolic waste produces which stimulate pain nerve endings (lactic acid, histamine, kinins, cellular proteolytic enzymes)  May be felt in neck, side of face, left arm as the nerves carrying the pain sensations all arise from the same area of the spinal cord
48
Treatment
 Vasodilator drugs (coronary)  Vasodilator drugs (systemic)  Beta blockers (inhibit sympathetic stimulation)  Re-establish blood flow to ischemic area

Physiology II (20 decks)

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