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Functional cardiac disorders Flashcards

1
Q

what is CAD

A

atherosclerosis of coronary arteries- disease of the intima (inner lining)

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2
Q

what kind of disorder is CAD and how does it start

A

it is chronic and progressive

inflammation starts the process

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3
Q

what is the first stage of the CAD patho chain

A

inflammation-> endothelium damage-> lipids deposited-> lipids are oxidized and attract macrophages-> monocytes enter intima-> become macrophages which ingest LDL-> transformed into foam cells-> foam cells release cytokines-> cause inflammation and injury

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4
Q

what is the second stage of CAD patho

A

fatty streak starts causing narrowing

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5
Q

what is a fatty streak

A

yellow, lipid filled smooth muscle cell- an organized collection of foam cells

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6
Q

what is the third stage of CAD patho

A

fibrous plaque causes further narrowing

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7
Q

what is fibrous plaque

A

fatty streak + collagen + elastic fibers

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8
Q

what is the fourth stage of CAD patho

A

complicated (advanced) lesion hemorrhages causes clot formation and obstruction

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9
Q

what is complicated (advanced lesion

A

fibrous plaque (all the before things) hemorrhages

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10
Q

what is the incidence of CAD

A

1 killer in us and other developed counteries

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11
Q

what are the 3 most dangerous risk factors for CAD

A

smoking
HTN
hyperlipidemia

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12
Q

what are the other risk factors for hyperlipidemia in CAD

A

age,
male gender under 60,
genetic predisposition (under 35),
hyper lipidemia

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13
Q

what causes hyperlipidemia in CAD

A
  1. increase in dietary fat intake
  2. diabetes and genetics
  3. lipoproteins (lipids, phospholipids, cholesterol and triglycerides bound to carrier proteins
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14
Q

what are found in a blood lipid profile

A

total cholesterol
triglycerides
LDL
HDL

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15
Q

why does type 1 affect CAD

A

increased blood glucose accelerates CAD

2x men, 4x women

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16
Q

why does htn affect CAD

A

increased peripheral vascular resistances increases workload of heart and accelerates process of atherosclerosis

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17
Q

why does smoking affect CAD

A
  1. nicotine- causes release of epi and increases hr and vasoconstriction
  2. increased platelet adhesiveness- increases clot formation
  3. CO- attaches to Hgb
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18
Q

women and CAD

A 
women have a higher morality rate after acute MI
#1 killer of women all cancers together
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19
Q

how does cocaine and meth affect CAD

A

increases BP hr and causes vasoconstriction of coronary arteries

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20
Q

how does hyperhomocysteinemia affect CAD

A

causes injury to arterial walls

treat/prevent with folic acid (folate)

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21
Q

what is homocysteine

A

an amino acid from animal protein normally broken down in the liver with help of vitamin b6 b12 and folic acid.. increased amount CAD

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22
Q

how do we measure what is the role of inflammation in the development of CAD

A

c reactive protein– high sensitivity– increases measures inflammation

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23
Q

what is myocardial ischemia

A

local and temporary deficiency of blood supply due to obstruction of coronary circulation

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24
Q

how does CAD lead to angina

A

CAD-> myocardial ischemia after 10 seconds-> angina from lactic acid production during anaerobic respiration

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25
what are the classical (transient) signs of myocardial ischemia
3-20 mins pain- substernal pain, discomfort, heaviness, pressure, tightening, squeezing or aching may radiate to neck, left arm, jaw, teeth, back
26
what are the non classical signs of myocardial ischemia
indigestion upper back pain jaw pain ONLY increasing fatigue
27
what are the types of angina
stable | unstable
28
describe stable angina
predictable similar events initiate attack (stress activity) similar type of sensation with each attack relief WITH REST and nitrates
29
describe acute coronary syndrome
sudden coronary artery obstruction due to thrombus formation over atherosclerotic plaque
30
what kind of angina is with acute coronary syndrome
unstable- unpredicable sensation often OCCURES WITH REST | indicates advanced CAD
31
what is an MI
CAD that leads to myocaridal ischemia which leads to irreversible hypoxia and cellular death
32
what is the cause of MI
narrowed coronary artery and clot formation with 100% of coronary artery occluded
33
describe cellular injury in MI
1. first 30-60 seconds of hypoxia with EKG changes | 2. cells without o2 and nutrients lose contractility
34
describe cellular death (myocyte death) with MI
after 20 minutes (irreversible hypoxia injury) | death and necrosis
35
describe remidelng with MI
scar formation and loss of function of cardiac cells leads to thin poorly contracting ventricular walls
36
what is cell membranes rupturing mean with cellular death for MI
intracellular enzymes spill out into blood stream
37
what is the zone of ischemia in MI
outside ring | colateral circulation causes healing
38
what is the zone of injury in MI
middle ring | colateral circulation causes healing
39
what is the zone of infarction in mi
inner ring | doesn't heal and becomes scar tissue
40
describe the scar formation of an mi
zone of infarction-- 1. weak and mushy 10-14 days post MI 2. strong scar 6 weeks but does NOT contract/pump
41
clinical mani of classical MI
1. substernal pain an discomfort, heaviness, pressure, tightening, squeezing, aching 2. may radiate to neck, left arm, jaw, teeth, back 3. indigestion, nausea, vomiting 4. diaphoresis 5. cool clammy skin 6. change in BP or HR and rhythm NO RELIEF WITH NITRATES
42
what lab data is collected to diagnose an MI
1. enzyme increase of CK- MB (creatinine phosphokinase) is released when cells die 2. Tropinin increase- protein in cardiac cell '' 3. WBC increase- reflects inflammatory response 4. glucose increased- elevates with stress
43
what does a 12 lead EKG do
identifies if and where a MI occurred
44
what are the post MI complications
1. heart failure/ cardiogenic shock | 2. arrhythmias/dysrhythmias
45
why is heart failure/ cariogenic shock a post MI complication
decreased ejection fraction- % of blood the left ventricle ejects normal is 50-60%
46
why is arrhythmias/dys a post MI complication
disturbance of cardiac rhythm occurs with 80-90% of MIs
47
what is heart failure
inability of heart to maintain adequate cardiac output to support body functions (heart fails as a pump)
48
what is the ejection fraction of heart failure
less than 40% (60-80 norm)
49
what does the 40% ejection fraction of heart failure lead to
results in ventricular remodeling where the heart chamber walls become thin, dilated and poorly contract
50
what is preload
amt of blood coming into the heart LV
51
what is afterload
load against which the heart must pump against
52
what is the incidence of heart failure
increased incidence because people are surviving MI
53
what are the four compensatory mechanisms in heart failure
ventricular hypertrophy SNS stimulation ADH Renin release
54
how does ventricular hypertrophy not help HF
heart enlarges to increase CO which increased the workload of the heart
55
how does SNS stimulated not help HF
increases HR and SV which increases workload of the heart
56
how does ADH not help HF
water is retained increasing BV and increases the workload of the heart
57
how does RENIN release not help HF
release of angio II leads to vasoconstriction and increases workload on the heart
58
left sided HF turns into what also
right sided HF
59
left sides was also called
congestive HF
60
what are the causes of LVHF
1. MI- no contractility area 2. hypertension- increase in SVR (vascular resistance) 3. aortic stenosis or incompetence- increase in SVR
61
what is backward effect in LVHF
decreased emptying of the left ventricle-> increases volume preload in left ventricle-> increaded volume preload in left atrium-> increased volume in pulmonary veins-> increased volume in pulmonary cap beds-> movement of fluid from caps to alveoli activation-> rapid filling of alveolar spaces-> pulmonary edema-> RVF (right ventricle failure)
62
what is the forward effect in LVHF
decreased cardiac output-> decreased perfusion of tissues of body-> decreased BP-> decreased glomerular filtration rate-> decreased urine output-> renin activation-> sodium and water retention
63
what are the mani of LVHF
1. decreased BP 2. dyspnea 3. lung crackles (rales) 4. frothy sputum 5. fatigue, exercise intolerance
64
what are the two causes of RVHF
1. pulmonary artery hypertension (COPD, pulmonary emboli) | 2. LVHF (most common)
65
what is the backward efffects of RVHF
decreased emptying of RV-> increased volume preload in the RV-> increased volume preload in the right atrium-> increased volume in the vena cava-> increased volume in the systemic venous circulation-> increased volume in the distensible organs (liver, spleen)-> increased cap pressure-> peripheral, dependent edema
66
what is the forward effects of RVHF
decreased volume from the RV to the lungs-> decreased return to left atrium and decreased left ventricular cardiac output-> all the forward effects of LVHF
67
what are the clinical mani of RVHF
1. jugular venous distension 2. increased central venous pressure 3. peripheral edema 4. abd. distention from liver and spleen 5. wt gain 6. fatigue, exercise intolerance
68
p wave
impulse from SA (normal pacemaker) through atria and atrial contraction (atrial depolarization)
69
PR interval
beginning of P to beginning of QRS (impulse from SA through AV)
70
QRS
impulse through ventricles (v depolarize causing v contraction)
71
ST segment
end of s to beginning of t wave (time between depolarization and repolarization of ventricles)
72
t wave
depolarization of ventricles
73
what are the clinical non classical of MI
1. weakness 2. fatigue 3. dyspnea 4. upper back pain 5. no symptoms

patho final (3 decks)

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