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BMS200 > Week 6, Lec 2 > Flashcards

Week 6, Lec 2 Flashcards

1
Q

what is edema

A

excess fluid in interstitial spaces

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2
Q

causes of edema

A

▪ blood hydrostatic pressure increase (arterial or venous)
▪ drop in blood oncotic pressure
▪ increased vascular permeability
▪ blockage of lymphatic flow

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3
Q

transudate vs exudate for edema fluid

A

transudate= low in protein
exudate= high in protein

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4
Q

transudate

A

transudate - edema fluid that is low protein, low cellular content, caused by pressure imbalances.

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5
Q

exudate

A

edema fluid (typical of inflammation) - High protein, high cellular content, caused by inflammation and vessel damage.

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6
Q

what is cause of transudate vs exudate

A

transudate from pressure imbalances

exudate from inflammation and vessel damage

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7
Q

what are starling forces

A
  • Describe the movement of fluid across capillary walls
  • Explains how fluid moves between blood vessels and surrounding tissues.
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8
Q

what do starling forces balance

A

between two pushing forces (hydrostatic pressures) and two pulling forces (oncotic pressures).

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9
Q

starling forces variables in equation

A

leakiness of capillary wall, hydrostatic pressure, osmotic pressure, fluid in capillary, fluid in interstitial space, how much protein leaks through capillary wall

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10
Q

what is oncotic pressure

A

the pull force that draws water into the blood vessels. Mainly created by large proteins.

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11
Q

what is hydrostatic presure

A

the push force that moves water out of the blood vessels into the surrounding tissues. It is generated by the pressure of the blood against the walls of the vessels, especially in the arteries.

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12
Q

hydrostatic pressure vs oncoticc pressure; which is push force and which is pull force

A

hydrostatic- push
oncotic- pull

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13
Q

4 things that can cause ederma

A
  1. increased hydrostatic pressure (arteriolar dilation, increased venous pressure, hypervolemia)
  2. decreases oncotic pressure (hypoproteinemia)
  3. increased capillary permeability
  4. lymphatic obstruction
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14
Q

disorders that are associated with edema

A

venous thrombosis, congestive heart failure, ascites, inflammation, post surgical lymphedema, malnutrition, nephrotic syndrome etc.

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15
Q

which is higher in arteries; oncotic pressure or hydrostatic pressure

A

hydrostatic pressure > oncotic pressure

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16
Q

which is higher in veins; oncotic pressure or hydrostatic pressure

A

oncotic pressure > hydrostatic pressure

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17
Q

which is higher for veins and for arteries; oncotic pressure or hydrostatic pressure

A

veins: oncotic pressure > hydrostatic pressure

arteries: hydrostatic pressure > oncotic pressure

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18
Q

in arteries since hydrostatic pressure > oncotic pressure then where is fluid driven into

A

interstitituim (surrounding tissue)

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19
Q

in veins since oncotic pressure > hydrostatic pressure then where is fluid go

A

filtered fluid is recaptured by osmosis, any excess is recovered by the lymphatic system

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20
Q

describe the starling forces in the arteries

A
  • Pc (Capillary hydrostatic pressure) is higher than πc (Capillary oncotic pressure).
  • This means that the force pushing fluid out of the capillary (Pc) is stronger than the force pulling fluid back into the capillary (πc).
  • As a result, fluid is driven into the interstitium (surrounding tissue). This fluid helps nourish tissues.
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21
Q

describe the starling forces in the veins

A
  • The capillary oncotic pressure (πc), driven by proteins like
    albumin, pulls fluid back into the capillary from the
    interstitial space
  • Not all fluid reenters the capillary; some excess fluid is
    absorbed by the lymphatic system to prevent tissue swelling (edema).
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22
Q

4 causes of edema

A
  1. increased hydrostatic pressure
  2. increased sodium and water retention
  3. reduced lympahtic drainage
  4. decreased oncotic pressure
  5. damage to the endothelium or just excessive leakiness can obviously lead to edema
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23
Q

example of increased hydrostatic pressure

A

malignant hypertension

where extreme increases in blood pressure overwhelm the normal balance of fluid movement across the capillaries.

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24
Q

what is increased hydrostatic pressure causes by

A

can be caused by a generalized global increase in arteriolar blood pressure

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25
Q

what endocrine cause can increase hydrostatic pressure

A

excess levels of aldosterone, ADH, angiotensin II, and catecholamines

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26
Q

a decrease in what can increase hydrostatic pressure

A

Decreased venous drainage which can be regional (i.e. a single obstructed vein) or global (i.e. congestive heart failure) can increase hydrostatic pressure

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27
Q

endocrine causes of increased sodium and water retention

A
  • syndrome of inappropriate ADH secretion
  • adrenal cortical pathologies – too much aldosterone
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28
Q

what pathologies can impair sodium elimination

A

kidneys (i.e. decreased perfusion)

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29
Q

2 main things that can cause reduced lymphatic draingage

A
  1. malignancies
  2. surgeries

▪ malignancies that infiltrate
the lymph nodes
▪ surgeries that resect the lymph nodes

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30
Q

rare cause of reduced lymphatic drainage

A

▪ Rarely infections that cause intense fibrosis of lymph nodes and their channels
* infestation by a parasitic organism – filiariasis

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31
Q

What plasma protein is most responsible for blood oncotic pressure?

A

albumin

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32
Q

what is nephrotic syndrome

A

excess leakage of protein from the glomerulus (renal capillary complex)

  • Protein filters from blood, through glomerular capillary –> protein enters the renal tubules and is excreted in the urine –> decreased oncotic pressure
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33
Q

causes of decreased oncotic pressure

A

nephrotic syndrome

hepatic failure

protein losing enteropathies or malnutrition

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34
Q

where is edema most noticable

A

areas inferior to the heart

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35
Q

renal diseases can cause

A

generalized edema that is apparent in areas that contain “looser” connective tissue

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36
Q

anasarca is

A

generalized edema

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37
Q

most severe forms of edema

A

pulmonary and brain edema

Unique features of the interaction of the microvasculature and air spaces (lungs) and the inflexible cranial cavity (brain) result in more severe consequences

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38
Q

anasarca

A

refers to severe, generalized edema, which is the widespread swelling of the body due to the accumulation of excess fluid in the interstitial spaces. It can affect various parts of the body, including the limbs, abdomen, and face.

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39
Q

angioedema

A

s a condition characterized by the rapid swelling of the deeper layers of the skin and mucous membranes, often affecting areas such as the face, lips, tongue, throat, and sometimes the abdomen. It is similar to hives (urticaria) but occurs in deeper tissues.

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40
Q

hyperaemia and congestion are both from

A

locally increased blood volume

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41
Q

what is hyperemia

A

arteriolar dilation (e.g., at sites of inflammation or in skeletal muscle during exercise) leads to increased blood flow

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42
Q

what happens to tissue in hyperaemia

A

affected tissues turn red (erythema) because of the engorgement of vessels with oxygenated blood

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43
Q

example of hyperemia

A

Example is the return of blood flow to tissue that is warming after being out in the cold

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44
Q

congestion

A

a passive process resulting from reduced outflow of blood from a tissue (sometimes called passive hyperemia)

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45
Q

hyperemia vs congestion

A

hyperemia= arteries dilate

congestion= passive hyperemia

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46
Q

types of congestion

A

can be systemic (heart failure) or local (venous obstruction)

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47
Q

what do tissues look like in congestion

A

▪ Congested tissues take on a dusky reddish-blue color (cyanosis) due to red cell stasis and the accumulation of deoxygenated

▪ Eventually red blood cells can extravasate, causing hemosiderin deposition in tissues

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48
Q

what is hemosiderin

A

degradation product of hemoglobin found mostly within macrophages

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49
Q

hyperaemia vs congestion

A

Hyperemia: Increased blood flow due to arteriolar dilation, typically resulting in a healthy, oxygen-rich appearance; often temporary.

Congestion: Blood pooling due to impaired venous outflow, often leading to a darker appearance and potential tissue damage; usually more chronic.

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50
Q

chronic passive congestion (long-standing congestion) is from

A

Stasis of poorly oxygenated blood causes chronic hypoxia

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51
Q

effects of chronic passive congestion

A

▪ Result in degeneration or death of cells and tissue fibrosis

▪ Capillary rupture at sites of chronic congestion → small foci of hemorrhage

▪ phagocytosis and catabolism of erythrocyte debris → Accumulations of hemosiderin-laden macrophage

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52
Q

acute vs chronic pulmonary congestion

A

▪ Acute: Alveolar capillaries engorged with blood
▪ Chronic: Septa become thickened and fibrotic

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53
Q

chronic pulmonary congestion

A

Septa become thickened and fibrotic

  • Alveolar spaces contain hemosiderin-laden macrophages (“heart failure cells”)
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54
Q

acute hepatic congestion

A

Hepatocytes degenerate, sinusoids and
venules are distended with blood
* Those near the hepatic artery circulation undergo less severe hypoxia and develop fatty change

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55
Q

in congestive failure what appearance does the liver have

A

nutmeg appearance

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56
Q

causes of pulmonary venous congestion

A

left heart failure, mitral stenosis or regurgitaation

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57
Q

appearance of pulmonary venous congestion

A

Engorgement of pulmonary capillaries and venules, alveolar edema, heart failure cells, brown induration

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58
Q

clinical features of pulmonary venous congestion

A

Shortness of breath (dyspnea), wheezing, difficulty breathing with lying flat (orthopnea)

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59
Q

causes of hepatic venous congestion

A

Right heart failure, constrictive pericarditis

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60
Q

appearance in hepatic venous congestion

A

Enlarged liver, centrilobular necrosis, nutmeg liver

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61
Q

clinical features in hepatic venous congestion

A

Right upper abdominal pain, elevated liver enzymes, ascites, peripheral edema, jugular venous distension

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62
Q

causes of deep vein venous congestion

A

Blood clot formation (DVT), incompetent valves

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63
Q

appearance of deep vein venous congestion

A

Dilated and tortuous veins, venous ulcers, potential of thrombus formation

64
Q

clinical features of deep vein venous congestion

A

swelling, pain, tenderness, skin changes

65
Q

white vs red infarct

A

White Infarct: Pale, necrotic tissue due to arterial occlusion in solid organs with single blood supply; minimal to no hemorrhage.

Red Infarct: Dark red tissue with hemorrhage, often occurring in organs with dual blood supply or due to venous obstruction.

66
Q

white infarct location vs red infarct location

A

white= Organs with a single blood supply, such as the kidney or spleen.

red= Organs with a dual blood supply, such as the lung, intestine, or testis.

67
Q

main mechanism of white vs red infarct

A

white= Arterial occlusion (atherosclerosis, thrombosis, or embolism)

red= venous occlusion

68
Q

damage in white vs red infarct

A

white= abrupt, severe

red= slow, gradual

69
Q

pulmonary infarcts

A

complication of a pulmonary embolus in the setting of CHF (congestive heart failure)

  • Difficulty providing oxygenated blood to the larger lung structures (bronchi, bronchioles)
  • Necrosis & hemorrhage in the affected lungi
70
Q

splenic infarct (is it white or red)

A

Wedge-shaped, white infarcts located under the capsule

71
Q

clinical events that cause shock

A

▪ severe hemorrhage or dehydration
▪ extensive trauma or burns
▪ myocardial infarction
▪ massive pulmonary embolism
▪ Sepsis and anaphylaxis

72
Q

what disturbances are in shock that leads to circulatory system failing to supply adequate microcirculation and perfuse vital organs

A

hemodynamic and metabolic disturbance

73
Q

shock; what happens when myocardial pump fails

A

decrease blood volume
increase vasodilation
increase vascular permeabilty

74
Q

distributive shock is which 2 types of shock

A

anaphylactic and neurogenic

75
Q

5 categories of shock

A

cardiogenic
hypovolemic
septic
anaphylactic
neurogenic

76
Q

cardiogenic shock examples

A

myocardial infarction
myocarditis
cardiac tamponade
pulmonary embolus

77
Q

hypovolemic shock examples

A

hemorrhage
diarrhea
dehydration
burns

78
Q

septic shock cause

A

severe infection

79
Q

anaphylactic shock example

A

type 1 hypersensitivity rxn

80
Q

neurogenic shock exmaple

A

brain damage

spinal cord injury

81
Q

hypovolemic shock is

A

too little fluid in vessels

▪ Hemorrhage, dehydration, third-spacing of fluid

82
Q

disruptive shock is (neurogenic or anaphylactic)

A

Too many vessels dilated, not enough blood to keep the pressure up

anaphylaxis, spinal shock

83
Q

cardiogenic shock is

A

heart isn’t working

▪ Heart attack, heart failure,
dysrhythmias

84
Q

obstructive shock is

A

Heart is working, but blood can’t leave the heart

Cardiac tamponade, pulmonary embolus, pneumothorax

85
Q

septic shock is

A

Shock is due to poor blood distribution AND inflammatory damage – from infection (sepsis)

response to infection leads to widespread inflammation, causing significant changes in blood circulation and resulting in a dangerously low blood pressure and inadequate blood flow to vital organs.

86
Q

why is shock fatal

A
  • Shock is fatal primarily due to inadequate tissue perfusion leading to cellular death, multiple organ dysfunction, systemic inflammatory responses, and failure of compensatory mechanisms.
87
Q

septic shock pathophysiology

A

▪ Dysregulated vascular reflexes! inappropriate vasodilation and often edema, sometimes due to damage to the endothelium
▪ Higher levels of pro-inflammatory cytokines ! adverse impacts on tissues such as the heart and kidneys
▪ Movement of leukocytes into a wide range of organs ! dysfunction
▪ Inappropriate activation of the coagulation and complement cascades

88
Q

stage 1 shock vs stage 2 shock

A

stage 1 is compensated; tachycardia and normal blood pressure

stage 2 is decompensated; tachycardia and hypotension

89
Q

stage I shock

A

compensated
▪ Tachycardia, but blood pressure is normal

90
Q

stage II shock

A

decompensated
▪ Body is no longer effectively compensating for the
reduced flow to tissues
▪ Tachycardia and hypotension
▪ Much more difficult to reverse at this stage

91
Q

clinical findings in hypovolemic and cardiogenic shock

A

▪ hypotension
▪ a weak, rapid pulse
▪ tachypnea
▪ cool, clammy, cyanotic skin

92
Q

findings in septic shock

A

▪ hypotension
▪ a weak, rapid pulse
▪ tachypnea
▪ cool, clammy, cyanotic skin
—-»»but skin may initially be warm and flushed because of peripheral vasodilation

93
Q

what layer of the heart is effected in ishcemic heart disease

A

myocardium

94
Q

what happens in ischemic heart disease

A

▪ Supply of blood to the myocardium is inadequate for
metabolic demands of the heart

  • Blood supply is either completely blocked or reduced
95
Q

most common cause of ischemic heart disease

A

atherosclerosis of the coronary arteries

  • Other causes – aneurysms, autoimmune attack or coronary vessels, strange episodes of vasospasm
96
Q

what is the leading cause of death worldwide

A

ischemic heart disease

97
Q

pathogenesis of ischemic heart disease

A

Progressive narrowing of coronary arteries –> hypoperfusion of myocardium –> heart failure

Sudden occlusion of a major coronary artery resulting in an infarct

  • An atherosclerotic plaque ruptures–> acute clot formation–> blocks the artery or gives rise to an embolus that blocks blood flow further downstream
98
Q

What are factors that acutely affect the heart’s metabolic demands?

A

heart rate
wall tension
contractility (via intracellular Ca2+)

99
Q

most common cause of ischemic heart disease

A

coronary atherosclerosis

100
Q

decreased oxygen supply of oxygen causing ischemic heart disesa

A

–> conditions that influence blood supply (atherosclerosis, thromboembolli, coronary artery spasm)

–> conditions that influence availability of oxygen in the blood (anemia, cyanide, carbon monoxide)

101
Q

increase oxygen demand and increased cardiac work causing ishemic heart disease

A

hypertension, valvular stenosis, thiamin deficiency, hyperthyroid

102
Q

Atherosclerosis is the major cause of

A

ischemic heart disease (90% of cases)

103
Q

stable angina

A

lumen of large coronary artery reduced by 50-75% and symptoms when increase activity/exercise

104
Q

unstable angina

A

lumen reduced by 80-90% and symptoms at rest

105
Q

stable vs unstable angina

A

stable is only during exercise, unstable at rest

106
Q

stable angina

A

If there is a plaque or thrombosis causing occlusion,
the obstruction is thought to be stable/unchanging

107
Q

what type of angina in acute coronary syndrome

A

unstable angina

108
Q

unstable angina

A
  • Could be a thrombus that forms and is broken down
    constantly over a plaque
  • Could be a very significant (limits a lot of flow, lumen is only 10-20% of regular diameter) stable occlusion
109
Q

acute coronary syndromes

A

▪ Unstable angina
▪ Non-ST elevation myocardial infarction
▪ ST-elevation myocardial infarction

110
Q

Prinzmetal angina (vasospastic or variant angina)

A

a type of unstable angina, but has a much better prognosis

111
Q

cause of Prinzmetal angina (vasospastic or variant angina)

A

coronary artery spasm

112
Q

when does prinzmetal angina occur? what does it respond to? who does it occur in?

A

Occurs early morning; unrelated to exertion

Does not usually cause infarction

Responds well to vasodilators
Nitroglycerine, calcium channel blockers

Typical patient population – younger ( < 60 years) women

113
Q

adaptations to chronic heart ischemia

A

hypertrophy, changes in cardiac myocyte contraction, develop coronary collateral circulation

coronary collateral circulation
▪ Extensive collateral connections develop in hearts with severe coronary atherosclerosis –> provide enough arterial flow to prevent infarction completely or to limit infarct size if occlusion occurs

114
Q

which vessels of the heart are most threatened in acute infarct

A

sub-endocardial vessels

pressure in these vessels during systole is highest

115
Q

fixed coronary obstruction would cause what type of angina

A

stable anging

116
Q

severe fixed coronary obstruction (chronic ischemic heart disease )causes what type of angina

A

unstable; bc lumen so narrow there would be problems at rest

117
Q

plaque aggregates and acute coronary syndromes and thrombus cause what angina

A

unstable angine

118
Q

what happens in first few minute then 1 hour of heart attack/ myocardial infarction

3 days?

1 wk?

A

few mins= cells and mitochondria swell, lose glycogen

1 hr= irreversible myocyte injury from ishemia

3 day= neutrophils

1 wk= macrophages replace neurophils, myofibroblasts deposit collagen and make scar tissue

119
Q

first few mins of myocardial infarction/ heart attack

A

swelling of cells and mitochondria, loss of glycogen

▪ Reversibly injured myocytes show subtle changes of sarcoplasmic edema, mild mitochondrial swelling, and loss of glycogen
▪ “stunned myocardium” = cells that are not dead, but cannot contract

120
Q

30-60 mins of myocardial infarction/heart attack

A

30to60minutes of ischemia myocyte injury has become irreversible

▪ mitochondria are greatly swollen and deformed
▪ Nuclei show clumping and margination of chromatin and
the sarcolemma is focally disrupted
▪ Disruption of cell membranes ! release of intracellular substances into the circulation
▪ Findings of coagulative necrosis

121
Q

necrosis mechanisms

A

▪ Depletion of ATP
▪ Mitochondrial damage
▪ Calcium accumulation
▪ Oxidative stress / free radicals ▪ Membrane damage
▪ Denatured proteins
▪ DNA damage

122
Q

how are mitochondria membrane damaged

A

decreased oxygen, free radial damage

123
Q

what can cause the mitochondrial permeability transition pores to open? what does this lead to?

A

increased cytosolic calcium

causes leakage of H+ and calcium

124
Q

mitochondrial permeability transition pores open when damaged and…

A

▪ Loss of mitochondrial membrane potential
▪ Releases H+
▪ Further increase in
cytoplasmic calcium
* Mitochondrial calcium “dumped” into cytosol
▪ Inability to generate ATP and ultimately necrosis

125
Q

day 2-3 of myocardial infarction/heart attack

A

▪ Neutrophils enter necrotic tissue - only gain access at the edge of the infarct, where blood still flows
▪ Interstitial edema and microscopic areas of hemorrhage may also appear
▪ muscle cells are more clearly necrotic, nuclei disappear and striations become less prominent

126
Q

day 5-7 of myocardial infarction/heart attack

A

▪ neutrophils have been replaced by macrophages, myofibroblasts begin depositing collagen (scar tissue)
▪ Dangerous period – the wall is weak

127
Q

week 1 and later of myocardial infarction/heart attack

A

▪ Collagen deposition with notable myofibroblasts and macrophages!
▪ Week 3: mostly scar tissue, new vessels and macrophages have disappeared from the infarct
▪ Later: scar becomes more “solid” as it is remodelled

128
Q

what is a repercussion injury (in myocardial infarction)

A

damage to cardiomyocytes that occur after blood
flow is restored to ischemic tissue

129
Q

what occurs in a repercussion injury

A

cardiomycoytes damages when restore blood flow because contraction bands necrosis

  • Reperfusion injury = damage to cardiomyocytes that occur after blood
    flow is restored to ischemic tissue
    ▪ Many myocardial cells will undergo contraction band necrosis when blood flow is restored
  • Contraction band = hypercontracted and disorganized sarcomeres with thickened Z disks.
  • Happens when calcium floods in across disrupted sarcolemma and ROS are generated by damaged mitochondria that suddenly have access to oxygen
  • Can lose some myocardial cells even after blockage is removed (but still advantageous to restore blood flow)
  • Seems that inflammatory damage contributes to reperfusion injury as well
130
Q

ST-Elevation Myocardial Infarction (STEMI

A

ST-Elevation Myocardial Infarction (STEMI) is a type of heart attack characterized by a significant elevation of the ST segment on an electrocardiogram (ECG). This indicates a complete blockage of a coronary artery, leading to a severe reduction in blood flow to a portion of the heart muscle.

131
Q

transmural infarcts

A

▪ Large, “permanent” occlusion of a coronary artery
▪ Thought to be same entity as an ST-elevation infarct (STEMI)

132
Q

non transmural infarcts

A

▪ Can have a variety of pathological patterns
▪ Global hypoxia, many small vessels occluded, transient occlusion
▪ Thought to be the same entity as a non-ST-elevation infarct (NSTEMI)

133
Q

transmural vs non transmural infarcts

A

trans are permeant occlusion

non trans are transient occlusion

134
Q

NSTEMI

A

Non-ST-Elevation Myocardial Infarction (NSTEMI) is a type of heart attack that occurs when there is a partial blockage of a coronary artery, resulting in reduced blood flow to the heart muscle. Unlike ST-Elevation Myocardial Infarction (STEMI), NSTEMI is characterized by the absence of significant ST segment elevation on an electrocardiogram (ECG).

135
Q

what is the most common vessel involved in myocardial infarction?

A

Anterior descending branch of left coronary artery (50%)

Right coronary artery (30-40%)

Left circumflex artery (15-20%)

– Anterior descending branch of left coronary artery (50%)
– apical, anterior, and anteroseptal wall left ventricle infarcts
– Right coronary artery (30-40%)
– infarct of the posterior basal left ventricle and the posterior 1/3 to 1/2 of the interventricular septum (“inferior” infarct)
– Left circumflex artery (15-20%) – lateral left ventricle wall.

136
Q

symptoms of ishcemic heart disease

A
  • Asymptomatic
  • Dyspnea, Fatigue
  • Palpitations
  • Diaphoresis
  • Congestive heart failure symptoms
  • Pain – chest pain = angina pectoris
    – Different patterns of chest pain – referred to left arm/ shoulder, retrosternal, interscapular, can also appear similar to gastro-esophageal reflux
    – Pain is typically “crushing” or squeezing in character – rarely described as sharp
137
Q

acute ischemic heart disease presentation

A
  • Stable angina
  • Unstable angina
  • Myocardial infarction (two types, ST elevation and non-ST elevation infarcts)
  • Sudden cardiac death
138
Q

chronic ischemic heart disease presentation

A
  • Heart failure
    ▪ Particular type of heart failure sometimes referred to as ischemic cardiomyopathy
139
Q

stable angina symptoms

A

▪ Chest or arm pain (or discomfort)
▪ Reproducibly associated with physical exertion or stress
* Pattern is consistent with previous episodes

140
Q

how long to relieve stable angina? what can relieve it?

A

▪ Relieved in a short time period (3 – 20 min) by:
* Rest
* Nitroglycerine

141
Q

symptoms of unstable engine

A

▪ New onset chest pain/discomfort, or presents differently than
before
▪ Is severe, and/or pain is accelerating in intensity (crescendo pattern)

142
Q

when does unstable angina occur? how long to relieve unstable angina? what can relieve it?

A

▪ Occurs at rest or not relieved by nitroglycerine/rest

143
Q

what 2 things make up acute coronary syndrome (ACS)

A

unstable angina and myocardial infarction (heart attack)

144
Q

What happens in ischemic heart disease

A

sudden cardiac death (but can be resusucitated)

no acute infarcts

sudden onset of dysrhythmia (due to longterm coronary ischemia)

dysrhythmia is fatal unless aggressive resuscitation measures are undertaken

145
Q

myocardial infarction clinical presentation

A
  • Often the pain of an MI is more severe than stable, unstable angina
  • MIs can masquerade as heartburn
  • Atypical presentations during an MI are not uncommon
    ▪ Interscapular pain
    ▪ Discomfort vs. pain
    ▪ Sometimes dyspnea, acute severe fatigue is the main complaint
146
Q

ischemic heart disease ECG findings

A

ST segment elevation, ST segment depression, T wave change, pathological Q wave, bundle branch blocks, atrial and ventricular arrhythmias

147
Q

cardiac enzymes in ishcmeic heart disease

A

troponin (T and I), CK-MB most reliable,

148
Q

most reliable cardiac enzyme for diagnosing ischemic heart disease

A

creating kinase CK-MB

149
Q

imaging for ischemic heart disease

A
  • Angiogram
  • Echocardiogram
  • Nuclear medicine imaging
    ▪ Certain isotopes are taken up more avidly by damaged/ ischemic cardiac tissue
150
Q

what is the treatment principle for ischmeic heart Disease

A

Treat causes of imbalance between energy supply and demand to the myocardium

151
Q

treatment for ischemic heart disease

A

ASA (antiplatelet agent to reduce thrombus)

antihypertensives

beta blcokers

calcium channel blockers (reduce contractility)

nitroglycerine (decrease pre and after load)

control glucose and lipids

152
Q

nitroglycerine effects

A

Decreases preload, coronary vasodilator, decreases afterload

153
Q

NSTEMI vs STEMI which drugs are needed

A

NSTEMI – no “clot-busting” drugs like tissue plasminogen activator

– STEMI – “clot-busting” drugs can be life-saving
– Thrombolytic drugs end in –plase (reteplase, alteplase,
used to use streptokinase)

154
Q

what is stent useful for

A

STEMI and NSTEMI (myocardial infarction)

155
Q

causes of death in myocardial infarction

A

▪ Death occurs acutely in 25% - 35% of cases due to dysrhythmia (ventricular fibrillation), heart block, heart failure, asystole (cardiac arrest)

▪ Also a high mortality days – months post-infarct
* Life-threatening dysrhythmias
* Cardiac rupture – highest risk at 3 – 7 days post-MI due to coagulative ! liquiefactive necrosis in the wall of the myocardium or at the attachment point of a papillary muscle
* Poor wall motion ! clot development (more later)
* Pericarditis

BMS200 (46 decks)

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