Week 6, Lec 2 Flashcards
(155 cards)
1
Q
what is edema
A
excess fluid in interstitial spaces
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
3
Q
transudate vs exudate for edema fluid
A
transudate= low in protein
exudate= high in protein
4
Q
transudate
A
transudate - edema fluid that is low protein, low cellular content, caused by pressure imbalances.
5
Q
exudate
A
edema fluid (typical of inflammation) - High protein, high cellular content, caused by inflammation and vessel damage.
6
Q
what is cause of transudate vs exudate
A
transudate from pressure imbalances
exudate from inflammation and vessel damage
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.
8
Q
what do starling forces balance
A
between two pushing forces (hydrostatic pressures) and two pulling forces (oncotic pressures).
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
10
Q
what is oncotic pressure
A
the pull force that draws water into the blood vessels. Mainly created by large proteins.
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.
12
Q
hydrostatic pressure vs oncoticc pressure; which is push force and which is pull force
A
hydrostatic- push
oncotic- pull
13
Q
4 things that can cause ederma
A
- increased hydrostatic pressure (arteriolar dilation, increased venous pressure, hypervolemia)
- decreases oncotic pressure (hypoproteinemia)
- increased capillary permeability
- lymphatic obstruction
14
Q
disorders that are associated with edema
A
venous thrombosis, congestive heart failure, ascites, inflammation, post surgical lymphedema, malnutrition, nephrotic syndrome etc.
15
Q
which is higher in arteries; oncotic pressure or hydrostatic pressure
A
hydrostatic pressure > oncotic pressure
16
Q
which is higher in veins; oncotic pressure or hydrostatic pressure
A
oncotic pressure > hydrostatic pressure
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
18
Q
in arteries since hydrostatic pressure > oncotic pressure then where is fluid driven into
A
interstitituim (surrounding tissue)
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
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.
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).
22
Q
4 causes of edema
A
- increased hydrostatic pressure
- increased sodium and water retention
- reduced lympahtic drainage
- decreased oncotic pressure
- damage to the endothelium or just excessive leakiness can obviously lead to edema
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.
24
Q
what is increased hydrostatic pressure causes by
A
can be caused by a generalized global increase in arteriolar blood pressure
25
what endocrine cause can increase hydrostatic pressure
excess levels of aldosterone, ADH, angiotensin II, and catecholamines
26
a decrease in what can increase hydrostatic pressure
Decreased venous drainage which can be regional (i.e. a single obstructed vein) or global (i.e. congestive heart failure) can increase hydrostatic pressure
27
endocrine causes of increased sodium and water retention
* syndrome of inappropriate ADH secretion
* adrenal cortical pathologies – too much aldosterone
28
what pathologies can impair sodium elimination
kidneys (i.e. decreased perfusion)
29
2 main things that can cause reduced lymphatic draingage
1. malignancies
2. surgeries
▪ malignancies that infiltrate
the lymph nodes
▪ surgeries that resect the lymph nodes
30
rare cause of reduced lymphatic drainage
▪ Rarely infections that cause intense fibrosis of lymph nodes and their channels
* infestation by a parasitic organism – filiariasis
31
What plasma protein is most responsible for blood oncotic pressure?
albumin
32
what is nephrotic syndrome
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
33
causes of decreased oncotic pressure
nephrotic syndrome
hepatic failure
protein losing enteropathies or malnutrition
34
where is edema most noticable
areas inferior to the heart
35
renal diseases can cause
generalized edema that is apparent in areas that contain “looser” connective tissue
36
anasarca is
generalized edema
37
most severe forms of edema
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
38
anasarca
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.
39
angioedema
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.
40
hyperaemia and congestion are both from
locally increased blood volume
41
what is hyperemia
arteriolar dilation (e.g., at sites of inflammation or in skeletal muscle during exercise) leads to increased blood flow
42
what happens to tissue in hyperaemia
affected tissues turn red (erythema) because of the engorgement of vessels with oxygenated blood
43
example of hyperemia
Example is the return of blood flow to tissue that is warming after being out in the cold
44
congestion
a passive process resulting from reduced outflow of blood from a tissue (sometimes called passive hyperemia)
45
hyperemia vs congestion
hyperemia= arteries dilate
congestion= passive hyperemia
46
types of congestion
can be systemic (heart failure) or local (venous obstruction)
47
what do tissues look like in congestion
▪ 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
48
what is hemosiderin
degradation product of hemoglobin found mostly within macrophages
49
hyperaemia vs congestion
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.
50
chronic passive congestion (long-standing congestion) is from
Stasis of poorly oxygenated blood causes chronic hypoxia
51
effects of chronic passive congestion
▪ 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
52
acute vs chronic pulmonary congestion
▪ Acute: Alveolar capillaries engorged with blood
▪ Chronic: Septa become thickened and fibrotic
53
chronic pulmonary congestion
Septa become thickened and fibrotic
* Alveolar spaces contain hemosiderin-laden macrophages ("heart failure cells")
54
acute hepatic congestion
Hepatocytes degenerate, sinusoids and
venules are distended with blood
* Those near the hepatic artery circulation undergo less severe hypoxia and develop fatty change
55
in congestive failure what appearance does the liver have
nutmeg appearance
56
causes of pulmonary venous congestion
left heart failure, mitral stenosis or regurgitaation
57
appearance of pulmonary venous congestion
Engorgement of pulmonary capillaries and venules, alveolar edema, heart failure cells, brown induration
58
clinical features of pulmonary venous congestion
Shortness of breath (dyspnea), wheezing, difficulty breathing with lying flat (orthopnea)
59
causes of hepatic venous congestion
Right heart failure, constrictive pericarditis
60
appearance in hepatic venous congestion
Enlarged liver, centrilobular necrosis, nutmeg liver
61
clinical features in hepatic venous congestion
Right upper abdominal pain, elevated liver enzymes, ascites, peripheral edema, jugular venous distension
62
causes of deep vein venous congestion
Blood clot formation (DVT), incompetent valves
63
appearance of deep vein venous congestion
Dilated and tortuous veins, venous ulcers, potential of thrombus formation
64
clinical features of deep vein venous congestion
swelling, pain, tenderness, skin changes
65
white vs red infarct
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
white infarct location vs red infarct location
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
main mechanism of white vs red infarct
white= Arterial occlusion (atherosclerosis, thrombosis, or embolism)
red= venous occlusion
68
damage in white vs red infarct
white= abrupt, severe
red= slow, gradual
69
pulmonary infarcts
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
splenic infarct (is it white or red)
Wedge-shaped, white infarcts located under the capsule
71
clinical events that cause shock
▪ severe hemorrhage or dehydration
▪ extensive trauma or burns
▪ myocardial infarction
▪ massive pulmonary embolism
▪ Sepsis and anaphylaxis
72
what disturbances are in shock that leads to circulatory system failing to supply adequate microcirculation and perfuse vital organs
hemodynamic and metabolic disturbance
73
shock; what happens when myocardial pump fails
decrease blood volume
increase vasodilation
increase vascular permeabilty
74
distributive shock is which 2 types of shock
anaphylactic and neurogenic
75
5 categories of shock
cardiogenic
hypovolemic
septic
anaphylactic
neurogenic
76
cardiogenic shock examples
myocardial infarction
myocarditis
cardiac tamponade
pulmonary embolus
77
hypovolemic shock examples
hemorrhage
diarrhea
dehydration
burns
78
septic shock cause
severe infection
79
anaphylactic shock example
type 1 hypersensitivity rxn
80
neurogenic shock exmaple
brain damage
spinal cord injury
81
hypovolemic shock is
too little fluid in vessels
▪ Hemorrhage, dehydration, third-spacing of fluid
82
disruptive shock is (neurogenic or anaphylactic)
Too many vessels dilated, not enough blood to keep the pressure up
anaphylaxis, spinal shock
83
cardiogenic shock is
heart isn't working
▪ Heart attack, heart failure,
dysrhythmias
84
obstructive shock is
Heart is working, but blood can’t leave the heart
Cardiac tamponade, pulmonary embolus, pneumothorax
85
septic shock is
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
why is shock fatal
* 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
septic shock pathophysiology
▪ 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
stage 1 shock vs stage 2 shock
stage 1 is compensated; tachycardia and normal blood pressure
stage 2 is decompensated; tachycardia and hypotension
89
stage I shock
compensated
▪ Tachycardia, but blood pressure is normal
90
stage II shock
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
clinical findings in hypovolemic and cardiogenic shock
▪ hypotension
▪ a weak, rapid pulse
▪ tachypnea
▪ cool, clammy, cyanotic skin
92
findings in septic shock
▪ hypotension
▪ a weak, rapid pulse
▪ tachypnea
▪ cool, clammy, cyanotic skin
---->>>>but skin may initially be warm and flushed because of peripheral vasodilation
93
what layer of the heart is effected in ishcemic heart disease
myocardium
94
what happens in ischemic heart disease
▪ Supply of blood to the myocardium is inadequate for
metabolic demands of the heart
* Blood supply is either completely blocked or reduced
95
most common cause of ischemic heart disease
atherosclerosis of the coronary arteries
* Other causes – aneurysms, autoimmune attack or coronary vessels, strange episodes of vasospasm
96
what is the leading cause of death worldwide
ischemic heart disease
97
pathogenesis of ischemic heart disease
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
What are factors that acutely affect the heart’s metabolic demands?
heart rate
wall tension
contractility (via intracellular Ca2+)
99
most common cause of ischemic heart disease
coronary atherosclerosis
100
decreased oxygen supply of oxygen causing ischemic heart disesa
--> conditions that influence blood supply (atherosclerosis, thromboembolli, coronary artery spasm)
--> conditions that influence availability of oxygen in the blood (anemia, cyanide, carbon monoxide)
101
increase oxygen demand and increased cardiac work causing ishemic heart disease
hypertension, valvular stenosis, thiamin deficiency, hyperthyroid
102
Atherosclerosis is the major cause of
ischemic heart disease (90% of cases)
103
stable angina
lumen of large coronary artery reduced by 50-75% and symptoms when increase activity/exercise
104
unstable angina
lumen reduced by 80-90% and symptoms at rest
105
stable vs unstable angina
stable is only during exercise, unstable at rest
106
stable angina
If there is a plaque or thrombosis causing occlusion,
the obstruction is thought to be stable/unchanging
107
what type of angina in acute coronary syndrome
unstable angina
108
unstable angina
* 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
acute coronary syndromes
▪ Unstable angina
▪ Non-ST elevation myocardial infarction
▪ ST-elevation myocardial infarction
110
Prinzmetal angina (vasospastic or variant angina)
a type of unstable angina, but has a much better prognosis
111
cause of Prinzmetal angina (vasospastic or variant angina)
coronary artery spasm
112
when does prinzmetal angina occur? what does it respond to? who does it occur in?
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
adaptations to chronic heart ischemia
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
which vessels of the heart are most threatened in acute infarct
sub-endocardial vessels
pressure in these vessels during systole is highest
115
fixed coronary obstruction would cause what type of angina
stable anging
116
severe fixed coronary obstruction (chronic ischemic heart disease )causes what type of angina
unstable; bc lumen so narrow there would be problems at rest
117
plaque aggregates and acute coronary syndromes and thrombus cause what angina
unstable angine
118
what happens in first few minute then 1 hour of heart attack/ myocardial infarction
3 days?
1 wk?
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
first few mins of myocardial infarction/ heart attack
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
30-60 mins of myocardial infarction/heart attack
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
necrosis mechanisms
▪ Depletion of ATP
▪ Mitochondrial damage
▪ Calcium accumulation
▪ Oxidative stress / free radicals ▪ Membrane damage
▪ Denatured proteins
▪ DNA damage
122
how are mitochondria membrane damaged
decreased oxygen, free radial damage
123
what can cause the mitochondrial permeability transition pores to open? what does this lead to?
increased cytosolic calcium
causes leakage of H+ and calcium
124
mitochondrial permeability transition pores open when damaged and...
▪ 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
day 2-3 of myocardial infarction/heart attack
▪ 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
day 5-7 of myocardial infarction/heart attack
▪ neutrophils have been replaced by macrophages, myofibroblasts begin depositing collagen (scar tissue)
▪ Dangerous period – the wall is weak
127
week 1 and later of myocardial infarction/heart attack
▪ 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
what is a repercussion injury (in myocardial infarction)
damage to cardiomyocytes that occur after blood
flow is restored to ischemic tissue
129
what occurs in a repercussion injury
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
ST-Elevation Myocardial Infarction (STEMI
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
transmural infarcts
▪ Large, “permanent” occlusion of a coronary artery
▪ Thought to be same entity as an ST-elevation infarct (STEMI)
132
non transmural infarcts
▪ 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
transmural vs non transmural infarcts
trans are permeant occlusion
non trans are transient occlusion
134
NSTEMI
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
what is the most common vessel involved in myocardial infarction?
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
symptoms of ishcemic heart disease
* 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
acute ischemic heart disease presentation
* Stable angina
* Unstable angina
* Myocardial infarction (two types, ST elevation and non-ST elevation infarcts)
* Sudden cardiac death
138
chronic ischemic heart disease presentation
* Heart failure
▪ Particular type of heart failure sometimes referred to as ischemic cardiomyopathy
139
stable angina symptoms
▪ Chest or arm pain (or discomfort)
▪ Reproducibly associated with physical exertion or stress
* Pattern is consistent with previous episodes
140
how long to relieve stable angina? what can relieve it?
▪ Relieved in a short time period (3 – 20 min) by:
* Rest
* Nitroglycerine
141
symptoms of unstable engine
▪ New onset chest pain/discomfort, or presents differently than
before
▪ Is severe, and/or pain is accelerating in intensity (crescendo pattern)
142
when does unstable angina occur? how long to relieve unstable angina? what can relieve it?
▪ Occurs at rest or not relieved by nitroglycerine/rest
143
what 2 things make up acute coronary syndrome (ACS)
unstable angina and myocardial infarction (heart attack)
144
What happens in ischemic heart disease
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
myocardial infarction clinical presentation
* 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
ischemic heart disease ECG findings
ST segment elevation, ST segment depression, T wave change, pathological Q wave, bundle branch blocks, atrial and ventricular arrhythmias
147
cardiac enzymes in ishcmeic heart disease
troponin (T and I), CK-MB most reliable,
148
most reliable cardiac enzyme for diagnosing ischemic heart disease
creating kinase CK-MB
149
imaging for ischemic heart disease
* Angiogram
* Echocardiogram
* Nuclear medicine imaging
▪ Certain isotopes are taken up more avidly by damaged/ ischemic cardiac tissue
150
what is the treatment principle for ischmeic heart Disease
Treat causes of imbalance between energy supply and demand to the myocardium
151
treatment for ischemic heart disease
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
nitroglycerine effects
Decreases preload, coronary vasodilator, decreases afterload
153
NSTEMI vs STEMI which drugs are needed
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
what is stent useful for
STEMI and NSTEMI (myocardial infarction)
155
causes of death in myocardial infarction
▪ 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
