ICD Flashcards
IHD
diference between ischema and hypoxia
Gropup of clinical pathological syndrome that results from 2conditions
Ischemia
imbalance of o2 demand and suply
Deficient nutrient tansport
impaired metabolic waste washout
Hypoxia
only imbalance is present
Withc heart is proned to ischemia more than the other
left ventricle
0,5 cm RV 1,5 LV — left ventricle is thicker
125 LV / 25mhg / RV — because of this R myocardium contracts less strongly so it will squeeze less the cappilary —- because of this there is less work in the Right Ventricle
RV squeezes its microvasculature less than LV
CONCLUSION
RV needs less O2
RIGHT VENTRICLE
Occurs when there is hypertrophy of the right ventricle like in cor pulmonale
CAD
Stable atheroma will be a fixed obstruction will oclude the artery 70% => vasodilatators that heart produce will not be efficient on the part of the vessel with atheroma. => ischemia at adrenaline rush
Can produce angina, but not as dangerous as unstable even medium
In 90% => ischemia even at rest
Unstable atheroma (more macrophages, more foam cells, less fibrous cap) proned to acute disruptions /
1.Acute diruptions:
- erosion / ulcerations, if thrombogenous BM is uncovered
- fissuring/fracture / Fatty material exposed => Highly trombogenous
- Intaplaque haemorage (from plque or from blood flow)
1+2 can lead to 2=>5
2.Platlet adesion
NO disfunctional so adesion will be failitated
Platlet release: PF 3/4 , 5HT, Adrenaline (see pic) and platlet agregate TXA2=> strong adeshion factor and VASCOCONSTRICTOR!!!!
Platlet make plaque verry dynamic (smoking sticks the platlet on the plaque) - after 1 year of quiting chances of MI will be reduce 50%
3.Platlet plug
4.Coagulation
Coagulation process is converting soluble fibrinogen in unsoluble fibrin
3+4 Lead to 5. Thrombus
Usualy unstable atheroma can lead to dynamic changes (emboli, Thromus formation )
Thrombus may rupture and embolise
Plaques with thin cap, more foam cells, more fat, more macrophages (metaloproteinase digest the fibrotic cap) are proned to rupture
Weakest point is the edge of the plaque Shear forces of bloodflow, macrophages enter more,
ATHEROEMBOLISM
Plaque can rupture and content can oclude smaller distal artery
STATINS
- Reduce cholesterol that enter plaque so are more stabile (less colesterol suply to plaque)
- STATINS HAVE ANTIINFLAMATOR REACTION ON PLAQUE (less proteinases from macrophages)
- Proper use of them can regress the problem of plaque
External triggers that lead a plaque to rupture
Peak time of MI
Tachicardia & Vasoconstriction can rupture soft plaques in coronary ( And thrombus formation )
Adrenaline uprise
- BP up (hearts plaques)
- Platlet stickability up
- Vasoconstriction may make plaque suffer and rupture
Peak time for MI is in the morning 6AM - 12AM due adrenaline surge
Peak time increase MI and sudden cardia death
A.C.S => Acute coronary syndromes
- in what part of day they will ocur
- Biomarker of Plaque inflamatory activity
UNSTABLE ANGINA
ACUTE MIOCARDIAL INFARCTION
SUDDEN CARDIA DEATH
Are more common in the morning and in patients with inflamatory plaque
Determine inflamatory activity in plaque you can tell what is the risc for developing MI from Angina or recurence of MI
BIOMARKER THAT TELL THE STATUS OF PLAQUE
CRP
Macrophages from the plque (mre in unstable) will secrete cytokines, that will stimulate liver to produce C.R.P
Other causes of IHD besides athero
Coronary
Blood
Coronry osteal stenosis
Ex:
- Syphilitic 3o can extend towards ostium
- Aortic dissection can extend to coronary
Coronary vasculitis
Afect wall => Afect intima => Oclusion
- PAN
- Kawasaki dissease
Coronary artery embolism
- Thromboembolism
- from left atrium (includeing acute Infective endocarditis)
- Fat embolism
- Love to stick to platlets and inactivates it (petechiae can apear)
- CNS
- Paradoxical emboli
- DVT emboli go to arterial through Left to Right shunt
Polycitemia
- Thick blood so it moves verry heard
- Hb > 18gr
- RBG > 7.000.000
O2 suply reduced
Usualy interplay with other causes
- Severe anemia (if coupled with increased demand ex:hypertroph sympath)
- CARBOXYHEMOGLOBULINEMIA
- SEVERE PULMONARY DISEASE -
Hypotension
Develop infarcts Mi , stroke, in patient under anhestesia due severe prolonged hypotension : Circumferential subendocardial infarction zone 1/2/3 zone 1 most less vascularised and with systole is the most squesed (subendocardium) : deepest layer of myocardium is most proned to ischemia.
In patient with multiple atheromatous lesions >50 do not let BP drop to low
IREVERSIBLE DAMAGE OCURS AFTER 20-40 minutes and continues 6H if coolaterals are available 12H OF TOTAL OCLUSION
If you give in 20 minutes you save all the myocardium
Ater 30 m - 12H will be a increase in cell death
Aortic Stenosis
LVH + Less BP Aorta + Squeeze of vessel in myocardium
Syndrome X
Repeated Ishemic atack without evidence of vessel narrowing
Dilatation of smaller vessels is problematic, and vessels are filled with delay on angiography
