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Learning objectives:
1. Define an electrocardiogram (ECG) and electrocardiography
2. Describe how dipoles generated by the heart produce the waveforms of the ECG
3. Describe the components of a normal electrocardiogram of a typical bipolar leads (limb II)
4. Differentiate between intervals and segments
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Study Resources:
1. Chapter 11, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 9, Human Physiology - From Cells to Systems, Lauralee Sherwood, 9th edition
3. Chapter 29, Ganong’s Review of Medical Physiology, 26th edition
4. Electrocardiogram, StatPearls - https://www.ncbi.nlm.nih.gov/books/NBK549803/
5. ECG in Medical Practice by ABM Abdullah, 4th edition
6. ECG Basics, http://www.nataliescasebook.com/tag/e-c-g-basics
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RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
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Drugs acting on Renin Angiotensin Aldosterone system
1. Dr Htet Htet
MBBS, MMedSc
CVS Pharmacology (IV)
Drugs acting on Renin-Angiotensin-Aldosterone System
All rights reserved.
2. At the end of the lecture, students should be able to
List the drugs act on RAA system.
Explain the physiological role of RAA system.
Describe the pharmacology of ACEI, ARB and renin
inhibitors.
3. Learning outline
1. What is RAA system?
2. What are the drugs acting on RAA system?
3. Pharmacology of
a. Renin inhibitor
b. ACEI
c. ARB
d. Aldosterone antagonists.
4. What is RAA system?
Renal arterial
pressure
Sympathetic
stimulation
Sodium
delivery
5.
6.
7. A parallel system for angiotensin generation exists in
several other tissues (eg, heart) and may be responsible
for trophic changes such as cardiac hypertrophy.
14. Angiotensin
I
ACE
ACEI
Angiotensin
II
Sympathetic
activation
Aldosterone
production
Vasodilation
in both
arteries and
veins
ADH
production
from anterior
pituitary
Na+ & H2O
reabsorption
from renal
tubules
K+
retention
Water
retention
from the
renal tubules
BP
Causes delay
in cardiac
remodeling
process
Useful in post
myocardial
infarct
patients
Causes delay
in diabetic
nephropathy
Useful in
hypertensive
patients with
nephropathy
Preload
and
afterload
of the
heart
Cardiac
workload
Congestiv
e heart
failure
15. Due to inhibition in bradykinin breakdown – high level of
bradykinin – leads to cough (untoward effect).
16.
17. Therapeutic uses
1. Systemic hypertension
2. Hypertensive patients with post MI
3. Hypertensive patients with diabetes mellitus
4. Post MI patients
5. Congestive heart failure
6. Diabetic nephropathy patients (not with chronic renal
failure)
7. Progressive renal insufficiency
18. Systemic hypertension
ACEI are used in hypertension because
sympathetic activation
Causes vasodilation of both arteries and veins
Decrease sodium and water retention.
Patients with high renin activity are most effective but all
hypertensive patients can have benefit.
19. Hypertensive patients with post MI / post MI patients
ACEI can delay the cardiac remodeling process and this effect
makes ACEI useful for patients with post MI or hypertensive
patients with post MI.
Hypertensive patients with diabetes mellitus patients
particularly useful
diminish proteinuria and stabilize renal function (even in the absence
of lowering of blood pressure)
now recommended in diabetes even in the absence of hypertension.
20. Congestive heart failure
Can decrease cardiac workload by arterial and venous dilatation –
(which is useful effect in heart failure) + delay cardiac remodeling
Therefore, extremely useful in the treatment of heart failure
It can also reduce the incidence of diabetes in patients with high
cardiovascular risk.
21. Different preparations of ACEI
Captopril – effective drug which decreases BP by two actions – 1.
by decreasing Ang II 2. by increasing bradykinin.
Enalapril is a pro drug, which converts to enalaprilat.
Lisinopril is a lysine derivative of enalaprilat.
Benazepril, fosinopril, moexipril, perindopril, quinapril,
ramipril, and trandolapril are other long-acting members of the
class. All are prodrugs, like enalapril, and are converted to the
active agents by hydrolysis, primarily in the liver.
22. Status of ACEI
Angiotensin II inhibitors lower blood pressure principally by
decreasing peripheral vascular resistance. Cardiac output and
heart rate are not significantly changed.
Unlike direct vasodilators, these agents do not result in reflex
sympathetic activation and can be used safely in persons
with ischemic heart disease.
23. Untoward effects of ACEI
1. Severe hypotension (who are hypovolemic as a result of diuretics,
salt restriction, or gastrointestinal fluid loss)
2. acute renal failure (particularly in patients with bilateral renal
artery stenosis or stenosis of the renal artery of a solitary kidney)
3. Hyperkalemia (more likely to occur in patients with renal
insufficiency or diabetes)
4. dry cough sometimes accompanied by wheezing, and
angioedema (Bradykinin and substance P seem to be responsible)
24. 5. ACE inhibitors are contraindicated during pregnancy because
of the risk of fetal hypotension, anuria, and renal failure,
sometimes associated with fetal malformations or death.
6. Minor toxic effects seen more typically include altered sense of
taste, allergic skin rashes, and drug fever, which may occur in
up to 10% of patients.
7. Captopril, particularly when given in high doses to patients with
renal insufficiency, may cause neutropenia or proteinuria.
25. Drug interaction
ACEI + potassium sparing diuretics – can worsen hyperkalaemia.
ACEI + NSAIDs – may blunt the antihypertensive effect of ACEI.
26. Angiotensin receptor blockers (ARB)
Losartan and valsartan were the first marketed blockers of the
angiotensin II type 1 (AT1) receptor.
Candesartan, eprosartan, irbesartan,telmisartan, and
olmesartan are also available.
27. Mechanism of action of ARB
blockers of the angiotensin II type 1 (AT1) receptor.
have no effect on bradykinin metabolism and are therefore
more selective blockers of angiotensin effects than ACE
inhibitors.
They also have the potential for more complete inhibition of
angiotensin action compared with ACE inhibitors because there
are enzymes other than ACE that are capable of generating
angiotensin II.
29. Angiotensin
I
ACE
ACEI
Angiotensin
II
Sympathetic
activation
Aldosterone
production
Vasodilation
in both
arteries and
veins
ADH
production
from anterior
pituitary
Na+ & H2O
reabsorption
from renal
tubules
K+
retention
Water
retention
from the
renal tubules
BP
Causes delay
in cardiac
remodeling
process
Useful in post
myocardial
infarct
patients
Causes delay
in diabetic
nephropathy
Useful in
hypertensive
patients with
nephropathy
Preload
and
afterload
of the
heart
Cardiac
workload
Congestiv
e heart
failure
30. No inhibition in bradykinin breakdown – less chance of cough
Angiotensin receptor blockers provide benefits similar to those
of ACE inhibitors in patients with heart failure and chronic
kidney disease.
31. Adverse effects
The adverse effects are similar to those described for ACE
inhibitors, including the hazard of use during pregnancy. ***
Cough and angioedema can occur but are less common with
angiotensin receptor blockers than with ACE inhibitors
32. Pharmacokinetics of ACEI and ARB
Drug Half-life
(hr)
Bioavailabili
ty
(%)
Dosage requirement in moderate
renal insufficiency
Captopril 2.2 65 Yes
Lisinopril 12 25 Yes
Losartan 1-2 36 No