Please enable JavaScript.
Coggle requires JavaScript to display documents.
Angina Treatment (Bahouth) (Pathophysiology of cardiac ischemia in…
Angina Treatment (Bahouth)
Tx. Approach
Increase coronary blood flow
Nitrates
MOA
nitrosovasodilators undergo denigration to release NO
NO activates
guanylate cyclase
-
increase
cGMP
cGMP activates
protein kinases G
producing:
venodilation and coronary vasodilation
CV effects
Veno
dilation
decrease
preload
decreased
pressure during diastole in ventricles of heart
reduced wall stress and MvO2
coronary
vaso
dilation
redistribute of BF to areas of ischemia
selective dilation of epicardial and
collateral coronary
vessels
prevents or reverses coronary vasospasm
Hemodynamics
unchanged
BP and HR
decrease
pulmonary vascular resistance
slight decrease
CO (
reduce O2 demand
)
SE
Hypotension
at
higher
doses of nitrates -
arterial vasodilation
:forbidden:
CI
with PDE5 inhibitor
increase cGMP by preventing metabolism
potential for augmented cGMP response to nitrates
profund Hypotension
myocardial ischemia
HA
due to dilation of meningeal arteries
use aspirin or acetaminophen
reduce dose
Drug rash
seen with long acting nitrates, cutaneous nitrates
continuous Nitrates exposure leads to loss of efficacy
recommended 8-12hrs 'nitrate free' (sleeping time)
CCB
DHP
-dipine
reduced afterload, coronary vasodilation
more potent vasodilator = reflex cardiac stimulation
direct and indirect effects balanced
unchanged HR, myocardial contractility, AV node
reduce MvO2 by
reducing afterload
= reduce O2 demand
combo with
beta blocker
for coronary vasodilation, reduced afterload; sinus bradycardia; SA/AV block;
valvular insufficiency:
reduce afterload
Non-DHP (Verapamil, Diltiazem)
text
coronary vasodilation
- prevents or reverse vasospasm
decrease HR, myocardial contractility, slowed AV conduct
reduce MvO2 by
reducing
HR, contractility
, afterload and O2 demand
tx. for
Asthma/broncospastic COPD; severe peripheral vascular dz with rest pain depression; labile (variable glucose levels) insulin dependent diabetes
health patients with normal heart
Reduce myocardial oxygen consumption (mvo2) by
beta blockers
decrease HR
Negative chronotropic effect
decrease myocardial contractility
Negative inotropic effect
combo with
Nitrates
- reduces LVEDP, LV volume, dilates coronary a.
DHP CCB
- prevent coronary vasospasm, reduce systemic vascular resistance
Prevents reflex tachycardia and positive inotropic effect of nitrates and DHP-CCBs
reserved CCB for beta-blocker intolerance or add-on therapy if angina is uncontrolled by beta-blocker and nitrate
cardiac affect -
beta1AR
reduce resting HR, myocardial contractility -
inhibit SA node
stop increasing HR, contractility in response to exercise -
block SA/AV node
reduce myocardial oxygen consumption
Non-cardiac affect -
beta2AR
responsible for many SE: bronchospasm, hypoglycemia, lethargy, confusion, nightmares, alopecia (hair loss)
:forbidden:
CI
with SA/AV block; sinus bradycardia; decompensated CHF; labile or brittle diabetes;
asthma
; COPD
abrupt WD beta-blocker may induce rebound tachycardia, unstable angina, MI
decrease ventricular workload
- wall stress
veno
dilation
reduced
preload
vaso
dilation
reduced
afterload
use in
MI
;
in acute MI/unstable angina use
beta-blocker IV + PO
provided no CHF, hypotension or sinus bradycardia/heart block
prevent platelet deposition/aggregation
Aspirin
all patients with CHD should receive aspirin therapy unless contraindicated
beta-blocker reduce CHD events; Nitrates do NOT!
ACE improve survival post-MI with LV dysfunction and reduce MI in high risk patient
revascularization: coronary angioplasty, CABG
Pathophysiology of cardiac ischemia in Coronary Artery Disease syndrome
ischemia
to the heart causing
pain
due to coronary a. obstruction limits blood supply to part of myocardium
unstable angina
atherosclerosis and thrombosis blocks the blood flow
high correlation with MI
recurrent angina associated with
minimal exertion
prolonged and frequent pain
due to plaques and subsequent platelet aggregation
use
beta blocker with nitartes, ASA and heparin
variant or Prinzmetal's angina
vasospasm
blocks blood flow
normal coronary angiograms & excellent prognosis
not an increase in myocardial oxygen demand
(
beta blocker ineffective
)
exertional angina
exercise induce
due to atherosclerosis, vascular obstruction (
surgical, angioplasty
)
coronary circulation can meet
oxygen demands
of myocardium at rest
use
beta-blcoker
to reduce HR and myocardial contractility
antianginal drugs on survival and prevention of recurrent cardiac events in patients with CHD
PK profile of nitrate preparation
Mucosal
SL Nitrostat
short half-life (30min)
buccal nitrolingual spray
short half-life (30min)
SR Nitrogard
long half-life (5hr)
quick onset (1-3 min)
PO
longer onset (15-60min) and half-life (hrs)
Isosorbide dinitrate
Nitro-SR capsule
Isosorbide mononitrate
half-life 8-12hr
eccentric dosing 8am-3pm
Transdermal
patch, nitro
half-life 24hr
remove at night
nitro 2% ointment
≠ in USA
IV
nitroglycerin
titrate dose upward as needed to maintain effect
Preventing MI and CHD with angina
LDL reduction with HMG-RI:
Statin
reduce LDL and increase HDL
HDL raising/TG lowering
Thrombolytic therapy: reduce mortality 20%-27% within 1st year