Pre-Hospital Medications Part 2

What superficial main coronary arteries supply the heart with it’s own blood supply?

left coronary artery

right coronary artery

left coronary artery include?

anterior descending artery

circumflex artery

right coronary artery includes?

posterior descending arterior

marginal artery 

stroke volume

is the amount of blood ejected by the heart with each beat (average 70ml)

ejection fraction

is the amount of blood ejected from the heart with each beat compared to the amount left remaining (normally between 50-70%)

preload

is the volume of blood delivered to the heart, or left ventricular end diastolic pressure

which is dependant on venous return

afterload

is the resistance against which the ventricles must fight to contract and expel blood

depends o peripheral vascular resistance

heart rate

is the number of beat per minute

sympathetic and parasympathetic innervation

cardiac output

amount of blood pumped by the heart per minute (average 5L/min

C0=HR x SV

blood pressure

the pressure exerted by blood against arterial walls

BP= CO x PVR

stable angina

partial obstruction of blood flow through coronary arteries commonly due to atheroma

atherosclerotic plague is “stable”

clinical manifestations are present under increased o2 demand and blood flow becomes adequate once O2 demand returns to normal

pain may be relieved by rest, use of vasodilators

unstable angina

partial obstruction of blood flow through coronary arteries commonly due to atheroma

atherosclerotic plague is “unstable”

plague may ulcerate or rupture resulting in inflammation and platelet aggregation in vessel wall, thrombus formation

may lead to total coronary artery obstruction

clinical manifestations can occur in the absence of stimulus, may have no relief with vasodilators 

Myocardial infarction

has a similar mechanism as angina, but occur when a coronary artery is completely or near-completely occluded, resulting in permanent damage to the heart muscle

blood flow may be lost due to:

obstruction by thrombus

severe vasospasm

thromboembolus

congestive heart failure

failure of the heart to function as an effective pump

in acute exacerbation- decreased cardiac output may be caused by:

severe tachycardia

myocardial infarction

hypertension

reduced blood flow to vital organs/tissue activates RAAS and SNS, which further increase workload on the heart

overtime, LV hypertrophy occurs which also increases myocardial oxygen demand

forward effects of CHF

decreased CO results in hypotension and cellular hypoxia (cardiogenic shock)

backward effects

because blood is not pumped out of the left ventricles efficiency, blood backs up in pulmonary circulation and causes congestion (cardiogenic pulmonary edema) due to the increase in pulmonary capillary hydrostatic pressure

Pharmacokinetics of nitroglycerin

is lipid-soluble and rapidly absorbed across capillary membranes when administered sublingually

orally, the bioavailability of nitroglycerin is less than one percent due to the hepatic first pass effect

administered sublingually or topically, plasma concentrations are able to reach therapeutic level

half-life of nitroglycerin is short due to it’s rapid metabolism in the liver

action of nitroglycerin

once administered, nitroglycerin is converted to nitric oxide

nitric oxide acts on smooth muscle of arteries and veins causing them to dilate

dilation of veins (greatest effect)

dilation of arteries

dilation and coronary arteries 

nitroglycerin action: dilation of veins

dilation of veins increases venous capacitance and a pooling effect a blood return to the heart is slowed down

nitroglycerin action: decreased pre-load

less blood return to the heart- decreased ventricular en-diastolic pressure

less volume/LVEDP- less workload on the heart

less workload on the heart- decreased oxygen demand

nitroglycerin action cardiac ischemia (dilation of arteries)

most effective at higher doses

dilation of arteries- decrease in PVR/afterload

decreased PVR/afterload- decreased workload on the heart

decreased workload on the heart- less oxygen demand 

nitroglycerin action cardiac ischemia (dilation of coronary arteries)

increases the amount of oxygenated blood perfusing the myocardium

may result in increased perfusion to ischemic myocardial tissue which will slow down the progression of ischemia to necrosis

also increases cardiac efficiency by improved oxygenation

nitroglycerin action for CHF

the mode of action for nitroglycerin in the treatment of CHF is the same as in the treatment of cardiac ischemia, but the decreased afterload becomes more important than in ischemia

decreased afterload- decreased workload on the heart and reduced oxygen demand

improved pumping efficiency will result in a decrease in pulmonary edema and improved diffusion across respiratory membrane

it will also decrease pre-load which will benefit the CHF patient

decreased blood return to the left ventricle

less blood forced into the pulmonary circulation- decrease in pulmonary hydrostatic pressure

what side effect is of significant concern when nitroglycerin was delivered?

hypotension

pharmacokinetics of ASA

rapidly absorbed (passive diffusion) by the stomach and intestines with an oral bioavailability of 68%

ASA binds to albumin is the plasma, with more drug being unbound (available) as drug concentration increases

distribution is widespread, will cross placental barrier

pharmacodynamics and action of ASA

cyclooxygenases (COX) is an enzyme involved in inflammation and blood clotting

COX is necessary for the formation of prostaglandins, which are inflammatory mediators

the primary action of ASA is inhibition of COX, and resultant anti-inflammatory properties

COX also plays an important role in blood clotting

COX activate thromboxane A2 which causes platelets to stick together at a site of vessel damage

platelet aggregation is an important part of the formation of thee fibrin clot

the action of ASA in inhibiting COX and thromboxane will prevent platelet aggregation

ASA and thrombolytics

one of the primary treatment options for ACS is thrombolysis

thrombolytic agents breakdown clots, and are much more effective when administered early in clot development, as clots become more resistant to lysis over time

increased thrombin may accumulate locally as a clot dissolves leading to more platelet aggregation and limiting the effectiveness of the drug- ASA administered in the pre-hospital setting can prevent this and increase the efficacy of the thrombolytic 

cardiovascular effects of cocaine

increases myocardial oxygen demand by increasing HR and BP

decreases myocardial oxygen supply by coronary vasoconstriction

promotes coronary thrombosis by activating platelets (even in the absence of atherosclerosis)

associated with coronary atherosclerosis even in young users with relatively few risk factors

myocardial oxygen demand may exceed supply, leading to ischemia an infarction

cocaine has sodium-channel blocking effects and can cause wide-complex tachyarrhythmias