Blood Flashcards
BP =
CO x SVR
CO is
The volume of blood thats being ejected by the heart per minute
SVR is
Systemic vascular resistance , this is the resistance that blood encounters through blood vessels
Cardiac output contributes of
Stroke Volume and Heart Rate
i.e. 70ml x 70 times a minute = 5L per minute
Systemic Vascular Resistance consists of:
Constricted vessels have increased SVR, increasing BP
Factors which affect Stroke Volume
Blood volume, Contractility
Factors that affect BP
Blood volume, contractility, heart rate, SVR
Aim of anti HTN drugs that affect SVR
Reduce SVR by dilating blood vessels
BP is dropped by reducing contractility how
reducing the calcium, calcium influx causes muscles to contract
Anti HTN Drugs that concentrate on reducing blood volume
Inhibiting the renin-angiotensin-aldosterone system (which, when stimulated increases blood volume)
OR
Giving a patient a diuretic which increases u/o, reducing blood volume
Three types of HTN
Primary (Essential) HTN
Secondary HTN (due to underlying cause)
Malignant HTN (associated with organ damage)
Beta Blockers action
adrenergic receptors names
Alpha 1
Alpha 2
Beta 1
Beta 2
Beta 3
adrenergic receptors names specifically on the heart and kidneys
beta 1
beta 2 affects
vascular smooth muscle, bronchioles of the lungs, skeletal muscles
beta 3 affects
fat cells
selective beta 1 blockers
LOL’s
atenolol
metorpolol
specifically bind to the beta 1 receptors in the heart and kidneys
what affect does beta 1 betablockers have on the kidneys
binds to the specific b1 receptors on the kidneys releasing less renin by the kidneys
non specific beta blockers name
propanolol
non specific betablocker affects
b1 b2 b3
issue with giving b2 to what patients
those with restrictive lung diseases
ACE stands for what
angiotensin converting enzyme
what does ACE inhibitors do
blocks angiotensin 1 converting into angiotensin 2
angiotensin 2 affects within the body
vasoconstricts the vessels, increasing SVR
releases aldosterone
aldosterone affect within the body
promotes NA reabsorption in the kidneys, more NA = more water in the blood= more blood volume,
also stimulates the release of ADH
angiotensin 2 inhibitors aim
to stop all of the processes done by angiotensin 2 and aldosterone
ace inhibitor aim
to stop angiotensin 1 converting to angiotensin 2
name of angiotensin 2 inhibitor
candersartan
Ca channel blocker aim
inhibiting the depolarisation of the AV SV node, slowing HR down, reducing contractility
Nifedepine
prodomently acts on calcium channels found on the vascular smooth muscle blocking Ca affect, dilating blood vessels - decreasing SVR - decreasing bp
also acts on aldosterone receptor antagonist aswell
veramapil (nifedpine like drug)
- blocks ca channels at the nodes, acts on conductive tissue, reducing arrhythmias, common anti arrhythmias.
Diltiazem aim
blocks the ca channels at coronary vasculature
diuretic process
acts on the nephrons, reducing na reabsorption, increasing urine amount
thiazides diuretics work where
at the distal convulated tubules, they are longer acting, more effective, stops na being reabsorbed
