Yet more cardio class stuff lol Flashcards
The QT interval is too long if it is more than
0.42 seconds
preload
initial stretching of cardiomyocytes before contraction
CO =
HR x SV
after load
load against which the muscles tries to contract
increase in TPR then an increase in aortic pressure leads to ventricle having to work harder to open aortic valve so less energy so SV
decreases
Vessels/ Veins (capacitance vessels) effect
preload
resistance vessels (arterioles) effect
afterload
the fast depolarising stage of cardiac AP is due to
an increase in Na+
resting membrane potential is set buy
leaky potassium channels
depolarisation is due to the opening of
K+ leaky channels
plateau phase is due to
calcium
contractility is the effect of the sympathetic system
releasing noradrenaline which increase calcium available for EC coupling
Beta 1 adrenoreceptors
increase HR and increase Contractility
Valsalva manœuvre will
increase vagal tone
parasympathetic
MAP +
CO x TPR
Blood clot is
fibrin clot + platelet plug
prostacylcins and NO will
reduce platelet aggregation
heparin
inactivates thrombin
fibrinogen to fibrin transformed by
thrombin
Noradrenaline acting on alpha 1 receptors will
reduce flow
increase TPR
Angiotensin II released in response to
low blood volume
Angiotensin II leads to
arteriolar constriction
ADH is released in response to
low blood volume
ADH release causes
arteriolar constriction
so increased TPR
atrial niuretic peptide is released in response to
high blood volume
atrial niuretic peptide release causes
arteriolar dilation
an increase in hydrostatic pressure (standing up) will…
reduce
SV
EDV
VR
Preload
MAP
Reflex response ill…
increase sympathetic tone
decrease vagal tone
an increase in sympathetic tone will
increase HR, CO, SV, contractility
Long term BP is controlled by what 4 things?
aldosterone
angiotensin II
atrial niuretic peptide
vasopressin (ADH)
an increase in thoracic pressure will decrease
VR
EDV
SV
CO
MAP
Baroreceptors are
sensors located on blood vessels that detect changes in BP
Aortic arch 1
nothing
maxillary artery
aortic arch 2
nothin
maxillary artery
aortic arch 3
internal carotid
aortic arch 4
aortic arch
aortic arch 5
nothing
aortic arch 6
pulmonary arteries
angiotensin II stimulates the release of …… and …….
aldosterone
ADH
ADH is produced in response to
low blood volume
ADH is produced in the
hypothalamus
ANP is released in response to …. and …..
increase blood volume
increased distension of atrium
ANP inhibits….
renin release
Anticoagulants 2 main drugs
heparin
warfarin
low molecular weight heparin is often used in
venous thromboembolism
Beta blockers work by
antagonising the sympathetic system
beat blockers example
propranolol
beta blockers are often used in
angina
hypertension
post MI
be careful when using beta blockers in
asthma
heart block
ACE inhibitors are often used in
hypertension
heart failure
post MI
Loop diuretics are used to treat
heart failure
Thiazide like diuretics are used to treat
IHD
hypertension
heart failure
Vasodilators example
nitrates
vasodilators (such as nitrates) are used in
IHD
hypertension
heart failure
Statins work by reducing
LDL cholesterol
Statins example
simvastatin
Sodium channel blockers are also known as
anti-arrhythmias
anti platelets are given following an
MI or stroke
anti platelets examples (2)
aspirin
clopidogrel
Calcium antagonists treat
hypertension and angina