cv Flashcards
chonotropic
relating to Heart rate
ionotropic
relating to force of heart contraction
how do MI, ACS, angina, IHD, CHD and atherosclerosis , atherogenesisrelate?
IHD (ischeamic heart disease) is the same as CHD (coronary heart disease) and is the same as coronary atherosclerosis.
These terms refer to MI (heart attack) and ACS (acute coronary syndrome, = unstable angina) and stable angina.
atherosclerosis (formation = atherogenesis) is the cause for angina, ACS, and MI .
types of angina
5
what they are
stable angina (=pectoris) - painful periods are regular
unstable angina (=ACS, = crescendo angina) - painful periods are increasing in severity / frequency/ occurring at rest
prinzemental’s (=variant) = spasm of coronary arteries
microvascular = stenosis of small coronary vessels – increase in resistance and pressure
decubitus = when lying down/recumbent
excarbeating factors of angina (4)
- cold
- exercise/activity
- post prandial
- stress
opioid vs opiate
opiates are naturally occurring, acting on opioid receptors.
opioid is a synthetic/partially synthetic molecule - may act/ replicate opiates to get same response
orthopnea=
sob when lying down
paroxysmal nocturnal dyspnoea
sudden attacks of severe sob and coughing occurring at night
stage 1 hypertension
stage 2 hypertension
stage 3 hypertesnion
1
- clinic : 140/90 - 160/100
- ABPM: 135/85 - 150/95
2
- clinic: 160/100 - 180/110
- ABPM: 150/95 +
3
- clinic: 180/110 +
gangrene
tissue death due to ischeamia/ infarction
typically feet
what is amourosis fugax
blindness due to lack of blood flow
atrophic skin
- eg of disease its seen in
thin skin (eg PAD)
CRP blood test
c-reactive protein
detects inflammation, released after tissue injury
quite vague, non-specific but can be used to rule things out (eg claudication)
ESR blood test
erythrocyte sedimentation rate measure degree of inflammation such as cancer, autoimmune etc non specific (excludes claudication)
haematoma vs haemorrhage
both refer to localised bleeding from a blood vessel. haematoma is associated with clotted bleed whereas haemorrhage implies ongoing bleed
usually large vessels i think
haemoptysis
coughing up blood
early diastolic murmur
mitral stenosis
opening snap could be considered early diastolic (valves closer together so friction sound when blood is pushed through (diastole = blood moves from a –> v)
then mid diastolic as well
aortic regurgitation
mitral stenosis’ murmur =
opening snap (early diastolic)
— valves closer together so friction sound when blood is pushed through (end of diastole)
blood moves from a –> v in disatole
then mid diastolic (rumble) to end of diastole
early systolic click murmu
mitral valve replacement (working fine)
click= metal
mitral valve replacement murmur
early systolic click
ejection systolic crescendo-decrescendo murmur
aortic stenosis
- systole as after aorta is after ventricles. de/crescendo is due to the rise/fall of pressure
aortic stenosis murmur
ejection systolic crescendo-decrescendo murmur
systole as after aorta is after ventricles. de/crescendo is due to the rise/fall of pressure
pansystolic murmur
mitral /tricuspid regurgitation
-valves flap through ventricular systole blood moving past them
- maybe also MI/angina
mitral regurgitation murmur
pansysolic murmur
ANP raised
- suggests
- causes what
atrial dysfunction
high BP
causes kidney to excrete more in order to correct for high BP
CK MB
- when
Is a marker of damaged heart muscle
raised in MI
troponin I elevated when
MI
sepsis =
systemic inflammatory response associated with an infection
where in the blood vessel does atherosclerosis occur
intima
pericarditis ecg
Saddle shaped ST and PR depression
Saddle shaped ST and PR depression
pericarditis
hyperkalemia ecg
Tall tented T waves + pathological Q waves + flattened - absent p waves
Tall tented T waves + pathological Q waves + flattened - absent p waves
hyperkalemia
stemi ecg
st elevation
st elevation ecg
stemi
angina ecg
st depression
st depression ecg
angina
general heart block ecg
increase PR interval
increased pr interval
heart block
more than one atria p wave to each QRS block
2nd degree heart block
no relation between p and QRS
3rd degree heart block
3 rd degree heart block ecg
no relation between p and QRS
2nd degree heart block ecg
more than one atria p wave to each QRS block
mobitz type 1
pr interval increases gradually until QRS dropped/missing (p wave not conducted)
mobitz type 2
pr interval does not increase, it is constant. and then a qrs beat dropped/missing (p wave not conducted)
atrial fibrillation
irregularly irregular
atrium contracts rapidly irregularly, uncoordinately
av node responds intermittently - only some conducted to ventricles (irreg vents)
atrial fibrillation ecg
absent p wave rapid heart rate irregular QRS jaggedy no isoelectric baseline
absent p wave rapid heart rate irregular QRS jaggedy no isoelectric baseline
atrial fibrilation
atrial flutter ecg
saw tooth
narrow tachycardia
flutter waves
atrial flutter
regularly irregular
due to re-entry circuit in RA from AV back to sinus
atrial fib/ flutter - which is reg?
atiral fib= irregularly irregualr
atrial flut = regularly irregular
saw tooth
narrow tachycardia
flutter waves
atrial flutter
p waves
atrial depolarization
SAN –> AVN
general direction is SE so + on trace
PR inteval
- length?
SAN to ventricle muscle including AV node delay
should be 120-200ms (3-5 small squares)
QRS
ventricular depolarization
AVN to septum and ventricles
septum is SE so big postive up to R then negative as goes opposite direction up ventricle walls
narrow is good
T wave
ventricular repolarization
time of ECG square
small square = 0.04s
big square = 0.2s (5 small squares)
how long does ECG measure for
10s
lead 1
lateral
lead 2
inferior
lead 3
inderior
aVR
not a heart face, it is aorta
aVL
lateral
aVF
inferior
v1
septal
v2
septal
v3
anterior
v4
anterior
v5
lateral
v6
lateral
inferior heart – vessel?
R coronary
R marginal branch of it
lateral hear – vessel?
L circumflex
septal heart – vessel?
LAD
anterior heart – vessel?
LAD
ecg rate calculation
- ) number of R peaks x 6 (ecg is 10s–> min)
- - reg/irreg HR
2) 300 / distance between R peaks in large squares
- – reg HR only
IHD race risk facotrs
SE asia
AF-CArib
QRISK2
aim for?
risk of CV ecent in next 10 y
aim for <10%
ACE i action
Inhibits angiotensin converting enzyme which converts angiotensin 1-2 in the RAAS system. Effect is to less aldosterone so reduce reabsorption of sodium and water in the kidneys so lowers BP,
also vasodilates
ACE I names
“-pril”
ramipril
ACE i side effects
Decreased angiotensin 2 formation
- Hypotension
- Hyperkalemia (aldosterone blocked aldosterone causes K+ excretion). this is esp bad for bilateral renal artery stenosis)
- Acute renal failure (less kidney perfusion due to efferent arteriole constriction)
Increased (brady)kinin production (normally ACE converts kinin to inactive peptides– metabolism) - not with ARB as doesn’t stop ACE’s other action (brady(kinin) causes)–
- Cough !
- rash
- allergic reaction
contraindications for ACEi
- Pregnancy (teratogenic)
- Hyperkalemia
- Renal dysfunction (hyperkalemic S/E esp bad for bilateral renal artery stenosis)
- Afro-carribean patients
- —- Have Salt sensitivity so less renin
- —– means lower angiotensin 1 so already repressed RAAS so medication is less effective for other patients
- asthma? cos of cough side effect?
ARB action
Stops angiotensin 2 binding to peripheral AT1 receptor
does not stop ACE’s other function of bradykinin metabolism, so no high bradykinin so no cough
ARB names
” -sartan”
ARB side effects
- painful breast tissue
- Breast tissue increase in males
- Hypotension (esp volume depleted patients)
- Hyperkalemia (aldosterone causes K+ excretion). this is esp bad for bilateral renal artery stenosis
- Renal dysfunction
- Rash
- Angio -oedema
No cough as ACE still able to do other function : convert kinin to inactive peptides so no (brad)kinin hanging about
ARB contraindications
Pregnancy
Renal issue
Hyperkalemia
postural hypotension
alpha blockers example
doxazosin
alpha blockers action
block adrenoreceptors - which act on smooth muscle so decreases preripheral resistance (vasodilation)
clopidogrel =
antiplatelet
ticagrelor=
antiplatelet
B blocker name
“-onol”
“-olol”
“-llol”
metoprolol bisoprolol
B blocker action
Block noradrenaline attaching to B adrenoceptors by continued binding to them
Decreases cardiac output (less oxygen demand for the heart)
Decreased HR (chronotropic)
Decreased heart contractility (inotropic)
Lower HR means better oxygen distribution
(beta1 receptors)
(beta 2 receptors – vasodilation)?
Block reflex sympathetic responses which stress heart in HF
Propanolol best B blocker for post MI arryhtmia as also blocks sodium channels (also in class 1 = soidum channel blockers , as well as b blocker class 2 )
B blocker contraindications
Asthma !!!!!! (bronchospasm)
COPD
PVD - peripheral vascular disease
B blocker side effects
Fatigue Headache Sleep disturbances inc nightmares Bradycardia Hypotension Cold peripheries Erectile dysfunction
calcium channel blockers types with examples
all = L type CCB
1) phenylalkyonines (verapamil, diltiazem)
2) dihydropiridines -“dipine”. (amlodipine)
3) benzothiazapines
* in maudative-
dihy. . = multi purpose - including hypertension (amlodipine)
Non-dihy.. = specific to heart, not hypertension (diltiazem)
CCB action
Increase cGMO and reduces intracellular Ca2+ concentration
inhibits opening of voltage gated Ca channels (L type) in vascular smooth muscle), so lower calcium entry so less Ca available for contraction so decrease in peripheral resistance
vasodilation
prevents artery and heart hardening
1)phenylalkyonines (verapamil) cardiac:
Decreases CO- negatively chronotropic (decrease HR)
Negatively inotropic (reduce force of contraction)
Doesn’t act on calcium channel at rest (more effective)
type 4 anti arrythmia drugs
2) dihydropiridines (class 1 ?) -“dipine”. (amlodipine) - vascular:
Vasodilates peripheral arteries so decreases peripheral resistance
Acts on calcium channel at rest (less effective)
- good for coronary spasm angina (not sure why)
3) benzothiazepines - both heart and vascular effects - between 1 and 2
corticosteroid 2 examples
prednisolone
hydrocortisone
corticosteroid action
Dampens immune system
- Suppress prostaglandin and leukotryin mediators
digoxin action
inhibit Na/K pump (blocks Na out and K in action)
So more Ca in heart
– Increased force of contraction (ionotropic)
Increased vagus (parasympathetic supply increased) stimulation ACh released (increases)
- Bradycardia (chonotropic)
- Slows AV node conduction
this is a cardiac glycoside (class 5 ) antiarrythmia drug
digoxin side effects
More ectopic activity (extra beats)
Narrow therapeutic range
- Vom
- Nausea
- Diar
- confusion
diuretics types and names
1) thiazides - distal tube “-thiazide”
2) loop diuretics- loop of Henle”-mide”
3) k (spironolactone)
diuretics action
Pass more urine, more electrolytes lost
Decrease blood pressure
1) thiazides = block sodium and chloride reabsorption at the Na/Cl luminal co transporter
2) loop diuretics block Na / K/ 2Cl transporter (moving Na, K, 2 Cl into cells from urine via Na movement). This then reduces water outflow
nitrates action
Arterial and venous vasodilators
Reduce preload and afterload
(it’s the reduced preload that reduces anginal pain as less heart demand)
Lowers BP for IHD/ heart failure (not hypertension)
statins action
Lowers serum LDL cholesterol by reducing production in the liver
lidocaine action
sodium channel blocker (decrease Na)
class1 antiarrythmia drug
amiodarone action
prolong duration of action potential (by decrease K + )
type 3 antiarrythmia drug
amiodarone has long half life and is selective for long action potential
thiazides SE
hypokalaemia (increased K+ secretion)
chlorthalidone =
non thiazide drug (but still antihypertensive)
acts on DCT (reduce reabsorption)
for longer duration
indapamide =
non thiazide drug (but still antihypertensive)
acts on DCT (Reduce reabsorption)
also vasodilator
what effect do beta blockers have on RAAS
reduce plasma renin
spironolactone effect on RAAS
aldosterone antagonist
when is CCB contraindicated / cautioned
heart failure
as in cardiac muscle - negatively inotropic (contractility)
hypocalceamia ECG looks like?
- other causes for same ecg?
long QT (QT syndrome)
hypokalemia MI DM drugs - amiodarone, antidep congenital - romano-ward, jervell-large-neilson
