CVS Flashcards
Coronary arteries=
first branches of the aorta from the aortic sinus’
features of coronary arteries
ischaemic heart disease; stable angina symptoms
- Central chest pain and tightness
- Brought on by exercise and relieved by stress
- Radiations to neck, shoulder, elft arm
treatment for stable angina
- nitrates (sublingual GTN)
- B- blockers
- calcium channel antagonists
B blockers increase the length of diastole
- B- blood flow to the left coronary artery is compromised because diastole (relaxation) is shorter
- E - Dilation of systemic veins
- Dilating veins in systemic circulation reduces the return of blood to the right side of the heart which lowers preload, therefore force of contraction is reduced making the heart work less hard
- Constrict left coronary artery going into the myocardium
- Dilating veins in systemic circulation reduces the return of blood to the right side of the heart which lowers preload, therefore force of contraction is reduced making the heart work less hard
acute coronary syndromes
Unstable angina, NSTEMI, STEMI
Caused by plaque rupture and thrombus formation
- Continuum of increasing severity depending on extent, duration and location on the thrombus/blockage
Unstable angina vs NSTEMI vs STEMI
- Unstable angina- partial occlusion no death to muscle
- NSTEMI- death of cardiomyocytes but not full thickness
- Non- ST elevation myocardial infarction
- STEMI- full thickness death
Unstable angina
- Rapid onset pain at rest
- Severe central- may radiate less than MI
- Cause
- Disruption of atherosclerotic plaque and thrombus formation
- Limited duration and extent of obstruction
- May be ST depression and or T wave inversion
- No detectable necrosis (Troponin not elevated)
MI
- Acute severe central chest pain (crushing)
- Radiating to neck, left shoulder and arm
- Not relieved by reast
- Strong sympathetic reaction
- Sweating
- Pallor
- STEMI- full thickness necrosis of myocardial wall
- NSTEMI- more limited necrosis
typical ECF changes with STEMI
Q wave is a sign
of previous death of electrical tissue –> persists for years
E
lateral leads and which artery
I, aVL, V5-V6
- left circumflex
- LAD
inferior leads
II, III, aVF
- RCA and/ore LCx
anterior/septal leads
V1-V4
- LAD
E
time course of eleavtion in cardiac troponins and emzymes
troponin
Troponin I and T for cardiac
troponin C for skeletal muscles
heart failure can be due to
systolic dysfunction- inability to contract properly
- ejection fraction will be reduced (HFrEF)
diastolic dysfunction- inability to relax or fill properly
- ejection fraction may be preserved (HFpEF)
can be a combination
HFpEF
stroke volume will be reduced as well as EDV (a ratio) – so will be unchanged
frank starling curve
The higher the stroke volume, the stronger the contraction
120- 80/120
- D- 33%
- 120-80/120
- EDV volume- systolic volume = stroke volume
- Stroke volume/ EDV = ejection fractions
Left vs right vs congestive heart failure
Commonest cause of right sided heart failure is left sided heart failure
C
C
oedema is madfe worse by
fluid retention
B
B
C
B
D
D
- E
- P wave and QRS are independent of each other
- Therefore atria and ventricles depolarise separately
D
prolonded PR interval
ECG interval segment
B
Electrode placement
Ride your green bike
Z
ventricular depolarisation
what each part of the ECG relates to
- 300/2.5 = 125bpm
- Sinus tachycardia
prolonged PR interval
- Second degree heart block (Mobitz type 1)
- Progressive lengthening of PR interval
- until drop out of QRS complex
- Second degree heart block (Mobitz type 2)
- May need pacemaker
first degree AV block
- Third degree heart block
- QRS are wide because block is happening at more distal site, therefore broad complexes
A
