CVS Flashcards
Muscular arteries
Same as elastic, but less elastic membranes, more SMC and unmyelinated nerve endings
Structure of elastic arteries
TI endothelial, sub endothelium of CT
TM fence started elastic membranes, SMC, collagen
TA fibroelastic CT and vaso vasorum
Structure of arterioles
D<0.1mm
1-3 SMC
External elastic lamina is abscent
TA is scant
Length of systole and diastole
280ms
700ms
Spread of excitation down septum
Endocardial to epicardial
Define ionotropy and chronotropy
Ionotropy is contract ability
Chronotropy is rate
Receptor that is responsible for vasoconstriction
Alpha 1
Autonomic nervous system that dominates heart at rest
Natural heart rate
If parasympathetic knocked out
Parasympathetic dominates
60bpm
100bpm
The autonomic changes involved in increasing heart rate
Decrease in parasympathetic
Then increase in sympathetic
Link resistance, flow and pressure drop in arterioles
Flow constant in all CVS so due to high R, high pressure drop
Pulse pressure and average pressure
Pulse: difference between systolic and diastolic
Average: diastolic + 1/3’systolic pressure
Name the vasodilator metabolites
H+, K+, Adenosine
Define pre load and after load
Pre load- end diastolic stretch of myocardium
After load- force necessary to expel blood into the arteries
How the body prevents pulmonary oedema in excercise
Heart rate already high so stroke vol kept low but CO is high
How haemorrhage effects venous pressure
Decreased blood vol, decreased CO and arterial pressure, recognised by barro receptors that increase HR and TPR which lowers VP and hence AP even further
What is special about SAN myocardium a membrane potential
Less negative so fast Na chan remain inactive, only slow Na chan open during repolarisation so you get timed depolarisation
Causes of Arrhythmias
Ectopic Pace Maker activity
After Depolarisation
Reentry loop
Class 1 anti arrythmic
V gated Na chan blockers eg lidocaine, this prevents after depolarisations
Class 2 anti arrythmic
Beta adrenoceptor antagonists eg propranolol and atenolol
Decreases ionotropy and chronotropy so reduced O2 demand from myocardium
Class 3 anti arrythmic
K+ chan blockers! lengthened absolute refractory period preventing another AP too soon,
Not generally used
Class4 anti arrythmic
Ca2+ chan blockers eg Verapamil
Decreases HR and AV node conduction
Decreases contractile force
What does adenosine do as an antiarrythmic?
Resets the heart as it hyper polarises the cell
How do ACE inhibitors work?
Prevent vasoconstrictor angiotensin 2 so decreases pre and after load
Also decreases aldosterone and therefor blood vol.
What is the action of an organic nitrate spray?
SMC release NO2 -> NO which is a vasodilator
Primarily acts as a venodilator, then on coronary arteries
The colours of the limb leads
Red RU
Yellow LU
green LL
Bike RL
Placement of chest leads
1 is 4th intercostal space RHS of sternum
2nd is LHS of above
4th is 5th intercostal space mid clavicular line
6th is mid axillary
How to work out ECG rate
300/no of squares
What would a ventricular ectopic beat look like
Wider, taller and may be every 3rd or 4th
ECG of atrial fibrillation
P wave abscent, instead irregular fibrillation waves between QRS complexes
What does ventricular fibrillation look like on ECG
Uncoordinated contraction
1st degree heart block
PR interval elongated from 200ms, conduction delay
2nd degree T1 heart block
PR interval is erratic, gets longer till a QRS complex is dropped
2nd degree T2 heart block
Excitation sometimes fails to pass AVN or bundle of His
Compete 3rd degree heart block
No conduction at AVN, ventricles have ectopic pacemaker but beats are slower
Bundle branch block
Lengthened QRS complex
Blood flow of pulmonary cvs
Low r, short, wide vessels, low pressure
How is blood diverted from alveoli not well oxygenated?
Hypoxia pulmonary vasoconstriction
How does coronary endothelium produce a high basal flow?
Continuous production of NO
3 cerebral circulation protection mechanisms
Myogenic auto regulation: increased bp causes vasoconstriction across trans mural wall
Metabolic Regulation: increased CO2 causes vasodilation
Regional activity: highly active has high release of adenosine
Cushings reflex
Increased ICP decreases blood flow to vaso motor control regions and increases it’s sympathetic activity so increased arterial blood pressure
Chest pain from heart problems location
Central retrosternal
Signs of unstable angina
Ischemic chest pain at rest, depressed ST
Treatment of angina
Acute - Nitrate spray,
Prevent - beta and Ca chan blockers and oral nitrates
Prevention of cardiac event: aspirin, statins, ACE inhibitors
Cause of thrombosis from atheroma?
Exposure of thrombogenic necrotic core
She do you get NSTEMI MI
Infarct is not full thickness
Class 1 heart failure
None symptomatic but limitation of physical activity (LPA)
Class 2 heart failure
Slight LPA leading to symptoms, none at rest
Class 3 heart failure
Marked LPA and symptoms, none at rest
Class 4 heart failure
Inability to do activity without symptoms and some symptoms at rest
Congestive heart failure
Both sides of the heart failing
Describe RAAS
Renin angiotensin aldosterone system, makes HF worse
Decreased bp causes renin release from kidneys
Angiotensin 1 converted to angiotensin 2, this is a vasoconstrictor and causes release of aldosterone increasing blood vol
Action of cardiac glycosides
Increase CO and heart contractility by inhibiting Na/K pump so inhibits NCX so intra cellular Ca raises
Define shock
Inadequate distributed tissue perfusion
Cardiogenic shock
Inability to eject enough blood eg Arrhythmias
Mechanical shock
Restriction of filling the heart eg cardiac tamponade
Hypovolaemic shock
Loss of circulating fluid eg haemorrhage
Normovolaemic shock -
Fall in TPR eg sepsis
How to treat shock?
Fluids and adrenaline
Pericardial sac in to out
Serous, parietal, fibrous
Phrenic nerves
C3 C4 C5, motor and sensory to diaphragm, sensory to pericardium
Right phrenic nerve over RA
Left over left
How is heart attached to sternum?
Sternopericardiac ligament
