Cardiovascular Flashcards
What is the formula for cardiac output?
HR X SV
What increases stroke volume?
Increased end diastolic ventricular volume or decreased end systolic ventricular volume
What affects EDVV and ESVV?
EDVV- preload, compliance, diastolic filling time
ESVV- after load and contractility
What is the difference between bulk flow and osmosis?
Movement of fluid from hydrostatic pressure is bulk flow where as movement from oncotic pressure is osmosis
What does high hydrostatic pressure cause relative to ECF?
Filtration- blood out the capillary into ECF
How can heart contractility be increased?
Sympathetic nervous system- fight or flight
What changes occur in the CV at birth?
First breath leads to large drop in resistance to flow in pulmonary circulation
Increased venous return to left atrium = increased left atrial pressure closing foramen ovale
What is a vector of an ECG?
A vector is measuring the size of individual waveforms, observing direction and comparing size of deflections to give information on the flow of depolarisation
What does a vector show?
The vector points towards the most positive charge indicating the direction the action potential is moving
How can an estimate of a vector be made?
Comparing leads 1,2 and 3 it can be estimated by comparing the size of the deflection
The larger the deflection the more parallel the line
What is the mean electrical axis?
All the vectors create a PQRST waveform which can be averaged to give mean electrical axis
What is the mean electrical axis useful for?
Useful for looking for signs of chamber enlargement, cardiac displacement or interruption of the conduction pathway
What diagram is needed to work out the mean electrical axis?
Bailey’s hexaxial Diagram
What are the three techniques for estimating the mean electrical axis?
1) look for biggest QRS complex (note if +/-), this lead is most parallel to MEA so will be within 30 degrees
2) Look for isoelectric lead (lead with biggest deviation above the baseline equal to deviation above the baseline), this lead will be perpendicular
3) Quadrant graphing method- uses I and AVF to divide circle into 4 quarters
Describe how to estimate the mean electrical axis with the quadrant graphic method
Use lead I and AVF to divide the circle into quarters
Look at the traces for these leads and see if they have a positive or negative QRS
Draw arrows on the hexaxial diagram indicating the quadrant of the MEA
Then compare QRS in these two leads biggest is closer to MEA
What is the normal readings of MEA in dogs and cats?
Dogs- +40 to +100
Cats- 0 t0 + 160
What is the term used to describe an MEA out of the normal ranges?
Axis deviation- can be left of right
What causes axis deviations to MEA?
Heart isn’t sitting in the normal position in relation to limb leads
Size of the chambers of the heart is abnormal
The conduction pathway is abnormal so the AP is travelling a different route
What is the term for a fast and slow arrhythmia?
Slow- bradyarrythmia
Fast- taccyarrhthmias
What does an supraventricular, junctional, ventricular arrhythmia mean?
Supra- generated by atrium
Junctional- AV node/bundle
Ventricular- ventricle
What are the three premature complexes?
Supraventricular
Junctional
Ventricular
This is because they are when the heart should be depolarising
What is a supraventricular complex?
Normal QRS but in the wrong place, AP follows normal conductive route but no P as atria didn’t depolarise
What is a ventricular premature complex?
AP not following normal direction of travel, usually wider QRS as not following the purkinje fibres, no P wave and T wave in opposite direction to QRS
What is atrial fibrillation?
Arrhythmia associated with large atria, seen in small animals with stretched atriums and horses with normal huge hearts. The atrial myocardium begins to generate random wavelets which bombard AV node, some are conducted some not giving chaotic rhythm. There is no p wave and an irregular r-r interval
What is an atrioventricular block?
A cardiac cause of bradycardia, can be 1st, 2nd or 3rd degree. The conduction of the action potential is slowed or obstructed in the AV node/bundle
How can a 1st degree AV block be distinguished?
The PR interval Is prolonged indication slowing at this point
What is a 2nd degree AV block and what are the two types?
2nd degree AV block is when the conduction of the action potential through the AV node is partially blocked meaning that intermittently the P wave will fail to generate a following QRS complex
Types- Mobitz 1 and 2
What is the difference between mobitz 1 and 2?
Mobitz 1- aka Wenckebach, progressive lengthening of the PR interval until eventually there is a non-conducted P wave
Mobitz 2- P wave are at constant rate, intermittently there will be one or more non-conducted beat
What is a 3rd degree AV block?
Complete blockage at the AV node, so all PQRST are present but unrelated, the atria will depolarise at the rate by the SAN and the AV node will take over for the ventricles
What is a normal BP for dog or cat at rest?
120/80
What is the potential impact or consistently low or high blood pressure?
High- afterload increases, increased workload, stretching, hypertrophy, backwards heart failure, increased pressure on kidneys, eyes
Low- low perfusion to tissues, low production from kidneys, muscle wastage
What is the blood pressure formula?
Pa = CO x TPR
What factors influence stroke volume?
Contractability, Ventricular stretch
How is blood flow controlled locally and extrinsically?
Locally- metabolic auto regulation, paracrine control
Extrinsic- Preserve flow, Baroreflex, RAAS
Where are baroreceptors found and how does the baroreflex work?
Aortic arch and carotid sinus
Send imputes to CV centre in medulla oblongata, output via autonomic nervous system
Drop in BP, increases sympathetic decreases parasympathetic
Increase in BP decreased sympathetic increased parasympathetic
Where are different adrenergic receptors found in the CV system and what to they cause?
a1/2- found in blood vessels causes vasoconstriction
b1- found in cardiomyocytes casques increased contractility and HR
b2- in blood vessels causes vasodilation
All for fight or flight
Where are cholinergic receptors found in the CV system and what do they cause?
M2- in cardiac (nodal tissue), causes decreased contractility
M3- found in blood vessels (coronary arterioles) and cause vasodilation
Rest and digest
What is the function of nitric oxide and where is is released from?
Local factors which are released following increased speed of blood flow, causes vasodilation, also secreted by parasympathetic system
Briefly describe the RAAS system?
renin, angiotensin, aldosterone system- renin from the kidney causes angiotensin to convert to angiotensin I
angiotensin converting enzyme converts to angiotensin II in lungs
Ang II causes vasoconstriction and produces aldosterone
Aldosterone causes sodium then water retention in the kidneys, increasing thirst
What three factors change blood pressure?
Change in blood volume
Change in contractility
Change in blood vessel diameter
How does the kidney help regulate blood pressure?
Afferent arteriole detects changes in BP and secretes renin (RAAS)
Regulates sodium excretion
What are the three functions of Angiotensin II?
Vasoconstriction of non-essentials
ADH from pituitary
Increased sensation of thirst
How can cardiomyoctes contractility be influenced by adrenaline/noradrenaline?
Adrenaline binds to B1 adrenoreceptor on nodal tissue
This produces adenyl cyclase which converts ATP to cAMP
cAMP activates activates PK-A which phosphorylates Ca channels for Ca influx increasing contraction
How can cardiomyocytes therefore be affected by PDE3?
cAMP is broken down into AMP by PDE3, therefore anything affecting PDE3 will increase contractility
Other than B1 adrenoreceptors how else can contractility be affected?
a1 adrenoreceptors can be bound by noradrenaline, ang II, ET-1 which increases calcium release from sarcoplasmic reticulum
How can vascular smooth muscle be made to contract and how?
Stretch, electrical, chemical stimulus
Cause increased intracellular Ca2+, activation of myosin light chain kinase, phosphorylates myosin light chain increasing cross bridge formation
How can vascular smooth muscle be relaxed?
Increased cAMP inhibits myosin light chain kinase
Increases cGMP activation of MLCP which dephosphorylates MLC
