Cardiovascular overview 2 Flashcards
What is the equation for blood pressure?
BP/Pa = CO X TPR
Which blood vessels are the biggest influence on TPR?
Arterioles
How is TPR increased?
Vasoconstriction to non-essentail organs (everything except brain, heart and sk muscle)
Permanent fluctuations –> organ damage due to ischaemia
What are the 2 types of heart failure?
Primarily….
Backwards (CHF) or forwards (systolic). One usually leads to another and at the time of Dx, both are usually present.
What is forwards heart failure?
Systolic failure
Resulting in reduced CO, and reduced mean arterial pressure
What does forwards heart failure cause?
Decreased CO
Decreased stroke volume
Thready pulse, decreased CO, reduced perfusion therefore decreased capillary refill time, causes faint when exercising. (VASOVAGAL SYNCOPE)
Cold extremities
What is backward heart failure (CHF)?
Inability to cope with preload
Usually mitral valve disease- allows blood to flow back into left atrium during ventricular systole
What does backward heart failure generally cause?
Increased atrial and venous pressure, increased capillary pressure, fluid leaks into ISF
which leads to pulmonary oedema
What are the symptoms of left sided CHF/backwards HF?
Pulmonary oedema
Tachypnoea - inc RR
Dyspnoea - laboured breathing
Audible crackles on auscultation of the lungs
What are the symptoms of right sided congestive heart failure?
Increased systemic venous pressure often leads to effusions. Such as ascites (abdominal effusion)
inc SP = visible distension of jugular veins and
Splenomegaly
Hepatomegaly
Compensation for heart failures are often a viscious cycle. Why is this?
Increased work load on failing heart
Increases compensatory mechanisms
Cycle continues
What are the compensations for FHF? (systemic)
Non-essential organs vascoconstrict
RAAs system
Frank-Starlings mechanism - reduced CO = venous and atrial pressure rises, = greater preload which increases EDVV, therefore inc CO
Baroreflex (perceived drop in atrial BP) = sympathetic stimulation heart and BV to inc contractility, HR and conduction thereby inc CO)
Atrial and brain natriuretic peptides
Non-Essential organs vasoconstriction during heart failure. What does this lead to? Is this effective?
Increased TPR - increases HR and contractility
Not effective longterm - increases afterload on failing heart, leads to kidney failure and sepsis (lack of blood to GI system leads to bacterial increase)
How does the RAAS system try to compensate heart failure? Is this effective?
Ranin + AG = Ag1, lungs = Ag2
Ag2 binds to adrenal gladn releasing aldosterone = excretes K+, absorbed Na+ and water.
Increase blood pressure by sodium and water retention
Ag2 inc ADH release
Overall inc preload, SV adn CO therefore mean aterial pressure.
Heart has more work which leads to BHF/CHF
What are atrial and brain natriuretic peptides? What does their presence in blood suggest?
Proteins produced in atria/brain in response to stretching of myocardium
Indicates stretch of myocardium
What do ANPs and BNPs do?
Cause increased sodium in urine and therefore increased water in urine.
Causes body to think thirsty
Increases renin production
What is the Frank-Starling mechanism?
Heart changes force of contraction and stroke volume to match demand
Response to changes in venous return
What is the baroreflex?
Baroreceptors in carotid sinus and aortic arch detect stretch when blood pressure is increased
Baroreceptors fire more APs when more stretch detected
Cause an increase in HR
Where do APs originate? How are they propagated?
Nodes
Propagated from cell to cell via intercalated disks - allow cations to move and depolarise next cell
Very fast - act as one cell = function syncytium
Pacemaker cells have automacity - what is this?
Spontaneously depolarise and generate APs
Which node is responsible for sending APS in the heart?
SAN - fastest
AVN is slower (slower spontaneous depolarisation) but can take over if needed
What happens with ions during depolarisation?
Na and Ca move into cell, potassium moves out f cell
When do sodium channels open?
At negative membrane potential
Cause calcium channels to open
What is the pacemaker potential?
Difference in sodium channels
The outermsmbrane of each cardiomyocyte has what type of resting membrane potential?
What are the 2 differences between cardiomyocytes and muscle cells in terms of depolarisation?
Stable, negative resting membrane potential
They spontaneously depolarise unlike muscles which need stimuli
AP is much longer in cardiomyocytes
What is the refractory period? What is the significance of this in the heart?
Period where a new AP cannot be initiated until previous AP is completed
Prevent the heart from sustaining contractions (tetany) - allows relaxation phase to fill chambers
Skeletal muscle is capable of temporal summation. What does this mean?
Multiple APs can cause one contraction
What graph does an ECG produce? What position should an animal be in when taking an ECG and why?
Voltage against time
R lateral recumbency - heart is midline
What should the P:QRS ratio be in an ECG? What is P, Q, R, S and T?
1
P - atrial depolarisation
QRS - ventricle depolarisation
T - ventricle repolarisation
Why is atrial repolarisation not visible on an ECG?
Occurs during ventricular depolarisation
Very small amplitude - masked by large QRS complex
The ECG compares voltage at + and - electrodes. What does it measure? What can’t it measure?
Measures potential difference/amplitude and direction - peak –> towards positive electrode. Trough –> away from positive electrode
Can’t measure blood oxygenation or CO
What are augmented unipolar leads?
Compare one limb with average of other two - cover all angles
Increased height/voltage don an ECG shows what?
More tissue
Increase width on an ECG shows what?
Longer time period –> larger chamber
A change in ECG direction could indicate what?
Ectopic pacemaker
