Cardiology - Physiology Flashcards
What is CO equal to ? typical CO ?
CO = HR x SV
typical CO: 5L/min
What structures in heart have pacemaker potential ? (4) what determines which is the one that the heart follows?
heart follows rhythm of fastest pacemaker
- usually SAN, can be AVN, ventricular myocytes, purine fibres
What is chronotropy ? inotropy ?
Chronitropy: affecting HR
inotropy: alter force/energy of contraction
What is normal HR? what is the structure that normally controls this ?
normal HR 60-100 usually controlled by SAN (cluster of pacemaker cells in RA)
what is normal SAN pacing? what innervation brings it down ?
SAN pacing normally around 100 bpm but para innervation at rest brings it down
(has natural automaticity)
what is AVN function ?
pass on impulse from A => V (but with small delay due to lower conduction velocity (0.5s) => allows atria to finish contraction + AV valve to shut
describe the para effect on heart ? (chronic/ino)
para via vagus nerve (to SAN + AVN) => negative chronitropic effects (decrease HR)
describe the sympathetic effect on heart ? (chronology/ino)
via superical + deep cardiac plexus => +ve chrono + inotropic effects (increase HR and SV)
what are baroreceptors sensitive to ? where are they located ? what does increased firing mean ? what does this cause ?
baroreceptors (located in carotid sinus and aortic arch): sensitive to change in stretch + tension in arterial walls (then communicated to medulla)
- increased barorecepot firing => means increased arterial pressure detected => PSNS innervated => reduced HR + vasodilation
What is SV equal to ? (what blood in heart)
difference between end diastolic vol + end systolic vol
what is central venous pressure (CVP)
BP in vena cava, reflects amount of blood returning to RA)
how does increased CVP affect SV ?
increase CVP => increased diastolic filling => stretch myocytes => increase preload => increase SV
What is starlings law?
the more the hear chamber fills, the stronger the ventricular contraction => increase SV
How does increased TPR affect SV ?
increased TPR => increased after load = > reduce SV
How much blood does the heart pump around the body at rest ?
5L
when does most filling of the ventricles take place ?
ventricles fill during diastole and atrial systole (most filling is in diastole)
what is is-volumetric contraction ?
ventricles contract, hert valves remain shut => increase pressure
What is the outflow phase of the cardiac cycle ?
(systole)
ventricles contract further, valves open, blood exit
What are the phase 0 - 4 of cardiac muscle contraction ?
Phase 0: rapid depolarisation (rapid sodium influx)
Phase 1: early depolarisation (efflux of K)
Phase 2: plateau (slow influx of Ca)
Phase 3: Final depolarisation (efflux of K)
Phase 4: restoration of ionic concs (NA+/K+ ATPase)
Where is the AVN located ?
within AV septum - near opening of coronary sinus
what are the 2 AV bundles? where supply to ?
AV bundle (bundle of His)
- Right bundle branch (conducts impulse to RV)
- Left bundle branch (conducts impulse to LV)
What are gap junctions ? located where in cardiac context ? What does it allow for ?
regulated pores that connect adjacent cardiac myocytes
- located at the intercalated discs (at either end of the myocytes)
- allows for cell coupling => quick AP spread from cell to cell => unidirectional and synchronicity
What is the ventricular resting membrane potential
-70mV
What is blood flow ? and what is it equal to ?
vol of fluid passing a point per unit time
Flow = pressure / resistance
what is laminar flow ? describe it
velocity is highest in centre of vessel and lower closer to vessel wall (due to increased resistance)
where is turbulent blood flow more likely ?
when vessel branched/constricted => rougher flow
(bifurcations, atheroslecrotic)
What is resistance to blood flow dependant on ? (3) high or low of each of these increase resistance ?
what law ?
dependant on
- radius (increase)
- viscosity (decrease)
- vessel length (decrease)
what is virchows triad ?
what are the 3 factors ?
3 factors that reduce flow => increase thrombus risk
- stasis of blood flow
- hypercoagulability
- vessel wall injury
What is BP equal to ?
CO x TPR
(flow x resistance)
what is short term BP regulation controlled by ? detected by what ?
controlled by autonomic NS
- baroreceptors detect BP
What happens when there is increased baroreceptor firing ? what innervation ? what affect on BP does this have ?
increased firing => (medulla oblongata) PSNS via X nerve => reduce HR => reduce CO => reduce BP
what is involved in long term BP regulation ? (2) explain a bit
- RAAS: reinin is released in response to SNS stimulation
- ADH: produced in hypothalamus + stored/released from AP => increased water reabsorption
what are some of the complications of long term high BP ? (3)
- Macrovasc (storke, MI)
- Microvasc (neph/retinopathy)
- Heart (increase afterload => LV hypertrophy, dilated cardiomyopathy => HF)
What is Ficks law ?
rate of diffusion is proportional to conc difference + area available
(capillary exchange)
- capillaries have large SA + steep conc gradient + short diffusion pathway
what are starling forces ? name the 4
physical forces that determine the movement of fluid between capillaries and tissue fluid
- blood hydrostatic (pressure exerted by blood in capillaries against vessel wall)
- oncotic (pressure exerted by proteins in blood (pull fluid into blood))
- interstitial hydrostatic pressure
- interstitial oncotic pressure
what is kwashiorkor ? pathophys explain
malnutrition + low albumin => low oncotic pressure => muscles wasting + oedema (thin extremities + distended albumin)
what cells regulate arteriolar tone ?
smooth muscles cells in tunica media
describe the pressure in veins vs arteries ?
- Veins: low pressure, low resistance
- Arteries: high pressure, high resistance
do veins or arteries have higher capacitance ? what does this mean ?
veins have high capacitance (can distend with increasing BP)
what is CVP ? where is is measured from ?
Central venous pressure (CVP) is the BP in the vena cava (near RA)
What does coronary vessel perfusion occur during cardiac cycle ? where does blood enter through ?
occurs during diastole
- enters through aortic sinuses (openings behind the aortic valve leaflets)
What is the clever things about circle of willis being a circle ?
anastomoses between basilar _ internal carotid arteres
(this provides collateral flow in case one artery is blocked)
describe Cushings triad ? what does this indicate ?
- hypertension
- bradycardia
- irregular breathing
(indicates acute elevated ICP)
What are the actions of ANP (atrial naturieretic peptide)
- promotes excretion of NA (natriuretic)
- reduce BP
- Antagonise angiotensin II
What is endothelin ?
- potent long-acting vaso + bronchoconstrictor
- thought to be involved in pathogenesis of: primary HTN, HF, Raynaud’s
What vessel do the coronary arteries branch off from ?
branch off from the aorta
what are the branches from the aorta ? (3)
- brachiocephalic
- L common carotid
- L subclavian
at what vertebral level does the pulmonary truck split ? into what ?
splits at T5-6 into R + L pulmonary arteries
SVC is formed by the merging of which veins ?
brachiocephalic veins
what forms the R border of the heart ?
RA
what is the coronary sinus ? opens into where ?
recieves blood form the coronary veins and opens into RA
what forms majority of anterior border of the heart ?
RV
what are papillary muscles ? pull on what ?
papillary muscles pull on cord tendinae to prevent valve prolapse
Describe overview of conducting system of the heart ?
AP is created in SAN => wave of excitation spreads across atria => deli at AVN => conduction down bundle of His => purkinje fibres
what is the SAN ? where located ? what impact does SNS input have ?
collection of specialised pacemaker cells (in RA where SVC enters) which spontaneously generate electrical impulses
- excitation spreads across both atria via gap junctions (atrial systole)
- SNS => increased San firing rate
how long AVN delay ? why have this delay ?
node delays impulses by 120ms which allows time for atria to fully eject blood before ventricular systole
(lies near coronary sinus)
what is bundle of His ?
continuation of AVN dividing into 2 main bundles
(RBB conducts impulse to purkinje fibres of RV)
which part of the heart has fastest conduction rate ?
purkinje fibres
What is the pericardium ?
fibroserous, fluid filled sack that surrounds the hearts + roots of the great vessels
describe the two layers to the pericardium ?
- tough external fibrous pericardium
- internal serous pericardium (sub divided into visceral + parietal layers with pericardial cavity in between which contains small amount of lubricating serous fluid to minimise heart friction)
(fibrous layer => serous parietal layer => serous fluid => serous visceral layer)
functions of the pericardium ? (4)
- fixes the heart in places
- prevents overfilling
- lubrication
- protection from infection
what is the innervation of the pericardium ? where referred pain ?
phrenic nerve (C3,4,5)
- referred pain: shoulder pain
how many cusps does the pulmonary valve have ? aortic valve ?
semilunar valves
- pulm valve (3 cusps)
- aortic valve (3 cusps)
where do the Coronary arteries arise from ? when do they fill ?
L + R coronary arteries arise form the L + R aortic sinuses (small openings behind the L + R flaps of the aortic valve)
- fill during diastole
describe the veinous drainage of the heart ?
venous drainage mostly through coronary sinus
- cardiac veins => coronary sinus => RA
ECG changes ssen in II, III, aVF. what artery occluded ?
RCA (inferior)
ECG changes ssen in V3 + V4. what artery occluded ?
Distal LAD (anteroapical)
ECG changes ssen in V1 + V2. what artery occluded ?
LAD (anteroseptal)
ECG changes ssen in I, aVL, V5, V6. what artery occluded ?
circumflex artery
describe the ECG changes ? (like slow mo described)
V1-2: septal
V3-4: anterior
V5-6: Lateral
II,III, aVF: Inferior
I, aVL: Lateral
give examples for each of these categories of tachycardia:
- narrow regular
- narrow irregular
- wide regular
- wide irregular
- Narrow regular: sinus tachycardia, atrial flutter, paroxysmal SVT
- narrow irregular: AFib, AFlut with variable block
- Wide regular: monomorphic Vent tachycardia
- Wide irregular: Polymorphic Vent tachycardia (TdP), ventricle fib
normal PR interval ?
<200ms
what class drug is amiodarine ? what does it do ?
class III anti-arryhtmic
- prolongs cardiac action potential
