cardio physio Flashcards
what is the sequence of flow of electrical signals through the heart?
SA node→ AV node→ bundle of his→ left/right bundles→ purkinje fibres
what is the function of the AV node?
ensures atria & ventricles function in sync
- ensures complete atrial depolarisation before depolarisation spreads to ventricles
- ie atria contract→ ventricles contract (AV nodal delay)
what is the function of fibrous rings?
- electrically insulates ventricles from atria (AV node’s the only gate)
- prevents signals from travelling from atria→ ventricles directly
- ie allows AV node to regulate ventricular depolarisation
what is the function of bundle of his?
- specially rapidly conducting tissues
- allows synchronised contraction between & within ventricles
what are the consequences of RCA (right coronary artery) being infarcted?
RCA supplies SA node, AV node, RV and RA
- SA node compromised (fires impulses slower→ bradycardia)
- AV nodal block
what happens during AV nodal heart block?
- impulses from atria to ventricles blocked ie ventricular rate is no longer controlled by SA node (now controlled by downstream pacemaker discharging at slower rate)
- heart rate decreases
- ventricular stroke volume’s variable due to variable filling (no longer atria full→ ventricle pump)
how is heart rate regulated?
- by ANS
- through the vasomotor centre (VMC)
what factors indirectly increase heart rate (via VMC) (4)
- increased pain
- fall in arterial pressure
- increase H+ ions
- inspiration
what factors directly increase heart rate (3)
- catecholamines (stress hormones)
- increase temperature
- thyroxines (hormones regulating metabolism)
what are the sympathetic effects on the depolarising activity of SA node (2)
- resting membrane potential is more positive
- slope of depolarisation is steeper
threshold potential for SA to fire impulse is reached faster→ SA node fires more frequently!!
what causes upstroke in ventricular muscle action potential?
depolarisation of purkinje fibres→ depolarise muscles→ opens voltage gated Na+ channels→ INFLUX of Na+
what causes early fast repolarisation in ventricular muscle action potential?
K+ channels open→ EFFLUX of K+
what causes plateau in ventricular muscle action potential?
Ca2+ channels open→ INFLUX of Ca2+
(K+ efflux> Ca2+ influx→ gradual downward sloping)
what causes repolarisation (phase 3) in ventricular muscle action potential?
Ca2+ channels close→ Ca2+ influx stops→ K+ efflux continues
what gives rise to the P wave?
atrial depolarisation
what gives rise to the QRS complex?
ventricular depolarisation (atrial repolarisation is masked)
what gives rise to the T wave?
ventricular repolarisation
what is PR interval?
- start of P wave to start of QRS complex
- time taken for signal to travel from AV node to ventricles (conduction through AV node)
what are the pathologies of PR interval? (2)
- wide (>2 squares): P-mitrale/LA enlargement
- tall (>2 squares): P-pulmonale/RA enlargement
what is the QRS interval?
time for ventricular depolarisation
what is the RR interval?
- peak R to peak R
- time taken from one cycle to the next ie heart rate
- irregular: arrythmias
what is the QT interval?
- start of QRS to end of T
- time for ventricular depolarisation + repolarisation
what is the ST segment?
- end of QRS to start of T
what does a Tall QRS complex show? (increase voltage/amplitude)
hypertrophy
what does a tall T wave show?
hyperkalaemia
what does an elevated ST segment show?
myocardial infarction (STEMI)
what does a depressed ST segment show?
myocardial ischaemia
what are the functions of ECG? (4)
- suspect disturbances in cardiac rhythm & conduction
- localise & assess extent of IHD
- assess size of various chambers in the heart
- assess effects of changes in electrolyte concentrations in the body on heart function (esp K+)
what are the leads associated with antero-septal region? (4)
V1, V2, V3, V4
what supplies antero-septal region of the heart?
Left Anterior Descending (LAD) artery
what are the leads associated with antero-lateral region? (4)
1, aVL, V5, V6
what supplies antero-lateral region of the heart?
left circumflex artery
what are the leads associated with inferior region? (3)
2, 3, aVF
what supplies inferior region of the heart?
right coronary artery
what are the leads associated with posterior region?
none
what supplies posterior region of the heart?
right coronary artery
why are troponin levels elevated during myocardial infarction?
dead heart muscles release troponin into the bloodstream
what does starling’s law of the heart state?
the heart adjusts its pumping ability (SV) according to how much it’s filled (as volume of blood in ventricle increases, output/SV increases)
aka EDV increases→ SV increases
how is contractility regulated?
SNS (activated SNS→ NE binds to receptors on cardiac muscles→ influx of Ca2+→ increase contractility)
aka ESV decreases→ SV increases
how is contractility measured?
EJECTION FRACTION
EF = SV/EDV
(SV = EDV-ESV)
when does MV open?
start of diastole (pressure in atria>ventricles)
when does MV close?
start of ventricular systole (pressure in ventricles> atrium)
when does AV open?
start of ejection phase of ventricular systole (pressures in ventricles>aorta)
when does AV close?
end of ejection phase/systole (pressure in aorta>ventricles)
what causes 1st and 2nd heart sounds?
1st: closing of MV/TV (semilunar valves)
2nd: closing of AV/PV
marks the start and end of ventricular systole respectively
what causes 3rd heart sound?
- occurs after opening of mitral valve during EARLY diastole
- due to rapid inflow of blood from atrium into ventricle (woosh!!)
PHYSIO: children/young adults w hyperdynamic circulation
PATHO: adults (could indicate volume overload→ heart failure)
what causes 4th heart sound?
- occurs during atrial systole, LATE diastole
- due to decreased compliance of left ventricle (stiffening of walls)
- atria has to contract harder (increase pressure) to fully fill ventricle→ difficult to push blood→ turbulent flow
PATHO:
- e.g. hypertension→ ventricular hypertrophy
- e.g. cardiac ischaemia
what does JVP measure?
location indicates right atrial pressure: increase height of JVP, increase RA pressure
(IJV directly connects to SVC that directly drains to RA)
what does the a wave in venous pulse represent?
- upwards
- Right Atrial contraction (increase pressure in RA)
- atrial systole/ventricular diastole
what does a TALL/prominent a wave in venous pulse indicate?
- increase in pressure needed to fill RV
- RV hypertrophy or TV stenosis
what does the c wave in venous pulse represent?
(upwards)
- Right ventricular contraction (RV contracts→ TV pushes upwards into RA→ RA pressure increases slightly)
- ventricular systole
what does x wave in venous pulse represent?
(downwards)
- atrial relaxation (RA pressure decreases)
- ventricular systole
what does v wave in venous pulse represent?
(upwards)
- atrial filling (blood returns to body before TV opens→ RA pressure increases)
- atrial/ventricular diastole
what does a TALL/prominent v wave in venous pulse indicate?
- increase in pressure needed to fill RA
- TV regurgitation
what does y wave in venous pulse represent?
(downwards)
- passive ventricular filling (TV opens→ blood flows from RA to RV→ RA pressure decreases)
what causes cardiac murmurs? (3)
turbulent flow of blood
1. across incompetent/regurgitant valves
2. across stenosed/narrowed valves
3. increased blood flow through normal valves
what is ventricular septal defect?
- blood flows directly from LV to RV through VSD
- causes a systolic murmur
- oxygenation of blood unaffected (no cyanosis)
how could VSD lead to cyanosis?
increase blood flow to RV→ increase blood flow to lungs→ pulmonary hypertension→ increase P in pulmonary circulation→ RV hypertrophy→ shunt reverses when P in RV>LV→ deoxygenated blood flow from RV to LV→ cyanosis
what does the apex beat represent?
corresponds to ventricular systole (LV contracts→ taps against front of the chest)
what does an absent apex beat show?
RV hypertrophy
what does an apex beat that has shifted laterally & inferiorly show?
LV hypertrophy
what does a stronger/higher amplitude apex beat show?
increase in stroke volume
what causes physiological splitting of S2?
- slightly different closing times between AV (earlier) and PV (later) upon INSPIRATION
- inspiration→ increased venous return to right heart→ PV closes later, decreased return to left heart (less blood volume)→ AV closes earlier
describe the law governing rate of blood flow
ohm’s law
Q = (P1-P2)/R
aka cardiac output = arterial P/resistance
describe the formula for resistance in a blood vessel
poiseuille hagen formula
R= 8nL/pir^4
aka R is proportional to viscosity and length of tube, and inversely proportional to r
describe the formula for velocity of blood flow in a vessel
velocity = flow rate/total cross sectional area
what is the significance of velocity of blood flow in a vessel?
velocity determines whether blood flow is turbulent (blood flow velocity> critical velocity) or laminar
what is tissue perfusion?
rate of blood flow (delivery of blood) in capillary network
what are the factors affecting tissue perfusion?
blood flow in arteries
1. arterial bp (fall bp→ fall perfusion)
2. cardiac output (fall CO→ fall bp→ fall perfusion)
vasomotor tone of arteries (vasocontriction→ maintains bp→ ok perfusion)
what are the capillary causes of edema? (5)
- decrease in (inward) colloid osmotic pressure (inward pressure decrease→ net outward pressure increase→ fluid retention)
- increase hydrostatic (outward) pressures (vasodilation→ increased blood flow→ increased hydrostatic pressure)
- increase in capillary permeability
- increase in venous pressure (→ decrease ability of fluid to return back into capillaries due to impaired venous return)
- decrease in lymphatic flow eg. lymphatic obstruction
INCREASE NA+ AND H20 RETENTION
what is the formula for cardiac output?
volume of blood pumped out by the left ventricle per minute
CO = SV x HR
units: L/min
what are the factors affecting cardiac output? (3)
- preload (volume that the ventricle is filled with blood during diastole= venous return)
- afterload (pressure against which the heart pumps, depends on calibre aka peripheral/arteriolar resistance)
- heart! contractility and HR
what is the definition of heart failure?
failure of the heart to pump at sufficient rate to meet the metabolic requirements of tissues
causes of heart failure/fall in CO (4)
- fall in preload (volume) e.g. due to hemorrhage
- increase in afterload (resistance) e.g. due to hypertension→ remodelling of heart→ heart less effective
- heart decreased contractility due to myocardial infarction (heart muscle dies)
- bradycardia
what are the types of heart failure (4)
- right heart failure
- left heart failure
- HFrEF
- HFpEF
describe how right heart failure leads to its consequences
right heart fails→ backpressure in systemic venous circulation→ systemic venous pressure increases & JVP increases→ organs that can hold more volume thus enlarge→ GENERALISED/PERIPHERAL EDEMA (eg hepatosplenomegaly, pedal edema)
describe how left heart failure leads to its consequences
left heart fails→ backpressure effects in pulmonary venous circulation→ retention of fluid in pulmonary interstitium/alveoli→ PULMONARY EDEMA→ lung compliance decreases→ BREATHLESSNESS (exertional dyspnea & orthopnea cos when pt lies down the blood in legs return to RV→ LV→ increases backpressure effects in lungs)
describe HFrEF + causes + treatment
Heart Failure w Reduced Ejection fraction
- failure of heart to CONTRACT sufficiently (systolic)→ blood pools in heart and then lungs/veins
- when EF<40%
- causes: myocardial infarction, hypertension, arrhythmias
treatment:
- decrease blood volume (diuretics, ACE inhibitors)
- decrease afterload by using B blockers
describe HFpEF + treatment
Heart Failure w Preserved Ejection Fraction
- failure of heart to RELAX sufficiently (diastolic) for blood to fill ventricle frm atria (higher P needed to fill LV→ increase P in pulmonary venous system→ pulmonary edema & heart failure)
treatment:
decrease load by using diuretics
what is the definition of blood pressure?
capillary hydrostatic pressure that pushes fluid out of the capillaries into tissues
what is the formula for blood pressure?
BP = CO x PR (arterial tone)
what generates blood pressure (4)
- heart contraction
- heart valves ensuring unidirectional flow
- thick walls of arteries with low resistance
- arterioles at ends of arteries have high resistance to allow arteries to maintain high p
what is the formula for mean arterial pressure?
2/3 diastolic + 1/3 systolic
or
diastolic + 1/3 pulse pressure
what is hypotention/circulatory shock?
when bp is too low to maintain perfusion of tissues
systolic bp<80mmHg
diastolic bp<60mmHg
what are the types of circulatory shock (4)
- hypovolemic shock (fall in blood volume e.g. severe diarrhoea)
- cardiogenic shock (heart pumps inadequately e.g. MI, arrythmia)
- obstructive shock (acute blood flow obstruction eg pulmonary embolism)
- distributive shock (redistribution of blood out of arterial system e.g. anaphylaxis, sepsis)
what are the receptors in sensing fall in BP? (2)
- baroreceptors
- kidneys
what is the process of acute regulation of bp in hypotension?
BARORECEPTORS
carotid & aortic baroreceptors sense fall in bp→ send signals to Vasomotor Center→ stimulates ANS→ fall in PNS, increase in SNS→ increase SA node (increase HR & CO), vasoconstriction of arterioles (increase PR, increase BP), vasoconstriction of veins (increase venous return, increase SV)→ increase mean arterial pressure :)
what are the effects of hypotension + causes? (4)
- cold and sweaty (SNS stimulation)
- decreased urine output (reabsorption of fluid by kidneys)
- pale (vasoconstriction due to SNS)
- increase HR, strength of cardiac contraction (SNS stimulation)
what is the process & symptom of postural hypotension?
change in posture (sitting to standing)→ blood pools in legs→ decrease venous return→ decrease stroke volume→ fall in MAP→ fall in perfusion→ neurons fall in effectiveness→ pt feels faint
what is the process of long term regulation in hypotension?
KIDNEYS!! (Juxtaglomerular Apparatus via RAAS)
fall in bp→ sensed by JGA in kidneys→ secretes renin→ converts angiotensinogen to angiotensin 1 then angiotensin 2→ adrenal cortex releases aldosterone→ increases salt retention→ expands blood volume→ bp rises
what are the 2 main functions of angiotensin 2?
- stimulate synthesis & secretion of ALDOSTERONE from adrenal cortex→ increase Na+ reabsoption→ increase preload→ increase CO (starling’s law)→ increase TPR
- VASOCONSTRICTION of arterioles to increase TPR
how does the heart autoregulate blood flow in increased metabolic demand? (2)
- release Nitric Oxide (release Ca2+ in smooth muscle & inhibit release of NE from SNS→ vasodilation→ increase blood flow)
- release more metabolites (by muscle cells)→ activate NO release→ relaxation & vasodilation
how does the heart autoregulate blood flow in decreased metabolic demand?
increased myogenic response: stretch sensitive receptors sense wall stretching due to increase in pressure→ depolarisation & release of Ca2+→ vasoconstriction→ fall in blood flow
what are the effects of aging on CVS? (3)
- aging heart
- aging vessels
- aging baroreceptor reflex (decreased ability to respond to postural changes→ POSTURAL HYPOTENSION)
describe & explain the consequences of an aging heart (4)
fall in SV:
1. heart is stiffer→ higher filling pressures needed (ventricular filling compromised)→increase pulmonary pressures→ BREATHLESSNESS
2. ventricular filling further compromised by increase in duration of myocardial contraction that shortens diastolic filling time→ fall in SV
3. atrial systole compensates for reduction in ventricular diastolic filling→ ATRIAL ENLARGEMENT
4. heart less responsive to SNS stimulation→ fall in contractility→ FALL IN HR
fall in HR + fall in SV = fall in CO
describe and explain the causes of aging/stiffening vessels (3)
- progressive breakdown of elastic components in tunica media (replaced by cross linking collagen)
- endothelial dysfunction→ oxidative stress & inflammation→ fibrosis in arterial wall
- atherosclerotic deposits in tunica intima
what are the effects of stiffened aorta?
- decreased stretching that decreases outflow pressures→ INCREASED SYSTOLIC PRESSURES
- decreased elastic recoil→ DECREASED DIASTOLIC PRESSURES
= increased pulse pressure
why are older adults at higher risk for IHD? (5)
decreased supply
1. atherosclerosis→ decrease lumen of CA
2. stiffening of CA (less elastic)→ decreased compensatory dilation of arteries to deliver blood to heart
3. fall in diastolic pressures due to stiffening aorta→ fall in perfusion
increased metabolic demand of heart
4. increased afterload due to aortic stiffness & peripheral resistance
5. increased afterload→ventricular hypertrophy→ increased demand
what are the changes in stroke volume after exercise training?
- increased SVmax
- increased resting SV
what are the changes in heart rate after exercise training?
fall in resting HR
- @rest, HR falls to maintain the same CO (since SV increased)
same/decreased maximal HR
- too high of HR compromises ventricular filling→ inefficient
what are the changes in the heart after exercise training? (2)
left ventricular hypertrophy
- allows increased COmax (adaptive response)
- leads to further fall in HR (sinus bradycardia) as LVH→ increased SV→ fall HR to maintain CO
- lumen volume increases (vs hypertensive hypertrophy)
signs of first deg AV block
- PNS activated/increased to increase cardiac cycle duration to decrease HR→ fall in AV node firing
what are the blood volume/composition changes after exercise training? (2)
- overall increase in blood volume
- fall in hematocrit (increase in plasma vol> RBCs)→ decreased blood viscosity→ decreased peripheral resistance→ low resting BP
