5. Physiology III - Blood Pressure and Cardiac Cycle Flashcards
HEART RHYMTH is normally DETERMINED by PACEMAKER CELLS in the ….
SINO-ATRIAL NODE (SAN)
- which DEPOLARISE SPONTANEOUSLY
CARDIAC ELECTRICAL ACTIVITY is the result of the MOVEMENT of… across the cell membrane
IONS: Na+, K+, Ca2+
how is the RESTING MEMBRANE POTENTIAL / PHASE 4 in the SA NODE ACTION POTENTIALS and why
UPSLOPING, NOT flat
around -60 mV (less polarised than av node)
- GRADUAL RISE due to
gradual REDUCTION in OUTWARD K+ current
& INCREASE in INWARD current of Na+ and Ca2+
How are the ION CHANNELS in PHASES 0,2,3 of SAN ACTION POTENTIALS
0: Ca2+ channels open, LARGE Ca2+ INFLUX once threshold reached (slower rise)
(1: initial repolarisation)
2: (plateau as Ca2+ channels and K+ channels open) Ca+ channels start to close
3: Repolarisation as K+ EFFLUX (Ca2+ channels are closed, K+ channels open)
RESTING POTENTIAL in SAN
around -60mV
RESTING POTENTIAL in AV NODE
-85 / -90 mV
NON-PACEMAKER ACTION POTENTIALS (ie AV NODE) PHASES:
0: DEPOLARISATION as Na+ channels OPEN (FAST)
1: INITIAL REPOLARISATION (Na+ channels CLOSE, some K+ EFFLUX)
2: PLATEAU as Ca2+ channels open, Ca2+ INFLUX (and K+ efflux) (SLOW)
3: REPOLARISATION (Ca2+ channels CLOSE) K+ EFFLUX
- RESTING POTENTIAL (FLAT)
ECG is a … MEASUREMENT
VECTOR
- measures MAGNITUDE of Depolarisation and DIRECTION
CHANGES in the ECG are used to DIAGNOSE..
HEART ARRYTHMIAS (ABNORMAL RHYTHM)
ECG
P WAVE:
QRS:
T WAVE:
P: ATRIA DEPOLARISE
QRS: VENTRICLES DEPOLARISE
T: VENTRICLES REPOLARISE
how does the WAVE OF DEPOLARISATION SPREAD starting from SA NODE (PACEMAKER) FIRING
- ATRIA - DEPOLARISE
- AV NODE - DELAYS
- BUNDLE of HIS
- LEFT & RIGHT BUNDLE BRANCHES
- PURKINJE FIBRES
- VENTRICLES - DEPOLARISE (contract)
name of structure that Connects Right and Left ATRIA and allows Impulses to pass from right to left (from SAN) for simultaneous contraction
BACHMANN’S BUNDLE
define CARDIAC CYCLE
the sequence of….
sequence of ONE HEART BEAT ENDING to the BEGINNING OF ANOTHER
- Cardiac Diastole (whole heart relaxed)
- Atrial Systole (contract)
- Ventricular Systole (contract)
PHASES of CARDIAC CYCLE
- ATRIAL SYSTOLE
- ISOVOLUMETRIC VENTRICULAR CONTRACTION
no change in volume as valves are still shut - RAPID VENTRICULAR EJECTION
ventricular pressure overcomes pulmonary trunk or aorta pressure, so valves open - ISOVOLUMETRIC VENTRICULAR RELAXATION
while blood fills atria. no change in volume as atrioventricular valves shut - RAPID VENTRICULAR FILLING
atrial pressure overcomes ventricular pressure so av valves open, increase in volume as ventricles fill - atrial systole
what happens in CARDIAC CYCLE AFTER VENTRICULAR FILLING
ATRIAL SYSTOLE - atria CONTRACT
in a PHONOCARDIOGRAM what are the 1st, 2nd and 3rd SOUNDS picked up
1st: MITRAL VALVE CLOSING (bicuspid)
2nd: AORTIC VALVE CLOSING
3rd: Ventricular filling (rapid inflow of blood) during diastole
what is CARDIAC OUTPUT and how is it CALCULATED
VOLUME OF BLOOD PUMPED EACH MINUTE
CO = STROKE VOLUME X HEART RATE
in L/MIN
STOKE VOLUME (blood pumped out of left ventricle in one beat) is determined by which 3 FACTORS
- PRELOAD
volume of blood INTO VENTRICLE (that ventricle is able to pump) - CONTRACTILITY
force that the muscle can create - OUTLOAD
the arterial pressure (pressure of blood in aorta) that the ventricle must overcome to open the valve
does the LEFT VENTRICLE EMPTY COMPLETELY during SYSTOLE
NO
CALCULATION for STROKE VOLUME (amount of blood transferred from Left ventricle to arterial system in systole)
SV =
END DIASTOLIC VOLUME (EDV) - END SYSTOLIC VOLUME (ESV)
EDV - total volume of blood IN ventricle at end of diastole (dependent on PRELOAD)
ESV - volume of blood REMAINING in ventricle at the end of systole (dependent on AFTERLOAD)
what is the STROKE VOLUME in a HEALTHY PERSON
> 60 ml
(approx 80-90ml)
what is END DIASTOLIC VOLUME (EDV) and what is the approx amount
total VOLUME of BLOOD IN VENTRICLE at the END OF DIASTOLE (filling from aorta)
- dependent on PRELOAD
approx 140 ml
what is END SYSTOLIC VOLUME (ESV) and what is the approx amount
VOLUME of BLOOD REMAINING IN VENTRICLE at the END of SYSTOLE (after contraction, and expelling into aorta)
- dependent on AFTERLOAD
approx 50ml
what is EJECTION FRACTION and what is the normal %
STROKE VOLUME / END DIASTOLIC VOLUME
(proportion of blood in the ventricle that is pumped out)
normally 55-75 %
EJECTION FRACTION (EF) is an important measurement of…
CARDIAC EFFICIENCY
used to asses cardiac status in patients with heart failure
BLOOD PRESSURE is a MEASUREMENT of…
the FORCE AGAINST THE WALLS of the ARTERIES
as the heart pumps blood throughout the body
- measured in mmHg
what is SYSTOLIC PRESSURE (P systolic)
the MAXIMAL AORTIC PRESSURE following EJECTION from ventricle
(pressure in aorta after blood pumped out of ventricle)
what is DIASTOLIC PRESSURE (P diastolic)
the LOWEST AORTIC PRESSURE which occurs JUST BEFORE VENTRICLE EJECTS BLOOD INTO AORTA
as the left ventricle is relaxing and filling
what is NORMAL SYSTOLIC PRESSURE and NORMAL DIASTOLIC PRESSURE
p systolic: 120 mmHg
p diastolic: 80 mmHg
120/80
what is the DIFFERENCE between the SYSTOLIC and DIASTOLIC PRESSURE called and what is it normally
AORTIC PULSE PRESSURE
ranges between 40 and 50 mmHg
how do you calculate the MEAN AORTIC/ARTERIAL PRESSURE (MAP) - the average pressure (geometric mean) during the whole cardiac cycle
MAP =
CARDIAC OUTPUT X SYSTEMIC VASCULAR RESISTANCE (SVR)
- OHM’S LAW
based upon relationship between flow, pressure, resistance
MEAN ARTERIAL PRESSURE (MAP) is an estimate of LEFT VENTRICULAR PRESSURE and can be approximated by which EQUATION
MAP =
MAP = DIASTOLIC + 1/3 (AORTIC) PULSE PRESSURE
(as heart spends 2/3rd time in diastole)
= 80 + 1/3 (120-80)
= 93 mmHg
what BP is the cut off for HYPERTENSION (HIGH BP)
140/90 and HIGHER
(varies according to age)
what provides an INDIRECT MEASURE of CENTRAL VENOUS PRESSURE (CVP)
JUGULAR VENOUS PRESSURE (JVP)
aka jugular venous pulse
- from visualization of the internal jugular vein, using ultrasound probe
- patient placed at 45 degree angle
why does the INTERNAL JUGULAR VEIN act as a column for the blood in the right atrium
CONNECTS DIRECTLY to the RIGHT ATRIUM
WITHOUT any intervening VALVES
CARDIOVASCULAR SYSTEM is under AUTONOMIC CONTROL
SYMPATHETIC control acts on which RECEPTORS
- mostly cardiac BETA-1
- sometimes ALPHA-1 adrenoreceptors
CARDIOVASCULAR SYSTEM is under AUTONOMIC CONTROL
PARASYMPATHETIC control acts on which RECEPTORS
MUSCARINIC RECEPTORS
(M2 & M3)
Which NERVOUS SYSTEM controls ALL COMPONENTS of the HEART (SAN,AVN, VENTRICLES)
SYMPATHETIC
- via BETA-1 RECEPTORS
which does the PARASYMPATHETIC NERVOUS SYSTEM CONTROL in cardiac function
SA NODE & AV NODE
SYMPATHETIC NERVOUS SYSTEM controls heart by RELEASING…
NORADRENALINE
via Noradrenaline and Beta-1 Receptors, what is the affect of SYMPATHETIC NERVOUS SYSTEM
INCREASE HEART RATE (positive chronotropic effect)
and
INCREASE Cardiac CONTRACTILITY (force) (positive inotropic effect)
(fight or flight)
what does SYMPATHETIC NERVOUS SYSTEM cause by ACTIVATING ALPHA-1 RECEPTORS
VASOCONSTRICTION
PARASYMPATHETIC NERVOUS SYSTEM controls SAN and AVN by RELEASING…
ACETYLCHOLINE (Ach)
EFFECT of PARASYMPATHETIC NERVOUS SYSTEM via release of Ach and Muscarinic receptors..
DECREASES HEART RATE (Negative chronotropic effect)
PROLONGS DELAY at AV NODE (slowing down rate of transmission)
- VASODILATION
(little effect on contractility)
(rest and digest)
what are chronotropic effects
effects on Heart Rate
what are inotropic effects
effects on Contractility / Force
what is dromotropy
rate of Electrical Impulses
BP =
CO X SVR (systemic vascular resistance)
SVR aka PR (peripheral resistance)
(BP = CO X PR)
to Maintain normal BP, CO and PR/SVR are controlled by 2 overlapping mechanisms:
- SHORT-TERM BP REGULATION (Neural mechanisms)
- LONG-TERM BP REGULATION (Endocrine/Hormonal ie RAS system)
example of LONG-TERM BP REGULATION
RAAS SYSTEM
- angiotensin II is a potent VASOCONSTRICTOR
- angiotensin II also directly acts on kidney to INCREASE SODIUM REABSORPTION in the pct
- ALDOSTERONE release for NaCl and H2O retention at dct (increase expression of epithelial sodium channels)
- ADH for H2O REABSORPTION
RENIN is released from juxtaglomerular apparatus in response to…
- SYMPATHETIC STIMULATION (juxtaglomerular Beta1 receptors)
- REDUCED NaCl delivery to the DCT
- DECREASED BLOOD FLOW to the kidney (low CO)
SHORT-TERM REGULATION of BP is controlled by the AUTONOMIC NERVOUS SYSTEM.
CHANGES in BLOOD PRESSURE are detected by? where?
BARORECEPTORS
in AORTIC ARCH and CAROTID SINUS
SHORT-TERM REGULATION of BP is controlled by the AUTONOMIC NERVOUS SYSTEM.
changes in BP, detected by BARORECEPTORS in AORTIC ARCH and CAROTID SINUS, is RELAYED TO…
the CARDIOREGULATORY CENTRE in the MEDULLA OBLONGATA
SHORT-TERM REGULATION of BP is controlled by the AUTONOMIC NERVOUS SYSTEM.
CHANGES in Blood PH, O2 and CO2 Levels are DETECTED by…
CHEMORECEPTORS
(in aortic arch and carotid sinus)
INCREASED ARTERIAL PRESSURE STRETCHES the wall of the blood vessel, triggering BARORECEPTORS which feedback to the ANS to REDUCE HEART RATE, CARDIAC CONTRACTILITY and CARDIAC OUTPUT
via which nervous system FIBRES of which NERVE?
EFFERENT PARASYMPATHETIC FIBRES
- VAGUS NERVE
DECREASED ARTERIAL PRESSURE detected by BARORECEPTORS triggers which NERVOUS SYSTEM RESPONSE to INCREASE HEART RATE, CONTRACTILITY and CARDIAC OUTPUT and also VASOCONSTRICTION
SYMPATHETIC response
- via CARDIAC BETA-1 RECEPTORS
(noradrenaline)
& ALPHA-1 receptors for vasoconstriction
how does VASOCONSTRICTION (sympathetic) INCREASE BLOOD PRESSURE
via ALPHA-1 RECEPTORS
INCREASES PERIPHERAL RESISTANCE (PR) (aka SVR)
BP = CO X PR
