Cardio Flashcards
What are the relative intracellular and extra cellular concentrations of Na+, K+ and Ca2+?
- Na+ (o) >>> Na+ (i)
- K (i) >>> K+ (o)
- Ca2+ (o) >>> Ca2+ (i)
What are the components of the electrical conducting system of the heart?
START:
- SA node
- AV node
- Bundle of his
- bundle branches
- purkinje fibres
END
How does the SAN determine the heart rate? What are the intrinsic rates of other areas within the heart?
SAN determines HR dt pacing at higher rate than AVN.
Intrinsic rates:
- SAN: 60 – 99
- AVN: 40 – 60
- Bundle of his: 30 – 40
- Purkinje fibres: 20 – 30
What are the features of the pacemaker AP at the SAN/AVN?
- No evidence of RMP (but when AP blocked = -35mv), continual depolarisation before fast upstroke
- Split into 3 phases (0,3,4)
- Phase 0 (upstroke): VG L-type ca2+ channels (in), open at -45mV, inactivate slowly, blocked by CCB, especially diltiazem and verapamil
- Phase 3 (downstroke): delayed rectifier K+ channel (out)
- Phase 4 (slow depol. between upstrokes): leak dominated by Na+ (in) , if current, funny dt hyperpol. activated (-20mV)
What are the features of a myocyte AP?
- 5 Phases (0, 1, 2, 3, 4)
- Phase 0 (upstroke): VG Na+ (in)
- Phase 1 (dip): transient outward K+ current
- Phase 2 (plateau): L-type Ca2+ channels (in) balancing with K+ current (out)
- Phase 3 (drop): terminated by delayed rectifier K+ current (out)
- Phase 4 (diastolic): inward K+ recitifer (out) with If current (in)
What is the importance of the absolute refractory period?
- Period in which AP cannot be generated, prevents repeated, rapid contraction that would result in ~0 CO.
- Absolute, from Q wave to peak of T.
- Relative, from down slope of T – vulnerable period.
What is the process of EC coupling in cardiac muscle vs skeletal muscle?
- Ca2+ entry via L-type Ca2+ channels, not coupled with ryanodine receptor of SR Ca2+ entry leads to more ca2+ release from ryanodine-sensitive SR, Ca2+ induced Ca2+ release (CICR)
- Compared to muscle: Ca2+ release from SR -Ca2+ binds to troponin C, releasing tropomyosin from actin Myosin head binds to myosin binding sites on Actin
How does the time period of diastole and systole changing during the cardiac cycle with increasing HR?
Duration of systole quite constant, during of diastole varies with HR, such that ↓diastolic time with ↑HR
What are the pressure ranges in; RA, RV, AP, LV & aortic trunk
- RA: 2- 8mmHg
- RV: 0-40mmHg
- PA: 20-40mmHg
- LV: 0 – 120mmHg
- Aortic trunk: 0 – 120mmHg
Summarise the 7 phases of the cardiac cycle and the respective electrical activity at these time points.
- CARDIAC FUNCTION SAYS ROGER RABBIT STAYS ALIVE
- Isovolumetric contraction – RS phase
- Fast ejection – S-T phase
- Slow ejection – T wave
- Isovolumetric relaxation
- Rapid ventricular filling
- Slow ventricular filling
- Atrial contraction – P wave
What is the timing of the ventricular contraction (right versus left) and the valvular opening and closure?
Cycle starts in right atrium (pacing in SAN) and ends in right ventricle (delayed contraction)
How do you calculate the ejection fraction? What is a typical value? What value defines systolic dysfunction?
EF = ((SV/EDV) * 100), typically >55% with values <45% defining systolic dysfunction
What factors determine CO?
- HR and SV
- HR -> electrical properties
- Stroke volume -> preload, afterload, contractility, lusitropy
What is preload and how does it relate to SV?
- Preload is the LV EDV/EDP
- Determines cardiac muscle fibre length @ end-diastole
- Greater force production and therefore greater velocity of contraction -> longer ejection
What is afterload and how does it relate to SV?
- Pressure against which ventricle muscle contract to eject blood into aorta -> load given by peripheral vasculature.
- Afterload ↑ -> SV↓ dt increase in force required for contraction resulting in decreased contraction velocity and therefore less time to eject.
From a P-V diagram, how do you calculate cardiac work?
Work = area spanned by P-V diagram, or Work = ΔP. V
What are the two forms of work in the cardiac cycle and which phases of the cardiac cycle do they correspond with?
- External work -> physical, kinetic work, during ejection
- Internal work -> largely heat (comprised of isovolumetric work, sounds/murmurs, electrical activity and base metabolism. Corresponds to isovolumetric contraction.
- Internal is 5-20x > than external work
Compare the energy requirements of ↑CO by ↑SV versus ↑HR:
- ↑CO via ↑HR -> internal work -> greater energy requirement
- Energetically more costly
- ↑CO via ↑SV -> increase largely via ↑external work -> > energy efficiency by increases via SV
What effects to preload and afterload have upon internal and external work?
- Afterload -> ↑internal work dt ↑isovolumetric phase -> increase energy demands
- Preload -> ↑SV -> ↑external work -> energy efficiency (“cheap”)
What are the determinants of venous return and how can VR be mathematically determined?
- VR determined by mean systemic filling pressure
- RA pressure
- Resistance in the vasculature
Mathematically determined by VR = (Pmsf - PRA) / Rv
From what spinal levels are the sympathic innervations of the heart?
T1 -> T5
How do PsNS and SyNS modulate HR at rest?
Both PsNS and SyNS tonically active at rest, with predominant PsNS activity
Where are the arterial baroreceptors (responsible for the arterial baroreceptor reflex) located and what is their innervations?
- Aortic arch -> left vagus
- Cartoid sinus -> glossopharyngeal
What occurs during exercise to allow for increasing HR and also increasing BP?
Set-point for baroreflex shifts to a higher point, resulting in a higher HR being achieved at the same BP
What is the Bainbridge reflex?
- Tachycardia induced by increase in central venous pressure detected by low pressure stretch receptors in cardiac atria.
- Receptors activated by increase in atrial pressure -> signals medullary control centre -> decreases PsNS tone via vagus, functions to decrease pressure in SVC and IVC
What is respiratory sinus arrhythmia?
Increasing HR during expiration and decreasing during expiration.
What happens to the pulse wave as the measurement site moves towards the periphery?
- ↑ Systolic pressure
- ↓ slightly in diastolic pressure
- ↓ arterial pressure slightly
- incisura lost (notch) and second hump (due to reflection from resistive elements)
What does pulse wave velocity depend upon?
- Stiffness of vessels
- Increases from proximal to distal in arterial circulation
- Very low PWV in venous system.
Compare perfusion in the RCA and LCA during systole and diastole
Overall flow
- RCA: Smaller
- LCA: Larger (x6)
Maximal flow
- RCA: At fast ejection phase
- LCA: During early diastole
Cessation in flow
- RCA: None
- LCA: During isovolumetric phase, affects subendocardial vessels (more infarcts) much more than subepicardial
What is the purpose of autoregulation in the coronary vasculature and how does it operate?
Local blood flow regulation: defined as the intrinsic ability of an organ to maintain a constant blood flow despite changes in perfusion pressure.
F = (Pa - Pv) / R
- As perfusion pressure (PA-Pv) drops, resistance vessels dilate to decrease resistance to flow and maintain blood flow through the tissue
- The decrease in pressure dt the decrease in resistance is counteracted by the increased in flow.
- The converse is also true.
- Maintains constant blood flow over pressure range (range determined by maximal relaxation or contraction).
What effect does neural control of perfusion have upon the coronary vasculature?
Metabolic self regulation more important than neuronal control, as myocardial O2 demand and coronary flow linearly proportional -> denervation does not alter this (transplanted hearts don’t have problems with regulation of perfusion)
How does Pco2 and Po2 affect CBF?
- Pco2 is main determinant of CBF
- ↑ Pco2 -> vasodilation
- ↓ Pco2 -> vasoconstriction.
- Po2 has little effect on CBF, only at very low levels of PaO2
