Where does the L ventricle lie?
Under sternum and 4th intercostal space on left
What are the 2 different types of circulations?
Systemic (L.vent -> aorta)
Pulmonary (R.vent -> pulmonary arteries)
NB. same cardiac output in both circulations
Why are the lungs efficiently perfused at a lower pressure than the body?
Pulmonary vascular resistance is much lower than system vascular resistance because the total vascular resistance in the pulmonary vascular bed is much lower than that in systemic circulation.
What is the difference between systemic and pulmonary arteries?
Give their mean pressures.
Systemic: moderate size, thick muscular walls, mean: 100mm/Hg
Pulmonary: large diameter, thin elastic walls, mean: 15mm/Hg
What is Starling's Law of the Heart?
Ventricular contractile force increases with increased end diastolic volume.
Thus if more blood delivered to R.vent, it expands to greater diameter, and contracts more strongle.
What is preload, and what is it proportional to?
How does an increased preload demonstrate Starling's Law of the Heart?
What happens to an increased preload in heart failure?
Degree of stretching experienced by the ventricle during diastole. Proportional to end diastolic volume.
An increased preload -> increased end diastolic volume -> increased end-diastolic muscle fibre length -> increased stroke volume and C.O.
Heart failure: ventricles overstretched and weakened, increased preload -> enlarges heart -> weakens it further -> stroke volume decreases
Describe the mechanism underlying Starling's Law of the Heart
A & M filaments have excess overlap at rest, and stretching INCREASES amount of OVERLAP and thus INCREASES CONTRACTION FORCE.
Thus ventricular contractile force increases in proportion to end disatolic volume.
How is blood prevented from accumulating in the pulmonary or systemic circulation (due to uneven ventricular output)?
Averaged over several beats, the 2 ventricules eject the same volume of blood = balances the output of the 2 sides of the heart
Why is an enlarged heart (detected on an X-ray) a bad sign?
If ventricles enlarged with no corresponding increase in ventricular wall thickness = contracts more weakly than a smaller heart b/c muscle fibres stretched to point where Starling Law does not work anymore, and a LARGE END DIASTOLIC VOLUME produces a SMALLER STROKE VOLUME = heart failure
What is the stroke volume for a normal healthy adult male at rest?
Why is the stroke volume not the same as the end-diastolic volume?
What is the EDV ad ESV in a typical heart?
Always some blood left in the ventricle at end of systole - residual volume
What is afterload?
How is compliance connected to afterload?
Flow impedence (resistance) of aorta and large arteries. Depends on diameter and elasticity of tissue.
The HIGHER the compliance, the LOWER the afterload, and the LESS WORK the heart has to do
In older people the elasticity of the aorta declines.
a) why is this?
b) what happens to the afterload?
c) how does this affect the stroke volume?
a) elastic tissue progressively lost from the wall and replaced with collagen
b) afterload increases
c) longer period of isovolumetric contraction of the ventricle before aortic valve opens and shorter duration of ejection -> smaller stroke volume -> larger end systolic (residual) volume
an increased afterload decreases C.O.
What is ionotropy?
The contractility of the ventricular muscle. Can vary widely (neuronal and hormonal influence)
How will an increase in contractility affect residual volume and stroke volume?
What factors increase contractility?
Decreases residual volume and thus increase stroke volume
- Increased blood Ca2+
- beta-adrenergic agonists (e.g. adrenaline)
- drugs which stimulate Ca2+ entruy into myocardium (e.g. levosimendan)
- cardiac glycosides (e.g. digoxin)
- insulin & glucagon
A: pulmonary valve
B: aortic valve
C: mitral valve
D: tricuspid valve
A: tricuspid valve
B: mitral valve
C: aortic valve
D: pulmonary valve
What keeps the heart valves in position when closed?
What are these structures attached to?
Chordae tendinae - fibrous tedons attached to the valves
Papillary muscles (first part of ventricles to contract in systole)
How do papillary muscles work?
Pull on chordae tendineae and pull the valves closed.
A: opening of superior vena cava
B: tricuspid valve
C: myocardium of R ventricle
D: papillary muscles
E: mitral valve
F: chordae tendinae
G: interventricular septum
H: myocardium of L ventricle
Describe the cardiac cycle
Atrial systole (atriack contraction forces small amount of blood into ventricle) - AS ends, atrial diastole begins -> ventricular systole (phase 1: isovolumetric contraction - vent. contraction pushes AV valves closed but does not create enough pressure to open semilunar valves) (phase 2: vent. pressure increases and exceeds artery = semilunar open and blood ejected) -> ventricular diastole (isovolumetric relaxation - pressure in vent decreases, blood flows back against cusps of semilunar valves and forces them closed, and blood flows into relaxed atria) -> all chambers relaxed, passive ventricular fill
Why is atrial systole not needed at rest?
Why is it needed during exercise?
The elastic recoil of the ventricular walls as they enlarge during diastole is enough to suck blood into the ventricles without atrial contraction.
Needed during exercise b/c diastole is shortened with the increased heart rate - atria give blood extra push - helps fill expandind ventricles
What is AF?
How is it usually detected by the patient?
What would you see on an ECG?
Asynchronous contraction of atria
Dizzy/breathless during exercise
No P waves
A: mitral valve closes
B: aortic valve opens
C: aortic valve closes
D: mitral valve opens
E: isovolumetic contraction
F: isovolumetric relaxation
What is the first heart S1 lubb sound?
What is the second heart S2 dupp sound?
AV valve closure followed by opening of semilunar valves
Semilunar valve closure followed by opening of the AV valves
May be 3rd/4th sound (gallops)
What is the third heart sound S3, and what are the implications if heard in adults as opposed to young adults/children?
Where might S4 be heard?
Heard 1/3 through diastole, coincides with rapid ventricular filling due to turbulent flow in children/young adults. May be heard in adults with heart disease - serious heart damage, poss. valves.
S4: Immediately before first heart sound due to turbulent flow in ventricle, rare in normal adults.
Amplify with phonocardiogram to investigate.
Label A-D, the optimal stethoscope positions for hearing different sounds.
A: aortic semilunar
B: pulmonary semilunar
C: left AV
D: right AV
What is the jugular venous pulse?
What are the 3 peaks in a the JVP due to?
No valves between vena cava and R atrium, or pulmonary veins and L atrim, so when R. atrium contracts, a backpressure occurs in the jugular vein, can be felt as faint pulse.
a: atrial contraction just before tricuspid valve closes
c: pressure increasing in atrium just after the tricuspid closes b/c valve bulges back into the atrium
v: ventricles filling when tricuspid valve is closed. (venous pressure increases in people with heart failure)
Label what A-C show
A: a wave - atrial contraction before tricuspid valve closes
B: c wave - pressure rising in atrium just after tricuspid closes b/c valve bulges back into atrium
C: v wave - venous filling when tricuspid valve is closed
What three main factors mediate venous return to the heart?
1. one way valves in the veins
2. muscular pumps
3. thoraco-abdominal pump (during inspiration, pressures in thoracic cavity are reduced, pulling blood back into inferior vena cava. On exhalation thoracic pressures increase and this blood is forced into the R. atrium b/c/ veins squeezed).