Cardiac Output 2 Flashcards
how will the parasympathetic nervous system impact the heart at rest
decrease heart rate but not effect on stroke volume
decrease Na+ current by inhibiting HCN channels
intrinsic regulation
CVS is a closed system
amount of blood returning must = vol. blood ejected
Venous return = Cardiac Output
frank-Starling law
hearts intrinsic ability to adapt to changes in blood volume
greater degree of stretch = greater force of contraction of myocytes
how did otto frank and Ernest H Starling investigate the law
independent experiments investigating effects of filling pressure on stroke volume
mechanics of starling law
Actin and myosin are brought together as myocardium is stretched
– increased filling increases the stretch
increased overlap = more cross bridges formed -> more force made
the muscle stretch relationship with cross bridge relationship is similar to
force-length
preload
umbrella term to describe ventricular filling during diastole
– it is a catch term all to describe the end diastolic volume
what is ventricular filling affected by
the pressure in the atria, venous pressure, gravity and the volume of blood in the circulation
what will ventricular filling impact
stroke volume and cardiac output
great veins function
capacitance vessels for the storage of blood
– veins contain 60-70% of total blood volume at any given time
how does increased blood volume change venous pressure and preload
increased central venous
pressure and hence increased preload
– equally an increased venous tone will also increase the central venous pressure
how does gravity affect the blood returning to the heart
blood returning to the heart has to work against gravity
e.g. arterial blood to the brain
when upright, what factor is gravity for venous return and what is it the basis for
this is negative factor for venous return
– this is the basis for postural hypotension on standing
how is venous return affected in supine position
In the supine position venous return is increased
– this can contribute to pulmonary congestion and orthopoea (breathlessness when
lying flat) in heart failure
where do large veins pass through in limbs
• In limbs large veins pass between muscle blocks and are compressed as the muscle contracts
– to a lesser extent this happens as an adjacent artery pulsates
how does compression in veins affect blood distribution
This compression displaces the blood and the presence of the valves
mean it must go back toward the heart
– think of squeezing a tube of toothpaste
how does the thoracic and abdominal pressure change during inspiration
diaphragm flatten
raises abdominal pressure
lowers thoracic pressure
blood from abs to thorax
how does the thoracic and abdominal pressure change during inspiration
thoracic pressure increases
abdominal pressure decreases
stays below abdomen in legs
how do muscle and thoracic pump contribute to cardiac output in exercise
increase cardiac output in exercise
The Starling Law of the heart increases stroke volume by
changing the orientation of the fibres
what do iontropes increase and how
increase contractility by changing
Ca2+ signalling
what do changes in preload effect
the filling of the ventricle
– as preload increases so does filling
how will increased afterload affect the cardiac output
decrease cardiac output short term
as the stroke volume drops …
the end systolic volume rises
– atrial filling remains unchanged
– the end diastolic volume is increased
Increased end diastolic pressure, increases …
increases stretch of the ventricles
leading to a more forceful contraction
– cardiac output is maintained at greater work
typical daily water intake
~2.5 L most lost via kidney
how is water intake categorised
body water compartments
intracellular - 67%
extracellular 33%
Physiological control of blood volume
renin-angiotensin system
Antri-diuretic hormone
Atrial Natriuretic Peptide
RAS
Ang II - potent vasoconstrictor (increases resistance)
– stimulates aldosterone, increasing Na+ and water reabsorption from urine.
– net effect is expansion of blood volume and increase in blood pressure
ADH
released in response to high osmolality and/or low blood volume
– drives water reabsorption from kidney (decreases diuresis)
Atrial Natriuretic Peptide (ANP)
one of many natriuretic peptides (includes brain or BNP)
– opposite of the other two, inhibits salt reabsorption so promotes salt and water loss
heart failure
inability to maintain cardiac output
decrease cardiac output = decreased blood pressure
activate baroreceptor reflex
SNS induced increase in renin-angiotensin system
when there is heart failure how does the problem try to be address by activating SNS induced ATS
maintain stroke volume by volume expansion
will be a point where no further volume expansion can maintain stroke volume
excess blood volume
increased blood volume stretches atria activating sensory afferents to medulla
decrease SNS = less RAS, ADH greater filtration in kidney
also triggers release of ANP and BNP
