Lecture 10- Cardiac Phys II (Cardiac output) Flashcards
What is a cardiac cycle?
“A single cardiac cycle includes all of the events associated with one heartbeat.
Thus, a cardiac cycle consists of systole and diastole of the atria plus systole
and diastole of the ventricles”
Cardiac cycle refers to all events associated with blood flow
through the heart
What is the difference between systole and diastole?
– Systole (pronounced “sis-ter-lee”) – contraction of heart muscle
– Diastole (pronounced “dias-ter-lee”) – relaxation of heart
muscle
Go through the phases of the cardiac action potential and what does it tell you?
- rapid depolarization due to Na+ inflow when voltage-gated fast Na+ channels open
- plateau of membrane potential (a maintained depolarization) due to Ca2+ ions flowing in when voltage-gated slow Ca2+ channels open and K+ outflow when some K+ channels open
- repolarization due to the closure of Ca2+ channels and K+ outflow when additional-gated K+ channels open
The atrial systole has which 3 parts of the cardiac cycle?
- arteriol systole
- ventricular systole
- relaxation
Go through the process of the cardiac cycle and all its phases
- Depolarization of SA node
- atrial depolarization (pwave) - Ventricular filling – mid-tolate diastole
– Heart blood pressure is
low as blood enters atria
(passively) and flows into
ventricles
– AV valves are open, then
atrial systole occurs - At the end of atrial
systole, the ventricle contains
~130mL blood - QRS complex marks onset
of ventricular depolarization - Ventricular depolarization,
ventricle systole. Pressure ↑ in
ventricles putting pressure on AV
valves causing isovolumetric
contraction (ie all 4 valves closed,
ventricular volume same) - Ventricular contraction,
pressure
↑. When L ventricular pressure >
aortic pressure (~80mmHg) AND R
ventricular pressure > pulmonary
trunk pressure (20mmHg), aortic
valves open ventricular ejection - L ventricle ejects blood into aorta +
R ventricle ejects into pulmonary
trunk - T wave == onset of ventricular
repolarization - Ventricular repolarization
ventricular diastole. Ventricular
pressure ↓, blood in aorta and
pulmonary trunk flows back,
pressure equalizes, and all 4
valves close (isovolumetric
relaxation) - Ventricles relax, pressure ↓.
AV valves open, ventricles fill. P
waves appear, starting the next
cycle
What is the ventricle systole? What are the phases that make up the ventricle systole?
- Ventricular depolarization
ventricle systole. Pressure ↑ in
ventricles putting pressure on AV
valves causing isovolumetric
contraction (ie all 4 valves closed,
ventricular volume same) - Ventricular contraction pressure
↑. When L ventricular pressure >
aortic pressure (~80mmHg) AND R
ventricular pressure > pulmonary
trunk pressure (20mmHg), aortic
valves open ventricular ejection - L ventricle ejects blood into aorta +
R ventricle ejects into pulmonary
trunk - T wave == onset of ventricular
repolarization
What are the phases of the relaxation phase?
- Ventricular repolarization
ventricular diastole. Ventricular
pressure ↓, blood in aorta and
pulmonary trunk flows back,
pressure equalizes, and all 4
valves close (isovolumetric
relaxation) - Ventricles relax, pressure ↓.
AV valves open, ventricles fill. P
waves appear, starting the next
cycle
What is auscultation?
Auscultation (listening to the heart)
How are valves affected when blood is leaving and returning from the heart?
- when blood is returning to the heart and fills the atria it puts pressure against the arterioventricular valves
- as the ventricles fill, arterioventricular valve flaps hang limply into the ventricles
- when atria contracts blood is forced into the ventricles
- when ventricles contract, blood is forced against the arterioventricular valve cusps
- the arterioventricular valves close
- papillary muscles contract and chorsae tendineae tighten, this prevents valve flaps from everting into the atria
as ventricles contract and intraventricular pressure rises blood is pushed up against the semilunar valves and forces them to open
as ventricles relax and intraventricular pressure falls, blood flows back from arteries and fills the cusps of the semilunar valves and forces them to close
What are the first and second sounds associated with auscultation?
First sound (Lub) occurs
as AV valves close and
signifies beginning of
systole (contraction)
– Second sound (Dub)
occurs when SL valves
close at the beginning of
ventricular diastole
(relaxation)
Define cardiac output
Cardiac Output is the amount of blood pumped by each ventricle in one
minute
How is CO calculated?
CO is the product of stroke volume (SV) and heart rate (HR)
* HR is the number of heart beats per minute
* SV is the amount of blood pumped out by a ventricle with each beat
Cardiac reserve is the difference between resting and maximal CO
CO=SV x HR
What is SV? How is it calculated? What is SV affected by?
SV = end diastolic volume (EDV) minus end systolic volume (ESV)
– EDV = amount of blood collected in a ventricle during diastole
– ESV = amount of blood remaining in a ventricle after contraction
At rest, SV is 50–60% of the EDV because 40–50% of the blood remains in
the ventricles after each contraction (ESV)
SV is affected by three factors:
1. Preload – degree to which ventricles are stretched by the blood
2. Contractility – cardiac cell contractile force
3. Afterload – back pressure exerted by blood in the large arteries leaving the
heart
What are intrinsic and extrinsic mechanisms of cardiac output?
What does the Frank-Starling law tell us about the heart?
Preload (degree of stretch) of cardiac muscle cells before they contract is the
critical factor controlling SV
The volume of blood ejected by the ventricle depends on the volume
of blood present in the ventricle at the end of diastole
Slow heartbeat and exercise (more next time) increase venous return to the
heart (filling time is longer), increasing SV
Blood loss and extremely rapid heartbeat (eg >160bpm) decrease SV (short
filling time
What is contractility?
Contractility is the increase in contractile strength, independent of stretch and
EDV
How does contractility increase and what affects its decrease?
Increase in contractility comes from:
– Increased sympathetic stimuli
– Certain hormones
– Ca2+ and some drugs
Agents/factors that decrease contractility include:
– Acidosis
– Increased extracellular K+
– Calcium channel blockers (more in the lecture bites)
What is the extrinsic mechanism of the ANS?
How do the sympathetic and parasympathetic nervous system affect the heart? How do they impact the myocardium and the SA node
The heart is innervated by both
-Sympathetic fibers (upper thoracic
region)- Noradrenaline is the postganglionic transmitter
-Parasympathetic fibres- Vagal
nerve-. Acetylcholine is the as a
post-ganglionic transmitter:
*SA node is innervated by both
parasympathetic and sympathetic
nerve fibres.
*The myocardium is innervated by
sympathetic nerve fibres only.
What does sympathetic stimulation do?
Sympathetic stimulation releases
noradrenaline and initiates a cyclic AMP
second-messenger system
What are positive and negative chronotropic factors?
Positive chronotropic factors increase heart rate
– Caffeine
Negative chronotropic factors decrease heart rate
– Sedatives
What impact do the SNS and PNS have on the heart?
Sympathetic nervous system (SNS) stimulation is
activated by stress, anxiety, excitement, or exercise
(more in the lecture bites)
Parasympathetic nervous system (PNS) stimulation
is mediated by acetylcholine and opposes the SNS
What causes vagal tone and what is it?
– PNS dominates the autonomic stimulation, slowing
heart rate and causing vagal tone
Define blood pressure
Blood Pressure (BP) = measure of the force of blood against the
walls of the arteries.
How is BP fluctuation expressed?
BP fluctuates, and is expressed as two numbers:
(1) systolic = max pressure in the arteries when the heart
contracts
(2) diastolic = min pressure in the arteries when the heart is
at rest between beats
What is the normal BP range?
Normal BP ~120/80 mmHg (millimeters of mercury).
High blood pressure (hypertension): ≥ 140/90 mmHg
increased risk of heart disease/stroke.
Low blood pressure (hypotension): ≤ 90/60 mmHg
dizziness, fainting, etc.
How is BP distributed across the CV system?
Blood leaves the aorta and flows through the systemic circulation (~120/80 mmHg)
Pressure falls progressively as the distance from the left ventricle increases.
BP ↓ to 35 mmHg as blood passes from
arteries through arterioles and into
capillaries, where the pressure fluctuations
disappear.
Venous end of capillaries, blood pressure
↓ 16 mmHg.
Blood pressure continues to drop as blood
enters systemic venules and then veins
because these vessels are farthest from
the left ventricle.
Finally, blood pressure reaches 0 mmHg
as blood flows into the right ventricle
How do you calculate Mean arterial pressure and why is it important to measure it in certain circumstances?
MAP= (2xdiastolic BP) +systolic BP/3
- MAP more accurate indicator of perfusion or the blood flow to organs
and tissues than systolic or diastolic blood pressure alone. - MAP is considered a more important indicator of a patient’s CV status
(for monitoring hypertension, hypotension). - MAP is an indicator of organ perfusion in critical care.
- MAP is monitored during surgical procedures (+ sepsis, trauma,
critical illness etc.)
What factors affect blood pressure by increasing it?
Increase in blood volume –> increase in BP
Increase in blood volume (eg water retention, renal disorders, heart failure,
medications, pregnancy):
-Heart pumps harder to circulate the increased blood volume –> increase in
BP
- Increased blood volume –>blood vessels dilate –>increase in vascular
resistance –>increase in BP
What factors decrease blood pressure?
Decrease in blood volume –> decrease in BP
Decrease in blood volume (eg haemorrhage, dehydration, medications,
malnutrition)
- Heart does not have to pump as hard to circulate the blood through the body –> decrease in BP
-Decreased blood volume–> blood vessels to constrict –> decrease in
vascular resistance –> decrease in BP
What neuronal systems affect blood pressure? What are the different receptors involved? What makes up the input centre and what are the output effectors?
At the input to cardiovascular centre nerve impulses are recieved from higher brain centres such as cerebral cortex and limbic system and also
Proprioceptors – these monitor muscle movement to feedback activity
Baroreceptors – these are pressure-sensitive receptors in larger arteries in neck/chest
Chemoreceptors – these monitor blood pressure (and breathing, etc) through chemical composition of blood by monitering [H+], PCO2, PO2
Output effectors gain increased frequency of nerve impulses resulting in:
decreasted heart rate via vagus nerve (parasympathetic)
increased heart rate and contractility via signal from cardiac accelorator nerves (sympathetic)
and vasoconstriction of blood vessels sent via the vasomotor nerves (sympathetic)
What is the endocrine system?
- Endocrine system: hormones help regulate BP and blood flow by altering cardiac output, changing
systemic vascular resistance, or adjusting the total blood volume
What parts of the endocrine system affect blood pressure? how?
- Renin–angiotensin–aldosterone (RAA) system – monitors drop in blood flow/blood volume via kidneys–> increase BP
- Adrenaline/noradrenaline – increase HR in times of stress–>increase BP
- Antidiuretic hormone (ADH) – released by pituitary gland during dehydration. Causes
vasoconstriction –> increased BP (also decrease urine output) - Atrial natriuretic peptide (ANP) – released during drop in blood volume –>decrease BP
