Cardio 3 Flashcards
Pulmonary Circulation Pressures (4)
1= ventricular filling 2= isovolumetric ejection 3= ventricular ejection 4= isovolumentric ventricular relaxation
Cardiac Output (CO)
The amount of blood pumped out of each ventricle in 1 minute.
Cardiac Output (CO) equation
CO= HR x SV
Normal resting CO
= 70 beats/min x 70 ml/beat
≈ 5 L/min
During intense exercise CO can increase to
30 – 35 L/min
CO regulated to match demands of tissues
o Increased by: (3)
o Decreased by: (2)
Physical activity, Metabolic status, Drugs
Blood loss, Heart Disease
Control CO by changing (2)
HR and SV
Factors that increase HR are called
+ chronotropic agents
Factors that decrease HR are called
- chronotropic agents
HR is mainly controlled by input from the nervous
system: (2)
SNS increases heart rate (AR and Contractile
Cells)
PSNS decreases heart rate (AR Cells only)
Major Factors Influencing Heart Rate (3)
increase activity of sympathetic nerves to heart
decrease activity of parasympathetic nerves to heart
increase plasma epinephrine
stroke volume equation
SV= EDV-ESV
SV is altered by: (3)
o Δ preload (EDV)
o Δ afterload (Blood Pressure)
o Δ contractility (Force of Contraction)
At rest, cardiac muscle sits at a length that is
less than
optimum
Starling’s Law of the Heart (4)
↑ EDV
↑ stretch of myocardium moves resting cardiocyte length toward optimum
↑ SV
VR =
Rate at which blood is
returned to the heart from
veins
Veins
Flaccid vessels and can hold
up to 60% of total blood
volume (Peripheral Venous
Pool)
Veins:
ΔP to return blood to the heart
from capillaries
very small
Veins:
One-way Valves to facilitate
blood movement back to heart
increase VR by: (3)
- increase Skeletal muscle pump
- increase Thoracic Pump
- increase Venoconstriction via Sympathetic NS
(1-3 Dependent on one-way valves in veins)
decrease VR by: (2)
- valsalva maneurver
2. *Extremely high HR (tachycardia) – decrease CO by decrease EDV
SV α 1/–
HR
CO α
HR (at normal HR)
HR has greater affect on CO
than SV unless extremely
tachycardic
increase in HR results in decrease CO (decrease SV, decrease EDV)
Afterload is the
pressure that the ventricles must overcome to force open the aortic and pulmonary valves.
Anything that increases
systemic or pulmonary
arterial pressure can
increase afterload
hypertension
↑afterload causes
↓SV
after load is a NOT a major factor in
healthy subjects
Contractility
Ability of heart to contract at any given resting
fiber length
The ventricles are never completely empty of
blood (ejection fraction), so a more forceful
contraction will
expel more blood with each
pump.
Contractility is varied by
controlling the amount of Ca++ that
enters contractile cell via L type voltage gated
Ca++ channels (Graded Contractions)
+ inotropic agents
increase contractility and increase ejection
fraction
(ex. Sympathetic Stimulation, Epinephrine)
- inotropic agents
decrease contractility decrease ejection
fraction
(ex. β1 Blockers, Ca++ channel blockers)
At rest,
amount of
ACh ? NE
>
Cardiac Muscle vs. Skeletal Muscle
Similarities (2)
Sarcomeres = functional unit
Length/Tension
Cardiac Muscle vs. Skeletal Muscle
Differences: (4)
Stimulus (Intrinsic: Extrinsic) Ca++ release from SR (10% ECF/90% SR : 100% SR) Summation/tetanus (No: Yes) Muscle Twitch (Graded: All or None)
