Cardiac Output Flashcards
Cardiac Output function
VITAL to homeostasis
Controls amount of blood flow to the tissues. Prevents undue stress on the heart.
Depends on venous return, which, in turn, depends on the rate of flow to the tissues.
Rate of flow to tissues depends on tissue needs (i.e. it depends on Total Peripheral Resistance). Therefore, cardiac output is proportional to the energy requirements of the tissues.
HR factors
Primarily varied by altering balance of parasympathetic and sympathetic influence on SA node.
Sympathetic stimulation speeds it up
Parasympathetic stimulation slows heart rate.
Average End Diastolic, Stroke Volume, End Systolic Volume, and Ejection Factions
- EDV - 120-130ml
- SV output - 70 ml
- ESV - 50-60ml
- Ejection Fraction - 60 % [70/120]
The volume of blood pumped each minute
CO = SV x HR
COis cardiac output expressed in L/min (normal ~5 L/min) Note difference between CO & CI.
SV - is stroke volume per beat.
HR- is the number of beats per minute.
Stroke Volume
The volume of blood pumped out by each ventricle per each contraction.
Determined by extent of venous return and by sympathetic activity.
Intrinsic control of Cardiac output
Heart muscle operates short of its optimal sarcomere length.
Stretch it by bringing more blood back to the heart
Increase in stroke volume, increases contractility.
Extrinsic control of Cardiac output
NE from sym. + Epi. from adrenal medulla →↑ opening of Ca++ channels → more Ca++ inside → ↑ force of contraction
Factors that increase Cardiac Output
- SNS - (Epi, Nor Epi)
- T3 + T4 (metabolic increase)
- Increase in Body Temp
- Increase in Calcium.
- decrease in PO2 - (hypoxia)
- Increase in CO2
- decrease in pH
Factors that decrease Cardiac Output
- PSNS - (Ach)
- Decrease in Calcium
- Increase in Potassium
Factors that increase Preload
- Increase in EDV - Venous return
a)muscular activity
b) respiratory pump
(deep inspiration - increase in abdominal pressure; decrease in thoracic pressure)
c) SNS - Nor Epi on smooth muscle
venomotor tone / constriction - Filling time -
Increased HR - decreases filling time.
How MI’s affect preload
The heart muscle has scar tissue and will not stretch as much, decreasing preload.
Frank Sterling’s Law
Greater the stretch, the greater the force of contraction.
[more stretch allows for more cross-bridging which increases preload and SV]
Ejection Fraction (EF)
- % of the EDV that is pumped by the ventricle (important clinical parameter) the EF should be about 55-60%
[ SV/EDV ]
Increases during exercise.
SV determinants
- Preload - The amount of myocardial stretch (EDV)
- Contractility - intrinsic strength of cardiac muscle.
- Afterload - amount of of resistance the ventricles need to overcome to send blood to the aorta and pulm. trunk. [arterial pressure, valvular pressure]
Contractility determinants
- SNS - Epi, Nor Epi act on ß1 adrenergic receptors - which increases Ca2+ levels, increases contractility and increases SV.
- Hormones - T3 and T4 stimulates genes in cardiac cells and proteins which increase ß1 receptors and increases cont. and SV.
- Increase in Glucagon.
- Drugs - ( Digitalis, epi, atropene)
Afterload determinants
[Increase in afterload, decreases SV]
- Stenotic valves
- vessel occlusion
- HTN
- plaque buildup
Increases back pressure in arterioles; increases BP
Heart Rate
Heart rate is directly proportional to cardiac output
Adult HR is normally 80-100 beats per minute (bpm.)
Heart rate is modified by autonomic, immune, and local factors.
An increase in parasympathetic activity via M2 cholinergic receptors in the heart will decrease the heart rate.
An increase in sympathetic activity via B1 and B2 adrenergic receptors throughout the heart will increase the heart rate
Cardiac Reserve
the difference between resting and maximal CO.
CO limits
Normal CO – 5 L/min
Plateau – 13 L/min
Hyper-effective heart plateau – 20 L/min
Hypo-effective heart plateau – 5 L/min
Hyper-effective heart conditions
- Nervous excitation
- Cardiac Hypertrophy
- Exercise – Marathon runners may get 30 to 40 L/min
- Aortic Valve Stenosis
Valvular disease
Increased output pressure
Congenital heart disease
Myocarditis
Cardiac anoxia
Toxicity
The result of Cardiac muscle fiber stretch
Cardiac fibers contract MORE FORCEFULLY when stretched thus ejecting MORE
BLOOD (increased SV)
If SV is increased, then ESV is decreased!!
Slow heartbeat and exercise
Slow heartbeat and exercise increase venous return (VR) to the heart, increasing SV.
VR changes in response to blood volume, skeletal muscle activity, alterations in cardiac output
⬆️VR , ⬆️EDV, ⬆️ SV
and vice versa. (Proportional relationship)
Blood loss and extremely rapid heartbeat decrease SV