3 Control of Cardiac Output Flashcards
Blood flow to most tissues is controlled by…
tissue needs
microvessel feedback
Arterial Pressure is regulated…
indepedent of either local blood flow or cardiac output control
Cardiac Output
-quantity of blood pumped into aorta each minute (L/min)
4-6 L/min at rest, increase 4-7x with exercise
CO = HR x SVR
What regulated Cardiac Output?
1.) intrinsic cardiac regulation of pump in response to changes in volume of blood flow to heart
2.) autonomic nervous system - contractility & HR
+= contractility, preload, HR, SV
-= aferload
Stroke Volume
SV = EDV - ESV
-can increase with HR, but non sustain w/o help from other mechanisms
Sympathetic Innervation of CO
increase, 100%
T1-T4 = cardiac accelerators
Parasympathetic
slow down, can reach 0
medulla - vagal
Heart Rate
more effect on CO than SV
high HR = low SV
Bowditch (Treppe) Effect
-an increase in HR will also increase inotropy
-stairway phenomenon
r/t increase intracellular Ca++ with high Hr
Preload
- initial stretching prior to diastole - sarcomere length
- considered to be the end-diastolic pressure when ventricle has become filled
- cannot measure directly
LVEDV
Left Ventricular End Diastolic Volume
-after contraction
LVEDP
Left Ventricular End Diastolic Pressure
-after contraction
PCWP
Pulmonary Capillary Wedge Pressure
CVP
Central Venous Pressure
Determinants of Preload
Venous Blood Pressure
- vasomotor tone
- venous volume (respiration, gravity, exercise)
Frank Starling Mechanism
- Intrinsic ability of heart to adapt to increasing volumes and pump out what it received.
- increased venous return = increased preload -> increased SV
Afterload
- what muscle has to contract against
- resistance in circulation, not pressure
- r/t wall stress
LaPlace’s Law
wall stress = ventricular pressure x ventricular radius divided by wall thickness
Increased Afterload will lead to…
increased aortic pressure increased systemic vascular resistance aortic valve stenosis ventricular dilation **shift Frank Starling curve down and to the right
Anrep Effect
- an abrupt increase in afterload can cause a modest increase in inotropy
- scare = sympathetic activation -> increase inotropy in response to sudden increase in aortic pressure
Contractility is highly related to….
-fiber length - think preload and sarcomere length
increased inotropy = increased ventricular SV
Contractility Definition
the inherent capacity of the myocardium to contract independently of changes in afterload or preload.
- d/t intrinsic cellular mechanisms that regulate interaction between actin and myosin (independent of sarcomere length)
- CICR, calcium availability
Factors Regulating Inotropy
\+ Systemic Activation \+ Catecholemines \+ Heart Rate \+ Afterload (Anrep) - Systolic Failure - Parasympathetic Activation