Physio lecture 1 Flashcards
3 principle components of CV system
Func impacted by
Heart (pump)
Blood vessels/vascular system (tubes)
Blood (fluid connective tissue)
CV func impacted by endocrine, nervous and urinary systems
Blood formed of
cells and cell fragments in liquid called plasma
erythrocytes
leukocytes
platelets
What is hematocrit
% of blood volume that is erythrocytes
RBCs func
contain?
shape?
Func: gas transport!
contain large amounts of hemoglobin
Biconcave shape -high surface area for improved diffusion
Platelets
contain?
produced when?
role in?
-Circulating, colorless, non-nucleated fragments that contain granules-smaller than RBCs
-produced when large bone marrow cells (megakaryocytes) pinch off into circulation
-role in clotting
Blood vessels
arteries and veins do what
exception to rule?
Arteries carry blood away from heart (oxygenated)
veins carry to the heart (deoxygen)
except:
Pulmonary arteries- carry deoxy blood to lungs to get oxygen.
Pulmonary veins-carry oxygen blood to heart to get delivered to body
Pressure
what is it
blood flows from..
-force exerted by blood -measured in Hg
High pressure area to low pressure area
Flow
what is it
-volume of blood moved per unit time (velocity)
ml/min
Resistance
what is it
-describes how difficult for blood to flow between two points at any given pressure difference
measure of friction that impedes flow
Resistance
factors that determine it
-blood viscosity
-total vessel length
-radius of vessel (radii of vessels is NOT constant- determines changes in resistance)
Epicardium
what kind of tissue
fibrous outer layer
Myocardium
composed of?
acts as?
middle layer
cardiac muscle
contractile layer
Endocardium
continuous with?
inner layer
continuous with lining of blood vessels entering and leaving heart
Atria
L and R what they receive from where
R atrium gets deoxy blood from systemic and coronary circulations
L atrium gets oxyg blood from pulmonary circulation
Ventricles
whole shabang
R ventricle pumps deoxy blood to lungs
L ventricle pumps oxy blood to rest of body including myocardium
R and L sides of heart- which circuit is which
Right-Pulmonary circuit
Left-Systemic circuit
Valves
2 AV- open in diastole (tricuspid and mitral)
2 semilunar- open in systole (pulmonic and aortic)
S1 (lub)-closure AV valves
s2 (dub)-closure semilunar
Coronary arteries
supply
max when
-supply oxygenated blood to myocardium
-max in diastole and min in systole
Left CA also has LAD(widowmaker)
Right CA
Cardiac veins
do what
coronary sinus
-drain deoxy. blood from myocardium
-runs parallel to arteries
-CS- collects blood from veins and returns to R atrium
Innervation
Para
Symp
Para- vagus nerve -decreases HR and force of contraction
Symp- cardiac splanchnic nerves- increases HR and force of contraction
Visceral afferent pain fibers follow symp pathways to T1-4 (referred chest pain from MI)
Other visceral afferents (stretch, baroreflexes, chemoreflexes) conveyed to brainstem via vagus nerve
Cardiac muscles
-arranged in tight layers that circle chambers
-every heart cell contracts with every beat of the heart
-LIMITED healing ability
Cardiac communication
-1% of cells do not contract, instead excite
-Conducting system is in electrical contact with muscle via gap junctions
-this system INITITIATES heartbeat and spreads AP through heart
Conducting system sequence
- SA node-pacemaker, initiates HB, altered by ANS
- AV node -receives pulses from SA and passes to bundle of His
- Bundle of His- transmits impulses to IV septum-> Purkinje fibers to distribute impulse to ventricular muscle
Nodal cells APs
SA- NO steady resting potential, undergoes slow depolarization called -Pacemaker potential
—AUTOMATICITY!!!!
Other cells slower, they are driven to threshold by APs from SA
Faster conduction wins!
Excitation-contraction coupling
-Small amount of Ca enters cell through channels during plateau of AP
-Trigger Ca binds to ryanodine and triggers release of lots of Ca
-This causes a contraction
Systole vs diastole
Period of ventricular contraction and blood ejection ->Systole
Period of ventricular relaxation and blood filling ->Diastole
Periods during systole
-Isovolumetric ventricular contraction: ventricles contracting but BLOOD CANNOT leave since VALVES are CLOSED
-ventricular ejection: muscles fibers shorten and blood is forced out. Aortic and pulmonary valves open by RISING PRESSURE
SV is volume of ejected blood from each ventricle during systole
Periods during diastole
-Isovolumetric ventricular relaxation: valves close and NO BLOOD enters or leaves ventricles
-Ventricular filling: AVs are open, blood flows into ventricles
Atria contract at end but a lot of filling is passive
CO formula
CO= HR x SV
volume of blood pumped out per unit time
norm: 5 L/min
Resting= SV constant
blood loss=SV declines and CO maintains by increasing HR
Regulating HR
SA node fires 60-100 x/min
Para(vagus nerve) causes HR decrease
symp causes increase HR
Chronotropic effects
Major factors: increase Epi, increase symp nerves, decrease para nerves-> SA node increased HR
SV control
-volume of blood each ventricle ejects during contraction
SV= EDV-ESV
70 ml/beat avg.
Regulation:
Preload: changes EDV
afterload: arterial pressures against which ventricles pump
Frank Starling
Ventricle contracts more forcefully when filled to greater degree during diastole
OPTIMAL LENGTH- increasing EDV leads to this greater stretch and forceful contraction
increase in venous return forces increase CO by increasing EDV and therefore SV
Symp Regulation SV
NE acts on beta-adrenergic receptors to increase ventricular contractility (Inotropic)
Symp stimulation of myocardium causes powerful contraction but ALSO the contraction and relaxation occurs more quickly
Ejection Fraction
Quantifies contractility
EF= SV/EDV
avg. 50-75%
increased contractility causes increased EF
this can dx HF
Effects of afterload on SV
-increased arterial pressure reduces SV
-arterial pressure that constitutes load is termed afterload
greater load= less contracting fibers can shorten at a given contractility
