Cardiology Flashcards
intercalated disks
gap junctions and localized mechanical adhesions
accessory/auxiliary hearts
secondary/local hearts that assist with the pumping of blood through localized parts of the body
myocardium
the muscle tissue of a heart
isovolumetric contraction/isometric contraction
period where ventricular pressure is greater than atrium (atrio-ventricular valves close) but lower than aorta (aortic valve not pushed open) = volume in ventricle is constant
ventricular ejection
marked by opening of aortic valve and ends when it closes
isovolumetric relaxation
ventricular pressure falls with both inflow/outflow valves closed
ventricular filling
ventricular pressure below atrial pressure, inflow valve opens
cardiac output
volume of blood pumped per unit time; cardiac output = heart rate * stroke volume
in mammals/birds, ventricular myocardium is compact :
muscle cells are close together and blood cannot flow from ventricular lumen among myocardial cells
coronary artery
branch from systemic aorta that carries oxygenated blood to capillary beds throughout the myocardium
coronary veins
carries blood from myocardium into the right atrium
pacemarker
cell or set of cells that spontaneously initiates the rhythm of depolarization of the heart
myogenic
electrical impulse to contract originates in muscle cells
neurogenic
each impulse to contract originates in neurons
conduction
the process by which depolarization spreads through vertebrate/myogenic hearts
P wave
depolarization of myocardium of the 2 atria
QRS complex
depolarization of myocardium of the 2 ventricles (ventricular contraction)
T wave
repolarization of the ventricles
regulatory neurons
CNS neurons that modulate heart action
intrinsic controls
occur without the mediation of hormones or extrinsic neurons
Frank-Starling mechanism
intrinsic control, stretching of cardiac muscle leads to increased force of contraction
perfusion
the forced flow of blood through blood vessels
blood pressure
produced by the heart and is the principal factor that causes blood to flow through the vascular system, amount of pressure by which the blood exceeds the ambient pressure
systolic pressure
the highest pressure attained at the time of cardiac contraction
diastolic pressure
the lowest pressure reached during cardiac relaxation
fluid-column effects
in an unobstructed vertical column, fluid exerts increasing pressure as height is increased
open circulatory system
blood leaves discrete vessels and bathes at least some nonvascular tissues directly
- hemocoel: open space where fluid is “dumped”
- hemolymph: fluid that comes into direct contact with cells, cannot differentiate as blood in vs. out of vessel because it occupies both of these spaces
closed circulatory system
always a barrier separating blood from other tissues
vascular endothelium
single-layered epithelium lining all blood vessels
arteries
thick walls lined with muscle and elastic tissue
pressure-damping effects
effect of arterial elasticity - reduces variations in arterial pressure over the cardiac cycle
pressure-reservoir effects
effect of arterial elasticity - maintains pressure in arteries even when heart is at rest between beats
microcirculatory beds
consist of arterioles, capillaries, capillary beds, venules
arterioles
walls have smooth muscle and connective tissue, smooth muscle is involved in vasomotor control of blood distribution (changes luminal radius of blood vessel to direct blood flow)
capillaries
walls consist of vascular endothelium, usually fenestrated (physical gaps in the wall), the primary site of oxygen, water, and exchange of other materials between blood and tissues
capillary bed
consist of many capillaries that branch and anastomose among the cells of a tissue, walls contain aquaporins which facilitates osmosis between blood and tissue fluid outside capillaries
angiogenesis
the process of forming new capillaries and other microcirculatory elements
venules
small vessels with thin walls containing muscle and connective tissue
veins
blood is low pressure, contains passive one-way valves, capacitive properties allows holding of blood that cannot be housed elsewhere in the circulatory system
ultrafiltration
pressure-driven bulk flow of fluid out of the blood plasma across the capillary walls
colloid osmotic pressure
difference in osmotic pressure of blood plasma to extracellular tissue fluid (plasma has more dissolved proteins)
Starling-Landis hypothesis
overall effect is a net loss of fluid to interstitial fluid, which is picked up to the lymphatic system
pulmonary circuit
blood leaving heart to go to lung
branchial circuit
in water breathers, heart to gills
systemic circuit/circulation
blood to body tissues
lobster heart (open cardiovascular system)
- heart contraction squeezes hemolymph which eventually spills into hemocoel
- ostium = pore/opening on heart where hemolymph re-enters, has valves that prevent hemolymph from leaving during contraction
- spring-like ligaments/suspensory ligaments connects heart to structures around it, stretched during contraction
fish heart
- 2 chamber heart: 1 atrium and 1 ventricle
- sinus venosus: collects blood, pacemaker of heart beat
- atrium: muscular, contracts, job is to fill the ventricles, primer pump
- ventricle: muscular, contracts, power pump
- bulbus arteriosis (teleosts) or conus arteriosus (elasmobranchs, lungfish, bowfin)
- aorta
bulbus arteriosis (in teleosts)
- not muscular, elastic
- valves keep blood moving toward the aorta
conus arteriosis (in elasmobranchs, lungfish, bowfin)
- muscular, contractile ability
- also helps depulsate and decrease pressure of ventricle’s blood surge
circulatory plan of water breathers
heart, O2 source, and tissues in series with each other, low pressure blood going into system circuit limits metabolism (limits rate of blood being pushed through circulation)
-heart is also perfused with low O2 blood, limits heart’s ability to pump blood
circulatory plan of air and water breathing fish (fish with ABO - air breathing organs)
heart, O2 source, and tissues in parallel with each other
-heart receives low O2 venous blood mixing with high O2 blood from O2 source (heart gets more O2 than water breathers)
shunting
the ability of blood to follow pulmonary/branchial circuit or systemic circuit
pulmonary vasomotor segment in lungfish heart
band of muscle that surrounds ductus (leading to aorta/system circuit) and pulmonary artery. contraction controls shunting, when breathing air, pulmonary artery opens and ductus closes
when amphibians hold breath:
blood is shunted to systemic circuit via pulmonary-to-systemic shunt (constriction of pulmonary blood vessels, higher resistance=less blood flow in pulmonary circuit)
right ventricle of crocodilian heart leads to:
pulmonary artery and left aorta (systemic arch)
left ventricle of crocodilian heart leads to:
right aorta (systemic arch)
Foramen of Panizza
hole between L & R aorta, outside of heart, allows mixing between blood
cogwheel valves (in crocodilian heart)
2 swellings near pulmonary artery in right ventricles, active valves, contracts when breath holding and closes pulmonary artery, this generates high pressure in right ventricle which pushes blood out at high pressure to left aorta (shunts low O2 blood into systemic circuit)
pulmonary valve + aortic valve
- semilunar valves
- tricuspid
atrioventricular (AV) valves
- prevents backflow from ventricles to atria
- right AV = tricuspid
- left AV = bicuspid/mitral valve
cordae tendinae
connected to mitral/bicuspid valve on left side of heart, prevents prolapsed valve, attached to papillary muscle on ventricular valves
fetal pulmonary to aortic shunt
right atrium to right ventricle to ductus arteriosus to aorta
foramen ovale
- valve in fetal heart
- provides a passage between right and left atrium, so that blood can pass to left ventricle and then aorta (another shunt passage to systemic circuit)
fetal circulatory system changes after taking first breath:
- pulmonary pressure falls (stops all shunting passages)
- left pressure > right pressure (can’t be pushed through foramen ovale, closes and becomes nonfunctional)
- pulmonary artery blood flows to the lungs instead of the aorta (lower pressure in lungs)
- smooth muscle in ductus arteriosus squeezes closed and forms ligamentum arteriosis
dihydropyridine receptors
voltage gated calcium channels on T-tubules of cardiac muscle, not linked to ryanodine receptors on sarcoplasmic reticulum (entry of calcium binds to ryanodine receptors and causes release of intracellular calcium stores=calcium-induced calcium release)
cardiac glycosides
- modifies internal calcium levels
- ex. digitalis (foxglove), oubain, digoxin blocks Na-K pump
- increased intracellular Na causes Na/Ca pump to increase such that intracellular Ca rises and can bind to ryanodine receptors (causes increased heart rate and force of contraction)
what are 2 kinds of cardiac muscle?
1) working myocardium (lots of myofibrils, lots of SR, prolonged action potential)
2) pacemakers (depolarize spontaneously, conducting action potentials, don’t contract)
what are the 4 types of pacemaker cells?
1) sinoatrial node (SA) node (right atrium)
2) atrioventricular node (AV)
3) bundles of HIS
4) Purkinje fibres
AV nodal delay
AV nodal link between atria and ventricles is very high resistance, requires more time for membrane depolarization to reach threshold. This causes atrial contraction to occur before AV node initiates ventricular contraction
amplitude of electrocardiogram signal that reaches body surface is influenced by:
- mass of muscle
- rate of depolarization
Einthoven’s Triangle
-leads placed on left arm, right arm (reference=0), left leg (sense)
PR segment
2 electrodes are seeing the same signal, caused by AV nodal delay
ST segment
plateau of ventricular action potential
TP segment
diastole (ventricular relaxation)
chronotropic
effect on heart rate
inotropic
effect on strength of contraction
lusitropic
effect on relaxation
dromotropic
effect on rate of spread of cardiac action potential
parasympathetic control of heart rate
- cholinergic (ACh) neurons
- main=vagus nerve, mostly affects pacemakers
- increases K+ conductance (slower rate of rise of pacemaker potential)
- slows heart rate, rate of depolarization, increases AV nodal delay
sympathetic control of heart rate
- adrenergic (NE) neurons
- activated by catecholamines
- acts on pacemakers and working muscle
- decreases K+ conductance
- easer for pacemaker potential to rise, increased heart rate, increased spread of depolarization, decreased AV nodal delay
- catecholamines binding to B1 receptors on working muscle activates protein kinases that phosphorylate Ca channels and troponin, causes increased Ca entry and increased binding of Ca to troponin, increased force of contraction (inotropic effect)
stroke volume
blood ejected per beat (mL/beat)
heart rate
contractions/min
cardiac output
heart rate * stroke volume = mL/min
Frank/Starling Relationship or Law of the heart
higher end-diastolic volume is proportional to stroke volume, until end-diastolic volume reaches a very high volume and causes congestive heart failure
sympathetic stimulation increases heart contraction force, what effects does this have on a SV vs. EDV figure?
causes an upward shift, potential treatment for congestive heart failure
what affects end-diastolic volume?
EDV is a function of how much blood is returned to the heart (venous return) and is affected by:
- squeezing veins (sympathetic stimulation of smooth muscle around the veins)
- skeletal muscle contraction helps with venous return
- respiratory pumping (inspiration decreases intra-thoracic pressure and right atrium pressure and increases venous return)
- cardiac suction (elastic recoil of the heart)
- valves in veins (passive structures that help return blood to the heart)
