Exam 2 - CV Intro Flashcards
8 functions of cardiovascular system
- Gaseous exchange
- Removal of CO2, lactic acid, urea
- Delivery of major nutrients (building blocks)
- Delivery of micronutrients (vitamins, metals)
- Delivery of hormones
- Defense
- Thermal exchange
- Maintaining tissue hydration
3 hemostatic mechanisms to prevent blood loss
- vascular spasm
- formation of a platelet plug
- coagulation (clotting)
CV system 4 important variables and what determines each
- cardiac output (heart)
- resistance (arterioles)
- capacity (veins, venules)
- blood volume (balance between fluid supply and fluid loss - kidneys)
what modulates gene expression in the intima of vascular endothelium?
shear stress
what three substances does the intima of vascular endothelium produce?
- prostacyclin (PGI2) - vasodilator, inhibitor of platelet aggregation
- NO - vasodilator, inhibitor of platelet aggregation and leukocyte-endothelial cell adhesion
- endothelin - vasoconstrictor
describe structure of capillaries
- just intima (no media or adventitia)
- surrounded by pericytes (Rouget cells)
functions of pericytes (5)
- regulation of tight and adherens jxns
- angiogenesis
- regulation of ECM protein secretion
- contractile - regulate capillary diameter/blood flow
- phagocytosis
describe the structure/purpose of the media of vascular endothelium
smooth muscle - responsible for vasoconstriction and vasodilation
in general, what mainly controls vasoconstriction?
- sympathetic nerve stimulation (a1 adrenergic receptors)
- vasoconstrictors:
- -thromboxane A2 (TXA2)
- -vasopressin (ADH)
- -angiotensin II
- -endothelin
- -epinephrine (adrenaline)
in general, what mainly controls vasodilation?
- metabolically generated substances:
- -H+
- -CO2
- -adenosine
- vasodilators:
- -prostacyclin
- -NO
- loss of sympathetic tone
in large vessels, where is the vasa vasorum contained?
within the adventitia
what are the three major bypasses that virtually remove the liver and lungs from fetal circulation?
- ductus venosus (bypasses liver)
- foramen ovale (shunt from RA -> LA)
- ductus arteriosus (bypasses pulmonary circuit)
describe the changes in pressure that occur with birth
loss of placenta -> increase in systemic resistance -> increase in systemic and left heart pressure -> LA pressure increases -> foramen ovale closes
ventilation of lungs -> decrease in pulmonary resistance (availability of oxygen -> relieves hypoxic pulmonary vasoconstriction) -> pulmonary and right heart pressure decrease
describe the four structural changes that occur at/after birth
- ductus venosus closes -> ligamentum venosum
- higher pressure in LA closes foramen ovale -> fossa ovalis
- blood flow reverses through ductus arteriosus -> closes -> ligamentum arteriosum
- -also bradykinin in high O2 conditions = vasoconstrictor - LV increases in mass b/c pumping at higher pressure, while RV decreases in mass b/c pumping at lower pressure
post-ductal vs. pre-ductal coarctation of the aorta
post-ductal:
- most common
- stenosis past ductus arteriosus
- normal flow reversal
- live to about 40
pre-ductal:
- stenosis before ductus arteriosus
- flow reversal doesn’t always occur - fetal direction of flow persists and ductus arteriosus remains patent (here causes a right to left shunt though)
three congenital conditions that result in left to right shunts
- patent ductus arteriosus
- except with pre-ductal coarctation - VSD
- ASD (most common = patent foramen ovale)
(from left heart/aorta, which are normally high pressure, to the right heart/pulmonary trunk, which are normally low pressure)
two congenital conditions that result in right to left shunts
- pre-ductal coarctation w/ patent ductus arteriosus
- Tetralogy of Fallot (blue baby syndrome; PROVE)
-Pulmonary stenosis
-RV hypertrophy
-Overriding aorta
-VEntricular septal defects
(blood shunted from R -> L, bypassing lungs w/o getting O2)
describe the relaxation of cardiac muscle
- cAMP-dep PK phosphorylates Troponin I
- SERCA pumps Ca2+ back into SR (activated when phospholamban is phosphorylated)
- then Ca2+ is sequestered in SR by calsequestrin
- some Ca2+ is pumped out of cell (Na-Ca exchanger, calcium ATPase)
what is a positive lusitropic effect and what neurotransmitters can cause this?
= acceleration of cardiac muscle relaxation
catecholamines - phosphorylate phospholamban and phosphorylate troponin I
(during rapid HR, this allows rapid relaxation to still get adequate ventricular filling b/w pumps)
what does the strength of cardiac muscle contraction depend on?
sarcoplasmic [Ca2+]
more Ca2+, stronger contraction
effects of extracellular [Ca2+] on myocardial contractility
decreased EC Ca2+:
-decreased contractility -> arrests heart in diastole
increased EC Ca2+:
-increased contractility initially -> arrests heart in systole
what are some positive inotropic agents and how do they work?
- catecholamines (epi, norepi, dopa) - increase Ca2+ influx
- digitalis/digoxin - inhibit Na-K pump, which reduces Ca2+ efflux via Na-Ca exchanger
what are some negative inotropic agents and how do they work?
-Ca-channel blockers - block Ca2+ entry
what causes S1?
closure of the mitral and tricuspid valves
what causes S2?
closure of the aortic and pulmonic semilunar valves
what is the best indicator of RA pressure?
right internal jugular pressure
what are some factors that increase central venous pressure?
- decreased CO
- increased blood volume
- venous constriction
- changing from standing to supine body posture
- arterial dilation
- forced expiration (Valsalva)
- muscle contraction (abdominal and limb)
four major determinants of CO
- preload (inflow)
- afterload (outflow)
- HR
- myocardial contractility
what is heterometric autoregulation?
Starling Law
-the more the cardiac muscle can stretch, the stronger the contraction
(increasing preload will increase SV, and therefore CO)
two factors that affect preload
- blood volume
- venous capacity
what is the mean filling pressure?
the pressure that the arteries and veins will equilibrate at if the heart stops and flow ceases
does aortic valve stenosis cause HTN?
no - although it does increase afterload
