Cardiovascular Flashcards
varicose veins are the result of ___ ___
valve incompetency
the SA node provides stimulus for heart to pump at what rate?
60-100 bpm
“neurohumoral” refers to what?
renin-angiotensin-aldosterone system
most of the blood entering the right ventricle enters (actively/passively)
passively
cause of increased right atrial pressure
right ventricular congestion (due to left ventricular insufficiency)
result of increased right atrial pressure
peripheral edema
right side of heart is (low/high) pressure
low
cause of increased left atrial pressure
left ventricular congestion (due to HTN, injury, etc)
result of increased left atrial pressure
pulmonary edema/congestion
purpose of chordae tendonae
prevent valvular prolapse (of AV valves) –> ensure one-way blood flow
purpose of sinuses of Valsalva
protect right and left coronary arteries from excessive increases in pressure/volume
location of sinus of Valsalva
surrounding leaflets of semilunar valves
rate of ventricular automaticity
20-30 bpm
rate of AV node automaticity
40-60 bpm
rhythmicity def
regularity of impulse generation by cardiac automatic cells
conductivity def
ability to transmit an electrical impulse across a distance
excitability def
ability to respond to a stimulus (i.e. catecholamines)
arteries have a (low/high) volume, (low/high) pressure flow
low volume, high pressure
where in circulation does regulation of blood pressure occur?
alpha and beta (1) receptors on arterioles
___ are the major site of exchange in circulation, due to their ___
capillaries, fenestrae
laminar flow properties
unidirectional, smooth, fastest in the center of vessel, some frictional resistance along sides
veins have a (low/high) volume, (low/high) pressure flow
high volume, low pressure
function of skeletal muscle pump
facilitating venous return by massaging the veins with muscular movement; forces blood to flow away from wherever the vein is being sqeezed, but it can only go in the direction that the venous valves allow: towards the heart
function of thoracic pull
movement of diaphragm creates a vacuum, assisting in “pulling” blood towards thoracic cavity
which coronary artery is most often affected by disease
left anterior descending artery (?)
lymphatic vessels empty into the
super vena cava
pulmonary circulation is ___ pressure, ___ volume, and ___ resistance
low, low, low
pulmonary hypertension leads to right ventricular ___
hypertrophy
cor pulmonale def
right ventricular hypertrophy caused by pulmonary hypertension; most often the result of left heart failure but can also be caused by chronic lung disease
stimulation of beta 1 receptors (norepinephrine) of heart
increased heart rate, increase stroke volume, vasoDILATION of coronary arteries; increase conduction through AV node
sympathetic response is stimulation of ___ receptors
adrenergic (beta and alpha)
describe cascade of cellular effects of beta 1 receptor stimulation in heart muscle
norepi binds to b1 receptor, a g-protein linked receptor; activation of adenylyl cyclase; formation of cAMP –> increase in inotropy, lusitropy, and chronotropy
inotropy def
strength of cardiac contraction, affected by # of Ca 2+ ions and adrenergic stimulation
lusitropy def
relaxation of contracted cardiac muscle
chronotropy def
rate of cardiac contraction
parasympathetic response is carried out by the ___ nerve
vagus
type of receptors that create a parasympathetic response
cholinergic/acetylcholine
ACh ___ heart rate
decreases
ADH effects (2)
water reabsorption in kidneys and vasoconstriction –> increase BP
factors that stimulate release of renin
drop in BP (detected by JGA); decreased serum NaCl; beta-adrenergic stimulus (norepi); decreased angiotensin II; decreased serum K+
angiotensin II effects
vasoconstriction; stimulates release of aldosterone and ADH; promotes growth of cardiovascular tissues; increased sympathetic output (catecholamines)
purpose and MOA of ACE inhibitors
for managing HTN; inhibits the action of angiotensin converting enzyme (ACE) in converting ang I to ang II
true or false: chronic elevation of aldosterone is independently damaging to cardiac tissues
true
Poiseuille’s law
Resistance is dependent on: viscosity of the blood, the length of the vessel; it is inversely proportional to the fourth power of the lumen’s radius –> small changes in radius create BIG changes in resistance
cardiac output formula and normal range
CO = SV x HR; normally about 5 L/min
stroke volume determinants and normal range
SV = (end-diastolic volume) - (end-systolic volume); or
SV = preload - afterload
normal is 50-70 mL
ejection fraction formula
EF = (end-systolic volume) / (end-diastolic volume)
cardiac index formula and normal range
CI = CO/surface area
normal CO = 5L/min, normal surface area = 1.78 m^2
(5 L/min) / (1.78 m^2) = 2.8 L/min/m^2
normal is 2.8-3.6 L/min/m^2
Starling’s law
the volume of blood in the heart at the end of diastole (the length of its muscle fibers) is directly related to the force of contraction during the next systole –> preload and contractility affect SV and therefore CO
sinus of Valsalva allows blood to enter the coronary arteries during what cardiac phase?
left ventricular diastole
beta 1 receptor stimulation causes vaso-___
DILATION (think “beta makes it bigger”)
alpha receptor stimulation causes vaso-___
CONSTRICTION (think “a is to c as b is to d”)
cardiac reserve def
the degree to which the heart is able to increase CO in response to increased activity
tissue ischemia causes vaso-___
dilation
ischemia def
inadequate perfusion of tissues (not enough blood flow)
ischemia is (reversible/irreversible)
reversible
pathogenesis of coronary artery disease
atherosclerosis of coronary arteries causes cardiac ischemia
pathophysiology of atherosclerosis
- endothelial injury (can be caused by HTN, diabetes, etc.)
- platelets adhere to site of injury
- macrophages enter site and eat lipids of tunica intima, forming foam cells
- build up of foam cells creates protrusive fatty streak
- protrusion interrupts laminar flow –> turbulent flow
- turbulent flow causes further injury to endothelium
- fatty streaks continue to grow together forming fibrous plaques, result of collagen destruction and LDL oxidation
modifiable risk factors for CAD/atherosclerosis
hyperlipidemia, obesity, hypertension, smoking, stress
cardiac markers
CPK, LDH, MB-CK, troponin
viral pericarditis patho
decreases cardiac conductibility
preload def
degree of myocardial stretch at the end of ventricular diastole
afterload def
amount of force necessary for ventricles to eject blood; determined by systolic pressure, ventricular wall thickness, and radius of aorta/pulm arteries
forward vs backward heart failure
forward: poor ventricular contractility
backward: poor ventricular filling
two hormones that directly contribute to ventricular remodeling
ang II and aldosterone
thrombus vs embolus
thrombus is the blood clot; when it dislodges, it is an embolus
atherosclerotic lesions tend to develop at what areas in the arteries?
points of branching, where there is more turbulent blood flow
arterial occlusion will present with ___, while venous occlusion will present with ___
pain (claudication), edema (local)
arterial aneurysm pathogenesis
medial layer of artery deteriorates, causes dilation/ballooning of weakened arterial wall
aortic aneurysms most commonly occur at:
places below the renal arteries
function of pericardial fluid (2)
suspension, lubrication
why is a slower heart rate more efficient?
the slower the heart rate, the more time per beat the sinus of Valsalva is open, allowing more blood to perfuse the coronary arteries
the dicrotic notch is caused by:
the aortic valve snaps shut at the end of ventricular systole, the elastic force of the aortic walls recoiling after being pumped full of blood briefly increases pressure
assess the health/efficacy of the AV node with ___ on EKG
P-R interval
EKG changes with 1st degree AV block
AV node is delaying conduction –> long P-R interval, but still one P wave per QRS
EKG changes with 2nd degree AV block
AV node is intermittently blocking conduction –> some long P-R intervals, some “lonely” P waves that are not followed by QRS; causes atrial flutter
EKG changes with 3rd degree AV block
AV node totally obstructs conduction –> no SA node control of ventricular beats. Marching P waves at SA rhythm (60-100 bpm), but no QRSs; ventricular beats elicited by Perkinje fibers, so very slow HR
what makes the SA node the “pacemaker”?
the cells of the SA node have the fastest automatic depolarization/repolarization cycles, and all other cells depolarize according to the rate of the fastest cells
In coronary artery disease, smooth muscle cell apoptosis or macrophage apoptosis may lead to development of:
calcification
ventricular septal defects are most often found in (membranous/muscular) septum, and people with genetic ___ are at high risk of developing them
membranous; trisomies
most common cause of abdominal aortic aneurysm
arteriosclerosis (smoking is a HUGE risk factor)
Tetralogy of Fallot
VSD, pulmonary valve stenosis, misplaced aorta, right ventricular hypertrophy
rheumatic heart disease most often affects which valve?
mitral (left AV)
serous pericarditis is/is not usually a big problem
is not
Marfan’s syndrome characteristics
floppy mitral valve; long, thin chordae tendonae; mid-systolic click
