Disorders of the CV & Peripheral Vasc Systems Flashcards
heart rate and force of contraction are controlled by
cardiac control center in medulla
amount of volume of blood ejected by a ventricle in one minute
cardiac output
volume pumped from one ventricle in one contraction
stroke volume
cardiac output is calculated with
heart rate and stroke volume
pressure of blood against the systemic arterial walls
blood pressure
Inner layer of the heart
endocardium
separated the left and right sides of the heart
septum
connections to prevent muscle cells from separating during contraction
Desmosomes
sympathetic innervation does what to the heart
increases heart rate
parasympathetic stimulation by vagus nerve
decreases heart rate
branch off the aorta immediately above the aortic valve
right and left coronary arteries
left coronary artery divides into
left anterior descending/interventricular artery.
left circumflex artery.
coronary artery that circles the exterior of the heart in the left atrioventricular sulcus
left circumflex artery
coronary artery that follows the anterior interventricular sulcus downward over the surface of the heart
left anterior descending
coronary artery that follows the right atrioventricular sulcus on the posterior surface of the heart
right coronary artery
anastosomes
direct connections between small branches of the left and right coronary arteries near the apex
collateral circulation
alternative source of blood and nutrients. vessels expand or extend to meet metabolic needs of the cells.
brings blood o the right side of the heart and inferior portion of the left ventricle, posterior interventricular septum
right coronary artery
brings blood to the anterior wall of the ventricles, anterior septum, bundle branches
left anterior descending artery
brings blood to left atrium, lateral and posterior walls of the left ventricle
circumflex artery
Blood supply to the SA node
mainly right coronary artery, left circumflex in some
AV node blood supply
right coronary artery
blockage of the right coronary artery results in disturbances to the
AV node - arrhythmias
blockage to the left coronary will impair
pumping capability of the left ventricle - CHF
illustrate the conduction activity of the heart
ECG
auscultation of heart murmurs reveals
valvular abnormalities
reflected sound waves to record the image of the heart and valve movement
echocardiography
assessing general cardiovascular function and checking for exercise-induced problems
exercise stress test
show the shape and size of the heart, pulmonary congestion associated with heart failure
chest x-ray
assesses the size of an infarct in the heart, the extent of the myocardial perfusion, and function of ventricles
nuclear imaging
illustrates various levels of a tissue mass
tomographic studies
can identify dead or damaged areas of myocardial tissues and may be used to assess the extent of myocardial damage after MI
nuclear imaging
assesses cardiac ischemia at test
SPECT - single proton emission computed tomography
visualizes the inside of the heart, measures pressures, assesses valve and heart function
cardiac catheterization
way of visualizing the blood flow in the coronary arteries
coronary angiography
visualizing blood in the peripheral vessels
doppler studies
assess serum triglyceride and cholesterol levels and levels of sodium, potassium, calcium, and other electrolytes
blood tests
current oxygen level and acid-base balance in patients with shock or myocardial infarction
arterial blood gas determination
drugs that resist peripheral resistance systemically, cause decrease in blood pressure, dizziness/syncope, flushed face
vasodilators
drugs used to treat hypertension and dysrhythmias, reduce number of angina events
beta blockers
beta blockers mechanism of action
block the beta1-adrenergic receptors in the heart and prevent the SNS from increasing heart activity
drugs that block the movement of calcium ions into the cardiac and smooth muscle fiber
calcium channel blockers
drugs that decrease cardiac contractility, antiarrhythmic for atrial activity, antihypertensive, vasodilator
calcium channel blockers
CCB that is effective in selectivity for the myocardium and reduce both conduction and contractility
diltiazem
CCB that slows the heart rate by depressing the action of the SA and AV nodes
verapamil
CCB effective as peripheral vasodilators
nifedipine
CCB effective in lowering blood pressure
amlodipine
cardiac glycoside, as a treatment for heart failure and as an antiarrhythmic drug for atrial arrhythmias, increases the contractility
digoxin
drug that must be monitored for signs of toxicity and why
digoxin - effective dose is close to toxic dose
examples of antihypertensive medications
adrenergic or sympathetic-blocking agents, calcium blockers, diuretics, ACE inhibitors, and angiotensin II receptor blocking agents
may act on the SNS centrally (brain), may block peripheral alpha1-adrenergic receptors, may act as vasodilators
adrenergic-clocking agents
preferred in the treatment of patients with hypertension and CHF
ACE inhibitors
act by blocking the conversion of angiotensin I to angiotensin II by renin from the kidney
Angiotensin-converting enzyme inhibitors (ACE inhibitors)
how do ACE inhibitors work?
reduce peripheral resistance (vasoconstriction) and aldosterone secretion (decreasing sodium and water retention) - decrease in preload and after load.
remove excess sodium and water from the body through the kidneys by blocking the reabsorption of sodium or water
diuretics
used to reduce the risk of blood clot formation in coronary or systemic arteries or damages or prosthetic heart valves
anticoagulants
prescribed when diet and exercise are ineffective in reducing blood levels
statins
how do statins work
reduce low-density lipoprotein (LDL) and cholesterol content of the blood by blocking synthesis in the liver
relaxation phase of cardiac activity
diastole
cardiac contraction
systole
atria fill, all valves are closed
diastole
increased atrial pressure opens AV valves, ventricles fill
diastole
atria contract and empty, ventricles are full
systole begins
ventricles begin contraction, pressure closes AV valves, atria relax
systole
ventricles contract, increased pressure in ventricles, aortic and pulmonary valves open, blood ejected into aorta and pulmonary artery
systole
ventricles empty, ventricles relax, aortic and pulmonary valves close
diastole
lub corresponds with
closure of AV valves at the beginning of ventricular systole
dub corresponds with
semilunar valves close with ventricular diastole
heart rate measured at the heart itself
apical pulse
difference in rate between the apical pulse and the radial pulse
pulse deficit
volume of blood ejected by a ventricle in one minute
cardiac output
volume pumped from one ventricle in one contraction
stroke volume
Cardiac Output =
HR x SV (stroke volume)
average cardiac output
4900-5000 mL/min (70bpmx70mL)
Heart rate is influenced by
sympathetic nervous system, epinephrine
stroke volume is influenced by
venous return, blood volume, sympathetic nervous system, peripheral resistance
the ability of the heart to increase output in response to increased demand
cardiac reserve
mechanical state of the heart at the end of diastole with the ventricles at their maximum volume
preload
force required to eject blood from the ventricles
afterload
determined by the peripheral resistance to the opening of the semilunar valves
afterload
pressure exerted by the blood when ejected from the left ventricle
systolic pressure
pressure sustained when the ventricles are relaxed
diastolic pressure
difference between the systolic and diastolic pressures
pulse pressure
force opposing blood flow, the amount of friction with the vessel walls encountered by the blood
peripheral resistance
changes in blood pressure are detected by the
baroreceptors
signals into the baroreceptors are relayed to
vasomotor control center in medulla
what does the vasomotor control center in the medulla do?
adjusts the distribution of blood to maintain normal blood pressure
Two ways in which blood pressure is elevated by increased SNS stimulation
- SNS and eps act at the beta1-adrenergic receptors in the heart to increase rate and force contraction.
- SNS, epi, and norepi increase vasoconstriction by stimulation the alpha1-receptors in the arterioles of the skin and viscera. Reducing capacity of the system and increases venous return.
increases water reabsorption through the kidney, thus increasing blood volume
Antidiuretic hormone (ADH)/Vasopressin
increases blood volume by increasing reabsorption of sodium ions and water
aldosterone
cause for angina
deficit of oxygen to the hear
deficiency of blood
ischemia
death of myocardial tissue due to ischemia
myocardial infarction
right heart failure
right ventricle cannot maintain its output, less blood proceeds to left side of heart and systemic circulation - forward effect
left heart failure
normal blood volume of blood returning from lungs cannot enter left side of heart - causes congestion in pulmonary circulation, increased capillary pressure, possible pulmonary edema
structural defects in the heart that develop during the first 8 weeks of embryonic life
cardiac anomalies
acute systemic inflammatory condition resulting from abnormal immune reaction occurring weeks after an untreated infection
rheumatic fever
what causes rheumatic fever
certain strains of group A beta-hemolytic streptococcus
general term for all types of arterial changes
arteriosclerosis
arterial changes characterized by the presence of atheroma
atherosclerosis
define atheromas
plaques consisting of lipids, cells, fibrin, and cell debris, often with thrombus attached
lipid subgroups assessed in serum lipids
total cholesterol, triglycerides, low-density lipoproteins, high-density lipoproteins
bad lipoprotein that promotes atheroma formation
low-density lipoprotein
where does LDL transport cholesterol
from liver to cells
where does HDL transport cholesterol
from peripheral cells to liver for catabolism and excretion
a bulge in the material wall
aneurysm
non modifiable atherosclerosis factors
age, gender, genetic of familial factors
predisposing or modifiable factors for atherosclerosis
obesity, smoking, sedentary lifestyle, DM, HTN, combination of these.
what causes angina
deficit of oxygen to the heart muscle
prolonged pain at rest and of recent onset
unstable angina
types of chest pain
classic/exertional angina, variant angina, unstable angina
vasospasm occurs at rest
variant angina
myocardial hypertrophy
heart has outgrown its blood supply
tachycardia associated with hypothyroidism can increase
Oxygen demand
pain described with angina
tightness or pressure that radiates to the neck and left arm
7 emergency treatments for angina
- rest, stop activity.
- sit upright.
- nitro SL.
- check pulse and resp.
- admin o2 if needed.
- hx of angina, nonresolving angina 3x NGSL > 5 mins - treat as MI.
- no pmhx angina, nonresolving angina NSGL > 2 mins - treat as MI.
three ways infarct may form
- thrombus obstructs an artery.
2.