Cardiovascular Flashcards
Hollow muscular organ with 4 chambers
Heart
The average heart weighs
300-400 grams
Right ventricular side pumps blood into
Pulmonary circulation
The left ventricular side pumps blood to
The body
Atria are
Volume reservoirs
Outer surface, thin transparent structure
Epicardium
Actual contracting muscle of the heart
Myocardium
Inner most layer consists of endothelial tissue
Endocardium
Pericardial layer encased the heart to protect it from
Trauma & infection
The pericardial layer space holds how much fluid
5-30 mL
Rupture of pericardial space
Tamponade
Which wall of the heart is the thickest
Left ventricle
The mitral & tricuspid valves are attached by
Chordae tendineae
What supplies the heart with blood
Right & left coronary artery
Left anterior descending artery is aka
Widow maker
What prevents the regurgitation into ventricles at the end of each contraction
Pulmonic & aortic valves
Coronary sinus empties into
Right atrium near inferior vena cava
Local & temporary defunct of blood supply due to coronary artery obstruction or blockage
Ischemia
The electrical impulse is initiated by
The SA node
Pacemaker
Pathway of electrical impulse
SA node through muscle fibers of atria, to AV node, bundle of HIS, to right & left bundle branches then through the purkinje fibers
The cardiac cycle starts with the
SA node
The conduction pathway starts with
Depolarization
The cardiac cycle ends with
Repolarization
Firing of SA nodes, depolarization of atrial fibers
P wave
Depolarization from AV node through the ventricles
QRS complex
Replorization of ventricles
T wave
(if seen) may represent repolorazation of Purkinje fibers or hypokalemia
U wave
Myocardium contracts blood ejected from ventricles, aorta fills
Systole (S1)
Myocardium relaxes, allows for filling of ventricles
perfusion of coronary artery
Diastole (S2)
Volume blood ejected with each contraction
Stroke volume
Amount of blood pumped by left ventricle into aorta in one minute
Cardiac output
Cardiac Output= ? X ?
Stroke volume x heart rate
The more myocardial fibers are stretched the greater the force of contraction
Frank Starlings Law
Stroke volume is affected by
Preload
Contractility
Afterload
What can effect the stroke volume
Hypothermia Hypovolemia Stress Anemia Vasodilation
CO divided by BMI
Cardiac index
Percentage of end diastolic blood volume ejected during systole that can be measured
Ejection fraction
Ability of heart to increase CO in response to various situations
Cardiac reserve
Blood vessels with thick walls composed elastic tissue
Arteries
Blood vessel, little elastic tissue, more smooth muscle
Arterioles
Blood vessels, large diameter thin walled. Low pressure, high volume
Veins
Blood vessels, small vessels collect blood from capillary beds
Venules
Blood vessels, thin walls made of endothelial cells
Capillaries
Regulation of the cardiovascular system is done by
Autonomic nervous system
Chronotropic effect
Heart rate
Inotropic effect
Myocardial Contractility
Specialized nerve endings affected by changes in arterial B/P
Baroreceptors
Where are baroreceptors
Located in wall of aortic arch & carotid sinuses
Located in terminal sections of vena cava & right atrium
Stretch receptors
Respond to pressure changes (volume) which reflect circulatory volume status
Stretch receptors
Located in aortic arch & carotid body
Chemoreceptors
Initiate changes when decreased arterial O2 pressure & plasma pH, increased arterial CO2 pressure. Increase cardiac activity
Chemoreceptors
Measurement of pressure exerted by blood against walls of arterial system
Blood pressure
Difference between systolic & diastolic
Pulse pressure
Orthostatic B/P
Take laying, sitting, standing
Physical exam
Inspection
Palpation
Percussion
auscultation
Sustained heavy breaths
Heaves
Yellow plaque cholesterol filled nodules on eyelids & ears
Xanthomas
Diagonal earlobe crease
McCarthy’s sign
Reflects volume & pressure circumstances on right side of heart, visible while laying down
JVD
PMI
Apical pulse
5th ICS MCL
Pulsations in epi gastric region may reflect
AAA
abdominal aortic aneurysm
What are you looking for when you palate pulses
Rate
Rhythm
Quality
Insoluble yellow brown protein gives skin reddish brown pigmentation
Hemosiderin
Discrepancy between apical & radial pulse
Pulse deficit
S1is the closure of
Tricuspid & mitral valve
Beginning of systole
Lub
S2 is closure of
Aortic & pulmonic valves
Beginning of diastole
Dub
Heard early in diastole results from vibrations produced during rapid early ventricular filling into dilated ventricle
S3
Ventricle gallop
Lub——-dub–Dee
Heard in pt’s with heart failure
Vibrations produced in late diastole occurs during atrial contraction
Forces blood into a ventricle that resists filling
S4
Atrial gallop
Dee–Lub——-dub
Acute MI, angina, ischemia
Audible vibration from turbulent blood flow in heart & great vessels
Murmur
Cause of murmur
Increased velocity of blood through normal & abnormal valves
Turbulent glow in dilated chamber
Grade III/VI
Easily audible
Moderately loud
Same intensity as S1 & S2
Sound that initiates ventricular systole
Tricuspid & mitral valves close
S1
Decrease of volume is an _____ in pulse deficit
Increase
Sound of ventricular diastole
Aortic & pulmonic valves close
S2
Inflammation of pericardial sac
Short, high pitch squeaky sound
Pericardial friction rub
Hypo kinetic
Weak pulse
Hyperkinetic
Bounding pulse
Weak & strong beats alternate
Pulses alterans
Greater than 10 mmHg drop in SBP during normal inspiration
Pulses paradoxus
chest xray can show
cardiac contours, heart size, configuration and anatomic changes
what is the most important diagnostic test to determine extent and treatment for MI
serial EKG
p wave
impulse though atria
QRS wave
impulse through ventricles
T wave
electrical recovery or repolarization
holter monitor
keeps diary of activities and sympotms
what is different in elderly with a stress test (tredmill test)
HR does not increase right away
If your pt has a c/o chest pain while doing the stress test what would you do
stop the test immediatley
uses ultrasound waves to record movement of structures of heart
Echocardiogram
what test shows the best view of the heart
Transesophogeal echocardiogram (TEE)
probe introuduced into esophags @ level of heart-posterior view
TEE
IV injection radioavtive isotopes
nuclear cardioplogy
what is used to rule out blood clots incase of a-fib
TEE
analyze cardiac enzymes and proteins to diagose acute MI or other cardiac disorders
cardiac markers
name the cardiac markers
creatine kinase (CK) myoglobin cardiac specific troponins homocystine c-reactive protein (CRP) B-type natriuretic peptide (BNP)
creatnine kinase
levels rise 4-12 hours, peak 18-24, may return to normal 2-3 days after MI, drawn @ timed intervals
myoglobin
levels tise within 30-60 minutes, peak 6-7 hours, return to baseline 24 hours
what is the most specific to finding myocardial damage
Troponin I
troponin I
levels rise 3-12 huors, peak 24-48, returnes to normal in 5-14 days
homocystine
shows irritation to blood vessels
produced by liver, shows risk for CAD
C-reative protein (CRP)
sevreted in response to increased ventricle volume & pressure occurs in heart failure
BNP- b-type natriuretic peptide
triglycerides
40-190
women can be as low as 10
marker for heart failure, grade of heart failure
BNP
PTT-partial thromboplastin time
normal clotting 21-35 seconds, monitor response of heparin
protrombin time
normal range 10-14 seconds, monitored oral anti-coagulation therapy
*coumadin
what medications can affect prothrombin time
vitamin K, antibiotics
INR international normalized ratio
best means standardizing PT to monitor oral anticoagulant therapy
theraputic level of digoxin
0.8-2 ng/ml
passing catheter into artery or vein in arm or leg into the heart, measures blood pressure & flow in chambers of heart & O2 saturation
cardiac catheterization
what may a pt experience during a caridac cath
hot flushing, nausea
what do you monitor post cath
bleeding, site, pulses below site
injection or radiopaque contrast mediumdirectly into coronary arteries by same procedure as cardiac cath
coronary angiography
invasive study to record intracardiac electrical activity using catherters with multiple electrodes inserted into femoral vein into right side heart
electrophysiology studies
atheromas
fatty deposits
a type of blood vessel disorder that is included in the general category of atherosclerosis
CAD
what is the leading cause of all cardiovascular disease deaths & deaths in general
heart attacks
focal deposits of cholestrol and lipids primarily within the intimal wall
atherosclerosis
what are the two main causes of atherosclerosis
HTN
hyperlipidemia
development of atherosclerosis lesions involves
the presence and effects of fat substances in arteries
stages of atherosclerosis
fatty streak
raised fibrous plaque
complicated lesion
stenosis of what percentage is concidered dangerous
75%
collateral circulation is attributed to two factors
inherited predisposition and the presence of chronic ischemia
what is collateral circulation
when arteries in heart branch around the blocked area of the artery to aabove the affected area of the artery
name nonmodifiable risk factors for CAD
age
race
gender
genetic predisposition
name modifiable risk factors for CAD
elevated serum lipids
HTN
smoking
physical inactivity
bind with protien to form lipoprotein to be able to transport in blood throughout the body
lipids
smoking causes
vasoconstriction
what can pts work ok that hey can change for health promotion
stress factors
drugs that restrict lipoprotein production are
Statins
Lipitor
drugs that increase lipoprotein removal
Bile acid sequestrants
Questran
drugs that decrease cholesterol absorption
Ezetimibe (zetia)
niacin
increse HDL level
fibric acid derivatives
increases HDL level, can be used to statins
results when the lack of oxygen supply is temporary and reversible
chronic stable angina
develops when the oxygen supply is prolinged and not immediately reversible
acute coronary syndrome
what are the 3 things that make up acute coronary syndrome
unstable angina
non ST segment elevation myocardioal infarction (NSTEMI)
ST segment elevation (STEMI)
for ischemia to occur the artery is usually ____% or more stenosed
75%
most common clinical manifestation of Chronic stable angina is
Chest pain or discomfort
chest pain occuring intermittently over a long period of time with the same pattern of onset, duration and intensity of symptoms
chronic stable angina
is stable angina predictable
yes
silent ischemia
occurs without symptoms
occurs only at night
nocturnal angina
chest pain while lying down, relieved by standing or sitting
angina decubitus
occurs at rest usually in response to spasm of major coronary artery
prinzmetals angina
what is the drug therapy goal of chronic stable angina
decrease O2 demand, increase O2 supply
what is the 1st line of treatment for chronic stable angina
asa
side effects of nitrates
HA
hypotension
what dialates coronary arteries to increse oxygen supply
nitrates
-olol
beta blockers
decrease HR
decrease force of contraction
decrease rate of AV conduction
beta blockers
-pines
calcium channel blockers
calcium channel blockers
decreases conductivity of the heart
decreases demand for O2
decreases contractility
what should you do prior to giving a beta blocker
HR
B/P
is cardiac catheterization a surgery or diagnostic study
diagnostic study
percutaneous coronary intervention (PCI)
surgical intervention alternitive
ballon angioplasty or stent or both
if a stent placement is done what must be taken after surgery
anticoagulants
the plaque is shaved off using a type of rotational blade
atherectomy
used to precisely dissolve the blockage
laser angioplasty
develops when ischemia is prolonged and not immediatley reversible
acute coronary syndrome
manifestations of unstable angina
new onset
occurs @ rest
has worsening pattern
result of sustained ischemia, greater than 20 mintues causing irreversible myocardial cell death
MI
transmural MI
entire thickness of myocardium
subendocardial MI
damage has not penetrated through entire thickness
most MIs involve what area of the heart
left ventricle
infarction in the anterior of the heart is occlusion of
LAD
infarction in the inferior of the heart is
right coronary artery
infarction in the posterior of the heart is
circumflex
infarction of the lateral of the heart is
circumflex
the hallmark of an MI
severe immobilizing pain
total occlusion anaerobic metabolism and lactic acid accumulation
MI
symptoms of MI
increase of HR then a decease crackles JVD peripheral edema S3 or S4
angina
relieved by position or nitro
MI
not relieved by nitro or position
in an attempt to compensate for infarcted muscle, normal myocardium will
hypertrophy and dialte
S3 indicates
heart failure
what is the most common complication of MI
dysrhymias
a complication that occurs when the pumping power of the heart has diminished
CHF
occurs when inadequate oxygen and nutrients are supplied to the tissues because of severe LV failure
cardiogenic shock
causes mitral valve reguritation
papillary muscle dysfunction
results when infarcted myocardial wall becomes thinned and bulges out during contraction
ventricular aneurysm
inflammation of visceral and or parietal pericardium
acute pericarditis
what is the best way to diagnos
echocardiogram
sudden severe chest pain
pulmonary embolism
what is the window for MI
90 minute window from ER to cath lab
MONA
morphine
oxygen
nitrates
asa
CABG coronary artery bypass graft
uses arteries or veins for grafts
6 areas of optimal function for cardiac rehab
physiologic psychologic mental spiritual economic vocational
unexpected death from cardiac causes
sudden cardiac death
CAD accounts for ____% of sudden cardiac death
80%
most sudden cardiac death is caused by
ventricular dysrhythimas
what kind of presentation of coronary artery disease are found in women
atypical
what is found to be the single most powerful predictor of CAD in women
DM
what is the most powerful contributer for women under 50 for CAD
smoking
precardia
area over heart
increase cardiac output
increase cardiac rate
increase cardiac contractility
ace inhinitors
anfiotension converting enzyme
any structural or functional cardiac disorder that impairs the ability of the ventricle to fill or eject blood
heart failure
is heart failure a disease
no its a syndrome
inability to contract/fill effectivly bc of a stiffened ventricle
ventricular dysfunction
decrese in the left ventricular ejection fraction
systolic failure
inability to relaz between beats and fill during diastole
diastolic failure
diastolic failure is found more in
the elderly
when HR increases and CO does what and why
decreases bc of shortened fill time in ventricles
what do compensatory mechanisms do
are activated to maintain adequate CO
what are the compensatory mechanisms in heart failure
sympathetic nervous system kidneys release renin proinflammaroty cytokines endothelin is stimulated by ADH, angio II ventricular dilation increase muscle mass natriuetic peptides
most common type of heart failure
left sided HF
signs of L sided heart failure
increse HR crackles S3 &S4 changes in mental status restlessness pulsus alterans PND
pumping failure
left sided heart failure
backup of blood into the right artrium and venous systemic circulation
right sided HF
what symptoms will you find with acute decompensated HF
blood tinged sputum
bc of pulmonary edema
what is the earliest symptom of CHF
fatigue
sidden weight gain of greater than 3 pounds may indicate
an exacerbation of HF
what in CHF will you get restlessness, confusion and decreased memory
due to the decrease of O2 to the brain
thrombus
clot
embolus
traveling clot
what labs would you check for kidney
BUN
creatin
what labs would you check for liver
ALT,
AST
what labs would you check for heart
BNP
troponin
CK-MB
what labs would you check for hypoxia
ABG’s
% of blood ejected during systole
ejection fraction
BEADS
beat blockers ejection fraction ace inhibitors, ARB's discharge instructions smoking cession
what is the #1 choice for elderly with heart failure
dirretics
bc decreases preload and pulmonary congestion
what would you do to decrease venous return
high fowlers
IV nitro
primary intervention for HF
maintain oxygenation
for digoxin what does the HR have to be or else you have to hold the medication
60 bpm
first line of therapy for HF
ace inhibator
Lovastatin
mevacor
statin
antihyperlipidemic
decreases LDL, increases HDL
what is the treatment for prinzmetals angina
calcium channel blocker
metoprolol
lopressor
beta blocker
increases blood supply by decreasing O2 consupmtion, B/P, HR,
nesiritide
natrecor
b-type natiuretic peptide
helps with diuresis, vasodialtor
morphine
opiate
heparin
prevents blood clots, doesnt take care of ones already there
vasotec
enalapril
ACE inhibitor
renin/angiotension II suppressor
capoten
captopril
ACE inhibitor
renin/angiotension II suppressor
nadolol
corgard
beta blocker
antihypertensive
Stroke volume
Preload
Contractility
After load
Statin
Inhibit the action of an enzyme that controls the rate at which the body produces cholesterol
Lower LDL
raise HDL
Medications ending in _____ are statins
- Statin
- ol
- or
Creatine kinase
Shows acute MI if elevated
Myoglobin
Functions as an oxygen bonding muscle protein
It’s released when ischemia, trauma or inflammation of muscle occurs
Troponin I
Stays elevated for days
Homocysteine
Amino acid
High levels irritate blood vessels
C-reactive protein
Produced by liver
Inflammation in body
B-type natriuretic peptide
BNP
Hormone secreted by ventricular tissues in heart
Secreted in response to increased ventricular volume & pressure that occur when pt is in heart failure
PTT helps monitor pt’s response to
Heparin
PT helps monitor pt’s response to
Coumadin
PTT time should be
21-35
PT time should be
10-14
An INR level for a pt on Coumadin should be?
If the pt has a mechanical prosthetic heart valve the INR should be?
- 0-3.0
2. 5-3.5
Diuretics
Reduce preload by decreasing total blood volume
ACE inhibitors
Dilate blood vessels & decrease vascular resistance thereby reducing work load
Vasodilators are used if
Pt’s can’t tolerate ACE inhibitors
They increase cardiac output by decreasing after load
Stroke volume is affected by
Preload
Contractility
After load
Lack of contractile motion (ventricles)
Akinesis
Reduced inward wall motion
Hypokinesis
Paradoxical wall motion (systolic bulging)
Dyskinesis
Local & temporary deficiency of blood supply due to obstruction
Ischemia
Tissue death
Infarction
Regulation of the cardiovascular system is done by
Autonomic nervous system
Autonomic nervous system regulates
HR
chronotropic effect
Sympathetic nervous system
Increases HR
Contractility
Vasoconstricton
What is the first line of defense for chronic stable angina
Asa
What is the best way to diagnosis acute pericarditis
Echo
Amount of blood the heart pumps in one minute
Cardiac output
