Cardiovascular Flashcards by B -

Hollow muscular organ with 4 chambers

Heart

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The average heart weighs

300-400 grams

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Right ventricular side pumps blood into

Pulmonary circulation

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The left ventricular side pumps blood to

The body

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Atria are

Volume reservoirs

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Outer surface, thin transparent structure

Epicardium

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Actual contracting muscle of the heart

Myocardium

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Inner most layer consists of endothelial tissue

Endocardium

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Pericardial layer encased the heart to protect it from

Trauma & infection

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The pericardial layer space holds how much fluid

5-30 mL

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Rupture of pericardial space

Tamponade

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Which wall of the heart is the thickest

Left ventricle

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The mitral & tricuspid valves are attached by

Chordae tendineae

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What supplies the heart with blood

Right & left coronary artery

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Left anterior descending artery is aka

Widow maker

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What prevents the regurgitation into ventricles at the end of each contraction

Pulmonic & aortic valves

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Coronary sinus empties into

Right atrium near inferior vena cava

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Local & temporary defunct of blood supply due to coronary artery obstruction or blockage

Ischemia

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The electrical impulse is initiated by

The SA node

Pacemaker

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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

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The cardiac cycle starts with the

SA node

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The conduction pathway starts with

Depolarization

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The cardiac cycle ends with

Repolarization

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Firing of SA nodes, depolarization of atrial fibers

P wave

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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

Decrease of volume is an _____ in pulse deficit

Increase

Sound of ventricular diastole | Aortic & pulmonic valves close

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

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

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

symptoms of MI

``` increase of HR then a decease crackles JVD peripheral edema S3 or S4 ```

angina

relieved by position or nitro

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

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?

2. 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

Cardiovascular Flashcards

(264 cards)