1. Snapping sound first heard at the systolic pressure. Clear tapping, repetitive sounds for at least two consecutive beats is considered the systolic pressure.

heart Flashcards by Stephanie Browning

What are the signs and symptoms of heart disease commonly elicited during hx

Angina, Orthopnea, Palpitations, Edema, Fatigue & Weakness,

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Angina

Chest pain d/t hypoxia

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Orthopnea

Difficulty breathing in recumbant position

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Palpitations

being aware of heart beating; have to change rate, regularity, force of contraction in some way to make you be aware of it

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Edema

Accumulation of fluid in interstitial space

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Peripheral Edema

may be indication of cardiovascular disease;congestive Heart Failure. Seen in damage to R side of heart

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Pulmonary Edema

Seen with damage to L side of heart

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Fatigue and Weakness

decreased muscle perfusion d/t change in cardiac output (decreased CO2 decrease in perfusion)

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stroke Volume

The amount of blood pumped by one ventrivle duringeach heart beat. SV=EDV-ESV

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Good Stroke volume for adult

approx. 70mL

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Bad Stroke Volume for Adult

approx. 40 mL

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Hypertension vs. Hypotension

140/90 HTN; 120/80 Norm; 90/60 HoTN

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Pulse Pressure

difference btw systolic and diastolic. 120/80 PP=40

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Korotkoff 1st sound

Snapping sound first heard at the systolic pressure. Clear tapping, repetitive sounds for at least two consecutive beats is considered the systolic pressure.

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Korotkoff 2nd sound

sounds are the murmurs heard for most of the area between the systolic and diastolic pressures

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Korotkoff 3rd sound

A loud, crisp tapping sound.

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Korotkoff 4th sound

at pressures within 10 mmHg above the diastolic blood pressure, were described as “thumping” and “muting”.

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Korotkoff 5th sound

sound is silence as the cuff pressure drops below the diastolic blood pressure. The disappearance of sound is considered diastolic blood pressure – two mm Hg above the last sound heard.

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Define Pulse Pressure

difference between systolic and diastolic pressure

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Calculate Pulse Pressure for 120/80

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Kussmaul’s sign

increased venous pressure with inspiration opposite of what it should be (decrease) = (big jugular veins); deep rapid respiration commonly seen in conditions causing acidosis

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s1 Lub sound correlates with

onset of venticular systole

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S1 sound what is closing

AV Valves

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gallop rhythm

3rd heart sound due to rapid ventricle filling; blood rushing into ventricle

atrial gallop

4th heart sound heard when there is increased ventricle resistance to atrial filling

friction rub

extra cardiac sound, also; rubbing together of inflamed viscera extra cardiac sound, also; rubbing together of inflamed viscera extra cardiac sound, also; rubbing together of inflamed viscera extra cardiac sound, also; rubbing together of inflamed viscera Fibro pirulent exudate

EKG

noninvasive way to gain info about electrical activity of heart and

P Wave

atrial depolarization

Wide Pwave

hypertrophy of the muscle so depolarization is taking longer (contracting)

Inverted P wave

impulse is not starting at the SA node, look for a slower HR as well

P-R Interval

Transmission of impulse thru atria, naturally slowed at the AV node; determines Heart Block; NORMAL 0.1-0.2

1st degree heart block

longer than normal p-r interval (0.1-0.2) | 0.4 seconds

2nd &3rd degree heart block

longer time to get through to SA node. 3rd degree completly blocked impulse not getting to SA node

Longer/wider PR interval

Heart block is occurring, block of conduction not physical block. Length corresponds to what degree of heart block

QRS complex

Ventricle depolarization

QRS wider

hypertrophy of the muscle so depolarization takes longer

QRS Double

ventricles not synchronized; bundle branch block in one ventricle

ST Segment

Time btw depolarization and repolarizing; isoelectric

Depressed ST segment

myocardial ischemia

elevated st segment

Myocardial infarction

T wave

ventricle repolarization

Twave inverted

ischemia; pt needs oxygen

Twave flattened

Hypervolemia less K+

spiked T wave

ventricle is repolarizing more quickly; correlated with INCREASED K+ HYPERKALEMIA

4 Determinants of Myocardial Oxygen demand

Rate, Force, Muscle Mass, Ventricle Wall Tension

Rate

greater HR, greater demand O2

Force

more forcefully contracted, the more O2 it needs

Muscle Mass

more muscle; more O2 it needs

Ventricle Wall Tension

more tension muscle exerts the more O2 it requires

Cardiac Ischemia

demand of oxygen is greater than supply

MI affects which ventricle

Left

Coronary atherosclerosis most likely to develop where?

hardening of the arteries ususally not in straightaway happens where vessles curve or branch

Explain the development of Atherosceirotic lesions

caused by lipid and fibrous calcium deposited in the vessels; slowly narrows the vessels; vessel loses ability to dilate in order to increase O2 supply in Left Ventricle for this tissue

4 Risk factors for Coronary artherosclerosis

Age, Race (African American), Family(runs in family may be d/t environment), Sex (F: immune before menopause- after menopause >risk than males. Younger female w/ CAD more likely to die

#1 symptom for pre-memopause women for CAD

Nausea

Other risk factors for CAD

hyperlipidemia(cholesterol & triglycerides

VLDL to CAD

very low density lipoproteins – little bit of protein and whole lot of triglyceride); triglycerides unclear how they give increase for coronary artery disease

LDL to CAD

Lots of Cholesterol & little protien High LDL=High Risk for CAD

HDL to CAD

Litlle Cholesterol and lots of protien; High HDL=No CAD or little risk