foundations: exam 3

systole

heart empties

diastole

fills

veins

-get rid of waste

-edema, lower pulse, PLUMBING

conduction system

-transmits electrical impulses

-generates impulses needed to initiate the electrical chain of events for a normal heartbeat

-SA NODE= PACEMAKER

what kicks in when the SA node fails?

1. AV node

2. bundle of HIS

electrocardiogram (ECG)

reflects electrical activity of the conduction system

normal sinus rhythm

-originates at the SA node, follows normal sequence through conduction system

-P wave

-PR interval

-QRS complex

-T wave

-QT interval

p wave

atrial depolarization/contraction

PR interval

impulse from SA→AV→B of HIS→ purkinje fibers (normal contrxn)

QRS complex

ventricular depolarization/condxn

T wave

ventricular repolarization/relaxation

QT interval

ventricles contracting, then relaxing

disturbances in conduction

-electrical impulses that do not originate from the SA node cause conduction disturbances

-dysrhythmias

why do dysrhythmias occur?

ischemia, caffeine, anxiety, drug toxicity, alcohol, electrolyte imbalances

examples of dysrhythmias

-a fib

-paroxysmal supraventricular tachycardia

-ventricular tachycardia and ventricular fibrillation

atrial fibrillation

most common dysrhythmia; atria are QUIVERING, ventricles beating VERY FAST (firing from everywhere)

paroxysmal superventricular tachycardia

sudden, rapid tachycardia (180-200s), caffeine, alcohol, smoking, breathing tx (B2b), BEAR DOWN, adenosine

v tach and v fib

LIFE-THREATENING, will die of low cardiac output IF UNTREATED

altered cardiac output

INSUFFICIENT CARDIAC OUTPUT

-left sided heart failure (decrease fxn of L vent)

-right sided heart failure (decrease fxn of R vent)

left sided heart failure

-left=lungs

-blood from lungs= breathing symptoms (SOB, hypoxia, confusion, pulm. congestion, cough, noct. dyspnea)

right sided heart failure

-right=rest of body

-peripheral edema, hepato/splenomegaly

impaired valvular function

cause hardening (stenosis) or impaired closure of valves (can cause murmur)

myocardial ischemia

-angina

-myocardial infarction/acute coronary syndrome

angina

-treated w/ vasodilators

-chest pain; only lasts 3-5 minutes from activity (goes away w/ rest) *imbalance in O2 supply & demand

myocardial infarction/ACS

-pain can radiate

-doesn’t go away

-HEART ATTACKS, sudden decrease in blood flow/perfusion to the heart

-typically from a blockage

assessment (cardio)

-in-depth history of a client’s normal and present cardiopulmonary function

-past impairments in circulatory/respiratory functioning (hereditary)

-methods that a client uses to optimize oxygenation

-review of drug (meds and illicit), food, and other allergies

-physical examination

-lab and diagnostic tests

-smoking history

-CONTRAINDICATION: VIAGARA (can be used for pulmonary hypotension)

cardio inspection

skin and mucus membranes, LOC, breathing pattern, chest wall movement (equal), general appearance (dipahoresis, color, facial exp), and circulation

cardio palpation

-chest, feet, legs, and pulses

-edema (swelling in extremities)

cardio auscultation

normal/abnormal heart sounds

for cardio, gray indicates what?

low perfusion

for cardio, blue indicates what?

low oxygen

cardio inspection and palpation

-client must be relaxed and comfortable

-PMI/Apical pulse (point of MAXIMAL impulse-mid clav line, 4-5 intercostal space)

-pulsation in abdomen: DO NOT PALPATE→ POTENTIAL AORTIC ANEURYSM (could rupture/pop)

cardio assessment- HEART

-compare assessment of heart fxns w vascular findings

-alterations in either system affect one another oftentimes

-pt of maximal impulse (apical)

-cardiac cycle

-locate anatomical landmarks

5 areas for listening to the heart

-aortic

-pulmonic

-erb’s point

-tricuspid

-mitral

aortic point

right second intercostal space

pulmonic point

left second intercostal space

erb’s point

S1, S2; left 3rd intercostal space

tricuspid point

lower left sternal border, 4th intercostal space

mitral point

left 5th intercostal space, medial to midclavicular line

normal heart sounds (regular vs irregular)

-dysrhythmia

-if HR is irregular, listen to apical pulse and radial pulse

-S1 and S2 sounds

extra heart sounds

-S3 and S4 sounds

-murmurs

-intensity

-pitch

-quality

murmurs

sustained swishing or blowing sound

cardio intensity

(grade)

-can palpate

cardio pitch

low, medium, high (loud→quiet OR quiet→ loud)

cardio quality

scored 1-6 (1: quiet, 6: intense)

normal heart sounds

-S1: mitral and tricuspid valve closing

-S2: pulmonic and aortic valve closing

abnormal heart sounds

-S3: heard after S2, heart trying to fill already distended ventricle (ventricular gallop: KENTUCKY)

-S4: heard before S1, atria trying to enhance ventricular filling (atrial gallop: TENNESSEE)

blood pressure

-readings tend to be higher in the right arm

-always record the highest reading

carotid arteries

-reflect heart fxn better than peripheral arteries

-assess for visible pulsation

-palpate one artery at a time

-commonly auscultated

bruit

-narrowed blood vessel creates turbulence, causing blowing/swishing sound

thrill

palpable, feels like purring cat

jugular veins

-most accessible

-right internal jugular vein follows more direct path to right atrium

-note distention

-assess pressure

assessment of vascular system

-assess each peripheral artery for elasticity of the vessel wall, strength, and equality

-elasticity (normally elastic, not hard)

-equality (at the same time→ not carotids!

strength of peripheral arteries

0: absent, not palpable

1: pulse diminished, barely palpable

2: expected/normal

3: full pulse, increased

4: bounding pulse

upper extremities (peripheral arteries)

-brachial artery channels blood to radial and ulnar arteries of forearm and hand

-if occluded: hand loses blood flow: pale, numb, cold, lower pulses, edema

radial pulse assessment

thumb side of wrist

ulnar pulse assessment

little finger side of wrist

brachial pulse assessment

inside of elbow (kids/babies less than 5 y/o)

assessment of lower extremeties

-femoral artery

-primary artery in the leg

-eclusion (no fxn/bloodflow to leg)

assessment of peripheral arteries

-femoral pulse

-popliteal pulse

-dorsalis pedis pulse

-posterior tibial pulse

(can’t feel pedal pulse? move up!)

if peripheral arteries aren’t palpable:

-ultrasound stethoscopes (doppler)

-use to amplify the sound of a pulse

-used to find a difficult pulse

-place gel on the pulse site or directly on the transducer

tissue perfusion

-inspect the skin color and characteristic of skin

-palpate pulses, temp, and capillary refill

-clubbing (wide, rounded fingernails)

-look for absence of hair, presence of ulcers

color assessment

venous: normal

arterial: pale

temperature assessment

venous: normal

arterial: cool

pulse assessment

venous: normal

arterial: decreased

edema assessment

venous: marked edema (d'/t venous circulation)

arterial: minimal

skin changes assessment

venous: brown (deficiency)

arterial: thin, shiny, decreased hair, thick nails

varicosities

-superficial, dilated veins

-blood pooling in veins

-should be typically on the front/medial shin (not on calf)

phlebitis

-inflammation of vein (s), typically after trauma (ex→ IV blood draw)

*should be unilateral

edema assessment

0+ no pitting edema

1+ mild pitting edema, 2mm depression that disappears rapidly

2+ moderate pitting edema, 4mm depression that disappears in 10-15 seconds

3+ moderately severe pitting edema, 6mm depression that may last more than 1 minute

4+ severe pitting edema, 8mm depression that can last more than 2 minutes

blood specimens

-troponin

-CKMB

-electrolytes (Na, K, Ca, Cl)

-myoglobin

-BNP: binatriuretic peptide

radiology

-CXR: can detect cardiomegaly)

-chest CT

-ECG/EKG

-echocardiogram (ultrasound of heart, looks at valves)

TELE ONLY SHOWS THE FRONT

stress tests

nuclear med or treadmill (see how heart handles stress)

cardiac catheterization

femoral artery, inject dye to find blockages and install a stint

what diet to cardio patients follow?

low sodium, limit red meat, low fat, high fiber, low cholesterol

cardio meds

-reduce afterload: force against which heart has to pump to eject blood LOW)

-metroprolol

-lisinopril

-losartan

-hydralazine

-furosemide, spironolactone, HCTZ, diuretic

CPR

1. circulation

2. airway

3. breathing

-defibrillation (automatic external defibrillator AED)

100-200/min, 30:2, 2in

cardiopulmonary rehab

-good for extensive heart damage

-controlled physical exercise, nutrition counseling, relaxation and stress management, medications, oxygen, compliance, systemic hydration

evaluation (cardio)

focus on evaluating how the disease is affecting day-to-day activities and how the client believes he or she is responding to treatment

cardio client outcomes

compare the client’s actual progress to the goals and expected outcomes of the nursing care plan to determine his/her health status

oxygenation

-ventilation

-perfusion

-diffusion

ventilation

gases move in/out of lungs (main inspiratory muscle: diaphragm)

perfusion

ability to pump OXYGENATED blood to tissues and DEOXYGENATED blood to the lungs

diffusion

moving respiratory gases from one area to another

work of breathing

effort required for inspiration and expiration

surfactant

chemical produced in lungs to help maintain alveolar surface tension

atelectasis

collapse of alveoli (no CO2-O2 exchange!)

accessory muscles

intercostal spaces and abdominal muscles

compliance

ability of lungs to extend in response to intraalveolar pressure (lungs don’t expand as much)

airway resistance

increased pressure as airway diameter decreases

hypovolemia

fluid LOSS and decreased circulating volume (shock, dehydration, bleeding from surgery)

decreased inspired oxygen concentration

limits O2 getting to alveoli

increased metabolic rate

increased O2 demands, pregnancy, wound healing

conditions affecting chest wall movement

pregnancy and obesity

musculoskeletal abnormalities

trauma, NM disease, and CNS alterations

influences of chronic diseases

COPD, emphysema, barrel chest

hypoventilation

-increased CO2, COPD (retain CO2)

-alveolar ventilation is inadequate to meet the oxygen demand of the body or eliminate sufficient carbon dioxide (too much artificial O2: stop breathing)

hyperventilation

-determined via ABG’s

-ventilation in the lungs removes carbon dioxide faster than it is produced by cellular metabolism )electrolyte imbalances, drugs (RESP ALKALOSIS)

hypoxia

-deficiency in O2 delivery

-inadequate tissue oxygenation at the cellular level

-cyanosis: LATE SIGN OF HYPOXIA (restless, agitated, decreased LOC, increased HR/RR, measured via SpO2)

PaCO2

arterial CO2 levels (35-45mm Hg)