Mod 7 Cardio

-Arteries: Thicker due to withstanding systolic prssure, feel the pulse of arteries.

-Veins: Thinner because blood flows back up through muscle use and gravity. IV fluids inserted and drawing blood.

1. Sinoatrial Node: Contraction begins.

2. Atrioventricular Node: in between the right atricum and ventricles

3. Bundle of His: Important because that's were all the heart blockages come through -->Left and right Bundle Branches

4. Finally the purkinje fibers:

cc’s blood ejected with each heartbeat (normal 70cc); this is the amount of mLs squirted out of the Left ventricle per each beat.

Liters of blood pumped by the ventricle per minute (normal 5 L); Heart rate times stroke volume = Cardiac Output

degree of stretch of the cardiac muscle fibers at the end of diastole (volume); prssure of blood coming into the heart itself; how much blooed even available to fill the heart. THe venous return plays into it.

the resistance to ejection of blood from the ventricle (blood pressure);  How hard the heart needs to beat to get the blood out of the heart. In chronic hypertension:  there is a high afterload and vasoconstruction in hypertension: tiny holes and less able to get a much blood out in the same amount of beats with less blood exiting, heart has to now work harder. therefore cardiac output is lower.

ability of the cardiac muscle to shorten in response to an electrical impulse; "How well heart can beat as a muscle, not the volume but its ability to contract"

the percent of end-diastolic volume ejected with each heartbeat (normal 50%): "Of the amount that left ventricle is SUPPOSED to squirt out, how much blood is actually getting out of the left ventricle because some blood does get left behind".

-Core value: If E.F. is lower than a certain value, then congestive heart failure is pretty bad so meds, diet modification and smoking cessation will be emphasized.

-how much of blood actually gets out of the heart when the heart beats; hoping for Greater than 30% at the very least!

-Done with 2D echo or cardiac ultrasound: person lays on side; not very invasive.

Cardiac Output = Stroke Volume x Heart Rate

• =>Control of heart rate
• -Autonomic nervous system and baroreceptors. Vagus nerve (cranial) slows heart rate (passing out during a BM-hypotensive).
• Baroreceptors: top of Aorta, sense pressure.

=>Control of stroke volume

• -Preload: Frank-Starling law
• -Afterload: affected by systemic vascular resistance (deals with left ventricle) and pulmonary vascular resistance
• -Contractility increased by catecholamines, SNS, some medications and decreased by hypoxemia, acidosis, some medications. (Increased by stimulation, decreased by alterations in pH and meds
• -Betablockers "LOL" meds. -Decreased SV means decreased CO.

• => Health history
• -Demographic information: some races are more likely to have hypertension and plaque formation such as blacks. lifestyle: poor social backround & stress increases plaque formation.
• -Family/genetic history
• -Cultural/social factors: recreational
• -Videogrames? hiking? Drinking?
• -Risk factors:Modifiable (smoking, diet, exercise) vs. Nonmodifiable (age, race, genetics, sex)

-Chest pain; can also manifest as GI upset, stabbing in back (know non-classic signs/symptoms)

-Dyspnea- Seen more commonly in woman. "I'm so short of breath, stomach hurts so bad" you should think: Myocardial infarction!!

-Peripheral edema and weight gain: If preload can't be handles by heart, the pressure will back up fluid into the tissues.

-Fatigue

-Dizziness (from blood not reaching the brain very well), syncope (temporary loss of Consciousness caused by drop in BP), changes in level of consciousness

• -Nutrition: sodium, fat, cholestrol?
• -Elimination: vagus nerve
• -Activity and exercise: 10 mins daily recommended as minimum
• -Sleep and rest: emotional stress can alter stress on cardio system
• -Cognition and perception: poor perfusion to brain can manifest in LOC
• -Self-perception and self-concept: because edema, can't eat the same things tht they used to.
• -Roles and relationships: support system and who relies on them if they're gone?
• -Sex and reproduction: lack of fatigue control, pregnancy can be danerous for heart, some men skin meds because of impotency effects.
• -Coping techniques and stress management: If you don't deal with stress well, more inflammation and plaque build up (cortisol intake)

-What type of health issues do you have? (breathlessness or fatigue?)

Are you able to identify any family history or behaviors that put you at risk for this health problem? (smoking leads to athlerosclorosis: artery hardeneing)

What are your risk factors for heart disease? What do you do to stay healthy? (self perception of heart risk factors. Do they exercise? Give up smoking?)

Do you have a cardiologist or primary health care provider? How often do you go for check-ups? (medication management)

What kind of tobacco or alcohol do you consume? (focus on servings: Beer=12, wine=4 0z, Hard alc=1 oz

• Hypertension
• Altered glucose metabolism: "Prediabetes"
• Dyslipidemia: Dysproportional ratio of HDL to LDL levels
• Obesity: Part of disease progression

-Waist circumference woman>35”,man>40”

-Fasting glucose > 110 mg/dL;

-B/P > 130/85

-Fasting triglycerides > 110 mg/dL 

-HDL cholesterol less than 40 mg/dL man-<50 woman

Cardiac biomarkers (related mostly to the heart)

CK and CK-MB: "MB" is specific to the heart, goes up after 4 hrs

Myoglobin

Troponin T and I: Levels chage at different time with ischemia, goes up in about 1-2 hours (quicker)

Lipid profile: picture of their cholestrol

Brain (B-type) natriuretic peptide: substance that is given out by the brain when there is congestive heart failure, nice way to scale how bad the person's congestive heart failure is. Desiredd rage is 100. BAD BNP: 900 or 1000--> Prescriptions to get rid of fluid and reduce the pressure.

C-reactive protein: sign of inflammation in heart or anywere, not super specific because it can be combined with other tests to point to malnutriton.

Picks up on normal heart rates or ectopies-different beats/rhytms.

=>12-lead ECG: shows directionality. One time full picture of heart electrical system and what direction. "leads" refer to the cords that connect to the stickers.

=>Continuous monitoring: hardwire (connected directly to the monitor) and telemetry (Box that pt wears in pocket that beams to receiver and someone keeps an eye, 3 or 5 leads)

=>Continuous ambulatory monitoring (24hr Holter): wears at home; can be ordered for three days to see patterns at home because at hospital you're just lying there. Get a log book tied to activity to see heart rate relationships.

=>Transtelephonic monitoring:wear a heart monitor that connects to landline or computer with internet whiiich connects to house that beams to cardiology office, good for rural areas; form of telehealth; adjust medications over the phone.

=>Wireless mobile monitoring: with internet, replace transtelephonic.

 Exercise stress testing: Have you go until you have chest pain or until you reach your maximum recommended heart rate. Put you on a treadmill, rise up walking rate to increase maximum heart rate with blood pressure cuff, is there any ectopy or change in rhytm? Look at electrical conductivity and structure of your heart; structural part: stop on treadmill, go on bed and check the blood flow while gasping (laying on left side)

Pharmacologic stress testing: drug injected IV to stimulate/ increase heart rate without working out. Informed consent.

(shape and size, location of heart-shows density not flow) and fluoroscopy (Blood flow through heart and vessels)

("sound": doppler type of testing, ultra sound of heart) and transesophageal echocardiogram( through the esophagus by starting inside of espophagus, invasive-ultrasound probe goes down until level of heart and gives ultrasound from INSIDE of the body instead of outside body. Gives a good picture of bottom and back of the heart like inferior myocardial infarctions)

Radioactive material injected into blood vessels of tissue, look for rate of uptake  to see how well tissue perfusion occurs and how well cardiac tissues are-alive/dead?

=>PURPOSE: Measure cardiac chamber pressures and assess patency of the coronary arteries; invasive, requires informed concent-Requires ECG and hemodynamic monitoring (blood pressure, volume, BV structure, CO, Stable BP?); emergency equipment must be available

=>Assessment prior to test; allergies (shellfish, iodine, betadine), blood work- Clotting, blood type cross (jjust in case) and dyes should be excreted through kidneys, so make sure no renal failure. Any damaged heart tissue alrady? Troponin levels

=> Procedure: Given something to calm them down before (ativan), get nummed up, incision made in femoral artery, probe goes up to the heart, imaging taken from outside-flouroscopy, as tube goes near heart-doctor squirts contrast to see how the contrast is going up the chambers of the heart, perfusiion through coronary arteries. Any blockage, leaks, blood flow in wrong direction? in real time! People in room need to wear lead aprons and scrubs, surgical gears--sterile area. Risk for bleeding. Some can do through brachial artery. Outside images to catch the flow of the dye. IV flowing with anticoagulant (heparin-wears off withint 15 to half an hour) or else clots will occur.

=> Assessment of patient after procedure: check for circulation (femoral artery, check pedal pulses on BOTH sides, capillary refil on toes, check for edemas later, BP drops?, pain), potential for bleeding-internal (hemastasis- bruising and down into inner groin,pseudoanyeurism- vessels bulging out lungs or groins) and externally, potential for dysrhythmias (anything that touches heart will cause dysrhythmias)

=> Activity restrictions: no walking, no pressure, flat on bed rest (sand bags)

=> Patient education before & after procedure: teach them they will have to stand still after procedure, wetness on groin or warmth on thigh-tell nurse. Using the restroom? Empty out now. For females: femal urinal while avoiding pressure on that one leg to keep the site clean. Men: condom cath.

Autonomic Nervous System

• Parasympathetic:
• Sympathetic: adrenaline, epinephrine, BV constricts

PQRST Wave

P wave: SA node (smaller)

QRS sizing (bigger impulse): AV node/Bundle of HIS

T wave: Heart resetting, repolarizing itself.

-Palpate location of brachial pulse then auscultate the BP

-Normal BP < 120/80

-Check both arms: if there's a problem with arteries going into the arm, it'll show by a difference of 20 point in each arm. Report them both. Could mean have atherlorsclerois on one vessel/ arm rather than another. Vasodilators managed.

-Mean arterial BP: 2/3 dias+ 1/3 sys "MAP on BP machines" between 70-90 is normal. Hemodynamics.

In suspected cardiac disease or when rhythm is irregular, count pulse rate for a full minute. "lucky 15 seconds"

Maintain fingers on the patient’s radial pulse while counting the respiratory rate so patient will not alter breathing self

-consciously Check the Temperature: can indicate cardiovascular inflammation and infection of heart; one type "endocarditis": one of the signs is a fever, pain.

Eyes: dilated, sign of BP meds too,

pallor-conjunctivae

Skin-diaphoretic, pale, flush?

Hair: brittle, dried out hair shows poor C.O.

Nails: lines, brittle more

1+ : indentation of 2mm (run fingers over skin to feel the "dip in" over the shin), Normal contours, associated with interstital fluid volume 30% above normal

2+: Deeper pit after pressing (4mm-enough to see), Lasts longer than 1+, fairly normal contour

3+: Deep pit (6mm), Remails several seconds after pressing, skin swelling obvious by general inspection

4+: Deep pit (8 mm), remails for a prolonged time after pressing, possibly minutes, Frank Swelling "soft ball looking"

Brawny edema: Fluid can no longer be displaced secondary to excessive interstital fluid accumulation, no pitting, tissue palpates as firm or hard, skin surface shiny, warm or moist, "so tight/waterballon/shiny-don't even try to pit it". You can tear the skin and interstital fluid can leak.

=>Apical Pulse:May be visible at the midclavicular line in the 5th left intercostal space, point of maximum impulse

Point of Maximum impulse (PMI): see a bit of pulsation, needs to be fairly slender

=>Other Arterial Pulsations Visible pulsations over the pulmonary arteries, the aorta or epigastric area

=>Jugular Veins (deeper than carotids): At a 45° angle in Semi-Fowler’s position, no jugular venous distension should be noted -Level of sternum (angle of Lousis; on bottom and bulged distension measure difference at 45 degree angle. Less than 4 cm is normal

**Inspection of Jugular Venous Pressure

=>Apical Impulse Normally radius is 1 cm (2 cm cross)Impulse is gentle and brief; at point of maximal impulseFeel for a thrill

• =>Carotid Pulse: Medial to sternocleidomastoid; really imporant-only feel one side at the time
• Carotid pulse and S1 occur at the same time (mitral and tricupside valves closing)

=>Extremity Pulses: Best palpated over arteries close to surface of body-pitting edema: sink fingers into tissue until you feel pulse

• 4 Point Scale
• 4+ = Bounding
• 3+ = Full, increased
• 2+ = Normal
• 1+ = Weak, barely palpable
• 0 = Absent, not palpable

• Supine position with HOB elevated 30°Examiner on patient’s right side“APE To Man” terminology for heart sounds
• Aortic
• Pulmonic
• Erbs point: "middle of heart"
• Tricupsid
• Mitral

• S1: ventricular contraction
• S2: When ventricles are relaxed and blood going to body. S2 louder at aortic valve.

• => Heart:
• S3 faint, rapid ventricular filling In early diastole. CHF gallop "horsey"; NOT NORMAL

S4 faint low pitched,after diastole Blood enters a noncompliant ventricle; ga

• => Murmurs: turbulent, clicks, buzzing-Describe: with Systole or diastole? or S1 or S2?
• -Intensity: loud or faint
• -Pitch: high or low (more difficult to determine)
• -Quality: harsh, blowing, rumbling, musical
• -May be normal in children, teenagers
• -May be functional: Increased blood flow, or weak valves
• -Pericardial Friction Rub: vibration of heart against pericardium, rubbing with each beat, can be painful due to inflammation

=> Arterial-Bruits heard over carotids "buzzing"

Count pulse for full minute

Monitor change in B/P (160), widened pulse pressure (systolic – diastolic)

Check B/P in lying, sitting, standing for postural hypotension; incrased risk for orthostatic hypotenison

Difficult to hear apical pulse, murmur may be present due to calcification of valvesCheck for s/s mental confusion, lethargy, weakness,CHF

• Interventions: Prevent falls (causes? Brady, postural hypotension, MI, meds)
• Dangle, move slowly
• Avoid long period of standing, blood pooling
• Teach foot pumping
• Seek help for change in health status, unrelieved indigestion, change in behavior

• **Cardiovascular Changes in the Elderly
• Variations in heart rate 50’s to >100
• Irregular heart rhythm because of early heart beats
• Harder to find apical impulse
• Harder to find Dorsalis pedis and posterior tibial pulses
• Blood pressure higher
• Dependent edema

Specialized nerve tissue responsible for creating and transporting electrical impulse (action potential)->depolarization and cardiac contraction.

• Started in Sinoatrial node “pacemaker”-> interartrial pathways to depolarize atria resulting in contraction

• AV node->Bundle of His->purkinje fibers. Right and left ventricular contractions are synched resulting in ejection of blood into pulmonary and systemic circulations.

Ends with repolarization when contractile fiber cells and pathways cells regain their resting polarized condition. Note a refractory period of no reaction to stimuli.

electrodes used to detect electrical activity of heart on body surface.  

P wave begins with firing of SA node; represent repolarization of atria

 QRS: depolarization from AV node through the ventricles.

 T wave: represents repolarization of the ventricle.

 U wave: may represent repolarization of the purkinje fibers or associated with hypokalemia.

 Heart rate: controlled primarily by Autonomic NS.

•  Factors that affect SV: Preload, contractility and afterload. Increasing any of these with increase oxygen demand.
• • Preload: volume of blood in the ventricles at the end of diastole, before the next contraction. Determines the amount of stretch placed on mycoradial fibers. Can be increase d by myocardial infarction, aortic stenosis, and hypervolemia.

• Contractility can be increased by epi and norepi (sympathemic) which raises SV by increases ventricular emptying.

• Afterload: peripheral resistance against which the left ventricle must pump. Affect by size of ventricle, wall tension and artierial BP. Elevated BP cause increased resistance that ventricles must meet to eject the blood. Eventually results in ventricular hypertrophy: an enlargement of the cardiac muscle tissue without an increase in CO or the size of chambers.

• Cardiac Reserve: The ability to respond to these demands by altering CO

• • Autonomic Nervous System:
•  Sympathethetic: increases HR., speed of impulse conduction though AV node, and force of atrial and ventricular contraction. Mediated by specific receptors for norepinephrine and epinephrine called Beta adrenergic receptors.
•  Parasympathetic: vagus nerve slows HR. by decrease impulses to SA node.

 On Blood Vessels:

• sympathetic NS stimulate Alpha adrenergic receptors which result in vasoconstriction; decreased stimulation of alpha adrenergic receptors results in vasodilation. .
• Parasympathetic nerves have a selective distribution in BV’s. Blood vessels have no Parasym stimulation.

 BARORECEPTORS: located in aortic arch and carotid sinus (at the origin of the internal carotid artery) are sensitive to stretch or pressure; stimulation of these receptors (volume overload) sends info to the vasomotor center at brainstem -> inhibition of sympathetic nervous system and increased parasympathetic influence to cause decreased HR. and peripheral vasodilation. Decreased arterial pressure causes opposite pressure.

 CHEMORECEPTORS: located in aortic/carotid bodies and the medulla; capable of causing changes in respiratory rate and BP in response to increased arterial CO2 pressure (hypercapnia) and to a lesser dree, decreased plasma pH (acidosis) and arterial Oxygen pressure (hypoxia). When chemoreceptors in medulla are triggered , they stimulator vasomotor center to increase BP

• Arterial blood pressure: measure of the pressure exerted by blood against the walls of the arterial system.

• Systolic Blood Pressure: peak of pressure exerted against the arteries when the heart contract.

• Diastolic BP: residual pressure in the arterial system during ventricular relaxation (or filling).

• Main factors influencing BP: Cardiac output and systemic vascular resistance (the force opposing the movement of blood; created primarily in small arteries and arterioles)

•  Measuring of arterial BP:
• • Invasively: catheter insertion into an artery attached to a transducer.
• • Noninvasively: Use a sphygmomanometer and a stethoscope. Sphygmomanometer consists of an inflatable cuff and pressure gauge. BP measured by auscultating for sounds of turbulent blood flow through a compressed artery. Brachial artery recommended. Inflate cuff to 20-30 mmHg higher above SBP (estimate by palpating brachial pulse).
• o Korokoff sounds:
• first phase/Systolic BP: tapping sound caused by spurt of blood into the constricted artery as pressure cuff is deflated slowly.
• Diastolic: when sound disappears (fifth phase)
• • Oscillometric measurements from automated device
• • Doppler ultrasonic flow meter: hand held transducer positioned over artery, cuff is applied over artery until sound disappears.

• • Pulse Pressure: difference between systolic and diastolic.
• Increased due to increased SBP may occur during exercise or atherosclerosis or larger arteries.
• Decreased: found in heart failure of hypovolemia.

• • Mean Arterial Pressure (MAP) average pressure within the arterial system that is felt by organs In the body.
• MaP greater than 60 is needed to adequately perfuse and sustain the vital organs of an average person. If it falls under -> ischemic.

 Greatest risk for Cardiovascular Disease is age; many of the physiologic changes in cardiovascular system of older adults are result of combined effects of aging process, disease, environmental factors, lifetime health behaviors.

•  Major changes in cardiovascular system: response to physical or emotional stress: blunted HR. response to changes in position.
•  Age related changes:
• collage in heart increases, elastin decreases (affecting stretch ability and reducing cardiac reserve)

o cardiac valves are thicker b/c lipid accumulation, valve calicification, degeneration of collagen and fibrosis affecting aortic and mintral valves-> regurgitation of vlood or narrowing of the valve orifice (stenosis) when it should be open -> “murmur”: turbulent blood flow across affected heart.

o SA node pacemaker cells decrease, may account for frequecey of sinus dysrhythmias in older adults).

o Cellular aging and fibrosis of conduction system: decreased amplitude of QRS comples, irregular cardiac rhythms, decreased maximal HR and variability.

o Beta adrenergic receptors decrease-> decreased response to physical and emotional stress, less sensitive to beta adrenergic agonist drugs.

o Lower max HR. results in only a two fold increase in CO (less blood for tissues).

o BVs less elastic, increase sensitivity to vasopressin (antidiuretic)-> progressive increase in SBP and decrease/no change in Diastolic-> increased Pulse Pressure.

o *Hypertension is NOT normal for aging; orthostatic hypertension may be related to meds or decreased baroreceptor function.

o Kyphosis: Altered chest landmarks for palpation, percussion, and auscultation. Distant heart sounds.

o Arterial stifferening due to loss of elastin, progressive fibrosis: increased systolic BP, possible widened pulse pressure, pedal pulses diminished, increased intermittent claudication.

o Decreased CO, HR., SV in response to exercise or stress: decreased response to exercise and stress; slowed recovery from activity

 Vital Signs: • Measure BP bilaterally, normally vary from 5-15 mmHg. There shouldn’t be more than a 20 mmHg difference from supine to sitting.

•  Inspection:
• • Skin color, hair distribution, and venous pattern, edemas (due to gravity, interrupted venous return or right sided heart failure), nail clubbing, varicosities, lesions-statsis ulcer.
• • Inspect large neck veins in 45 degree angle for distension and prominent pulsation-> Jugular Vein Distension (R sided heart failure)

•  Palpation:
• • Palpate upper and lower extremities for temperature, moisture, pulses and bilateral edema.
• • Edema: depress skin over the tibia/medial malleolus for five seconds.
• • Palpate the pulses in neck and extremities for information on arterial blood flow. Assess the rhythm. Palpate each carotid pulse SEPARATELY to avoid vagal stimulation and possible dysrhythmias. Determine symmetries of L & R arteries. Note rigidity/hardness. Capillary Refill: used to assess arterial flow to the extermities
•  “Thrill”: a palpable vibration. Means vessel wall is narrowed or bulging vibrates.

•  Auscultation:
• • Look for bruits!! “A buzzing or humming caused by abnormal flow through a narrowed artery or one with a buldging wall. Heard with stethoscope.
•  Auscultate major artieres: carotid, abdominal aorta and femoral arteries.

•  Inspection & Palpation:
• • Inspect/palpate the areas where the cardiac valves project their sounds by identifying the intercostal spaces.
• • “Angle of Louis” where the manubrium and sternum are noined; located at the level of the second rib. Palpable at midline of sternum.
• • Locate the following auscultory areas:

•  Aortic: second ICS to the right of sternum
•  Pulmonic: second ICS to the left of stesrnum
•  Tricupsid: fifth left ICS close to sternum
•  Mitral: left midclavicular line at the fifth ICS
•  Erb’s point: located at third left ICS near the sternum.
•  **Normally: no pulsations are felt. If abnormal pulsations or thrills felt: valvular disorder
• • Palpate epigastric area: lies on either side of the midline just below the xiphoid process. Pulsations seen in thin people

• Inspect precordium: located over heart for “heaves”: sustained lifts of the chest wall in the precordial area that can be seen or palpated. They may be caused by ventricular hypertrophy. Normally no pulsations should be felt here.

• Palpate Point of Maximal Impulse or “Apical Pulse” in supine positon, the pulsation of the apex. PMI lies medial to the midclavicular line in the fourth or fith ICS. Record palpated position in relation to the midclavicular line and ICS, when the PMI is below the firth ICS and left of the midclavicular line, the heart may be enlarged.

•  AUSCULTATION:
• • S1: first heart sound associated with closure of the Tricuspid and mitral valves; has a soft “lubb” sound. Signals beginning of systole.
• • S2: second heart sound; associcated with closure of the aortic and pulmonic valves. Sharp “dupp” sound. Signals the belonging of diastole
• • Have patient lie on left side to enhance the sounds at the mitral area.
• • Auscultate the apical pulse while simultaneously palpating radial pulse. “Pulse deficit” is the difference between these two pulses, can indicate cardiac dysrhythmias.

• • Extra sounds:
•  Normal: splitting of S2 which is beast heard at the pulmonic area during inspiration, abnormal is heard during expiration.
•  S3: low intensity vibration of the ventricular walls, usually associated with decreased compliance of the ventricles during filling. Heard right after S2, known as a “ventricular gallop”. May be normal in young adults. In adults, signify left sided heart failure or mitral valve regurgitation.
•  S4: low frequency vibration caused by atrial contraction, precedes S1 of the next cycle, known as an “atrial gallop”. May be normal in older adults with no evidence of heart disease, but pathological in patients with: CAD, cardiomyopathy, left ventricular hypertrophy, or aortic stenosis.
• • Murmurs: produced by turbulent flow across diseased heart valves
• • Pericardial Friction rubs: sounds caused by friction that occurs when inflamed surfaces of the pericardium (pericarditis) move against each other. They are high pitched scratchy sounds that may be transient or intermittent and may last several hours to days; heard best at the apex after expiration, with patient upright.
• • Document abnormal sounds: timing, location, positon of patient and any other abnormal findings.
• • Focused Assessment: Used to evaluate the status of previously identified cardiovascular problems and to monitor for signs of new problems.

Distended neck/jugular veins with patient sitting at 30 to 45 degree angle -> elevated right atrial pressure, right sided heart failure.

Bluish or purplish tinge in central areas such as tongue, conjunctivae, inner surface of lips-> inadequate oxygen saturation of arterial blood because of pulmonary or cardiac disorders (congentical defects)

Bluish or purplish tinge in extermities or in nose and ears -> reduced blood flow because of heart failure, vasoconstriction, cold environment

small red to black streaks under fingernails-> infective endocarditis (infection of endocardium, usually in area of cardiac valves)

obliteration of normal angle between bse of nail and skin -> Endocarditis, congential defects, prolonged oxygen deficience

Pallor, cyanosis, mottling of skin after limb elebation, dependent rubor (reddish blue discoloration), Glossy skin -> chronic decreased arterial perfusion.

Venous: necrotic crater like lesion usualy found on lower leg at medial malleolus, characterized by slow wound healing.

Arterial: Pale ischemic base, wel-defined edges usually found on toes, heels, lateral malleoli -> Poor venous return, varicose veins, imcompetent venous valves, Arteriosclerosis, diabetes.

visible dilated, discolored, tortuous vessels in lower extremities -> incompetent valves in vein.

sharp, brisk, pounding pulse -> hyperkinetic states (anxiety, fever), anemia, hyperthyroidism

weak, slowly rising pulse easily obliterated by pressure -> Blood loss, decreased cardiac output, aortic valve disease, peripheral arterial disease

Regularly irregular or irregularly irregular. Skipped beats -> Cardiac Dysrhythmias

regular rhythm but strength of pulse varies with each beat -> heart failure, cardiac tamponade

lack of pulse -> Atherosclerosis, trauma, embolus• Thrill: vibration of vessel or chest wall -> Aneurysm, aortic regurgitation, arteriovenous fistula

stiffness or inflexibility of vessel wall -> Atherosclerosis

>100 bpm -> Exercise, anxiety, shock, need for increased cardiac output, hyperthyroidism

<60 bpm; Resting, sleeping, SA or AV node damage, athletic conditioning, side effect of drugs ( Beta adrenergic blockers), hyperthyroidism

PMI is palpated/auscultated below the fifth ICS and to the left of the MidClavLine-> Cardiac enlargement as a result of coronary artery disease, heart failure, cardiomyopathy.

Hands and feet warmer than normal -> possible thyrotoxicosis

Hands/feet fold to touch, external clothing necessary for comformt -> Intermittent claudication, peripheral arterial disease, low cardiac output, severe anemia.

visible finer indetation after application of firm preeure, weight gain, tightening of clothing, includes shoes, marks or indentations from constricting garments -> interruption of venous return to heart, right sided heart failure.

Blanching of nail bed for more than two seconds after release of pressure -> possible reduced arterial capillary perfusion, anemia

measurable swelling of involved limb -> Venous thromboembolism, varicose veins, lymphedema

apical heart rate exceeds peripheral pulse rate -> cardiac dysrhythmias, most often atrial fibrillation, flutter or premature ventricular contractions.

Turbulent flow sound in peripheral artery -> arterial obstruction or aneurysm

extra heart sound, low pitched, heard in early diastole, Horsey gallop-> Left ventricular failure. Volume overload, Mitral, aortic, or tricuspid regurgitation. Possibly Hypertension.

Extra heart sound, low pitched heard in late diastole. Similar to a horsey -> Forceful atrial contraction from resistance to ventricular filling (ex: in left ventricular hypertrophy, aortic stenosis, hypertension, coronary artery disease)

Turbulent sounds occurring between normal heart sounds. Characterized by loudness, pitch, shape, quality, duration, timing => cardiac valve disorder, abnormal blood flow patterns.

High pitched, scratchy sound heard during S1 or S2 at the apex. Heard best with patient sitting and leaning forward, and at end of expiration => Pericarditis!

injured cells release contents including enzymes and other proteins into circulation; these are biomarkers to diagnose myocardial injury and infarction

• • Cardiac-specific Troponin: myocardial muscle protein reliseassed into circulation fter injury or infarction.
• Two types: Troponin T and Troponin I.
• 1. Detectable within hours (avg 4-6 hrs) of myocardial injury, peak at 10-24 hrs and can be detected for up to 10-14 days.
• 2. Biomarker of choince in diagnosis of myocardial infarction

• found as three isozymes, CK-MB (specific to heart)
• begins to rise 3-6 hours after symptom onset,
• peak in 12-24 hours and return to baseline within 12 to 48 hours after MI.
• Peak levels and return to normal can be delayed in a person with large MI.

low molecular weight heme protein found in cardiac and skeletal muslcle. Myoglobin elebationis a sensitive indicator of very early myocardial injury but lacks specificity for MI. Limited MI diagnosis.

protein produced by liver during period of acute inflammation; measured using high sensitivity test (hs-CRP); increased levels is an independent risk factor for CAD, may also predict the risk for future cardiac events in pts with unstable angina and MI.

an amino acid that is produced during protein catabolism.

Elevated levels been linked to higher risk of CAD, Peripheral vascc disease, and stroke. Elevated levels can either be hereditary or acquired from dietary deficiencies of Vitamin B/folate.

Marker of choice for distinguishing cardiac or respiratory dyspnea.

• consist of triclycerides, cholesterol and phospholipids.
• • Cholesterol: structural component of cell membranes and plsma lipotprotiens is a precursor of cortoicosteoriods, sex hormones and bile salts. Absorbed from food, and synthesized in liver.
• • Triglycerides: the main storage for of lipids; make up 95% of fatty tissue
• • Lipoproteins
• • Different classes of lipoproteins:
• 1. Chylomicrons: primarily exogenous triglycerides from dietary fat
• 2. Low Density Lipoprotien: mostly cholesterol with moderate amounts of phospholipids.
• 3. High Density Liprotiens: about 50% protein and 50% phsopholipds and cholesterol
• 4. Very Low Densiity Lipoproteins (VLDLs): primary endogenous triglycerides with moderate amounts of phospholipid and cholesterol

measures cholesterol, triglyceride, LDL, and HDL.

Elevated LDL and triglycerides are strongly associated with CAD.

• Increased HDLs decrease risk by protective role by mobilizing cholesterol from tissues.
• • Risk assessment: calculated by comparing the total cholestrerol to HDL ratio over time, increase in ratio indicates increased risk. Patient must fast before blood is drawn for a lipid panel so food intake does not affect results.
• 1. Major HDL protiein: Apolipoprotien A-I and Major LDL Protein: Apolipoprotein B

2. Increased levels of Lp (a), especially with increased levels of lactate dehydrogenase (LDH) have been linked with the progression of atherosclerosis especially in women.

3. Lipoprotien-Associated Phosopholipase A2: an inflammatory enzyme expressed in atherosclerotic plaques. Elevated levels of lp-PLA2 are related to an increased risk of CAD.

• A radiographic picture of the chest can show cardiac contours heart size and anatomic changes in individual chambers. The chest x ray records any displacement or enlargment of the heart, extra fluid around the heart (pericardial effusion) and pulmonary congestion.

• PQRST waveforms used to assess cardiac activity

• Event Monitor: portable unit that uses electrodes to store ECG data once trigged by the patient, disadvantage: if symptoms brief, they’ll be overlooked. Used for routine pacemaker checks over the phone to the doctor’s office.

• Loop Recorder: implanted into chest wall; used for patients who may have serious yet infreq arrhythmias. Worn for about a month.

• Uses ultrasound waves to record the movement of the stuctures of the heart. Contrast echocardiography involes the addition of an IV contrast agent (albumin microbubbles, agitated saline) to assist in defining the images, especially in technically difficult patients (obese).

• Gives information about abnormalities of (1) valvular structures and motion (2) cardiac cambrer size and contents (3) ventricular ands eptal motion and thickness (4) Pericardial sac and (5) ascending aorta

• Ejection fraction: percentage of end diastolic blood volume that is ejected during systole can me measure; gives info about the function of the left ventricle during systole.

• • Two most commonly used types of echocardiograms: motion mode (m-mode) and two dimentional (2D)
• 1. M mode: single ultrasound beam is directed toward the heart,, recording motion of the intracardiact structures and detecting wall thickness and chamber size.
• 2. 2D ECG sweeps the ultrasound beam through an arc, producing a cross sectional view. This shows correct spatial relationships among the structures.

• Doppler technology allows for sound evaluation of the flow or motion of the scanned object (heart valves, ventricular walls, blood flow). “Color flow imaging (duplex)” is the combination of 2D ECG with Doppler technoly, using color changes to demonstate the speed and direction of blood flow

• Stress Echocardiography: combination of treadmill test and ultrasound images, evalvuates the wall motion abnormalitieis. Uses a digital computer to comparie images before and after exercise to see wall function. Those who can’t exercise-> pharmacologic stress using IV drug (dobutammine)

• TransEsophageal ECG (TEE): provides more precise echocardiography of the heart than surface 2D echocardiography by removing interference from the chest wall and lungs. Uses a flexible endoscope proble with ultrasound transducer in the time for imaging of the heart and vessels. Frequently in outpatient setting for evaluation of mitral valve disease or endocarditis vegetation, thrombuses. Risks: low; include performation of esophagus, hemorrhage, dysrhythmias, vasovagal reactions and transient hypoxemia. Contraindicated: history of esophageal disorders, dysphagia, or radiation therapy to chest wall. Sedation required.

provides info on wall motion during systoles and diastole, cardiac valves and EF. Stress perfusion

• Detect MI areas in 3 D view, sensitive enough to find small MIs not apparent with single photon emission CT. Aids in final diagnosis of MI and assessment of EF.

Advantage: does not require any radiation, pacemakers and CIDs discouraged due to magnets.

Heart imaging test that uses CT technology with or without IV contrast to see heart anatomy, coronary circulation and great blood vessels.

• CT angiogram: is noninvasive test; done faster than cardiac cath with less risk and sicomformt, the gold standard to diagnose coronary artery stenosis.

common outpatient procedure,provides info about CAD, coronary spasm, congenital and valvular heart diseas, and ventricular function. Used to measure intracardiac pressures, O2 levels, CO, and EF. Inserting a radiopaque cath into the right or left side of heart (arm or leg vein)

contractile proteins that are released after an MI. Both troponin T and Troponin I are highly specific to cardiac tissue.

 NS: Rapid point of care (bedside) assays are available. Explain to patient the purpose of serial sampling in conjunction with CK-MB and serial ECGs

• Reference:

Troponin I: Negative <0.5 ng/mL, Indeterminate: O.5-2.3 ng/mL and Positive for Myocardial injury: >2.3 ng/mL

Cardio specific isozyme that is released in the presence of myocardial tissue injury. Contractions > 4 to 6% of total creatine kinase are highly indicative of MI. Serum levels increase within 4-6 hours after MI.

-> NS: Serial sampling often done in conjunction with troponin and ECGs.

• Low molecular weight protein that is 99-100% sensitive for myocardial injury. Serum concentrations rise 3- to 60 minutes after MI.
• Reference Interval: Male: 15.2-91.2 & Fem: 11.1-57.5 mcg/L (NS: cleared from the circulation rapidly, limited use in the diagnosis or cardiac injury/infarction)

Marker of inflammation that can predict risk of cardiac disease and cardiac events, even in patients with normal lipid values. High sensitivity CRP assay used. Lowest risk <1 mg/L, moderate risk: 1-2 mg/L, high risk: >3 mg/L

(NS: Stable levels that can be measure non fasting and any time during the day. May be more predictive risk factor of cardiovascular disease than LDLs for women. The average of two assays obtained 2 wk apart provides a more stable measuremet than one single measurement

Amino acid produced during protein catabolism that has been identified as a risk factor for cardiovascular disease. Homocysteine may cause damage to the endothelium or have a role in formation of thrombi.

Reference: Male: 5.2-12.9 mol/L & Female: 3.7-10.4.

(NS: Hyperhomocysteinemia resulting from dietary deficiencies is treated with folic acid, vitamin B6, and vitamin B 12 supplements)

Peptide that causes natriureisis. Elevation helps to distinguish cardiac vs respiratory cause of dyspnea.

Refeerence: >100 pg/mL

(NS: Infison of nesiritide (natrecor) elevates levels temporarily)

Aids in assessing the severity of heart failure in symptomatic and asymptomatic patients. References: <75 yrs old: 124 pg./mL and >75 yrs: 449 pg./mL

A blood lipid. Elevated cholestrerol is considered a risk factor for cardiovascular heart disease. References: < 200 mg/dL (NS: cholesterol levels can be obtained in a nonfasting state)

Mixtures of fatty acids. Elevations are associated with cardiovascular disease and diabetes.

• Reference: <150 mg
• (NS: Triglyceride and lipoprotein levels must be obtained in a fasting state –at least 12 hours, except for water. Alcohol should be withheld for 24 hrs before testing)

electrophoresis is done to separate lipoproteins into HDL and LDL. There are marked day to day fluctuation in serum lipid levels. More than one determination is needed for accurate diagnosis and treatment.

(NS: Risk for cardiac disease is assessed by dividing the total cholesterol level by the HDL level and obtaining a ratio. Low risk < 3, Increased risk: >5.)

• o Refererence:
• HDL: Male: >40 mg, Female: >50, Low risk for CAD: >60 and High risk for Cad <40  
• LDLs: Recomendded: <100. Optimal: 100-129. Moderate for CAD: 130-159, High risk for CAD: >160 mg

Patient is placed in two upright positions to examine the lung field and heart size. The two common positons are posteroanterior (PA) and lateral. Normal heart size and contour for the idividual’s age, sex and size noted.

(NS: inquire about frequency of recent x rays and possibility of pregnancy. Provide lead shielding to areas not being viewed, remove any jewely or metal objects tha may obstruct the view of the heart and lungs.)

Electrodes are plaed on the chest and extermities, allowing the ECG machine to record cardiac electrical activity from 12 different views. A resting 12 lead ECG can identify conduction problems, dysrhythmias, position of heart, cardiac hypertrophy, pericarditis, myocardial ischemia or infarction, pacemaker activity and effectivesness of drug therapy at one point in time.

(NS: Prepare skin and apply electrodes and leads. Position pt. supine (or with head of bed elebated, if short of breath) Infrom pt. that no discomfort is involved and to lie still to decrease motion artifact)

 Holter Monitoring: Recording of ECG rhythm for 24-48 hours and then correlating rhythm changes with symptoms and activities recorded in diary. Normal patient activity is ecourageed to stimulate conditions that produce symptoms. Electrodes are placed on chest, and a recorder is esed to store information until it is recalled, printed, and analyzed for any rhthm disturbance. It can be performed on an inpatient or outpatient basis.

(NS; prepare skin and papply electrodes and leads. Explain imporatnace of keeping an accurate diary of activites and symptoms. Tell pt. that no bath or shower can be taken during monitoring. Skin irritation may develop from electrodes. )

 Event Monitor or Loop recorder: Records rhthm distrubances that arnt frequent enough to be recorded in one 24 hour period. It allows more freedom than regular holter monitor. Some units have electrode s that are attached to the chest and have a loop of memory that captures the oneset and end of an event. Other types are placed directly on patient’s wrist, chest or figers and have no loop of memory, but record the patient’s ECG in real time. Recordings may be transmitted over the phone to a receiving unit.

(NS: Instruct in use of equipment for recording and transmitting of transient events. Teach pt. about skin prep for lad placement or steady skin contact for units not requiring electrodes. This will ensure the reception of opital ECG tracings for analysis. Instruct pt. to initiate recording as soon as symptoms begin or as soon therafter as possible.)Exercise/Stress testing: Common protocol uses 2 minute stages at set speeds and eleation of the treadmill. Pt. can exercise to either predictedpeak HR (calculated by 220-age) or to peak exercise tolerance. Terst is also terminated for chest discomfort, significant increase or diecrease in vital signs from baseline or significant ECG changes indicating cardiac ischemia. Vitals signs and ECG are monitored, eCG monitored after exercise for rhythm disturbances or if ECG changes occurred with exercise for return to baseline. Continual monitoring of vitals and ECG rhythms for ischemic changes is important in the diagnosis of CAD. An exercise bike may be used if the patient is unable to walk on the treadmill. (NS: Instruct pt. to wear comfortable clothes, shoes. Importance of reporting any symptoms that occurs. Monitor vitals and obtain 12 lead ECG before exercise during each stage of exercise, and after until all vitals and ECG have returned to normal. Monitor pts response throughout procedure. Contraindications: any reasons pt. is unable to reach peak exercise tolerance. Beta adrenergic blockers may be held 24 hour before the test bc they blunt the heart rate and limit the pt. ability to achieve maximal HR. Caffeine containing food and fluids are held for 24 hr.. Pts must refrain from smoking and strenuous exercise for 3 hours before test.

 Types: Contrast, M-Mode, two Dimensional, Color Flow imaging (duplex), real time 3D

• Transducer that emits and receives ultrasound waves is placed in four positions of the chest above heart. Transducer records sound waves that are bounced off the heart. Also records direction, flow of blood through heart and transforms it to audio and graphic data that measure valvular abnormalities, congenital cardiac defects, wal motion, EF, and cardicac function. IV contrast agent may be used to enhance images.

(NS: Place pt. in a left side lying position facing eequipment. Instruct pt. about procedure and sensations (pressure and mechanical movement form head of transduce) No contraindications to procedure exist.

Combination of exercise test and echocardiogram. Resting images of the heart arte taken with ultrasound, and then the patient exercises. Post exercise images are taken within one minute of stopping exercise. Differences in left ventriculwar wall motion and thickening before and after exercise are evaluation.

NS: Instruct and prep pt. for treadmill or bicycle. Inform of importance of timely return to examination table for imaging after exrercise. Contraindications include any reasons pt. is unable to reach peak exercise tolerance.

Used as a substitute for exercise stress test in individuals unable to exercise. IV dobutamine or dipyridamole is infused, and dosage is increase in 5 min intervals while echocardiogram is performed to detect wall motion abnormalities at each state.

NS: Instruct and prepare pt. for treadmill or exercise bicycle. Inform pt. of importance of timely return to examination table for imaging after exercise. Contraindications include any reasons patient is unable to reach peak exercise tolerance.

Probe with ultrasound transducer at the tip is swallowed while the physicians control angle and depth. As it passes down the esophagus, it sends back clear images of heart size, wall motion, valvular abnormalities, endocarditis vegetation and possible source of thrombi w/o interference from lungs or chest ribs. Contrast medium may be inject IV for evaluating direction of blood flow if an atrial or ventricular septal defect is suspected. Doppler Ultrasound and color flow imaging can also be used concurrently.

NS: Instruct pt. to be NPO for at least 6 hrs. before test. Remove dentures. IV sedation is administered and throat locally anesthetized. A bit block placed in mouth. Designated driver need if done in outpatient dept. Monitor vital signs and oxygen saturation levels and perform suctioning as needed during procedure. Assist pt. to relax. Pt. may not eat or drink until gag reflex kicks in. Sore throat temporary.

Study involves IV injection of radiactive isotopes. Radioactive uptake is counted over the heart by scintillation camera. It supplies info about myocardial contractility, myocardial perfusion and acute cell injury.

NS: Explain procedure to pt., women shouldn’t wear bras to decrease breast attenuation. Establish IV line for injection of isotopes. Explain that radioactive isotope used is a small diagnostic amount and will lose most of its radioactivity in a few hours. Inform the pt. that he or she will be lying still on back with arms extended overhead for 20 mins. Repeat scans are performed within a few minutes to hours after the injection.

MUGA, positron emission tomography, etc

A small amount of the patient’s blood is removed, mixed with a radioactive isotope and reinjected IV. With the ECG used for timing, images are acquired during the cardiac cycle. Indicated for patients with MI, heart failure, or valvular heart disease. Can be used to evaluate the effect of various cardiac or cardiotoxic medications on the heart.

NS: Explain procedure to patient. Establish IV line for removal of blood sample and reinjection of isotope. Establish ECG monitoring. Inform pt. that procedure involves little risk.

Used to detmine size or risk of infarction and to detmine infarction size. Small amounts of a radioactive isotope are injected IV and recordings are made of the radioactivity emitted over a specific area of the body. Circulation of the isotope can be used to detect coronary arty blood flow, intracardiact shunts, motion of ventricles, EF, and size of the heart chambers.

NS: Explain proceudure to pt. Establish IV line for removal of blood sample and reinjection of isotope. Establish ECG monitoring. Inform pt. that procedure involves little risk.

Nuclear imaging images taken at rest and after exercise. Injection given at maximum HR. (usually 85% of age predicted max) on bicycle or treadmill. Pt. is then requires to continue exercise for one minute to circulate the radioactive isotope. Scanning is done 15-60 min after exercise. A resting scan is performed 60-90 min after initial infusion or 24 hr. later.


NS: Explain procedure to pt. instruct pt. to eat only light meal between scans. Certain meds may need to be held for 1-2 days before the scan. Patients should not have caffeine 12 hr. prior. If target max HR. is not achieved with exercise, test may be changed to pharmacologic imaging.

Dipyridamole or adenosine is used to produce vasodilation when pts are unable to tolerate exercise. Vasodilation increased blood flow to well perfused coronary arteries. Scanning procedure is same. Aminophylline may be given to prevent or reverse side effects of Dipyridamole (shortness of breath, dizziness). Dobutamine is used if vasodilators are contraindicated.


NS: explain procedure to pt. instruct pt. to hold all caffeine products for 12 hours before procedure. Calcium channel blockers and beta adrenergic blockers should be held 24 hr. before the test. Observe pt. for side effects (shortness of breath,, dizziness, nausea)

Highly sensitive in distinguishing viable and nonviable myocardial tissue. Uses two radionuclides. Nitrogen 13 ammonia is injected IV first and scanned to evaluate myocardial perfusion. A second radioactive isotope, fluoro 18 deoxyglucose is then injected and scanned to show myocardial metabolic function. In the normal heart, both scans match but in an ischemic or damaged heart, they differ. The pt. may or may not be stressed. A baseline resting scan is usually obtained for comparison.

NS: Instruct pt. on procedure. Explain that pt. will be scanned by a machine and will need to stay still for a time. Pt.’s glucose level must be between 60-140 mg for accurate glucose metabolic activity. If exercise is included as part of testing, pt. needs to be NPO and refrain from tobacco and caffeine for 24 hr. before test.

Noninvasive imaging technique obtains info about cardiac tissue integrity, aneurysms, EF, cardiac output, and patency of proximal coronary arteries. It does not involve ionizing radiation and is an extremely safe procedure. It provides images in multiple planes with uniformly good resolution.

NS: Explain procedure and inform pt. that the small diameter of the cylinder, along with loud noise of the procedure may cause panic or anxiety drugs. Antianxiety drugs and distraction strategies (music) may be recommended. Pt. must lie still during test. Contraindicated for person with implanted metallic devices or other metal fragments unless noted to be MRI safe. Discuss any implants before scan

Used for imaging vascular occlusive disease and abdominal aortic aneurysms, same as MRI but with use of gadolinium as IV contrast medium.

NS: contraindications include any known allergies to contrast medium and persons with implanted metal devices.

Cardiac CT is heart specific CT imaging technology with or without IV contrast medium used to visualize heart anatomy, coronary circulation, and blood vessels.

• • Coronary CT angiography (CTA): Use of CT with injected IV contrast medium to obtain images of blood vessels and diagnose CAD.
• NS: Explain procedure to pt., metal objects should be removed. Pts should already have regular hearat rhythm to allow for accurate testing. A Beta adrenergic blocker may need to administered before the test to control HR. The pt. may need to be NPO for several hours before procedure.

• Calcium scoring CT/Electron Beam CT: aka ultrafast CT, uses a scanning electron beam to quantify calcification in coronary arteries and heart valves. Primary used for risk assessment in asympotomatics pts and to assess for heart disease in pts with atypical symptoms potentially related to cardiac causes.

NR: Explain procedure to pt. inform pt. that procedure is quick and involves little to no risk.

Involves insertion of catheter into heart to obtain information about oxygen levels and pressure readings within heart chambers. Contrast medium is injected to assist in seeing structures and motion of heart. Procedure is done by insertion of cath into a vein (for right side of heart) and/or an artery (for left side of heart).

NR: Check for sensitivity to contrast media. Withhold food and fluids for 6-12 hours before procedure. Give sedative and other drugs if ordered. Inform pt. about use of local anesthesia, insertion of catheter, feeling of warmth when dye is injected, and possible fluttering sensation of heart as catheter is passed. Note that patient may be instructed to cough or take a deep breath when dye is injected and that pt. is monitored by ECG through procedure.

• After procedure: frequently assess circulation to extremities used for cath insertion, check peripheral pulses, color, and sensation of extremity per agency protocol. Observe puncture site for hematoma and bleeding. Place compression device over arterial site to achieve hemostasis, if indicated. Monitor vital signs and ECG. Assess for hpotension or hypertension, dysrhythmias, and signs of pulmonary emboli.

During a cardiac catheterization, contrast medium injected directly into coronary arteries. Used to evaluate patency of coronary arteries and collateral circulation.

NR: Same as for Cardiac Cath.

During cardiac cath: a small ultrasound probe is introduced into contrary arteries. Ata are used to assess size and consistency of plaque, arterial walls and effectiveness of intracoronary artery treatment.

During Cardiac catheterization, a special wire is inserted into coronary arteries to measure pressure and flow. Information is used to determine need for angioplasty or stenting on non-signifcant blockages.

Peripheral vessel blood flow is assessed y injecting contrast media into the appropriate arteries or veins (arteriography and venography). Serial x-ray studies taken to detect and visualize and atherosclerotic plaques, occlusion, aneurysms, venous abnormalities or tramatic injury. NS: Check for allergy to contrast media. Give mild sedative, if ordered. Check extremity with puncture site for pulsation, warmth, color, and motion after procedure. Inspect insertion site for bleeding or swelling Observe patient for allergic reactions to contrast media.

Invasive and minimally invasive bedside hemodynamic monitoring is done usually intrarterial, pulmonary artery, and central vein catheters to monitor arterial BP, stroke volume variation, pulmonary artery pressure, pulmonary artery wedge pressure, cardiac output, and central venous pressure. Used to evaluate cardiovascular status and response to treatment.

NS: Pts requiring hemodynamic monitoring are critically ill and are monitored in intensive care units.