Cardiac Exam 2

functions of the cardiovascular system

-transportation of oxygen, nutrients, and hormones to the tissues
-transportation of CO2 and wastes away from the tissues and to the lungs/kidneys
-thermoregulation
-urine formation

general cardiovascular responses to exercise

-activation of the sympathetic nervous system
-increased cardiac output
-increased blood flow to skeletal muscle and skin
-decreased blood flow to the viscera, including kidneys
-maintained blood flow to the brain

oxygen delivery

-if there is inadequate oxygen delivery to the tissues, anaerobic metabolism will be triggered
-this is detrimental because it limits protein and fat metabolism and increases production of lactic acid

oxygen extraction ratio

-this is the percentage of oxygen delivered that was actually CONSUMED

three surfaces of the heart

-the heart is rotated to the left and tilted posteriorly
-sternocostal surface is the right side of the heart
-diaphragmatic surface is mostly the left ventricle, some of the right ventricle
-posterior surface/base is mostly the left atrium, some of the r

apex of the heart

-tip of the left ventricle
-located at the level of the fifth rib at the midclavicular line

base of the heart

-located at the level of the third rib

pericardium

-double-layered membrane surrounding the heart
-fibrous pericardium: outer layer
-serous pericardium: inner layer, made up of the partietal and visceral pericardium
-there is a small fluid-filled cavity between the parietal and visceral pericardium
-this

layers of cardiac tissue

-epicardium: outermost layer, same structure as the visceral pericardium
-myocardium: middle layer, composed of cardiac muscle tissue
-endocardium: innermost layer, epithelium that lines the chambers and valves
-endocarditis: inflammation of the endocardi

ventricles

-right ventricle: wall is very thin
-left ventricle: wall is very thick, needs more muscle to generate enough force to pump blood throughout the body
-the left ventricle is the workhorse, and most infarctions occur in the left

papillary muscle

-muscle that attaches to the ventricular wall and the chordae tendineae
-papillary muscles do NOT make the valves open and close, this is accomplished by pressure differences
-papillary muscles help to prevent the valve cusps from bulging upwards back int

four properties of cardiac muscle

-functional syncytium
-inherent spontaneous rhythmicity
-polarized irritability
-all or none law

functional syncytium

-the cells of the atria and ventricles contract simultaneously, functioning as if they were one cell
-this can be accomplished due to the branching of the muscle fibers and the intercalated disks, which allow for rapid transmission of the depolarization

inherent spontaneous rhythmicity

-the cells of the heart can depolarize on their own without outside nervous input
-this is why we can have heart transplants
-this is also why we can get arrhythmias

polarized irritability

-some parts of the heart are more excitable than others
-the most unstable resting potential is at the SA node
-sodium and potassium are very leaky here, so it's easy for depolarization to occur
-if the SA node is pacing the heart, HR will be around 60-90

all or none law

-there is no recruitment of motor units in cardiac muscle
-either all muscle fibers fire, or none do

filling of the ventricles

-about 70-80% of ventricular filling is PASSIVE
-the last 20-30% occurs when the atria go into systole and provide the atrial kick
-with atrial fibrillation, there is no active atrial output, so you only get about 70-80% of normal ventricular filling
-how

atrial fibrillation

-most common abnormal heart rhythm in the older adult
-the cells of the atria do not depolarize together, so there is no atrial kick

opening and closing of the heart valves

-the valves open and close because of pressure differences, NOT because of papillary muscle or contraction

ventricular diastole

-during diastole, the ventricles relax and ventricular pressure starts to drop
-once the pressure in the ventricles is less than the pulmonary artery and aorta, those valves close
-some blood in the ascending aorta falls backwards and is caught by the cus

ventricular systole

-during systole, the ventircles contract and pressure starts to build up
-once the pressure in the ventricles is greater than the atria, the tricuspind and mitral valves are forced closed
-for just an instant, all 4 valves are closed
-pressure continues t

smooth muscle in blood vessels

-there is a lot MORE smooth muscle fibers in the arterial side than venous side, so the veins are more compliant
-the arterioles are really the GATE KEEPERS to the capillaries
-this is because arterioles have the MOST smooth muscle fibers
-when a patient

bulk flow

-blood pressure is what pushes fluid out of the capillaries and into the interstitial space for nutrient delivery
-this is why MAP and perfusion pressure are so critical
-osmotic pressure is what sucks fluid from tissues back into the capillaries for wast

collateral circulation

-coronary arteries have collateral branches that are typically closed
-when faced with tissue hypoxia, these collaterals will open up
-furthermore, chronic hypoxia can stimulate the formation of new anastomoses

right coronary artery

-branches off the aorta at the aortic valve
-supplies the right atrium, right ventricle, left ventricular inferior wall, and posterior 1/3 of interventricular septum
-in 90% of the population, the RCA also forms the posterior descending artery and supplie

left coronary artery

-branches off the aorta at the aortic valve
-only about an inch long
-branches into the left anterior descending and circumflex arteries

left anterior descending artery

-supplies the left ventricular anterolateral wall (more anterior than lateral) and anterior 2/3 of interventricular septum
-it does not contribute as much to the nodes as the RCA and left circumflex

left circumflex artery

-supplies the left atrium, left ventricular anterolateral wall (more lateral than anterior), and left ventricular posterolateral wall
-in 10% of the population, the left circumflex artery also forms the posterior descending artery and supplies the left ve

cardiac metabolism

-the heart is NOT a picky organ
-the heart can use glucose, fatty acids, amino acids, and lactate for fuel
-at rest, the heart mostly relies on fatty acids
-during moderate exercise, the heart equally relies on fatty acids, glucose, and lactate
-during he

oxygen consumption

-the amount of oxygen required by the body for a given activity
-VO2 = CO * A-VO2
-CO measures the heart's ability to pump blood
-A-VO2 difference measures the peripheral tissue's ability to extract O2
-the delivery system is what limits VO2 in people wit

heart rate

-max HR decreases with age
-increased HR means increased oxygen demand by the heart
-increased HR leads to decreased diastolic filling time

nervous system control of the heart

-the heart is dually innervated by the vagus nerve and sympathetic nerves (beta 1's)
-at rest, the vagus nerve is the MAIN thing controlling your heart by holding the SA node back (intrinsic rate of SA node is 110-118)
-MOST of the time in a 24-hour perio

vagus nerve

-decreases HR, contractility, and speed of conduction through AV node

sympathetic nerves (beta 1's)

-increase HR, contractility, and speed of conduction through AV node

sympathetic receptors

-alpha receptors are abundant in the peripheral vessels and cause VASOCONSTRICTION
-beta 1 receptors are located in the heart
-beta 2 receptors are outnumbered by alphas in the periphery, but they are dominant in the coronary arteries and cause VASODILATI

heart transplant

-when a heart is transplanted, the vagus nerve and sympathetic nerves are cut
-therefore, after receiving the heart, the patient's resting HR will be at the intrinsic rate of the SA node
-HR can still be modulated via hormones in the systemic circulation

potassium

-normal range in adults is 3.5-5.0 mEq/L
-hyperkalemia is > 5.1 mEq/L
-hypokalemia is < 3.2 mEq/L and is MORE concerning
-hypokalemia can cause dangerous ventricular arrhythmias, cardiac irritability, ST segment depression, dizziness, hypotension, and dec

sodium

-normal range in adults is 134-142 mEq/L
-hypernatremia is > 150 mEq/L
-CHF and hypovolemia are causes
-older adults have a faulty thirst mechanism and often don't hydrate well

stroke volume

-SV reflects the effectiveness of the heart as a pump
-3 components of SV: preload, contractility, and afterload
-preload is determined by venous return and distensibility
-contractility is determined by EDV and ejection fraction
-afterload is mostly dete

ejection fraction

-EF = SV/EDV
-resting EF: 55-70% is normal
-resting EF < 55% is reduced
-should increase with exercise as SV increases beyond the increase in EDV due to sympathetic input

location of blood volume

-at any given moment, about 70% of your blood is located in your veins, available for quick return if needed
-10% is in the systemic arteries
-15% is in pulmonary circulation
-5% is in capillaries

A-VO2 difference

-the body PREFERS to meet oxygen demand by increasing CO rather than oxygen extraction
-at rest, skeletal muscle pulls out about 25% of oxygen
-however, skeletal muscle can triple this amount if needed
-at rest, cardiac muscle pulls out about 70-80% of ox

nitric oxide

-endothelium can produce and store nitric oxide, which causes LOCAL VASODILATION
-it is released in response to drug stimulation, as well as flow-mediated
-nitric oxide release is an important mechanism of enhanced blood flow

metabolite release

-the chemical envirionment near a working muscle can trigger LOCAL VASODILATION
-metabolites include decreased pH, increasd CO2, increased calcium (vasoconstrictor), increased ADP, decreased O2, increased magnesium (vasodilator), and increased body temper

baroreceptor reflex

-baroreceptors are stretch receptors located in the walls of the aorta and carotid arteries that pay attention to blood flow going by them
-when there is an increase in SV and BP (supine), the baroreceptors respond by signalling for an increase in vagal t

atrial stretch reflex

-this reflex contributes to diuresis if the patient is lying flat
-atrial stretch receptors sense plenty of blood going by
-therefore, there is an increase in atrial natriuretic factor, decreased ADH, and decreased renin
-all of these contribute to an inc

myocardial oxygen consymption

-the amount of oxygen required by the heart for a given activity
-MVO2 = CBF * A-VO2
-remember that cardiac muscle fibers already extract 70-80% of the oxygen that is delivered at rest
-therefore, coronary blood flow is CRITICAL to ensure adequate oxygen

coronary blood flow

-blood flow to cardiac muscle
-determined by driving pressure and resistance to blood flow
-driving pressure = systemic DBP - LVEDP
-NORMAL left ventricular EDP is less than 12
-resistance to blood flow depends on metabolic factors (hypoxia, anemia), mech

myocardial oxygen supply vs demand

-HR and SBP are on the demand side
-RPP = peak HR * peak SBP, which is a good index of myocardial oxygen demand
-contractility is also on the demand side, meaning the stronger the contraction is, the more oxygen is required
-left ventricular wall tension

P wave

-atrial depolarization

PR interval

-from beginning of P wave to the beginning of the QRS complex
-should be 0.12-0.20 seconds
-this is the amount of time it takes the depolarization to transmit from the SA node, through the atria, through the AV node, and to the ventricles
-the 0.1 second

QRS complex

-ventricular depolarization
-should be 0.06-0.10 s

ST segment

-from the end of the QRS complex to the beginning of the T wave
-should be on baseline

J point

-point at the end of the QRS and beginning of the ST segment

T wave

-ventricular repolarization
-ST segment and T wave are sensitive indicators of myocardial oxygen supply and demand status
-inverted T wave doesn't mean that the patient definitely has ischemia/infarction, it can be due to hyperventilation

QT interval

-from the beginning of the QRS complex to the end of the T wave
-looks at the amount of time for the entire ventricular cycle
-normal QT interval should be less than half the distance of the R to R interval
-physicians are concerned about prolonged QT int

blood pressure

-BP = CO * TPR
-baroreceptors are extremely important for monitoring blood pressure when changing positions
-however, the baroreceptors accommodate quickly and are not as effective in older patients
-RAAS is an important control of both blood pressure and

RAAS

-this system helps to regulate both blood pressure and blood volume
-it is triggered by firing of the sympathetic nervous system, which is MASS RESPONSE
-first, the kidney release renin into the bloodstream
-renin activates angiotensinogen into angiotensi

mean arterial pressure

-the average pressure pushing blood through the circulatory system
-MAP = DBP + 0.33(SBP - DBP)
-normal MAP is 70-110 mm Hg
-MAP < 60 means that there is INADEQUATE perfusion pressure
-the LOWER the MAP is, the more concerned you need to be about the vita

vascular area

-vascular area significantly goes up when you reach the arterioles, capillaries, and venules
-therefore, flow velocity is lower here to provide time for nutrient exchange

rate pressure product

-RPP = HR * SBP
-RPP is a great index of myocardial oxygen demand
-it increases with activity, but decreases at a given workload with training
-in cardiac rehab, we can't do a lot to increase blood supply
-however, we can LOWER the demand via exercise tra

hemoglobin

-12-16 g/dL in females
-14-17 g/dL in males

hematocrit

-this is the best index of O2 carrying capacity in the blood
-36-47% in females
-41-51% in males

SaO2

-percent of arterial hemoglobin oxygen saturation
-normal is greater than 94%
-patients with < 90% may require supplemental O2

SvO2

-percent of venous hemoglobin oxygen saturation
-normal is 60-80%
-this value provides you with a sense of how much oxygen is being extracted by the tissues
-remember that the body likes to meet its oxygen demand by enhancing CO, not by pulling out a humo

normal cardiovascular changes with aging

-blood vessel walls get thicker and stiffer
-decreased elasticity of major blood vessels
-the ventricles of the heart are less distensible
-fibrotic changes occur in the valves
-enlarged left atrium due to the rigid left ventricle, often results in an aud

consequences of cardiovascular changes with aging

-increased SBP
-increased afterload
-decreased HR max and SV at max effort (no big impact on resting values)
-slowed myocardial tension development
-decreased inotropic response to catecholamines
-decreased max cardiac ouput
-decreased VO2 max
-decreased

elderly vs young

-decreased HR at same %VO2 max in older patients, but similar at the same absolute work rate
-decreased CO at same relative and absolute work rates, so A-VO2 difference is higher
-decreased SV, increased BP, and increased TPR at the same relative and abso

orthostatic hypotension

-SBP decrease of greater than or equal to 20 or a DBP decrease of greater than or equal to 10 within 3 minutes of standing
-symptoms include dizziness, faintness, and lightheadedness

causes of orthostatic hypotension

-volume depletion (older patients are often on a diuretic and don't drink much)
-vasodilating drugs
-prolonged immobility
-slowed normal regulatory mechanisms (baroreceptor reflex)
-endocrine and metabolic disorders, such as diabetes
-nervous system disea

suggested interventions for orthostatic hypotension

-elastic stockings
-sleep with head of bed elevated about 15-20 degrees
-eat frequent small meals
-avoid valsalva maneuver
-avoid hot showers or excessive heat
-avoid sudden standing

arm vs leg exercise

-HR and BP are higher with arm exercise, at a GIVEN workload
-this is because a given workload is relatively higher for the arms than the legs
-therefore, there is no difference at the same RELATIVE workload
-we usually do about 40% of the work with the a

normal effects of dynamic exercise

-increased VO2
-increased CO
-increased HR
-increased SV, then levels off
-increased SBP
-no change in DBP
-decreased TPR
-left ventricular eccentric hypertrophy

effects of age, disease, and deconditioning

-decreased VO2 max
-increased VO2 at a given workload
-decreased CO
-decreased HR max
-decreased SV max
-decreased A-VO2
-increased BP
-increased TPR

normal effects of static exercise

-increased VO2
-increased CO
-increased HR that is greater than dynamics
-SV stays relatively the same
-huge increase in SBP
-increased DBP
-no change in TPR
-left ventricular concentric hypertrophy

general signs and symptoms of CVD

-weakness
-fatigue
-weight change
-poor exercise tolerance

integumentary signs and symptoms of CVD

-pressure ulcers
-loss of body hair

CNS signs and symptoms of CVD

-headaches
-impaired vision
-dizziness or syncope (especially in elderly)

respiratory signs and symptoms of CVD

-labored breathing
-productive cough

cardiovascular signs and symptoms of CVD

-chest pain
-palpitations
-edema
-claudication

genitourinary signs and symptoms of CVD

-uringary frequency
-nocturia
-concentrated urine
-decreased urinary output

musculoskeletal signs and symptoms of CVD

-myalgias
-muscular fatigue
-edema

gastrointestinal signs and symptoms of CVD

-nausea
-vomiting

NYHA classification

-classification of the severity of a patient's heart failure based on their function
-class 1: no limitation of activity
-class 2: slight limitation of activity
-class 3: moderate, marked limitations
-class 4: severe, symptoms at rest

pathogenesis of CAD

-the first step is injury to the endothelium
-fat deposition
-platelets adhere to damaged endothelium
-platelets release growth factors that stimulate production of connective tissue cells and attraction of smooth muscle cells
-sclerotic plaque forms
-the

vasospasm

-injured endothelium lacks the normal formation and release of nitric oxide
-therefore, these diseased vessels are more prone to spasm and they lack the normal ability to dilate

risk factors for CAD

-modifiable: physical inactivity, smoking, high cholesterol, hypertension, systemic inflammation, homocysteine, and sleep apnea
-nonmodifialbe: age, family history, ethnicity
-contributing factors: obesity, diabetes, response to stress, personality type,

physical inactivity

-one of the top modifiable risk factors for CAD
-has been likened to smoking a pack of cigarettes/day in terms of risk
-there is a linear drop in risk of MI with increased frequency of exercise
-the exercise required does not need to be of vigorous intens

smoking

-one of the top modifiable risk factors for CAD
-triples risk

high cholesterol

-one of the top modifiable risk factors for CAD
-the best predictor or risk when looking at cholesterol is the TC/HDL ratio
-ratio > 4.5 indicates increased risk of developing atherosclerosis
-most doctors try to keep the TC < 200, LDL < 100, and HDL betw

hypertension

-one of the top modifiable risk factors for CAD
-about 70% of patients over 65 have HTN
-HTN is NOT just a problem in the elderly
-high risk groups include African Americans, Hispanics, Pacific islanders, and Native Americans

systemic inflammation

-risk factor for CAD
-the liver puts out Crp in response to systemic inflammation
-excessively high levels of Crp indicate a tripled risk

homocysteine

-risk factor for CAD
-an amino acid that is produced from the breakdown of methionine, which is found in protein-rich foods such as red meat
-homocysteine appears to contribute to damage in the endothelium
-leafy greens can help to break apart homocystein

sleep apnea

-risk factor for CAD
-a disorder in which the person stops breathing for brief periods while asleep
-often seen in people with obesity

contributing factors for CAD

-obesity: particularly android
-response to stress: especially with HTN
-personality type: angry, hostile type A
-diabetes: number one cause of death in diabetics in MI
-hormonal status: premenopausal women are somewhat protected by estrogen, but HRT does

treating CAD

-most doctors won't intervene surgically until the vessel is occluced about 70%
-although it may take up to a year, the combination of moderate exercise, low fat diet, and stress management has proven to help reverse occlusion
-some studies show that exer

cardiopulmonary exam history

-medical diangosis
-risk factors
-medications
-lifestyle
-occupation
-diagnostic tests
-surgical history
-lab tests
-PFTs

cardiopulmonary exam subjective complaints

-chest pain: can be cardiac, pleural, or MSK (breathing won't impact ischemic pain)
-edema: could be R CHF (both legs). renal dysfunction, lymphedema
-fatigue: common but not specific
-lightheadedness and dizziness: make sure to check BP, could also be hy

cardiopulmonary exam inspection

-general appearance
-ROM
-strength
-functional activity level (HUGE part of our job)

cardiopulmonary exam auscultation

-heart sounds should be auscultated in patients with heart failure, as they may have an S3
-end inspiratory crackles are also common in left CHF

S1

-the first heart sound, heard when the atrioventricular (mitral and tricuspid) valves close and the ventricles go into systole
-systolic sound

S2

-the second heart sound, heard when the semilunar (aortic and pulmonic) valves close and the ventricles go into diastole
-diastolic sound

S3

-abnormal heart sound known as ventricular gallop that is associated with a dilated ventricle (eccentric hypertrophy)
-this sound follows S2
-it can be an early sign of CHF
-it may be present at rest, but it could also be brought on if the workload is too

S4

-abnormal heart sound known as atrial gallop
-associated with a rigid ventricle

aortic valve

-located at the second rib space, to the right of the sternum

pulmonic valve

-located at the second rib space, to the left of the sternum

tricuspid valve

-located at the 4th-5th rib space, at the lower left sternal border

mitral valve

-located at the 5th rib space, medial to the midclavicular line

activity assessment

-it is important to monitor a patient's HR, rhythm, BP, and symptoms in supine, sitting, standing, and during activity
-this is because you want to make sure that you correctly interpret the heart's response to a positional change or activity

resting heart rate

-normal RHR is 60-100 bpm
-bradycardia: could be due to training effects, medications, severe CAD, or not in sinus rhythm
-tachycardia: could be due to deconditioning, medications, CHF, anemia, hypoxia, or arrhythmia
-RHR < 50 or > 110, check with MD or R

rhythm

-without ECG monitoring equipment, you can only determine if the rhythm is regular or irregular
-regularly irregular: includes early beats and pauses
-irregularly irregular: only an average HR can be determined, A-fib is a common cause
-when a patient has

amplitude

-a strong pulse indicates a good SV or decreased peripheral resistance
-a weak pulse indicates a low SV or increased peripheral resistance

heart rate response during exercise

-HR should increase about 10 beats/MET unless patient is on a beta blocker
-HR increase during exercise can give you an idea of heart health (smaller increase in trained, greater increase in untrained)
-bradycardic response: > 10 bpm drop in HR with incre

RPE

-RPE can be used as an alternative to HR as a measure of exercise intensity
-rating should be based on total feeling of exertion and fatigue
-this is especially usefl for patients on beta blockers
-we usually want patients around an RPE of 13, which is st

heart rate recovery post exercise

-heart rate recovery reflects parasympathetic reactivation
-normally, HR should drop by more than 12 bpm after the first minute post-exercise
-a drop of 12 or fewer is abnormal, even in most patients with beta blockers

resting blood pressure

-normal resting blood pressure is less than 120/80
-hypertension is defined as SBP > 130 and/or DBP > 80
-SBP < 90 should be cautious with exercise, but SBP < 80 is often a contraindication to exercise
-SBP > 180 is a contraindication to exercise
-DBP < 6

blood pressure response during exercise

-SBP should increase about 7-10/MET, with no change in DBP
-hypotensive response: SBP drop of 10-20 with increased workload or DBP drop > 10 below resting, patient can continue exercise with drop of 10 if asymptomatic, but patient should be stopped with d

pulse pressure

-SBP - DBP
-normal is greater than 20
-should increase with exercise
-if it decreases with exercise to < 20, notify MD or RN
-the lower the pulse pressure is, the more concerned you need to be about tissue perfusion
-at the same time, you don't want the p

exercise recommendations based on hemoglobin and hematocrit

-the lower the hemoglobin is, the more concerned you need to be about exercise intolerance
-use a symptoms-based approach when determining appropriateness for activity
-most hemodynamically stable and asymptomatic patients will not receive a blood transfu

INR

-the higher the INR is, the more conservative you need to be
-normal is 0.9-1.1
-many patients post-op will have an INR of 2-3 to decrease risk of DVT and PE
-with INR < 4, you can do regular exercise without progression
-with INR 4-5, avoid resistive exe

modified chair step test

-this test is often used for the frail elderly who can't walk far enough for a 2-minute test to be useful
-this can be used as an exercise test, as well as a tool to guide exercise prescription
-four-stage test, with each stage lasting 3 minutes
-metronom

immediate signs and symptoms of exercise intolerance

-if any of these signs occur, you should lower the working HR to about 10 bpm lower than the HR at which the abnormal response occurred
-angina
-claudication
-lightheadedness
-appearance of distress
-abnormal BP response
-nausea/vomiting
-unusual fatigue

delayed signs and symptoms of exercise intolerance

-slow recovery post exercise, especially a delayed drop in HR beyond 5-10 minutes
-excessive fatigue lasting longer than 1-2 hours post activity
-insomnia
-weight gain due to fluid retention

chest x-ray

-cardiac enlargement: heart should be < 50% of the diameter of the whole chest
-localized chamber enlargement
-calcification in valves or coronary arteries
-pulmonary venous congestion
-alveolar edema
-enlargement of the pulmonary artery or dilatation of

Holter monitor

-continuous 24 hour ECG
-this is indicated for patients who report syncope, dizziness, dyspnea, and arrhythmias, but the signs disappear when seeing the doctor
-it is importnat for teh patient to document when they performed activities, what they, and if

electrophysiologic mapping studies

-patient is awake and the doctor tries to bring on the dysrhythmia by applying electrical stimulation
-when aberrant pathways are found, they are ablated

echocardiography

-ultrasound transducer shows dimensions and motions of cardiac structures, such as ventricular wall and valve motion
-it can also be used to estimate SV and EF
-if the doctor suspects a valve problem, echo is usually the first test because it is non-invas

MUGA

-non-invasive scan that is used to calculate EF
-radiolabeled blood is injected into the heart chamber
-LV EF is highly predictive of 1-year survival
-exercise LV EF is the strongest EF predictor of outcomes

MRI

-detect coronary artery obstruction
-sense wall motion abnormalities
-look for valve disease
-measure cardiac blood flow
-MRI is NOT good enough to replace cardiac catheterization

radionuclide studies

-these are often performed in conjunction with an exercise test
-whenever the test is about done, Thallium is injected via IV
-the doctor will look for an area where the Thallium wasn't picked up, which indicates poor perfusion to that area, called a cold

exercise stress test

-can be very helpful for determining exercise capacity
-can also help to aid in the diagnosis of cardiopulmonary issues

cardiac catheterization

-invasive diagnostic procedure in which a catheter is passed into a vein or artery and then guided into the heart
-every patient who is going to have cardiac surgery will have a cardiac cathether
-this way, the surgeon knows EXACTLY which coronary arterie

arterial line

-monitoring device consisting of a catheter that is inserted into an artery and attached to an electronic monitoring system
-provides continuous BP monitoring
-the transducer needs to be level with the right atrium for the measurements to be accurate
-if

pulmonary artery catheter

-catheter that is usually inserted through the subclavian or internal jugular veins
-used to monitor right atrial and pulmonary arterial pressures, fluid balance, CO, SVO2, and vascular resistance

pulmonary artery catheter with balloon inflated

-pulmonary artery catheter has balloon inflated and is migrated until it wedges into a capillary
-because the pulmonary veins do not have valves, the pressure in the left side of the heart should be the same as the pressure picked up in the balloon
-this

normal heart pressures

-right atrial pressure: 0-8 mm Hg
-right ventricular pressures: diastolic is 0-8, systolic is 15-30
-pulmonary artery pressures: diastolic is 5-15, systolic is 15-30
-pulmonary artery wedge pressure: 4-12, should be the same as the diastolic pressure on t

MAP

-MAP = DBP + 1/3(pulse pressure)
-normal MAP = 70-110
-MAP < 60 indicates inadequate perfusion pressure and is frequently a contraindication to exercise

thermodilution method

-temperature change of the blood can be used to measure cardiac output

cardiac index

-cardiac output per square meter (height)
-3.5 is normal
-< 2.2 indicates cardiogenic shock

cardiogenic shock

-shock caused by inadequate function of the heart, or pump failure

intra-aortic balloon pump

-used for unstable patients to assist the left ventricle to increase diastolic pressure and coronary blood flow
-the balloon inflates during diastole, and it's timed with the QRS
-the balloon deflates during systole to prevent high afterload
-inserted via

impella

-fairly new internal assistive device for the left ventricle
-it sucks blood through the port and pushes it into the aorta
-can deliver up to 5 L/min forward flow
-helps to unload the left ventricle