stress test to see ischemia
dual isotope for cardiac perfusion study
heart rate at the end of stage 1?
within stage 1, HR to 120
target heart rate
how big is the pt? BMI(body mass index)?
resting heart rate?
What is the mechanism / severity of exercise test, what scale do they use? 1 - 20
METS?
short access, horizontal and vertical access
rest vs. stress
motion correction
no gated image due to arrhythmia
flow limiting stenosis?
RAO, LAO, LAD, D2, FFR
signs of vascular disease?
pressure wire
residual pressure down stenosis
hyperemia
adenosine mimicking hyperemia
pharmacological stress vs. physiological stress
coronary heart disease
MI(myocardial infarction) => chronic heart failure
chest pain stress
baseline EKG change
baseline heart rate
stress test
EF, EDV, ESV, SV, mass
RAO caudal?
PLOM(posterolateral marginal) lesion?
pressure of "juicy" stent, looks like a thick vessel
flow limiting disease, LB gram?
small vessel disease
LVEDP(left ventricular end diastolic pressure), LAD, ischemic dilation
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Fainting or syncope (IPA: /ˈsɪnkəpi/ or /ˈsɪŋkəpi/) is a sudden (and generally momentary) loss of consciousness, or blacking out, due to a lack of sufficient blood and oxygen reaching the brain.
Factors that influence fainting are taking in too little food and fluids, low blood pressure, hypoglycemia, growth spurts, physical exercise in excess of the energy reserve of the body, and lack of sleep. Even standing up too quickly or being in too hot a room can cause fainting.
Recommended treatment is to allow the person to lie on the ground with his or her legs a little elevated. As the dizziness and the momentary blindness passes, the person may experience visual disturbances in the form of small bright dots (phosphene). These will also pass within a few minutes. If fainting happens frequently, or if there is no obvious explanation, it is important to see a doctor about it.
More serious causes of fainting include cardiac (heart-related) causes such as an abnormal heart rhythm (an arrhythmia), where the heart beats too slowly, too rapidly or too irregularly to pump enough blood to the brain. Some arrythmias can be life-threatening. Other important cardiac conditions that can manifest with syncope include subclavian steal syndrome and aortic stenosis.
Fainting can also be due to neurological disorders, stress, side effects of anaesthetics, etc.
Types
Fainting involves a temporary reduction of blood (and therefore oxygen) supply to the brain, resulting in a blackout. Many forms of syncope are benign and easy to associate with clear precipitants that can be avoided. Such precipitants can include many common situations and recreational drugs as well as therapeutic drugs.
Syncope can be brought on by a variety of heart-related and non-heart-related circulatory problems and activities, including simply getting up too quickly. Because of these many causes, there are subclassifications:
- vasovagal syncope, this is the common faint associated with a stress response of the autonomic nervous system which can either suddenly lower the pulse rate, the blood pressure or both together. It is one of the neurally-mediated reflex syncopes.
- carotid sinus syncope, also is associated with abnormal sensitivity to external pressure over the region of the nerve sensory organ at the bifurcation of the external and internal carotid arteries in the neck. Another reflex syncope.
- tussive syncope induced by coughing fits, also called larangeal syncope. (Layterm: tussive syncopathy)
- An article in the August 2005 edition of the UK medical journal The Lancet was entitled Laughter-induced syncope.
- micturition syncope a faint during or shortly after urination. It is also one of the neurally-mediated reflex syncopes.
Some of the other common medical conditions which may result in syncope are orthostatic hypotension (fall in blood pressure when standing) and heart rhythm problems (Cardiac arrhythmia).
Other ways people faint is when they have an overdose of stress or long term stress, which may lead to a heart attack or stroke. At this stage, action should be taken immediately.
Patients who experience syncope episode do not remember falling.
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In physiology, perfusion is the process of nutritive delivery of arterial blood to a capillary bed in the biological tissue.
Two main categories of functional magnetic resonance imaging (fMRI) techniques can be used to measure tissue perfusion in vivo. The first is based on the use of injected contrast agent that changes the magnetic susceptibility of blood and thereby the MR signal which is repeatedly measured during bolus passage. The other category is based on arterial spin labeling (ASL), where arterial blood is magnetically tagged before it enters into the tissue of interest and the amount of labeling is measured and compared to a control recording obtained without spin labeling.
Tests of adequate perfusion are a part of patient triage performed by medical or emergency personnel in a mass casualty incident.
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Nuclear Cardiology
Overview
There are two main types of nuclear tests performed in cardiology:
1) Myocardial perfusion studies- examines the blood flow to the heart muscle.
2) Dynamic studies- measures the contractile (pumping) function of the heart muscle.
Exercise Myocardial Perfusion Imaging
This test is performed with the isotope thallium or, at the present time, more often with technetium Sestamibi (MIBI). The test is performed in conjunction with a treadmill exercise test and is referred to as a "treadmill-thallium" test or a "treadmill-MIBI" test.
Myocardial perfusion imaging is performed:
- When the results of a routine treadmill study are equivocal
- When there is known coronary artery occlusive disease and it is desirable to know the extent and severity of the disease (so-called risk stratification).
- In some patients to determine the functional significance of coronary blockage observed on an angiogram
- To determine if coronary disease is the cause of, or associated with, abnormalities on the resting electrocardiogram
- To evaluate the results of coronary bypass surgery or coronary balloon angioplasty (PTCA)
Myocardial perfusion imaging is a non-invasive test and carries no risk beyond that of the treadmill testing itself. The radioactive isotope injected for the study produces less radiation than x-ray procedures such as a CAT scan or kidney study and is non-allergenic.
Dynamic Studies
Dynamic studies measure the contractile (pumping) function of the heart muscle. The test goes under several different names and abbreviations. At St. Luke's Episcopal Hospital, an early description of the test was a "left ventricular performance study" and this was abbreviated LVPS. Other Institutions call the test a MUGA scan and others refer to it as a radionuclide ventriculogram or radionuclide angiogram (RNA). All of these names describe the same test. In this test a small dose of isotope tracer is injected into the bloodstream, followed by imaging of the region of the heart to demonstrate the isotope particles within the chambers of the heart. The dose of isotope is sufficiently small such that a number of cardiac cycles must be measured to have a quantity of isotope to be recognized by the camera. A good study will give an accurate picture of the chambers of the heart and the contraction of the ventricles, especially that of the left ventricle. Accordingly, cardiac enlargement, hypertrophy (thickening), pumping function (ejection fraction, EF) and areas of previous myocardial infarction can be well identified.
The study can be performed as a resting study and also as part of a rest/exercise study to determine whether the above parameters of cardiac function are altered favorably or deteriorate during and after exercise. The usual form of exercise is semi-supine bicycle exercising since in this fashion, the upper portion of the body is stabilized and adequate images of the heart can be obtained during exercise. The test is non-invasive and carries no risk to the patient whatsoever, other than the risk of exercise as described in the treadmill testing section above.--------------------------------------------------------------------------
Shock is a serious medical condition where the tissue perfusion is insufficient to meet the required supply of oxygen and nutrients. This hypoperfusional state is a life-threatening medical emergency and one of the leading causes of death in a critically ill person. This primary cause may lead to many other medical emergencies, such as hypoxia or cardiac arrest.
Stages of shock
There are four stages of shock.[6]
- Initial - This is where the hypoperfusional states causes hypoxia, leading to the mitochondria being unable to produce adenosine triphosphate. Due to this lack of oxygen, the cell membranes become damaged and the cells perform anaerobic respiration. This causes a build-up of lactic and pyruvic acid which results in systemic metabolic acidosis. The process of removing these compounds from the cells by the liver requires oxygen, which is absent.
- Compensatory - This stage is characterised by the body employing physiological mechanisms, including neural, hormonal and bio-chemical mechanisms in an attempt to reverse the condition. As a result of the acidosis, the person will begin to hyperventilate in order to rid the body of carbon dioxide (CO2). CO2 indirectly acts to acidify the blood and by removing it the body is attempting to raise the pH of the blood. The baroreceptors in the arteries detect the resulting hypotension, and cause the release of adrenaline and noradrenaline. These cause widespread vasoconstriction resulting in an increase in not only blood pressure but heart rate. Renin-angiotensin axis is activated and antidiuretic hormone is released to conserve fluid by kidneys. Also, these hormones cause the vasoconstriction of the kidneys, gastrointestinal tract, and other organs to divert blood to the heart, lungs and brain. The lack of blood to the renal system causes the characteristic low urine production.
- Progressive - Should the cause of the crisis not be successfully treated, the shock will proceed to the progressive stage and the compensatory mechanisms begin to fail. Due to the decreased perfusion of the cells, sodium ions build up within while potassium ions leak out. As anaerobic metabolism continues, increasing the body's metabolic acidosis, the arteriolar and precapillary sphincters constrict such that blood remains in the capillaries. Due to this, the hydrostatic pressure will increase and, combined with histamine release, this will lead to leakage of fluid and protein into the surrounding tissues. As this fluid is lost, the blood concentration and viscosity increase, causing sludging of the micro-circulation. The prolonged vasoconstriction will also cause the vital organs to be compromised due to reduced perfusion.
- Refractory - At this stage, the vital organs have failed and the shock can no longer be reversed. Brain damage and cell death have occurred. Death will occur imminently.
Shock is a complex and continuous condition and there is no sudden transition from one stage to the next.
[edit] Types of shock
In 1972 Hinshaw and Cox suggested the following classification which is still used today.[1] It uses four types of shock: hypovolaemic, cardiogenic, distributive and obstructive shock:[2][3][4][5][7]
- Hypovolaemic shock - This is the most common type of shock and based on insufficient circulating volume. Its primary cause is loss of fluid from the circulation from either an internal or external source. An internal source may be haemorrhage. External causes may include extensive bleeding, high output fistulae or severe burns.
- Cardiogenic shock - This type of shock is caused by the failure of the heart to pump effectively. This can be due to damage to the heart muscle, most often from a large myocardial infarction. Other causes of cardiogenic shock include arrhythmias, cardiomyopathy, congestive heart failure (CHF), contusio cordis or cardiac valve problems.
- Distributive shock - As in hypovolaemic shock there is an insufficient intravascular volume of blood. This form of "relative" hypovolaemia is the result of dilation of bloodvessels which diminishes systemic vascular resistance. Examples of this form of shock are:
- Septic shock - This is caused by an overwhelming infection leading to vasodilation, such as by Gram negative bacteria i.e. Escherichia coli, Proteus species, Klebsiella pneumoniaewhich release an endotoxin which produces adverse biochemical, immunological and occasionally neural mechanisms which are harmful to the body. Gram-positive cocci, such as pneumococci and streptococci, and certain fungi as well as gram-positive bacterial toxins produce a similar syndrome.
- Anaphylactic shock - Caused by a severe anaphylactic reaction to an allergen, antigen, drug or foreign protein causing the release of histamine which causes widespread vasodilation. Leading to hypotension and increased capillary permeability.
- Neurogenic shock - Neurogenic shock is the rarest form of shock. It is caused by trauma to the spinal cord resulting in the sudden loss of autonomic and motor reflexes below the injury level. Without stimulation by sympathetic nervous system the vessel walls relax uncontrolled, resulting in a sudden decrease in peripheral vascular resistance, leading to vasodilation and hypotension.
- Obstructive shock - In this situation the flow of blood is obstructed which impedes circulation and can result in circulatory arrest. Several conditions result in this form of shock.
- Cardiac tamponade in which blood in the pericardium prevents inflow of blood into the heart (venous return). Constrictive pericarditis, in which the pericardium shrinks and hardens, is similar in presentation.
- Tension pneumothorax. Through increased intrathoracic pressure, bloodflow to the heart is prevented (venous return).
- Massive pulmonary embolism is the result of a thromboembolic incident in the bloodvessels of the lungs and hinders the return of blood to the heart.
- Aortic stenosis hinders circulation by obstructing the ventricular outflow tract
Recently a fifth form of shock has been introduced:[1]
- Endocrine shock based on endocrine disturbances.
- Hypothyroidism, in critically ill patients, reduces cardiac output and can lead to hypotension and respiratory insufficiency.
- Thyrotoxycosis may induce a reversible cardiomyopathy.
- Acute adrenal insufficiency is frequently the result of discontinuing corticosteroid treatment without tapering the dosage. However, surgery and intercurrent disease in patients on corticosteroid therapy without adjusting the dosage to accommodate for increased requirements may also result in this condition.
- Relative adrenal insufficiency in critically ill patients where present hormone levels are insufficient to meet the higher demands
In medicine, ischemia (Greek ισχαιμία, isch- is restriction, hema or haema is blood) is a restriction in blood supply, generally due to factors in the blood vessels, with resultant damage or dysfunction of tissue. It may also be spelled ischaemia or ischæmia.
Mechanism
Rather than in hypoxia, a more general term denoting a shortage of oxygen (usually a result of lack of oxygen in the air being breathed), ischemia is an absolute or relative shortage of the blood supply to an organ. Relative shortage means the mismatch of blood supply (oxygen delivery) and blood request for adequate oxygenation of tissue.
Ischemia can also be described as an inadequate flow of blood to a part of the body, caused by constriction or blockage of the blood vessels supplying it. Ischemia of heart muscle produces angina pectoris.
This can be due to:
- Tachycardia (abnormally rapid beating of the heart)
- Atherosclerosis (lipid-laden placques obstructing the lumen of arteries)
- Hypotension (low blood pressure, e.g. in septic shock, heart failure)
- Thromboembolism (blood clots)
- Outside compression of a blood vessel, e.g. by a tumor
- Foreign bodies in the circulation (e.g. amniotic fluid in amniotic fluid embolism)
- Sickle cell disease (abnormally shaped hemoglobin)
[edit] Consequences
Since oxygen is mainly bound to hemoglobin in red blood cells, insufficient blood supply causes tissue to become hypoxic, or, if no oxygen is supplied at all, anoxic. This can cause necrosis (i.e. cell death). Necrosis due to ischemia usually takes about 10-12 hours.
Ischemia is a feature of heart diseases, transient ischemic attacks, cerebrovascular accidents, ruptured arteriovenous malformations, and peripheral artery occlusive disease.
Tissues especially sensitive to inadequate blood supply are the heart, the kidneys, and the brain. Ischemia in brain tissue, for example due to stroke or head injury, causes a process called the ischemic cascade to be unleashed, in which proteolytic enzymes, reactive oxygen species, and other harmful chemicals damage and may ultimately kill brain tissue.
Restoration of blood flow after a period of ischemia can actually be more damaging than the ischemia. Reintroduction of oxygen causes a greater production of damaging free radicals, resulting in reperfusion injury. With reperfusion injury, necrosis can be greatly accelerated.
--------------------------------------------------------------------------The BMI has become controversial because many people, including physicians, have come to rely on it for medical diagnosis - but that has never been the BMI's purpose. It is meant to be used as a simple means of classifying sedentary (physically inactive) individuals with an average body composition.[citation needed] For these individuals, the current value settings are as follows: a BMI of 18.5 to 25 may indicate optimal weight; a BMI lower than 18.5 suggests the person is underweight while a number above 25 may indicate the person is overweight; a BMI below 15 may indicate the person has an eating disorder; a number above 30 suggests the person is obese (over 40, morbidly obese).
In physiology the term “weight” is used interchangeably with the “mass”. For a given body shape and given density, the BMI will be proportional to height e.g. if all body dimensions increase by 50%, the BMI increases by 50%.
Generally, a BMI chart displays calculated BMI as a function of weight (horizontal axis) and height (vertical axis) using “contour lines” for different values of BMI or colors for different BMI categories.
Thresholds
Given the reservations detailed below concerning the limitations of the BMI as a diagnostic tool for individuals, the following are common definitions of BMI categories:
-
- Starvation: less than 15
- Underweight: less than 18.5
- Ideal: from 18.5 to 25
- Overweight: from 25 to 30
- Obese: from 30 to 40
- Morbidly Obese: greater than 40
The U.S. National Health and Nutrition Examination Survey of 1994 indicates that 59% of American men and 49% of women have BMIs over 25. Extreme obesity — a BMI of 40 or more — was found in 2% of the men and 4% of the women. There are differing opinions on the threshold for being underweight in females, doctors quote anything from 18.5 to 20 as being the lowest weight, the most frequently stated being 19. A BMI nearing 15 is usually used as an indicator for starvation and the health risks involved, with a BMI <17.5 href="http://en.wikipedia.org/wiki/Diagnostic_and_Statistical_Manual_of_Mental_Disorders" title="Diagnostic and Statistical Manual of Mental Disorders">DSM criteria for the diagnosis of anorexia nervosa.
--------------------------------------------------------------------------A unit of metabolic equivalent, or MET, is defined as the number of calories consumed by an organism per minute in an activity relative to the Basal metabolic rate (BMR/RMR, see below). A single unit (1 MET) is the caloric consumption of that organism, or individual, while at complete rest. For example, one might consider the restful state following a quiet night's sleep as a good example of a single MET. This is a base-line unit for that one individual, and since each individual has a varying BMR, a MET is, therefore, variable from one person to the next. One might consider a single unit the energy required to just stay alive without doing anything more.
The unit is commonly used in the context of aerobic exercise to gauge the intensity of the workout. A workout of 2-4 METs is considered light, while intensive running (8 minutes/mile, or 12 km/h) or climbing can yield workouts of 12 or more METs.
Since METs are variable units, they can only be used in calculating relative energy expenditures in "context;" meaning within the parameters per individual, unlike caloric expenditures which are unitary standards not variable from one person to another. While exercising at 6 METs, a 200-pound (90 kg) man would burn considerably more calories than his 120-pound (55 kg) son doing the same exercise.
METs are particularly relevant to those who intend to lose weight, because they are a simple approximation of the rate at which exercise causes calories to be burned. Many modern exercise machines can indicate METs, although the numbers given are estimates since, as mentioned above, the rate at which calories are burned while at rest (the Basal Metabolic Rate or, more strictly, the Resting metabolic rate: RMR) varies from person to person.
--------------------------------------------------------------------------Basal metabolic rate (BMR) is the amount of energy expended while at rest in a neutrally temperate environment, in the post-absorptive state (meaning that the digestive system is inactive, which requires about twelve hours of fasting in humans). The release of energy in this state is sufficient only for the functioning of the vital organs, such as the heart, lungs, brain and the rest of the nervous system, liver, kidneys, sex organs, muscles and skin. BMR decreases with age and with the loss of lean body mass. Increased cardiovascular exercise and muscle mass can increase BMR. Illness, previously consumed food and beverages, environmental temperature, and stress levels can affect one's overall energy expenditure, and can affect one's BMR as revealed by gas analysis. It is measured when the person is at complete rest, but awake. An accurate BMR measurement requires that the person's sympathetic nervous system is not stimulated. Basal metabolic rate is measured under very restrictive circumstances. A more common and closely related measurement, used under less strict conditions, is resting metabolic rate (RMR).[1]
Physiology
Both basal metabolic rate and resting metabolic rate are usually expressed in terms of daily rates of energy expenditure. The early work of the scientists J. Arthur Harris and Francis G. Benedict showed that approximate values could be derived using body surface area (computed from height and weight), age, and sex, along with the oxygen and carbon dioxide measures taken from calorimetry. Studies also showed that by eliminating the sex differences that occur with the accumulation of adipose tissue by expressing metabolic rate per unit of "fat-free" or lean body weight, the values between sexes for basal metabolism are essentially the same. Exercise physiology textbooks have tables to show the conversion of height and body surface area as they relate to weight and basal metabolic values.
The primary organ responsible for regulating metabolism is the hypothalamus. The hypothalamus is located on the brain stem and forms the floor and part of the lateral walls of the third ventricle of the cerebrum. The chief functions of the hypothalamus are:
-
- control and integration of activities of the autonomic nervous system (ANS)
- The ANS regulates contraction of smooth muscle and cardiac muscle, along with secretions of many endocrine organs such as the thyroid gland (associated with many metabolic disorders).
- Through the ANS, the hypothalamus is the main regulator of visceral activities, such as heart rate, movement of food through the gastrointestinal tract, and contraction of the urinary bladder.
- production and regulation of feelings of rage and aggression
- regulation of body temperature
- regulation of food intake, through two centers:
- The feeding center or hunger center is responsible for the sensations that cause us to seek food. When sufficient food or substrates have been received and leptin is high, then the satiety center is stimulated and sends impulses that inhibit the feeding center. When insufficient food is present in the stomach and ghrelin levels are high, receptors in the hypothalamus initiate the sense of hunger.
- The thirst center operates similarly when certain cells in the hypothalamus are stimulated by the rising osmotic pressure of the extracellular fluid. If thirst is satisfied, osmotic pressure decreases.
- control and integration of activities of the autonomic nervous system (ANS)
All of these functions taken together form a survival mechanism that causes us to sustain the body processes that BMR and RMR measure.
--------------------------------------------------------------------------The "LAD", or left anterior descending artery (or anterior interventricular branch of the left coronary artery, or anterior descending branch) passes at first behind the pulmonary artery and then comes forward between that vessel and the left auricula to reach the anterior interventricular sulcus, along which it descends to the incisura apicis cordis.
In 78% of cases, it reaches the apex of the heart.
It supplies the anterolateral myocardium, apex, and interventricular septum. The LAD typically supplies 45-55% of the left ventricle (LV).
The LAD gives off two types of branches: septals and diagonals.
- Septals originate from the LAD at 90 degrees to the surface of the heart, perforating and supplying the intraventricular septum.
- Diagonals run along the surface of the heart and supply the lateral wall of the LV and the anterolateral papillary muscle.
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Coronary Blood Supply to the Heart*
|
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Right Coronary Artery, LAO/cranial view
LAO(left anterior oblique) projection
RAO(right anterior oblique) projection
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ANTIARRHYTHMICS
1. Amiodarone
· Used in a wide variety of atrial and ventricular tachyarrhythmias, and for rate control of rapid atrial fibrillation and atrial flutter, especially in patients with impaired LV function.
· Contraindications: thyrotoxicosis, cirrhosis, severe pulmonary disease. Use with caution in patients with sinus or AV node dysfunction.
· Typical IV loading dose: 150 mg IV over 10 min, followed by 1 mg/min x 6 hours, then 0.5 mg/min x 18 hours. Can repeat 150 mg IV over 10-30 minutes for recurrent arrhythmias.
· Typical PO loading dose:
- VT (10 grams): 1200 mg/d (divided doses) x 10d, 800 mg/d x 2-4 weeks, 600 mg/d x 2-4 weeks, then 400 mg/d maintenance.
- SVT or CHF (4 grams): 800 mg/d x 5 days, then 200 mg/d maintenance.
· Switching from IV to PO therapy: If on IV therapy for >2-3 weeks, start with maintenance PO dose. If on IV therapy <>
· If a patient on long-term oral therapy has recurrent arrhythmias, assume inadequate myocardial drug concentrations and repeat IV load.
· Dosing of digoxin and warfarin may need to be adjusted in patients treated with amiodarone.
· Short-term adverse effects: vasodilation, hypotension, negative inotropic effects, prolonged QT (although rarely causes torsades)
· Long-term adverse effects (dose-related): photophobia, visual blurring, halo vision, blue skin discoloration, photosensitivity, cough (interstitial pneumonitis), nausea, anorexia, constipation, increased AST and ALT, hypothyroidism (can also cause hyperthyroidism), ataxia, paresthesias, peripheral neuropathy, bradycardia, AV block.
2. Procainamide
· Usually load 1 gram IV over 1 hour (750 mg if elderly) then start Procan SR 750 mg PO qid.
· Monitor for QTc prolongation, prolongation of QRS >50%, hypotension.
· Follow levels of procainamide + NAPA (therapeutic range=10-20).
3. Adenosine
· Used to assess underlying rhythm and/or to break SVT.
· Use 6-12 mg rapid IVP if through peripheral line; 3-6 mg IVP through central line.
4. Lidocaine
· Used for VF/VT arrest, stable VT, and wide complex tachycardia of unknown type.
· 1.0-1.5 mg/kg IV, then maintenance gtt at 1-4 mg/min.
Desai AD, Chun S, Sung RJ. The role of intravenous amiodarone in the management of cardiac arrhythmias. Ann Intern Med 1997; 127:294-303.
PRESSORS AND CARDIAC DRIPS
Name | Receptors | Dose | Action | Side effects |
| Phenylephrine | a1 | 10-200 mcg/min | pure vasoconstrictor | vasospasm, ARF |
| Norepinephrine | a1, b1 | 1-30 mcg/min | vasoconstrictor, positive inotropy | arrhythmias, ARF, vasospasm |
| Dopamine | D1 | 1-2 mcg/kg/min | splanchnic vasodilation |
|
| b1 | 2-10 mcg/kg/min | positive inotropy | arrhythmias, tachycardia | |
| a1 | 10-20 mcg/kg/min | vasoconstriction | arrhythmias, tachycardia | |
| Dobutamine | b1, b2 | 1-20 mcg/kg/min | positive inotropy and chronotropy | hypotension |
| Epinephrine | a1, a2, b1, b2 | 0.25-4 mcg/min | positive inotropy, chronotropy, and vasoconstriction | arrhythmias, tachycardia |
| Amiodarone | K+-, Na+- channel blocker, b-blocker, Ca-blocker | 150 mg over 10 min, then 1 mg/min x 6 hr, then 0.5 mg/min x 18 hr | anti-arrhythmic, rate control | AV block, hypotension |
| Procainamide | Na channel blocker | 1 g over 20 min, then 1-4 mg/min | anti-arrhythmic | hypotension, prolonged QT |
| Lidocaine | Na channel blocker | 1-1.5 mg/kg, then 1-4 mg/min | anti-arrhythmic | seizures, AMS |
| Esmolol | b1>b2 blocker | 500 mcg/kg then 25-300 mcg/kg/min | rate control, anti-hypertensive | hypotension, CHF, bronchospasm |
| Propranolol | b-blocker | 0.5-2.0 mg, then 1-10 mg/hr | rate control, anti-hypertensive | hypotension, CHF, bronchospasm |
| Labetalol | a1, b1, b2 blocker | 2.5-10 mg, then 10-120 mg/hr | anti-hypertensive | hypotension, CHF, bronchospasm |
| Diltiazem | Ca-channel blocker | 0.25 mg/kg over 2 min, reload 0.35 mg/kg q15 min. prn, then 10-15 mg/hr | rate-control | hypotension, AV block |
| Verapamil | Ca-channel blocker | 2.5-5 mg, then 5-20 mg/hr | rate control | hypotension, AV block |
| Hydralazine | direct vasodilator | 2.5-20 mg q3 min, up to 400 mg, then 5-20 mg q6h | anti-hypertensive | hypotension, angina |
http://medicine.ucsf.edu/housestaff/handbook/HospH2002_C2.htm#LCA
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Fractional flow reserve (FFR) is defined as the ratio of the
maximal blood flow achievable in a stenotic vessel to the
normal maximal flow in the same vessel.
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Hyperaemia (AmE hyperemia) is the medical condition in which blood congests in a part of the body. The condition may be subdivided into active hyperaemia, in which blood collects in an organ due to increased blood flow, and passive hyperaemia, in which blood collects in an organ due to an obstruction in the outflowing veins.
Active hyperemia is also a term used to describe dilation of arteriolar smooth muscle to increase blood flow in response to an increase in metabolism. Reactive hyperemia is the same but in response to a profound increase in blood flow to an organ after being occluded. There will be a shortage of oxygen and a build-up of metabolic waste.
Active Hyperemia is a term used to describe a dilation of arteriolar smooth muscle to increase blood flow in response to an increase in metabolism. As tissue or organs increase their metabolic activity they will consume more oxygen and produce more metabolites (products of metabolism ). This leads to a decrease in oxygen and increase in metabolite concentration in the interstitial fluid surrounding the arterioles that supply the tissue. This leads to arteriolar dilation which permits more blood flow to the organ or tissue. This is a local control that is independent of nerves or hormones.
The effect of active hyperemia is most highly developed in the tissues that exhibit the largest range of metabolic activity (Skeletal muscle, cardiac muscle, and glands.)
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Adenosine is a nucleoside comprised of adenine attached to a ribose (ribofuranose) moiety via a β-N9-glycosidic bond.
Anti-inflammatory Properties
Adenosine is a potent anti-inflammatory agent, acting at its four G-protein coupled receptors. Topical treatment of adenosine to foot wounds in diabetes mellitus has been shown in lab animals to drastically increase tissue repair and reconstruction. Topical administration of adenosine for use in wound healing deficiencies and diabetes mellitus in humans is currently under clinical investigation.
[edit] Action on the heart
When administered intravenously, adenosine causes transient heart block in the AV node. It also causes endothelial dependent relaxation of smooth muscle as is found inside the artery walls. This causes dilatation of the "normal" segments of arteries where the endothelium is not separated from the tunica media by atherosclerotic plaque. This feature allows physicians to use adenosine to test for blockages in the coronary arteries, by exaggerating the difference between the normal and abnormal segments.
In individuals suspected of suffering from a supraventricular tachycardia (SVT), adenosine is used to help identify the rhythm. Certain SVTs can be successfully terminated with adenosine. This includes any re-entrant arrhythmias that require the AV node for the re-entry (e.g., AV reentrant tachycardia (AVRT), AV nodal reentrant tachycardia (AVNRT). In addition, atrial tachycardia can sometimes be terminated with adenosine.
Adenosine has a direct effect on atrial tissue causing a shortening of the refractory period. When administered via a central lumen catheter, adenosine has been shown to initiate atrial fibrillation because of its affect on atrial tissue. In individuals with accessory pathways, the onset of atrial fibrillation can lead to a life threatening ventricular fibrillation.
Fast rhythms of the heart that are confined to the atria (e.g., atrial fibrillation, atrial flutter) or ventricles (e.g., monomorphic ventricular tachycardia) and do not involve the AV node as part of the re-entrant circuit are not typically affected by adenosine.
Because of the effects of adenosine on AV node-dependent SVTs, adenosine is considered a class V antiarrhythmic agent.
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Coronary heart disease (CHD), also called coronary artery disease (CAD) and atherosclerotic heart disease, is the end result of the accumulation of atheromatous plaques within the walls of the arteries that supply the myocardium (the muscle of the heart). While the symptoms and signs of coronary heart disease are noted in the advanced state of disease, most individuals with coronary heart disease show no evidence of disease for decades as the disease progresses before the first onset of symptoms, often a "sudden" heart attack, finally arise. After decades of progression, some of these atheromatous plaques may rupture and (along with the activation of the blood clotting system) start limiting blood flow to the heart muscle. The disease is the most common cause of sudden death, and is also the most common reason for death of men and women over 65 years of age.
Overview
Atherosclerotic heart disease can be thought of as a wide spectrum of disease of the heart. At one end of the spectrum is the asymptomatic individual with atheromatous streaks within the walls of the coronary arteries (the arteries of the heart). These streaks represent the early stage of atherosclerotic heart disease and do not obstruct the flow of blood. A coronary angiogram performed during this stage of disease may not show any evidence of coronary artery disease, because the lumen of the coronary artery has not decreased in calibre.
Over a period of many years, these streaks increase in thickness. While the atheromatous plaques initially expand into the walls of the arteries, eventually they will expand into the lumen of the vessel, affecting the flow of blood through the arteries. While it was originally believed that the growth of atheromatous plaques was a slow, gradual process, some recent evidence suggests that the gradual buildup of plaque may be complemented by small plaque ruptures which cause the sudden increase in the plaque burden due to accumulation of thrombus material.
Atheromatous plaques that cause obstruction of less than 70 percent of the diameter of the vessel rarely cause symptoms of obstructive coronary artery disease. As the plaques grow in thickness and obstruct more than 70 percent of the diameter of the vessel, the individual develops symptoms of obstructive coronary artery disease. At this stage of the disease process, the patient can be said to have ischemic heart disease. The symptoms of ischemic heart disease are often first noted during times of increased workload of the heart. For instance, the first symptoms include exertional angina or decreased exercise tolerance.
As the degree of coronary artery disease progresses, there may be near-complete obstruction of the lumen of the coronary artery, severely restricting the flow of oxygen-carrying blood to the myocardium. Individuals with this degree of coronary heart disease typically have suffered from one or more myocardial infarctions (heart attacks), and may have signs and symptoms of chronic coronary ischemia, including symptoms of angina at rest and flash pulmonary edema.
A distinction should be made between myocardial ischemia and myocardial infarction. Ischemia means that the amount of oxygen supplied to the tissue is inadequate to supply the needs of the tissue. When the myocardium becomes ischemic, it does not function optimally. When large areas of the myocardium becomes ischemic, there can be impairment in the relaxation and contraction of the myocardium. If the blood flow to the tissue is improved, myocardial ischemia can be reversed. Infarction means that the tissue has undergone irreversible death due to lack of sufficient oxygen-rich blood..
An individual may develop a rupture of an atheromatous plaque at any stage of the spectrum of coronary heart disease. The acute rupture of a plaque may lead to an acute myocardial infarction (heart attack).
[edit] Pathophysiology
Limitation of blood flow to the heart causes ischemia (cell starvation secondary to a lack of oxygen) of the myocardial cells. When myocardial cells die from lack of oxygen, this is called a myocardial infarction (commonly called a heart attack). It leads to heart muscle damage, heart muscle death and later scarring without heart muscle regrowth.
Myocardial infarction usually results from the sudden occlusion of a coronary artery when a plaque ruptures, activating the clotting system and atheroma-clot interaction fills the lumen of the artery to the point of sudden closure. The typical narrowing of the lumen of the heart artery before sudden closure is typically 20%, according to clinical research completed in the late 1990s and using IVUS examinations within 6 months prior to a heart attack. High grade stenoses as such exceeding 75% blockage, such as detected by stress testing, were found to be responsible for only 14% of acute heart attacks the rest being due to plaque rupture/ spasm. The events leading up to plaque rupture are only partially understood. Myocardial infarction is also caused, far less commonly, by spasm of the artery wall occluding the lumen, a condition also associated with atheromatous plaque and CHD.
CHD is associated with smoking, obesity, hypertension and a chronic sub-clinical lack of vitamin C. A family history of CHD is one of the strongest predictors of CHD. Screening for CHD includes evaluating homocysteine levels, high-density and low-density lipoprotein (cholesterol) levels and triglyceride levels.
[edit] Angina
The pain associated with very advanced CHD is known as angina, and usually presents as a sensation of pressure in the chest, arm pain, jaw pain, and other forms of discomfort. The word discomfort is preferred over the word pain for describing the sensation of angina, because it varies considerably among individuals in character and intensity and most people do not perceive angina as painful, unless it is severe. There is evidence that angina and CHD present differently in women and men.
Angina that occurs regularly with activity, upon awakening, or at other predictable times is termed stable angina and is associated with high grade narrowings of the heart arteries. The symptoms of angina are often treated with nitrate preparations such as nitroglycerin, which come in short-acting and long-acting forms, and may be administered transdermally, sublingually or orally. Many other more effective treatments, especially of the underlying atheromatous disease, have been developed.
Angina that changes in intensity, character or frequency is termed unstable. Unstable angina may precede myocardial infarction, and requires urgent medical attention. It is treated with oxygen, intravenous nitroglycerin, and morphine. Interventional procedures such as angioplasty may be done.
[edit] Risk factors
The following are confirmed independent risk factors for the development of CAD, in order of decreasing importance:
- Hypercholesterolemia (specifically, serum LDL concentrations)
- Smoking
- Hypertension (high systolic pressure seems to be most significant in this regard)
- Hyperglycemia (due to diabetes mellitus or otherwise)
- Hereditary differences in such diverse aspects as lipoprotein structure and that of their associated receptors, homocysteine processing/metabolism, etc.
Significant, but indirect risk factors include:
- Lack of exercise
- Stress
- Diet rich in saturated fats
- Diet low in antioxidants
- Obesity
- Men or Women over 65
Congestive heart failure (CHF), also called congestive cardiac failure (CCF) or just heart failure, is a condition that can result from any structural or functional cardiac disorder that impairs the ability of the heart to fill with or pump a sufficient amount of blood throughout the body. It is not to be confused with "cessation of heartbeat", which is known as asystole, or with cardiac arrest, which is the cessation of normal cardiac function with subsequent hemodynamic collapse leading to death. Because not all patients have volume overload at the time of initial or subsequent evaluation, the term "heart failure" is preferred over the older term "congestive heart failure". Congestive heart failure is often undiagnosed due to a lack of a universally agreed definition and difficulties in diagnosis, particularly when the condition is considered "mild".
Signs and Symptoms
Left Heart Failure: Symptoms of decompensated heart failure include dyspnea (shortness of breath) on exertion, orthopnea (dyspnea that increases upon lying down), fatigue and paroxysmal nocturnal dyspnea ("cardiac asthma", shortness of breath that occurs hours or minutes after lying down). Nocturnal cough, Confusion and memory impairment (in advanced stages), and diaphoresis and cool extremities at rest.
Signs of decompensated left heart failure include: Displaced apex beat (usually to left due to cardiomegaly), Pathologic S3 Gallop, S4, Crackles at the lung bases due to pulmonary edema (fluid accumulation in the lungs), Dullness to percussion and tactile fremitus of lower lung fields. Increased intensity of pulmonic component of 2nd heart sound.
Right Heart Failure: Symptoms and Signs include: Peripheral edema (fluid build-up in dependent portions of the body), ascites (fluid in the abdominal cavity), nocturia (due to increased venous return with leg elevation), Jugular venous distention, Epistaxis (due to an increase in venous pressure), Hepatomegaly, hepatojugular reflux, and right ventricular heave.
Individuals with heart failure are sensitive to small shifts in their intravascular volume status (the amount of fluid in their circulatory system). Increasing the volume in their circulatory system can cause symptoms and signs of decompensated heart failure, while decreasing the volume in the circulatory system can cause hypotension.
Chest X-rays (CXRs) are frequently used to aid in the diagnosis of CHF. Signs of CHF on CXR are[1]:
- Vascular redistribution
- Peribronchial cuffing/interstitial edema (bat-shaped)
- Kerley B lines
- Consolidation of lower lung fields
- Cardiomegaly
EF(ejection fraction), EDV(end-diastolic volume), ESV(end-systolic volume), SV(stroke volume)
In cardiovascular physiology, end-diastolic volume (EDV) is the volume of blood in a ventricle at the end of filling (diastole). Because greater EDVs cause greater distention of the ventricle, EDV is often used synonymously with preload, which refers to the length of the sarcomeres in cardiac muscle prior to contraction (systole). An increase in EDV increases the preload on the heart and, through the Frank-Starling mechanism of the heart, increases the amount of blood ejected from the ventricle during systole (stroke volume).
Because nearly two-thirds of the blood in the systemic circulation is stored in the venous system, end-diastolic volume is closely related to venous compliance. Increasing venous compliance elevates the capacitance of the veins, reducing venous return and therefore end-diastolic volume. Decreasing venous compliance has the opposite effect. For example, activation of the baroreceptor reflex (occurring, for instance, in acute hemorrhage) causes venoconstriction, which decreases venous compliance, improves venous return, and therefore increases end-diastolic volume.
End-systolic volume (ESV) is the volume of blood in the ventricles just after systole. The amount of blood in the ventricle at the end of the cardiac ejection period and immediately preceding the beginning of ventricular relaxation; a measurement of the adequacy of cardiac emptying, related to systolic function. On an ECG the End-systolic volume will be seen at the end of the T wave. It will be the lowest volume seen throughout the ECG.
In cardiovascular physiology, stroke volume (SV) is the volume of blood ejected from a ventricle with each beat of the heart.
Calculation
Its value is obtained by subtracting end-systolic volume (ESV) from end-diastolic volume (EDV) for a given ventricle:
- SV = EDV − ESV
In a healthy 70-kg man, the left ventricular EDV is 120 ml and the corresponding ESV is 50 ml, giving a stroke volume of 70 ml.
[edit] Influence on cardiac output
Stroke volume, along with heart rate (HR), is one of the determinants of cardiac output (CO):
Therefore, if heart rate remains constant, a larger stroke volume will proportionately increase cardiac output. However, in normal resting individuals, increased stroke volume is often accompanied by a decreased heart rate in order to maintain constant cardiac output.
[edit] Determinants
Men, on average, have higher stroke volumes than women due to the larger size of their hearts. However, stroke volume depends on several factors such as heart size, contractility, duration of contraction, preload (end-diastolic volume), and afterload.
[edit] Exercise
Prolonged aerobic exercise may also increase stroke volume, which frequently results in a slower heart rate. Reduced heart rate prolongs ventricular diastole (filling), increasing end-diastolic volume, and ultimately allowing more blood to be ejected.
[edit] Preload
Stroke volume is intrinsically controlled by preload (the degree to which the ventricles are stretched prior to contracting). An increase in the volume or speed of venous return will increase preload and, through the Frank-Starling law of the heart, will increase stroke volume. Decreased venous return has the opposite effect, causing a reduction in stroke volume.
[edit] Afterload
Elevated afterload (commonly measured as the aortic pressure during systole) reduces stroke volume. Though not usually affecting stroke volume in healthy individuals, increased afterload will hinder the ventricles in ejecting blood, causing reduced stroke volume. Increased afterload may be found in aortic stenosis and arterial hypertension.
In cardiovascular physiology, ejection fraction (Ef) is the fraction of blood pumped out of a ventricle with each heart beat. The term ejection fraction applies to both the right and left ventricles; one can speak equally of the left ventricular ejection fraction (LVEF) and the right ventricular ejection fraction (RVEF). Without a qualifier, the term ejection fraction refers specifically to that of the left ventricle.
Overview
By definition, the volume of blood within a ventricle is known as the end-diastolic volume. Similarly, the volume of blood left in a ventricle at the end of contraction is end-systolic volume. The difference between end-diastolic and end-systolic volumes is the stroke volume, the volume of blood ejected with each beat. Ejection fraction (Ef) is the fraction of the end-diastolic volume that is ejected with each beat; that is, it is stroke volume (SV) divided by end-diastolic volume (EDV):
Acute myocardial infarction (AMI or MI), commonly known as a heart attack, is a disease that occurs when the blood supply to a part of the heart is interrupted. The resulting oxygen shortage causes damage and potential death of heart tissue. It is a medical emergency, and the leading cause of death for both men and women all over the world.[1] Important risk factors are older age, smoking, high LDL ("bad cholesterol") and low HDL ("good cholesterol"), diabetes, high blood pressure, and obesity.
The term myocardial infarction is derived from myocardium (the heart muscle) and infarction (tissue death due to oxygen starvation). The phrase "heart attack" sometimes refers to heart problems other than MI, such as unstable angina pectoris and sudden cardiac death.
Myocardial infarctions are usually accompanied by characteristic severe chest pain and autonomic phenomena such as looking pale, sweating and feeling sick.
Initial treatment measures for someone suspected of suffering from an acute myocardial infarction include oxygen, aspirin, glyceryl trinitrate and pain relief. While these are being administered, diagnostic tests are often performed, including serial electrocardiograms (ECG, EKG), X-rays and blood tests. Further treatment may include either medications to break down blood clots that block the blood flow to the heart, or mechanically restoring the flow by dilatation or bypass surgery of the blocked coronary artery. Coronary care unit admission allows rapid and safe treatment of complications such as abnormal heart rhythms.
The term "myocardial infarction" literally means that there is destruction of heart muscle cells due to a lack of oxygen. If these cells are not supplied with sufficient oxygen by the coronary arteries to meet their metabolic demands, they die by a process called infarction. Not all "heart attacks" lead to loss of heart muscle, particularly if the heart attack is aborted.
The decrease in blood supply has several consequences. Heart muscle which has lost blood flow long enough, e.g. 10–15 minutes, undergoes the ischemic cascade, dies (this is called necrosis) and does not grow back. A collagen scar, which does not have the ability to contract, forms in its place. Thus the heart ends up permanently weaker as a pump for the remainder of the individual's life. Recent studies indicate that apoptosis also plays a role in the process of tissue damage subsequent to myocardial infarction.[2]
Injured, but still living, heart muscle conducts the electrical impulses which initiate each heart beat much more slowly. The speed can become so slow that the spreading impulse is preserved long enough for the uninjured muscle to complete contraction; now the slowed electrical signal, still travelling within the injured area, can re-enter and trigger the healthy muscle (termed re-entry) to beat again too soon for the heart to relax long enough and receive any blood return from the veins. If this re-entry process results in sustained heart rates in the 200 to over 400 beats per minute range, a phenomenon called ventricular tachycardia (V-Tach) or ventricular fibrillation (V-Fib), then the rapid heart rate prevents the heart from pumping blood effectively. Heart output and blood pressure falls to near zero and the individual quickly dies. This is the most common mechanism of the sudden death that can result from a myocardial infarction.
The cardiac defibrillator device was specifically designed for stopping these too rapid heart rates. If used properly, it stops and resets the electrical impulses in all heart cells —in effect "rebooting" the heart— thereby stimulating the entire heart muscle to contract together in synchrony, hopefully stopping continuation of the re-entry process. If used within one minute of onset of V-Tach or V-Fib, the defibrillator has a high success rate in stopping these often fatal arrhythmias allowing a functional heart rhythm to return.
