Hemodynamic Disorders Flashcards
Hemodynamics:
the flow of blood
Systole:
the blood pumping phase of the cardiac cycle.
Diastole:
the chamber filling phase of the cardiac cycle
Preload:
the ventricular wall tension at the end of diastole (degree of myocyte stretch) determined by end-diastolic volume, reflected in end-diastolic pressure
Afterload:
the resistance the ventricle must overcome to pump its contents, determined by systolic blood pressure, reflected in ventricular systolic pressure
Myocardial contractility:
inotropic state determining the portion of the force of contraction independently of preload and afterload
Compliance:
the distendibility of the ventricle, determining the ease of filling it and, indirectly, the amount of filling and hence the amount of blood pumped
Heart failure:
inability of the heart to pump sufficient blood to meet the needs of the body
B-type natriuretic peptide:
a hormone secreted in heart failure in proportion to the severity
Mitral valve prolapse:
billowing of redundant mitral valve into the left atrium during systole thromboemboli from infective endocarditis
Rheumatic heart disease:
immune-mediated inflammation of the heart, especially valves, triggered by group A streptococcal infection
Libman-Sacks endocarditis:
autoimmune inflammation of the heart valves as part of systemic lupus erythematosus.
Marantic endocarditis:
non-bacterial thrombotic endocarditis, the deposition of blood clot on heart valves.
Vegetations:
colorful misnomer for blood clots on heart valves.
Osler nodes:
pea-sized tender nodules in fingers and toes from infected thromboemboli from infective endocarditis.
Janeway lesions:
hemorrhages on the palms or soles from infected thromboemboli from infective endocarditis.
Cor pulmonale:
heart disease caused by lung disease.
Arrhythmia:
disturbance in heart rhythm due to deranged cardiac electrical signaling.
PR interval:
time from start of P wave to end of QRS, normally 120-200 ms, indicative of conduction block around AV node if prolonged.
QT interval:
time from start of QRS to end of T wave, normally <440 ms, dangerous if prolonged due to risk of ventricular tachyarrhythmias.
Atrial fibrillation:
arrhythmia of chaotic atrial activation at a rapid rate causing an irregular heart rhythm due to variable conduction through the AV node.
Ventricular fibrillation:
immediately life-threatening arrhythmia of chaotic ventricular activation at a rapid rate with lack of cardiac pumping.
Channelopathy:
heart disease of arrhythmias due to defective cardiac myocyte ion channels, usually due to genetic mutations.
Torsades de pointes:
a polymorphic ventricular tachycardia with variation in QRS size and shape, creating an outline resembling a twisted ribbon on EKG
LV end-diastolic volume
150 ml
LV end-systolic volume
50 ml
Stroke volume
100 ml
Ejection fraction
67%
LV end-diastolic pressure
10 mm Hg
LV systolic pressure
130 mm Hg
RA pressure
3 mm Hg
RV systolic pressure
25 mm Hg
LA pressure
8 mm Hg
The greater the volume of blood delivered to the cardiac ventricles?
The more the cardiac myocytes (myofibers) are stretched and the greater the force of the next contraction.
Inotropic:
It means something like contractility-related.
The ventricular preload is measured by?
Both the ventricular end-diastolic pressure and end-diastolic volume are regarded as representing the preload.
Afterload is the resistance the ventricle?
Must overcome to pump out its contents during systole.
The force of ventricular contraction in systole is determined?
Preload, Afterload, Contractility, and Compliance
Compliance:
This is the stiffness of the ventricular wall.
What decreases ventricular compliance and what does it cause?
Fibrosis, amyloidosis or any other process causing interstitial infiltration by anything more rigid than normal decreases ventricular compliance. This restricts (impairs) cardiac pumping. This condition is referred to as restrictive cardiomyopathy.
Impaired cardiac filling?
Called diastolic dysfunction. Diastolic dysfunction does not typically reduce the ejection fraction.
Impaired cardiac pumping?
Called systolic dysfunction. Usually due to impaired contractility or greatly increased afterload, decreases the amount of blood ejected from the ventricle, the stroke volume, and the proportion of the end-diastolic volume ejected, the ejection fraction.
The five major categories of the factors determining the heart’s function as a pump, the cardiac output?
(1) preload, (2) afterload, (3) contractility, (4) compliance and (5) heart rhythm.
The most common cardiac hemodynamic disorder?
Cardiac failure is inability of the heart to pump sufficient blood to meet the needs of the body.
Cardiac failure epidemiology
More than half a million Americans are diagnosed with heart failure per year, and 5 million have it. Rises sharply in old age, from 0.8% of 50-59-year-old men and women to 6.6% of 80-89-year-old men and 7.9% of 80-89-year-old women.The prevalence in African-Americans is reported to be 25% higher than in whites.
Heart failure most common type?
Myocardial infarction, necrosis of part of the pump exceeding the ability of the surviving part to compensate. MI causes coronary artery disease, 17% due to smoking, 10% hypertension, 8% overweight, 3% diabetes mellitus and 2% valvular heart disease.
Chronic heart failure is most frequently caused by?
Old myocardial infarction(s), commonly multiple old myocardial infarctions. This is often called ischemic cardiomyopathy.
Coronary artery disease can also cause
Acute heart failure.
Myocardial infarction can develop heart failure how long?
In a few hours.
Uncontrolled severe hypertension can cause?
Heart failure by causing excessive afterload exceeding the ability of the heart to compensate rather than impaired contractility.
Stenosis of the aortic valve?
Can make it so hard to pump through a tiny opening that the excessive afterload exceeds the ability of the heart to compensate resulting in heart failure.
Heart failure due to aortic stenosis, severe hypertension or coronary artery disease typically causes the ejection fraction?
Lowers the ejection fraction.
Heart failure due to left ventricular hypertrophy, restrictive cardiomyopathy or pericardial disease is typically cause ejection fraction?
Preservation of the ejection fraction.
Congestive heart failure:
When the heart fails, blood backs up behind it waiting for take-off, resulting in congestion of the veins bringing blood back to the heart.
Most common cause Cardiomegaly?
Cardiomegaly due to heart failure is caused by dilation of the chambers much more often than thickening of the walls.
The most common symptom of heart failure is?
Dyspnea, the sensation of breathlessness, not getting enough air.
What increase in pulmonary venous pressure cause fluid to pass from the congested pulmonary veins into the interstitium.
When pulmonary venous pressure, which is normally 8 mm Hg, goes over 20 mm Hg, a transudate of fluid passes from the congested pulmonary veins into the interstitium.
Two most specific symptoms of heart failure?
Paroxysmal nocturnal dyspnea and orthopnea
Two most common symptoms of heart failure?
dyspnea and fatigue?
Signs of heart failure include?
Tachycardia, tachypnea, hypotension, pulmonary crackles, pulmonary wheezing, diaphoresis and gallops.
At what pulmonary venous pressure will transudate pass into the airspaces, and what can you hear when this happens?
25 mm Hg, transudate passes not only into the interstitium, but also into the airspaces. Crackles first heard at the lung bases.
Diaphoresis (sweating)?
Can be a sign of heart failure due to sympathetic nervous stimulation, a compensatory response.
A third heart sound (S3) early in diastole?
A dull, low-pitched sound attributed to rapid filling can be a sign of heart failure. Gallop
Dulled mental status due to inadequate cerebral perfusion and oliguria due to decreased renal perfusion?
Can also be signs of heart failure, but are not at all specific for heart failure.
The diagnosis of heart failure?
Often apparent from the history and physical examination.If not, chest x-ray findings of cardiomegaly (enlarged heart), pulmonary vascular congestion and interstitial or alveolar edema, Echocardiography, B-type natriuretic peptide (BNP) levels.
Biomarker of heart failure?.
Serum B-type natriuretic peptide, and the level correlates with the severity of the heart failure.
Hypertension causes?
Increased afterload; the left ventricle responds and compensates with concentric hypertrophy until it passes the limits of its ability to compensate.
The gallop associated with hypertensive heart?
An S4 gallop with the extra heart sound later in diastole than S3.
The atrial gallop of hypertensive heart disease sounds like?
Tennessee.
Hypovolemia is?
A hemodynamic disorder and one important to differentiate from cardiogenic hemodynamic disorders because the treatment is essentially the opposite.
The most common cause of hypovolemic shock?
Hemorrhage is the most common cause, but some cases are due to diarrhea or vomiting.
Acute heart failure has four profiles?
- Profile A Warm and Dry 2. Profile B Warm and Wet 3. Profile C Cold and Wet 4. L Cold and Dry.
Warm or cold in these profiles refers to?
The extremities. Warm extremities are either adequately perfused or abnormally perfused with peripheral vasodilation, the latter most commonly due to sepsis. Cold extremities are inadequately perfused and manifest peripheral vasoconstriction in response.
Wet or dry in these profiles refers to?
The patient as a whole. Wet patients have edema, jugular venous distension and pulmonary crackles indicative of volume overload and elevated left ventricular filling pressure. Dry patients lack these findings.
The warm and dry profile is most associated with?
Transient myocardial ischemia or heart failure from lung disease.
Warm and wet heart failure patients are?
Volume overloaded, but still managing to adequately perfuse their extremities.
Cold and wet patients are?
Fluid overloaded and no longer adequately perfusing their extremities.
Cold and dry profile is called?
“L” for “low” cardiac output; Can be mitral regurgitation and left ventricular dilatation, whose is suddenly active. Much more commonly, cold and dry patients with profile L have hypovolemia.
The cardiovascular control center?
In the medulla gets the message via the ninth and tenth cranial nerves.
Hypovolemia leading to shock elicits multiple cardiovascular compensatory responses.
Rapid breathing, increased sympathetic nervous activity and decreased parasympathetic nervous action, increases the heart rate, augments myocardial contractility and causes peripheral vasoconstriction. Increase RAAS.
Normal central venous pressure?
Essentially the same as right atrial pressure, 3 mm Hg.
In a fluid overloaded heart failure patient or a patient with right heart failure the central venous pressure will be?
Abnormally elevated.
In a hypovolemic patient, the central venous pressure?
Usually be low.
Hypovolemic shock treatment?
Fluids
Cardiogenic shock treatment?
Diuresis
Differentiating hypovolemic shock from cardiogenic shock is crucial because?
The treatments are opposite and mistaken diagnosis and treatment for one can be fatal for a patient who has the other.
The valve disease most commonly causing a hemodynamic disorder in the US?
Aortic stenosis.
Calcific aortic stenosis is?
The second most common valvular disease. (male/female ratio 3/1).
Calcific aortic stenosis there are three main causes?
(1) congenitally anomalous bicuspid valve (50% of cases), (2) “senile” degeneration, and (3) chronic rheumatic disease.
When the aortic valve opening is less than?
50% of normal size, significantly increased left ventricular pressure becomes necessary to push a normal stroke volume through it during systole.
Significantly increased left ventricular pressure?
This causes concentric left ventricular hypertrophy like hypertensive heart disease, with the same accompanying decrease in compliance.
Symptoms of calcific aortic stenosis
Angina pectoris (chest pain due to myocardial ischemia), syncope (loss of consciousness) and dyspnea (the sensation of being short of breath). Symptoms of aortic stenosis usually occur with exertion.
Signs of calcific aortic stenosis?
include a crescendo-decrescendo systolic (ejection) murmur, a weak delayed pulse and an atrial gallop.
Calcific aortic stenosis presents with angina, syncope or dyspnea and valve replacement after the development of symptoms?
Greatly improves survival.
Mitral regurgitation is?
The ejection of a portion of the left ventricular stroke volume backward into the left atrium due to insufficiency (incompetence) of the mitral valve.
The second most common valve disease causing a hemodynamic disorder in the US?
Mitral regurgitation
The most common cause of mitral regurgitation in the US?
Mitral regurgitation in the US is mitral valve prolapse, 67% (two-thirds) of cases. The second most common cause is ischemic heart disease,25% (one-quarter) of cases.
The pathophysiologic consequences of mitral regurgitation are?
(1) decreased forward stroke volume, (2) increased left atrial volume and pressure and (3) volume-related stress on the left ventricle because the added left atrial volume is returned to it along with the normal left atrial volume during diastole.
If mitral regurgitation is acute, left atrial pressure is?
Raised.
If mitral regurgitation is chronic, left atrial dilatation?
Allows it to hold the extra volume with less elevated pressure.
If rupture of a papillary muscle (due to myocardial infarction or infective endocarditis) causes sudden mitral regurgitation?
The resulting increased left atrial pressure, transmitted backward to the pulmonary circulation, may cause rapid pulmonary congestion and edema (“flash pulmonary edema”), a medical emergency.
The symptom of acute mitral regurgitation is?
Dyspnea.
The most common symptom of chronic mitral regurgitation is?
Fatigue (or “weakness”).
Severe chronic mitral regurgitation will cause heart failure manifested by?
Paroxysmal nocturnal dyspnea and orthopnea.
The sign of mitral regurgitation is?
An apical holosystolic (pansystolic) murmur, which sometimes has a harsh quality.
In severe acute mitral regurgitation, the murmur may be?
Decrescendo, reflecting the rapid equilibration between left atrial and ventricular pressures during systole.
Reduction of forward stroke volume from the normal of 100 ml to 75 ml or lower is associated with?
Clinical manifestations of heart failure.
25% reduction of forward stroke volume from the normal of 100 ml to 75 ml is associated with?
With clinical manifestations of heart failure.
Mitral valve prolapse is?
A billowing of redundant mitral valve into the left atrium during systole.
Mitral valve prolapse epidemiology?
It is the most common valvular disease (present in 2% of the population) with a slight female predominance (female/male ratio 3/2).
Mitral valve prolapse may occur with?
Connective tissue diseases such as Marfan syndrome.
Mitral valve prolapse gross pathology?
Features billowing, ballooning and floppy leaflet(s). Sometimes the chordae tendineae are elongated attenuated and vulnerable to rupture.
Mitral valve prolapse microscopic pathology?
Degeneration and attenuation of the outer zona fibrosa of the valve and expansion of the inner zona spongiosa with myxomatous tissue (resembling mucus microscopically).
Mitral valve prolapse symptoms?
Usually asymptomatic, but patients may experience chest pain or palpitations due to associated arrhythmias. It causes a midsystolic click and late systolic murmur.
Mitral valve prolapse diagnosis?
By physical examination, confirmed by echocardiography.
Mitral valve prolapse complications?
Uncommon, but include regurgitation (the most common), infection of the valve (endocarditis, rare), rupture of chorda (can cause rapid pulmonary edema, rare), atrial arrhythmias (rare) and ventricular arrhythmias (serious, but very rare).
Mitral valve prolapse is the most common?
Valve disease in the US and usually benign.
Acute rheumatic heart disease is?
An inflammation of endocardium, myocardium, and epicardium (pancarditis, “carditis”) following group A beta-hemolytic streptococcal pharyngitis.
Acute rheumatic heart disease is associated with?
Fever, polyarthritis, Sydenham’s chorea (a movement disorder), subcutaneous nodules, erythema marginatum (skin rash with advancing edge and clearing center).
The Jones criteria for the diagnosis of rheumatic fever are?
Evidence of streptococcal infection AND either 2 major or 1 major and 2 minor criteria:
The Jones criteria major criteria:
Carditis, Polyarthritis, Sydenham’s Chorea, Erythema Marginatum, Subcutaneous Nodules
The Jones criteria minor criteria:
Fever, Migratory Arthralgias, Prolonged PR Interval, High ESR or WBC count
Acute rheumatic fever is still common in?
Developing countries, but is now rare in the US. It is most common in children.
Acute rheumatic fever is an?
Autoimmune disease in genetically susceptible individuals due to molecular mimicry between bacterial and heart antigens.
Acute rheumatic fever gross pathology?
Tiny (1-2 mm) verrucous (wartlike) vegetations lined up on the line of valve closure, along with fibrinous pericarditis.
Acute rheumatic fever microscopic pathology?
(1) fibrin and platelet thrombi on valves and (2) Aschoff bodies, which are foci of fibrinoid necrosis with histiocytes and Anitschkow cells (with clumped chromatin resembling a caterpillar).
Acute rheumatic fever signs?
Various systolic and diastolic murmurs and a pericardial friction rub.
Acute rheumatic fever treatment?
Aspirin, penicillin and supportive care. 65% of cases will go on to mitral stenosis, 25% with aortic regurgitation or stenosis, too.
Chronic rheumatic heart disease is more common with?
Recurrent carditis, severe carditis, and carditis at an early age.
Chronic rheumatic heart disease symptoms
Usually occur an average of 20 years after carditis, but 50% have no history of it.
The pathology of rheumatic mitral stenosis is?
A slitlike fishmouth or round buttonhole stenosis with fibrous thickening and rigidity of valves with or without calcification. There is a fusion of commissures, along with thickening, retraction and fusion of chordae, and sometimes MacCallum patches (maplike areas of atrial endocardial thickening and fibrosis).
The pathology of rheumatic mitral stenosis complications are?
Left atrial hypertension, left atrial dilation, atrial fibrillation, left atrial thrombus formation, pulmonary hypertension, right ventricular hypertrophy and right heart failure.
Aortic regurgitation can be due to?
(1) insufficiency of a congenitally anomalous bicuspid valve, (2) endocarditis (inflammation [especially infective]) or (3) chronic rheumatic valve deformation. It can also be due to dilation of the aortic valve ring by aortic aneurysm or dissection.
Acute aortic regurgitation causes?
Increased left ventricular diastolic pressure because the left ventricle has not had time to dilate and accommodate the extra regurgitant volume. This causes increased left atrial pressure, pulmonary congestion and edema, manifested by dyspnea.
If acute aortic regurgitation is severe?
The best relief is sometimes surgical valve replacement, so it can be a surgical emergency?
Chronic aortic regurgitation causes?
Dilation of the left ventricle with increased muscle mass yielding increased compliance and less elevated left ventricular diastolic pressure.
The symptoms of decompensated aortic regurgitation are?
Fatigue, decreased exercise tolerance and dyspnea.
The signs of decompensated aortic regurgitation are?
A diastolic decrescendo murmur (sometimes with a blowing quality), a hyperdynamic bounding, but rapidly collapsing pulse (Corrigan pulse), head-bobbing with each pulse (de Musset sign) and multiple other eponymic signs.
It is characteristic of aortic regurgitation to have?
A wide pulse pressure due to increased systolic and decreased diastolic pressure from the abnormally large amount of blood ejected into the aorta in systole and back leak into the left ventricle in diastole.
Treatment of choice for symptomatic aortic regurgitation.
Aortic valve replacement
Surgical valve replacement provides?
Immediate relief of chronic disease but it replaces one chronic disease with another.
Complications of surgical valve replacement are common and serious:
Leak, Thrombosis, Embolism, Bleeding, Endocarditis, Total Rate
Surgical valve replacement for chronic valve disease is not a pure cure?
Rather more like the replacement of one chronic disease with another, on the average lesser one.
Libman-Sacks endocarditis is?
Autoimmune inflammation of heart valves that occurs as part of systemic lupus erythematosus.
Libman-Sacks endocarditis occurs?
In 50% of patients with lupus. It usually occurs simultaneously with pericarditis.
Lupus occurs predominantly in?
Females (female/male ratio 9/1), usually 15 to 45 years old, and lupus is three times more common in African-Americans.
Libman-Sacks endocarditis gross pathology?
Small to medium verrucous, berrylike or flat vegetations, commonly on multiple valves, most commonly mitral and tricuspid, on either or both sides.
Libman-Sacks endocarditis microscopic pathology?
Necrotic debris, fibrinoid material, degenerating leukocytes, fibroblasts and hematoxylin bodies (condensed naked nuclei of dead degenerated cells ingested by phagocytes).
Libman-Sacks endocarditis complications?
Chronic adhesive pericarditis, but not emboli from the vegetations.
Marantic endocarditis is?
Nonbacterial thrombotic endocarditis.
Marantic endocarditis occurs?
It is common. It occurs in 75% of patients with malignant tumors (especially adenocarcinomas, especially mucinous adenocarcinomas). It is also prevalent in patients with disseminated intravascular coagulation, chronic sepsis and Swan-Ganz right heart catheterization.
Marantic endocarditis pathology?
Features small (1 to 5 mm) fibrin and platelet thrombi, most commonly on the atrial side of the mitral valve, usually on the line of valve closure. The second most common site is on the ventricular side of the aortic valve.
Marantic endocarditis complications?
Iinclude systemic emboli, which occur in about half of cases (to kidneys, spleen, brain, gut and heart) and infection (converts it to infective endocarditis).
Marantic (non-bacterial thrombotic) endocarditis is?
Deposition of blood clot on heart valves, important because it is common, frequently embolizes and is the precursor to infective endocarditis.
Infective endocarditis is?
Uncommon (1/1000 hospital admissions). It is primarily a disease of adults, and a bit more common in males (male/female ratio 1.7/1).
Infective endocarditis pathogenesis of the disease is:
(1) valvular endothelial injury, (2) platelet and fibrin deposition, (3) microbial seeding, and (4) microbial multiplication (up to 1010 bugs/gram).
Infective endocarditis prognosis?
100% fatal if undiagnosed and untreated. It is only 20% fatal if diagnosed and treated appropriately (IV antibiotics and/or surgery).
There are three classifications of infective endocarditis?
First by clinical course: acute bacterial endocarditis (“ABE”) versus subacute bacterial endocarditis (“SBE”). Second by host substrate: native valve endocarditis (“NVE”) versus prosthetic valve endocarditis (PVE) versus endocarditis in intravenous drug users. Third based upon the specific infecting organism.
Portals of entry for the organisms causing infective endocarditis are?
Central venous catheterization, dental procedures, gingivitis, chewing, brushing teeth, surgery, bladder catheterization, endoscopy, shaving, intravenous drug abuse, etc.
It is important to communicate to the microbiology laboratory that blood cultures are for suspected endocarditis?
Because the laboratory will use special media and hold the cultures longer for the fastidious and slow-growing organisms that sometimes cause infective endocarditis.
Infective endocarditis is infection of thrombi on heart valves, important because prompt diagnosis?
Decreases the mortality from 100% to 20%.
Infective endocarditis gross pathology?
Features large (up to 3 cm), friable vegetations that are some combination of tan, gray, red or brown. The number of vegetations ranges from one to many, and they are usually located on the line of valve closure (the atrial side of atrioventricular valves, or ventricular side of semilunar valves).
As a general principle, the larger a vegetation?
The more likely it is infective. Infective endocarditis is destructive of tissue and may cause perforation of a valve, adjacent abscess, fibrotic scarring and calcification.
Infective endocarditis microscopic pathology?
Fibrin, platelets and masses of organisms, sometimes with necrosis and neutrophils. Later, lymphocytes, macrophages and fibroblasts may infiltrate and fibrosis may occur.
Infective endocarditis common symptoms?
Fever (felt by 80% of patients), chills (40%), weakness (40%) and dyspnea (40%).
Infective endocarditis common physical signs?
Heart murmur, splenomegaly, and petechiae (30%). Uncommon physical signs include Osler nodes (pea-sized tender finger/toe nodules) subungual splinter hemorrhages, changing heart murmur, Janeway lesions (small palm/sole hemorrhages), and Roth spots (white dots with surrounding hemorrhage in the retina) (2%).
Infective endocarditis common laboratory findings?
Elevated erythrocyte sedimentation rate (“ESR”), circulating immune complexes, anemia, and proteinuria.
Characteristic of endocarditis?
Continuous low-grade bacteremia.
Infective endocarditis diagnosis?
Blood cultures are critical for specific diagnosis. Blood cultures may be negative if the patient has already received antibiotics. In some cases, infective endocarditis is “culture-negative.”
If you astutely diagnose infective endocarditis?
Don’t wait for the echocardiographic confirmation; get the blood cultures, put “suspect endocarditis” on the microbiology laboratory requisition and start the antibiotic therapy.
The most common cause of right heart failure is?
Left heart failure.
Cor pulmonale is right heart disease caused by?
Pulmonary hypertensive diseases, especially emphysema, embolism and interstitial lung disease.
Acute cor pulmonale is characterized by?
Dilatation of the right heart chambers.
Chronic cor pulmonale is characterized by?
Hypertrophy.
Common causes of chronic cor pulmonale include?
Pulmonary emphysema, recurrent pulmonary thromboembolism, interstitial lung disease and the acute respiratory distress syndrome.
Leg edema, hepatomegaly, ascites and jugular venous distention can all be manifestations of?
Right heart failure.
Signs of right heart failure included?
Peripheral edema (especially of the legs), hepatomegaly, ascites and jugular venous distention.
The ultimate hemodynamic disorder is?
Asystole, total lack of cardiac pumping.
Slow death from heart failure is characterized by?
Progressive dyspnea due to pulmonary edema.
The incidence of sudden cardiac death increases with?
Age, reaching its highest rate in the elderly. Sudden cardiac death is up to 3 X more common in males.
The resting membrane potential depends on gradients between inside and outside the cells of three cations?
Sodium, potassium and calcium.
Diseases of these ion channels are called?
Channelopathies.
The cycle of depolarization phase 0:
Phase 0 lasts only a few thousandths of a second. It consists of a rapid influx of sodium down a concentration and electrical charge gradient into the myocytes. -90 mV to around +10 mV.
The cycle of depolarization phase 1:
Which is a rapid decrease in membrane potential to around zero mV. Phase 1 is carried out by an outflux of potassium ions.
The cycle of depolarization Phase 2:
Is a long plateau of slowly, ever so slightly decreasing membrane potential about two tenths of a second. Phase 2 is mediated by an approximately electrically balanced inflow of calcium and outflow of potassium.
Phase 2 is mediated by?
An approximately electrically balanced inflow of calcium and outflow of potassium.
The cycle of depolarization Phase 3:
Is a relatively rapid descent of the cell membrane potential back down to the normal resting potential. This is accomplished by continuing outflux of potassium after the calcium ion channels have closed. This ceases when the normal resting potential is reached.
The cycle of depolarization Phase 4:
Normal resting potential.
Calcium binding to ryanodine receptors causes?
The sarcoplasmic reticulum to release large amounts of calcium the mediate the actions of a troponin, actin and myosin, resulting in cell contraction.
A disease called familial catecholeminergic polymorphic ventricular tachycardia is associated with?
Mutations in the genes for ryanodine receptors.
Afterdepolarizations occurring in phase 2 or phase 3 are called?
“early”
Afterdepolarizations occurring in phase 4 are called? “
“delayed”
Early afterdepolarization during the “long” plateau phase 2 is associated with?
Increased calcium inflow, which can be due to defective calcium channels.
Early afterdepolarization during phase 3 can be due to?
Abnormal sodium inflow, which can be due to defective sodium channels.
Delayed afterdepolarization during phase 4 is associated with?
High intracellular levels of calcium, which can be due to marked catecholamine stimulation.
Whether early or delayed, afterdepolarizations can generate?
Spontaneous action potentials, which can be self-perpetuating and lead to tachyarrhythmias.
Cardiac arrhythmias causing sudden death can result from?
A mechanism of abnormal conduction called reentry.
If injury or necrosis of myocytes creates an area of signal blockage?
This can result in aberrantly conducted signals around the area of injury of necrosis.
If all the myocytes getting the abnormally conducted signal are in their refractory periods?
The aberrant signal ends.
If an injured or abnormally excited myocyte spontaneously initiates a signal that just so happens to encounter a pathway of myocytes that are finished with their repolarization and no longer refractory?
This abnormally conducted impulse can reenter the normal conduction pathway adding an extra impulse or repeatedly depolarize the myocytes in a reentrant pathway much shorter than the normal one.
Small patches of myocardial disease, especially scarring, are a common anatomic substrate for?
Fatal reentrant ventricular tachycardia.
Understanding how to diagnose the heart diseases that predispose to sudden cardiac death is key for life-saving prevention and this requires?
Knowledge of electrocardiography.
Normal electrical signaling in the heart starts?
In the SA node in the peripheral right atrium, traverses the atria until it reaches atrioventricular AV node.
where does the electrical signal in the heart experience a delay?
AV node
Once through the AV node, the impulse travels quickly through the?
Bundle of His (in females as well as males) and passes into left and right branches of the bundle of His.
The left bundle branch divides into two large hemibranches?
Anterior and posterior.
Three conducting fiber bundles are, and what are they sometimes called?
The right bundle branch and the left bundle branch anterior and posterior. These three conducting fiber bundles are sometimes called fascicles
Unifascicular block of conduction through one of the three bundles can allow an?
Impulse from the atria into the ventricles.
Bifascicular block can still allow an?
Impulse from the atria into the ventricles.
Trifascicular block has the same effect as?
AV node blockade in preventing signals from the atria to the ventricles.
Myocardial scarring from infarction can do this and is perhaps the most common cause, but amyloidosis can also do it?
AV node blockade
A cardiac arrhythmia, especially heart block, in a young African American suggests?
The possibility of cardiac sarcoidosis.
Each heartbeat is reflected on an electrocardiogram by?
3 major deflections.
What is the first wave and what does it represent?
The P wave, which represents the depolarization of the atria.
What comes after P wave and what does it represent?
The QRS complex representing the depolarization of the ventricles
What comes after QRS complex and what does it represent?
T wave representing repolarization of the ventricles.
There are three important intervals?
The PR interval, QRS interval, QT interval.
The PR interval is from the onset of, and what does it represent?
The P wave to the end of the QRS complex. It represents the length of time for signals to propagate from the SA node through the AV node and the ventricles.
Delays in getting through the AV node area cause?
Prolongation of the PR interval.
The normal PR interval is between?
120 and 200 milliseconds (0.12 and 0.20 seconds).
PR intervals longer than 200 milliseconds, but with all impulses from the atria getting through, are called?
First degree AV block or first degree heart block.
The duration of the QRS is the?
QRS interval.
The duration of the QRS is the QRS interval. The QRS interval is normally less than or equal to?
100 milliseconds (<0.1 seconds).
Longer QRS intervals, commonly called wide complexes, represent?
Aberrantly conducted impulses or impulses from abnormal places, and are generally a bad thing to have.
The QT interval is from the beginning of the?
QRS to the end of the T wave.
If the QRS is not widened?
The QT interval represents ventricular repolarization.
With faster heart rates repolarization is faster so the QT interval needs?
Corrected for the heart rate?
QT interval is normally less than or equal to?
440 milliseconds (<0.44 seconds).
A prolonged QT interval is?
A dangerous thing.
The most common cause of prolonged QT interval?
Myocardial ischemia (ischemic heart disease), but it can also be caused by blood electrolyte abnormalities (specifically, low potassium, calcium or magnesium) or by a channelopathy
Abnormalities in 12-lead electrocardiograms can reflect the?
Anatomic site of heart disease within the organ.
Abnormalities in leads V1-V4 reflect disease of the?
Anterior left ventricle served by the left anterior descending coronary artery.
Abnormalities in leads V5-V6 reflect disease of the?
Lateral left ventricle served by the left circumflex coronary artery.
Abnormalities in leads II, III and aVF reflect disease in?
Right coronary artery territory, the inferior left ventricle.
Acute blockage of a major epicardial coronary artery is associated with?
Elevation of the ST segment, the portion of the EKG tracing between the end of the QRS and the T wave. The T wave commonly becomes inverted, too.
Large transmural myocardial infarction can leave a permanently misshapen?
QRS complex with an abnormally large, long and deep initial downward deflection, a pathologic Q wave. Some Q waves are innocent, like some heart murmurs and some S3s and some S4s.
Tachyarrhthymias that originate above the ventricles is called?
Supraventricular
Supraventricular rhythm most common?
Top of this list is atrial fibrillation. Second most common is atrial flutter.
Atrial fibrillation rhythm?
Irregular; the rate is high or normal (range 60 to 220) and there are no P waves.
Atrial flutter results from?
Reentrant circuit around the tricuspid valve.
Atrial flutter rhythm
It usually features two P waves for each QRS and yields a heart rate right around 150/minute.
Supraventricular tachycardia results from?
Usually due to a reentrant pathway in the atria right near the AV node.
Supraventricular tachycardia responds?
Home remedy vagal maneuvers such as a Valsalva maneuver, carotid sinus massage or immersion of the face in a pan of ice water.
Ventricular tachyarrhythmias are?
Dangerous.
Ventricular tachyarrhythmias two major types are?
Ventricular tachycardia and ventricular fibrillation.
The QRS complexes of ventricular tachycardia are typically?
Wide, over 120 milliseconds (>0.12 seconds).
Ventricular tachycardia usually has a rate?
Less than 200/minute (USUALLY).
Normal heart rate for adults?
60 to 100/minute.
If all the QRS complexes look alike, it is called?
Monomorphic.
If the QRS complexes vary in morphology, ventricular tachycardia is called?
Polymorphic.
Ventricular tachycardia, especially polymorphic ventricular tachycardia, can?
Degenerate into ventricular fibrillation.
Ventricular fibrillation is?
Immediately life-threatening. It is a totally disordered rapid stimulation of the ventricles.
Ventricular fibrillation electrocardiogram shows?
A chaotic pattern without discrete QRS complexes.
Ventricular fibrillation causes the ventricles to?
Squirm like a bag of worms.
Ventricular fibrillation treatment?
Is electrical defibrillation. If no defibrillator is available, a punch to the sternum will occasionally terminate ventricular fibrillation.
Commotio cordis.
A punch or baseball to the sternum in an apparently healthy person can precipitate a fatal arrhythmia.
A prolonged QT interval, corrected QT (QTc), over 440 milliseconds is a signal of?
Dangerous heart disease.
The channelopathies are a heterogeneous group of hereditary diseases of?
Sodium, potassium or calcium channels, which cause sudden death in infants, children and young adults.
Channelopathies gross and microscopically pathology?
No visible abnormalities in the heart.
There are how many types of congenital long QT syndrome and they kill between?
13 types; between 3,000 and 4,000 children per year in the US. ”.
The characteristic arrhythmia associated with long QT syndrome is?
A form of polymorphic ventricular tachycardia called torsades de pointes, with frequent variations of the QRS size, morphology or both.
The most common type of congenital long QT syndrome?
Type 1, is caused by mutations in the gene for a subunit of the IKs potassium channel resulting in decreased outward potassium current, which impairs this repolarizing current, prolonging the QT interval, allowing early afterdepolarizations from multiple foci.
Some forms of congenital long QT syndrome are particularly prone to causing?
Sudden death at rest or during sleep.
Some forms of congenital long QT syndrome are particularly prone to causing sudden death at rest or during sleep. Approximately 10% of cases of sudden infant death syndrome are due to?
Channelopathies
The Brugada syndrome is primarily in?
Young adult Asian males.
The Brugada syndrome mutations?
Gene for a subunit of the cardiac sodium channel result in a variety of abnormalities including failure of expression, alterations in the voltage and time dependence of activation, and accelerated or prolonged recovery from inactivation.
The defective myocardial sodium channels reduce?
Sodium inflow currents, thereby reducing the duration of action potentials.
The Brugada syndrome rhythm?
Associated with persistently elevated ST segments (≥2 mm) descending with an upward convexity to an inverted T wave (classic “coved type” Brugada pattern) in leads V1-V3, and with ventricular fibrillation.
The Brugada phase 2?
Can be dramatically shortened, and may precipitate sustained ventricular arrhythmias.
Familial catecholeminergic polymorphic ventricular tachycardia may account for at least?
One in seven cases of sudden unexplained death.
Familial catecholeminergic patients have?
Normal QT interval and typically present with life-threatening ventricular tachycardia or ventricular fibrillation during emotional or physical stress, with syncope often being the first manifestation of the disease.
Familial catecholeminergic cases are due to?
The majority are due to mutations in the cardiac ryanodine receptor, the cardiac sarcoplasmic calcium release channel.
Familial catecholeminergic treatment:
Beta-blockade is effective for preventing life-threatening arrhythmias in some patients, but others require an implanted defibrillator.
Myocarditis is inflammation of the?
Heart muscle.
Myocarditis commonly occurs with?
Simultaneous pericarditis. Myocarditis is uncommon. There is a slight male predominance (male/female ratio 6/4).
Myocarditis is most commonly caused by?
Parvovirus B19 and human herpes virus 6 have become the most frequent agents. Viral myocarditis commonly occurs in young healthy individuals. It is usually a disseminated infection in neonates.
Viral myocarditis may have 2 phases:
(1) early: direct viral infection of myocytes and (2) later: auto-immune attack on myocytes.
Myocarditis pathology?
Pale mottled flabby dilated heart, with multifocal interstitial, usually mononuclear (primarily lymphocytic) inflammation. Myocarditis is associated with myocyte injury and necrosis.
Viral myocarditis is associated with?
Fever, chest pain, dyspnea, malaise, myalgia, tachycardia, a pericardial friction rub and various electrocardiographic findings.
Myocarditis definitive diagnosis?
Cardiac biopsy is required for a definitive diagnosis, but magnetic resonance imaging and other tests are emerging as alternatives.
Myocarditis prognosis?
90% of patients recover, but 10% progress to chronic dilated cardiomyopathy.
Right ventricular cardiomyopathy is an uncommon underdiagnosed cause of?
Sudden death in young adults, particularly with strenuous exertion.
Right ventricular cardiomyopathy mutations?
Genes encoding desmosomal proteins (including desmoplakin, plakoglobin, plakophilin 2, desmocollin 2, and desmoglein have been identified in many patients, but the disease appears to require a second “hit”.
Right ventricular cardiomyopathy disease begins in the?
Right ventricular apex and is characterized by fatty replacement of myocytes, frequently with lymphocytic infiltration and later fibrous scarring.
Right ventricular cardiomyopathy causes?
Reentrant ventricular tachycardia originating from the right ventricle.
Right ventricular cardiomyopathy rhythm ?
Inverted T waves in leads V1-V3 and occasionally what is called an epsilon wave, a terminal upward notch of the QRS in lead V1, reflecting abnormal right ventricular activation.
Right ventricular cardiomyopathy diagnose?
By echocardiography and sudden death prevented by an implanted defibrillator.
Sudden cardiac death of an infant, child or young adult is commonly due to familial disease and accurate diagnosis can yield life-saving interventions for?
Other family members.
