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270 Cards in this Set

  • Front
  • Back
What are the two principle mechanisms by which vascular pathology results in disease?
1) Narrowing or complete obstruction of vessel lumina, either progressively or precipitously
2) Weakening of vessel walls, causing dilation and/or rupture
What type of blood vessels are generally affected by atherosclerosis?
Elastic and muscular arteries
What type of blood vessels are generally affected by hypertension?
Small muscular arteries and arterioles
Describe the general components of a blood vessel cell wall from the lumen to the connective tissue.
1) Intimia (Endothelium, Internal elastic lamina)
2) Media (External elastic lamina)
3) Adventitia
How do the innermost SMCs of the Media in BV walls receive oxygen and nutrients?
By diffusion from the blood in the BV lumen via fenestrations in the internal elastic lamina
How do the outermost SMCs of the Media in BV walls receive oxygen and nutrients?
From small arterioles in the adventitia called Vasa Vasorum
What is another name for Large Arteries?
Elastic Arteries
What is another name for Medium-sized arteries?
Muscular arteries
What is another name for small arteries?
Arterioles
Describe the regulation point of resistance to blood flow in the cardiovascular system and the type of blood flow that is occurring there (i.e. steady vs. pulsatile).
The regulation point of resistance to blood flow happens across the arerioles where the pressure and velocity of blood flow are both sharply reduced. Here blood flow is steady as opposed to pulsatile.
Resistance in a tube is inversely proportional to what parameter?
Depending on the Coefficient.....the radius or the diameter to the 4th power (8/r^4, 128/D^4)...thus small changes in arteriolar lumen size have profound flow-limiting effects
Describe the cross sectional area, and rate of blood flow in capillaries. Is this helpful for diffusion of oxygen and nutrients?
The total cross-sectional area of capillaries is very large and the resulting flow is very slow. This is and ideal setting for rapid diffusion of nutrients and oxygen from blood to tissues
In the setting of inflammation where does most of the vascular leakage and leukocyte emigration occur?
This occurs preferentially in the postcapillary venules
Compare the physical properties of arteries and veins.
Relative to corresponding arteries, veins have larger diameters, larger lumina, and thinner, less well-organized walls
What do the less organized and structurally sound components of veins leave them vulnerable to?
Dilation, compression, and easy penetration by tumors and inflammatory processes
Which side of the cardiovasular system contains more blood, arteries or veins?
The venous system has a huge capacitance, containing approximately 2/3 of all systemic blood
Describe the venous pressure and flow velocities.
Venous pressure and flow velocities are very low, thus where venous blood has to flow against gravity (e.g. leg veins) reversed flow is prevented by valves
How does the lymphatic system return fluid and its components back to the blood?
Via the Thoracic duct
What are berry aneurysms and where do they most often occur?
They are small spherical dilatations typically occurring in the circle of Willis; when ruptured they can cause fatal intracerebral hemorrhage
What are ateriovenous fistulas, when do they cause problems and condition can they lead to?
They are small direct connections between arteries and veins that bypass the intervening capillaries. When they are large or extensive they can become significant by shunting blood from the arterial to the venous circulations. This can force the heart to pump additional volume and high-output cardiac failure can ensue
What is fibromuscular dysplasia and what condition might it be responsible for?
A focal irregular thickening of the walls of medium and large muscular arteries, including renal, carotid, splanchnic, and vertebral vessels. It may be developmental and is due to some combination of irregular medial and intimal hyperplasia and fibrosis, which may result in luminal stenosis. In the renal arteries may actually be the cause of renovascular hypertension
Where are Weibel-Palade bodies found and what do they produce?
They are found in endothelial cells as organelles that produce and store Von Willebrand factor
List some of the jobs that Vascular Endothelial cells perform.
1) Maintain a non-thrombogeneic/thrombogeneic blood-tissue interface
2) Modulate vascular resistance
3) Metabolize hormones
4) Regulate inflammation
5) Affect growth of other cell types (particularly SMCs)
6) Acts as a selectively permeable monolayer
What are some of the consequences of endothelial dysfunction?
Endothelium-dependent vasodilation, hypercoagulable states, and leukocyte adhesion
What is the job the smooth muscle cells of the Media layer (the predominant cell type in this layer) that makes up the walls of BV, other than vasoconstriction and dilation?
They synthesize ECM collagen, elastin, proteoglycans and elaborate growth factors and cytokines. **They can proliferate when appropriately stimulated
What type of vascular injury is associated with SMC growth and matrix synthesis?
EC loss or even merely dysfunction
When do blood vessels produce and Intimal Thickening response?
Intimal thickening is essentially the stereotyped response of the vessel wall to ANY vascular insult. Following endothelial injury SMCs or SMC precursor cells migrate into the intima, proliferate, and synthesize ECM, much the same way that fibroblasts fill in a wound, forming a neointima
What makes neotintimal SMCs distinct from medial SMCs?
Neointimal SMCs cannot contract like medial SMCs can, and they have a distinct proliferative and synthetic phenotype
How are SMCs recruited and activated to repair injuries to the vascular intima?
They receive signals from ECs, platelets, macrophages, and mediators derived from coagulation and compliment cascades
What does Arteriosclerosis mean?
It literally means hardening of the arteries
How many types of Arteriosclerosis are there falling under this general term reflecting arterial wall thickening and loss of elasticity?
There are three main types:
1) Arteriolosclerosis
2) Monckeberg medial calcific sclerosis
3) Atherosclerosis
What is arteriolosclerosis and which diseases is it most often associated with?
Arteriolosclerosis (hyaline or hyperplastic) affects small arteries and arterioles. It is most often associated with hypertension and/or diabetes mellitus
What is Monckeberg medial calcific sclerosis?
Monckeberg medial calcific sclerosis is characterized by calcific deposits in muscular arteries, typically found in older patients. Its not usually clinically significant.
Define the major modifiable risk factors associated with atherosclerosis.
Increasing age, male gender, family history, genetic abnormalities
Define the major potentially controllable risk factors associated with atherosclerosis.
Hyperlipidemia, hypertension, cigarette smoking, diabetes, C-reactive protein
Atherosclerosis is a disease of what type of vessels?
Disease of large vessels- elastic and muscular
Where are the favorite sites of Atherosclerotic plaques?
1) Abdominal aorta and iliac arteries
2) Proximal coronary arteries
3) Thoracic aorta, femoral, and popliteal arteries
4) Internal carotid arteries
5) Vertebral Basilar, and middle cerebral arteries
What are the risk categories associated total cholesterol levels?
<200 mg/dl DESIRABLE

200-239 mg/dl BORDERLINE HIGH

>239 mg/dl HIGH RISK
What are the risk categories associated LDL cholesterol?
<100 mg/dl OPTIMAL

130-159 mg/dl BORDERLINE

160-189 mg/dl HIGH RISK

>189 mg/dl VERY HIGH RISK
What are the risk categories associated with HDL?
<40 mg/dl HIGH RISK

>60 mg/dl LOW RISK
The clustering of which risk factors qualifies a person as having Metabolic Syndrome (aka at high risk for atherosclerotic disease)?
Obesity, High TG, Low HDL, High BP, Diabetes (fasting glucose >110 mg/dl)
What type of junctions does atherosclerosis like to occur?
At areas of vessel branching, because for some reason ECs are damaged by low shear stress and higher turbulence, like there are at branch points
Why is homocysteine believed to be a contributor to atherosclerosis?
-Because it is toxic to the vascular endothelium and thus promotes endothelial dysfunction
-Also prothrombotic, activates platelets, contributes oxidative stress, and promotes vascular SMC proliferation
Define what type of marker C-Reactive Protein (CRP) is, which organ produces it and why.
CRP is a marker of inflammation that is produced by the liver in response to acute injury, infection, and other inflammatory stimuli
What is C-Reactive Protein (CRP) used as an indicator for in the clinical setting?
CRP is used to indicate possible Coronary Heart Disease (CHD). CRP has a high sensitivity for CHD, and may actually be a strong predictor of CAD that LDL. This raises the concept that atherosclerosis may truly be an inflammatory disease.
Is Monkeberg's calcification a lumen-narrowing intimal disease?
No! it is not a lumenal disease. It is just a medial calcification.
Define Ischemic Heart Disease. (IHD or CHD)
The spectrum of disorders resulting from the imbalance between the myocardial need for oxygen and the adequacy of oxygen supply
What are four clinicopathologic syndromes that are associated with Ischemic Heart Disease (IHD)
1) Angina Pectoris
2) Myocardial Infarction
3) Chronic Ischemic Heart Disease
4) Sudden Cardiac Death
What are some of the causes of Angina Pectoris?
Coronary atherosclerosis, increased myocardial demand, vasospasm, coronary microvascular disease
What types of Angina are there?
Stable/Typical angina, Variant/Prinzmetal's angina, Unstable Angina
What typifies Stable Angina?
Pain on exertion, relief upon rest
What typifies Variant Angina?
Coronary artery vasospasm, can occur at rest
What typifies Unstable Angina (pre-infarction angina)?
The pattern of frequency occurs with increased frequency, less exertion, and prolonged duration
Which MI clinical markers are found almost exclusively in heart tissue?
Troponin I and T- others like Myoglobin and CK-MB can be contributed to serum from other places in the body
What features of the blood vessels are seen in Chronic Ischemic Heart Disease?
Moderate to severe coronary atherosclerosis, progressive ischemic atrophy and death of myocytes, patchy myocardial fibrosis, may see scar or scars from previous MI, also called Ischemic Cardiomyopathy
What is normally the mechanism of death associated with Sudden Cardiac Death?
Ventricular fibrillation
Which hormone of the induces glycogenolysis and lipolysis during fight or flight states?
Epinephrine
If the conditions around us never changed would sympathetic nervous system be vital to life?
No, but in a variable environment we would lose the ability to regulate body temp, regulate blood glucose, regulate vasomotor tone, and resist fatigue
The sympathetic tone exerted on blood vessels usually constricts flow to organs except which ones in particular?
Brain, skeletal muscle, heart, and liver
What are the exceptions to the rule that tissues generally have dual, antagonistic parasympathetic and sympathetic innervation?
Adrenal medulla, sweat glands, spleen, pilomotor muscles, and most blood vessels have SYMPATHETIC INNERVATION ONLY
Compare the selectivity of antimuscarinics with that of the antinicotinics.
The antimuscarinics work at muscarinic receptors pretty much all over the body, whereas antinicotinics work at only certain subsets of nicotinic receptors at a time
Is epinephrine receptor subtype-selective?
NO, it activates all adrenergic receptor subtypes
Which adrenergic receptor is predominant in skin?
Alpha 1
Which adrenergic receptor is more sensitive to stimulation, Alpha 1 or Beta 2, and why is this important?
Beta 2 is more sensitive to stimulation and this is important because this means that vasodilation must be considered even at low drug concentrations
What is calcific aortic stenosis and when does it most commonly occur in people? What are the calcifications due to?
It includes calcifications and thickening of the valves of the aortic cusp annulus and peak incidence is in the 7th-8th decade of life; calcifications occur as part of an inflammatory process
What is another type of aortic valve stenosis (congenital) that most commonly occurs in the 4th-5th decade of life?
Bicuspid aortic valve which may eventually become stenotic due to turbulence and thickening
What are the symptoms and median survival times associated with those symptoms in a patient with clinically significant aortic stenosis (1-.1.5cm^2)
Angina = 5 yrs
Syncope = 3 yrs
CHF = 2 yrs
Artial Fib = 6 months
Why are patients with severe aortic stenosis more likely to have bleeding problems? What is this syndrome called?
Because their Type 2A vonWillebrand factor gets broken down in the turbulent jet of Aortic Stenosis; this syndrome associated with AS is called Heyde's Syndrome
Explain how the Bernouli equation can take the peak velocity across a valve and predict presure gradient? What does this let us decide?
If you can measure the peak velocity across a valve we know from Bernouli's equation that G=4(V^2). From this we can figure out what the pressure gradient is across the valve and based on that we can calculate the approx. size of the stenosis of the aortic valve and know how emergent the patient's condition is.
What is the critical point of pressure gradient in aortic stenosis warranting surgery for a patient?
>80mmHg
How can a low cardiac output affect the calculations for the pressure gradient and severity of Aortic Stenosis?
A low cardiac output can make a pressure gradient seem less significant that it is, and appear that it correlates with a lesser degree of stenosis than it actually does. The standard chart that we have seen relating pressure gradients across the aortic valve to area of the aortic valve assumes a normal cardiac output.
What is the classic lesion of Rheumatic valvular heart disease?
Mitral valve stenosis
When replacing an aortic valve what two types are there to choose from?
Mechanical valve (lasts 17yrs) and a Tissue valve (10 yrs)
What complications are seen with Mechanical aortic valve replacement and what long-term pharmacological therapy is usually employed?
Clotting problems are commonly associated with replacement with mechanical valves in the heart and patients with mechanical valves are placed on long-term anticoagulation therapies
What is the metal-biconcave heart valve called?
A St. Jude heart valve
What is the egg-in-a-basket heart valve called?
Starr-Edwards heart valve
***What considerations must be given when evaluating a patient for valve replacement?
Age of pt. vs. durability of valve, risk of coagulation for mechanical valves, presence of atrial fibrillation, Ross procedure (autograft with P valve), Percutaneous AVR, infectious endocarditis prophylaxis
***Which heart patients are required to have infectious endocarditis prophylaxis before certain procedures?
Those with complex congenital heart disease, those who have had endocarditis before, and those who prosthetic heart valve replacements
What is the prognosis in acute aortic insufficiency?
This is uniformly fatal
What are the main causes of aortic insufficiency?
Disease of Leaflets (e.g. bicuspid or AV), or due to Dilatation of the Aortic Root (HTN!, aneurysm, Marfan syndrome, syphylis)
What are two classical signs in the patient presentation that you might see with Aortic regurgitation? What do they look like?
de Musset sign:
Rhythmic nodding or bobbing of the head in synchrony with the heart beat, a sign of aortic insufficiency --incompetence of the aortic valve with aortic regurgitation. The causes include syphilitic aortitis, rheumatic fever, and aortic aneurysm.

Quinke's sign: pulsation of the capillary beds in the nails
What is the main cause of mitral stenosis?
Rheumatic valvular heart disease, which is normal seen after an infection with Group A strep
Left Atrial Myxoma (a benign tumor of the left atrium- buzz word = tumor PLOP!) can mimic what valvular heart disease that is normally caused by what?
Mitral stenosis, which is normally cause by Rheumatic valvular heart disease from infection with Group A streptococcus
What is the most common problem associated with the Mitral valve?
Mitral valve regurgitation
What are the most common causes of Mitral valve regurgitation?
Mitral valve regurgitation is most commonly caused by myoxmatous degeneration of the valve, remodeling of the LV from chronic overload and hypertension, endocarditis, papillary muscle dysfunction due to ischemia
If you see Mitral valve disease in a patient with SLE (Lupus), what special condition should you think of?
Libman-Sacks valvulopathy with antiphospholipid antibodies, veruccoid lesions, and thickening of the valve. There is immunodeposition which is mediating these observed problems
What is a normal ejection fraction of the Left Ventricle?
~55-65%
If a patient has Mitral valve incompetence, how much on average, is ejection fraction going to be overestimated by?
~8% added to the Ejection Fraction
It makes sense that the Left Atrium will get bigger with a Mitral valve regurgitation because there is a chronic backing up of blood, but the Left Ventricle also goes through some hypertrophy...Why?
This happens because there is still a pre-load increase in the LV when the atrium now dumps all its blood, which is more that it would normally have, back into the LV and the LV has to work to expel it all
Explain how Mitral regurgitation could lead to right heart failure.
With more blood in the Left atrium pressure builds up back against the Pulmonary veins which are bringing blood back to the heart from the lungs. This pressure transmits back to the lungs and the pulmonary capillaries which are going to sclerose. This sclerotic reaction creates Pulmonary hypertension and eventually transmits the increase in pressure back to the Right Ventricle and we can see Right sided heart failure from this
When you hear about changes in the left atrium such as mitral valve stenosis, dilatation, or A-fib that may cause stasis of blood, what hemotologic problem should you think about?
Clot formation, and patients should most likely be on anti-coagulation therapy
What is the difference between Orthopnea and Paroxysmal Nocturnal Dyspnea?
Orthopnea means you have dyspnea everytime you lie down. PND wakes you up only after you have been lying down for extended periods (this is why it take a while to wake you up in the middle of the night). Its like delayed orthopnea
Explain the root cause of PND and why it does not happen during the day?
The root cause of PND is a weak heart. When a person lies down at night there is an increased venous return to the heart that was not experienced during the while standing (at that time, gravity kept much of the venous return in the legs and there is some edema). The weak heart cannot handle pumping out this increased venous return it experiences at night and so blood backs up in the LV and LA with resulting congestion in the lungs.
What is the hallmark of advancing disease with Mitral Stenosis?
Dyspnea upon exertion
What co-morbidity is commonly seen with that atrial dilation observed in Mitral valve stenosis? Why?
Atrial fibrillation; because the stretching of the atrial tissue leads to changes seen in the conducting fibers of the heart (SA node?)
What other valve, in addition to the Mitral valve can commonly be involved with Rheumatic valvular heart disease?
The Aortic valve contributing aortic regurgitation
What are keys to remember about Mitral Valve Stenosis?
-Prior to Mitral valve commissurotomy patients died a slow death from MS due to RIGHT sided heart failure (anasarca)

-In rheumatic heart disease MS most often coexists with AI

-There is a latent period of 10-15 yrs after RF before RVHD becomes apparent
What are keys to remember about Mitral Valve Regurgitation?
-Commonly found in the setting of hypertensive and ischemic heart disease

-Will lead to enlarged LA and will strain LV with overload as well

-Afterload reduction to favor forward flow is indicated

-The presence of Mitral Regurg will cause an overestimation of ejection fraction
What are keys to remember about Tricuspid Valve disease?
-It is most commonly due to regurgitation

-May be organic (RF, IE, Carcinoid) or function

-Often well tolerated

-Doppler echo can calculate PA pressure by measuring TR jet velocity

-Some medications can cause it (Ergot alkaloids for headaches, 5-HT active drugs, Pergolide, Phen/Fen)
Which valve does Carcinoid Heart Disease effect most and what can it cause? Where does the carcinoid production originate, where does it metastasize to, what is its biggest disseminator into the blood stream?
Carcinoid heart disease is most commonly associated with the Tricuspid valve and the right side of the heart. The original Carinoid producing lesion most commonly comes from neural crest amine cells in the GI tract and metastasizes to the liver, where the Carcinoid products are released into the blood stream and can get to the heart right heart valves and cause fibrotic thickening damage leading to Tricuspid S. and Tricuspid I. and Right sided heart failure.
What are some distinguishing features of Right sided heart failure do to Cardiac Carcinoid?
Flushing, Diarrhea, Bronchospasm, Hypotension, Tachycardia,
What are some causes of Pulmonic heart valve disease (rare)?
PS-Usually congenital malformations, and Carcinoid cause is possible

PI- usually from Pulmonary HTN of any cause

Phen/Fen- reported to cause plaques on heart valves and Pulmonary HTN
What is the most common cause of aortic stenosis in younger patients(i.e. 4th and 5th decade of life)?
Congenital Bicuspid aortic valve.
What is the definition of CHF?
The clinical syndrome resulting from deficient cardiac stroke volume, relative to body need, with an inability of the cardiac output to keep pace with venous return
What causes congestive heart failure?
The loss of a critical quantity of functioning myocardial cells after injury to the heart due to :
-Ischemic heart disease, hypertension, idiopathic cardiomyopathy, infections, toxins (drugs and alcohol), valvular disease, prolonged arrhythmias
Explain the mechanisms of impairment involved with CHF.
The mechanisms involved with CHF are decreased myocardial ability to contract, and excessive pressure-stroke-volume load on the heart
What are some of the compensatory mechanisms that develop in the heart as a result of CHF?
Myocardial hypertrophy (Frank-Starling Mechanism), Cardiac chamber dilatation (Ventricular Remodeling), Increased blood volume (Neurohormonal Activation-increased RAAS,, SNS, ADH)
What are the three types of Naturetic peptides known?
Artial Naturetic Peptide (ANP): predominantly found in the atria, diruetic and vasodilatory properties

Brain Naturetic Peptide (hBNP): predominantly found in the cardiac ventricles, diuretic and vasodilatory properties

C-type Naturetic Peptide (CNP): predominantly found in the central nervous system, limited maturetic and vasodilatory properties
Describe the effects seen from stimulation of AT1 receptors by ANGII.
Vasoconstriction, Na+ retention, increased aldosterone release, increased cellular growth, Increased sympathetic nervous activity
Describe the effects seen from stimulation by ANP and BNP.
Vasodilation, sodium excretion, decreased aldosterone levels, inhibition of RAAS, inhibition of SNS
Describe the effects seen from stimulation by CNP.
Vasodilation, decreased vascular smooth muscle growth, decreased aldosterone levels
What are some causes of left sided heart disease?
Ischemic heart disease, Hypertension, Aortic and mitral valve diseases, Cardiomyopathy
What are some of the more prominent symptoms of left sided heart failure?
Dyspnea, orthopnea, PND, hemoptysis, fatigue
Explain the hemodynamic basis for left sided heart failure symptoms.
increase in LV End Diastolic pressure --> increase in Left Atrial Pressure --> Increase in Pulmonary capillary pressure --> Pulmonary congestion
What are some of the causes of Right-sided heart failure?
Left-sided heart failure, Lung disease (cor pulmonale), tricuspid and pulmonic valvular disease
Explain some of the symptoms seen in Right-sided heart failure.
Peripheral edema, RUQ discomfort (hepatic enlargement/ nutmeg liver), anorexia and nausea, weight gain
What is a major blood marker that we use to gauge the degree of heart failure that is occurring? Where does it come from, is it produced, what are its levels correlated to?
The marker is BNP; it is found in the cardiac ventricles; it is made in response to stretch and increased volume found in the ventricles; BNP levels are correlated to LVEDP; the more BNP released, the more deformation and dilatation of the heart exists
You are able to use BNP as a prognostic indicator after what type of heart event?
Myocardial Infarction
When you are trying to distinguish whether or not a patient is having lung problems due to primary lung disease or CHF what is a marker you can use to point you in the direction of CHF?
BNP
What types of medications are involved in the management of CHF?
Digoxin(enhances contractility of the myocardium and reduces neurohormonal activation), Diruetics, ACE inhibitors, ARBs, Beta Blockers
What are the results of some of these actions that occur in the body during Non-progressive cardiogenic shock:
-Baroreceptor reflex
-Catecholamines
-RASS
-ADH
-Tachycardia
-Peripheral vasoconstriction
-Conservation of fluid by the kidneys
What features mark the progressive stage of cardiogenic shock?
-Hypoxia leading to anaerobic glycolysis with excess production of lactic acid
-Induction of metabolic lactic acidosis
-Acidosis leads to vasodilation with pooling of blood in the periphery, decreased CO -->anoxic injury to endothelial cells
-May lead to DIC
Describe the features of Irreversible Stage Cardiogenic shock.
-Widespread cellular injury with leakage of lysosomal enzymes
-Ischemic pancreas released myocardial depressant factor
-Complete renal shutdown (acute tubular necrosis)
What are some clinical findings that are seen in cardiogenic shock?
Ashen grey pallor, cool clammy skin, weak thready pulse, RAPID cardiac and respiratory rate, Decreased urine output, about 70-80% mortality
It does not happen often, but which metastatic cancers most often metastasize to the heart?
Lung cancer, Breast cancer, Melanoma, Leukemia and Lmphoma
What are some of the consequences of benign cardiac tumors?
Embolism, Valve damage, blood flow obstruction, congestive heart failure, arrhythmias, sudden death
Explain what tissues Cardiac Myxomas arise from and what other condition they might resemble.
Most arise from the left atrial endocardium and are composed of myxoma, endothelial, and smooth muscle cells with macrophages; they can often dip down into the mitral valve and resemble mitral valve stenosis
Describe the pathological changes that can occur in heart valves.
There can be:
-Damage to collagen resulting in weakness of leaflets
-Calcification, leading to thickening and sclerosis
-Fibrotic thickening
-Damage to chordae tendineae and papillary muscles
What condition does congenital bicuspid aortic valve predispose partients to earlier in life than would otherwise be expected?
Aortic calcification
What are some of the causes of Mitral Regurgitation?
Mitral valve prolapse, RHD, IHD, Mitral annular calcification, hypertrophic cardiomyopathy, infective endicarditis, CHF
When is mitral valve prolapse most commonly seen?
In Marfan's syndrome
What are the two ways in which RHD affects the heart?
1) Acute rheumatic carditis
2) Chronic valvular deformities
Explain the pathogenicity of Acute Rheumatic Fever (ARF).
Pathogenicity in the heart that occurs as a result of acute rheumatic fever probably occurs as a result of a hypersensitivity cross reaction. To Goupr A strep antigen. Host anitbody produced against M protein of Strep cross reacts with tissue glycoprotein in the heart, joints and other tissues. Onset occurs about 2-3 weeks after pharyngitis.
Where do the cross reacting antibodies produced from ARF react in the heart tissue?
PANCARDITIS: Endocardium (mitral and aortic valves), Myocardium (myocardial Aschoff bodies/diffuse inflammatory infiltrate), Pericardium (fibrinous pericarditis/effusion)
When do you see Anitschkow cells in the heart?
In RHD, in the myocardium with Aschoff bodies
What are some clinical features of Chonic Rheumatic Heart Disease?
Seen years to decades after ARF, results from irreversible deformity of valves caused by scarring of acute endocarditis, can lead to CHF, deformed valves increase risk of infective endocarditis, Mitral and Aortic valves are most commonly invovled
Does RHD usually cause Mitral Valve stenosis or regurgitation?
Stenosis
Is Mitral valve involvement after ARF more commonly seen in men or women?
Women
Is Aortic valve involvment after ARF more commonly seen in men or women? What type of problem is most commonly observed?
Men; Aortic stenosis
What is the mechanism by which valves stenose in response to ARF?
Commisural Fusion
What are some of the complications that can occur with Prosthetic Valves?
Mechanical deterioration, stiffening, and calcification (esp. with bioprosthetic), Thrombosis (esp. with mechanical), Infective endocarditis, Paravascular leaks, Hemolysis (esp, with ball and cage), Anticoagulant related hemorrhage, Noise
What is the first step in classifying Acute Coronary Syndrome(ACS)? What do we look for?
The first step in classifying ACS is looking at an Electrocardiogram. Here we are looking for an ST-elevation.
What is the second step in classifying Acute Coronary Syndrome? What do we learn from the results?
The second step in classifying ACS is looking at Cardiac markers. If they are negative then we classify the event as unstable angina. If they are positive we classify the event as an MI. Based on the results of the first step in classification we say if it is an ST or Non-ST elevated MI.
What does the ST elevation on an electrocardiogram represent?
Thrombus formation and occlusion of an epicardial coronary artery
What is the MONA treatement? When do you get it?
MONA = Oxygen. Aspirin (160-325mg), Nitro S/L, Morphine IV

Patients are given this when they present with a history of chest pain consistent with possible MI
Do patients with ST segment depression receive Thrombolytic Therapy?
NO! in that case there is no proof that there is a thrombosis exists. You only use thrombolytic therapy if there are two members of contiguous leads showing ST ELEVATION (90% thrombus)
What is the classification and course of treatment for a patient with no ST elevation and no cardiac markers present in the blood?
The classification is Unstable Angina with intermediate or low risk; Tx is to monitor closely, CXR, and evaluate for Non-Cardiac pain
What is the classification and course of treatment for a patient with ST depression/T inversion and no cardiac markers present in the blood?
The classification is Unstable Angina with high risk and ischemia present; Tx is anticoagulation therapy with Unfractionated or LMW Heparin, ASA, Beta Blockers, Nitro IV, consider clopidogrel or glycoprotein IIb/IIIa inhibitors, assess for reperfusion
What is the classification and course of treatment for a patient with ST depression/T inversion and cardiac markers PRESENT in the blood?
The classification is NSTEMI with ischemia and damage; Tx is anticoagulation therapy with Unfractionated or LMW Heparin, ASA, Beta Blockers, Nitro IV, consider clopidogrel or glycoprotein IIb/IIIa inhibitors, assess for reperfusion
What is the classification and course of treatment for a patient with ST elevation and cardiac markers PRESENT in the blood?
The classification is STEMI with ischemia, damage and thrombosis; Fibrinolytic treatment if appropriate, Beta blockers, Nitro IV Anticoagulation, ACE Inhibitors, Consider reperfusion
Which layers of the heart wall are effected when a patient undergoes an STEMI?
All layers, this is a transmural infarction
Which layers of the heart wall are affected when a patient undergoes an NSTEMI?
Only the subendocardial layer is most often what is affected
How quickly does Troponin begin to rise after an acute MI?
3-6 hours
When would you see peak Troponin levels after an acute MI?
12-24 hours
How long might elevated Troponin levels last after an acute MI?
I Week
On a 12 lead EKG what do leads II, III and aVF represent? What do the other leads represent?
Right Coronary Artery; Left coronary artery
What type of continuing pharmacological therapy are patients with stents put on?
Anticoagulation therapy to ensure that there is no problems with clot formation.
What are the three major complications associated with ST-elevation Myocardial infarction? How does these structural damages take place?
Vetricular septal rupture, Free wall rupture, Mitral Regurgitation (Papillary muscle rupture); these ruptures can only happen after coagulation, necrosis and softening have taken place, and this takes about 3-7days
What is required to have rupture defects associated with acute myocardial infarction and how long after the initial event does it take to see these changes?
To get rupture events associated with acute MI the there must be coagulation blockage, necrosis, and softening of the heart tissue. It takes about 3-7 days after the initial insult to see these changes and have the rupture take place
Occlusion of which coronary artery would most likely give rise Vetricular Septal rupture? What conduction problem might be associated with occlusion of this artery?
The Left Coronary artery; the conducting bundle fibers run along the ventricular septum and so with occlusion there might also be a problem with bundle branch block
Which coronary artery is associated with Free Wall rupture seen after an acute MI?
Left coronary artery, but can be seen in inferiorly with the Right coronary artery
Which coronary artery most lends itself to Papillary Muscle rupture associated with an acute MI (The Right or the Left?)?
The Right Coronary artery; the papillary muscles in the heart are seated posteriorly, and in 85% of patients the Posterior descending coronary artery arises from the Right coronary artery, so if you block the Right Coronary artery and the Posterior descending artery the papillary muscles will likely be affected
Which coronary artery is associated with Right Ventricular infarct?
Right coronary artery occlusion
What does the description of Dyskinesia mean when describing the walls of the heart and how does it form?
Dyskinesia usually means that there is an aneurysm in the wall of the heart the is being described (e.g. LV Aneurysm formation leads to LV dyskinesia) . The aneurysm formed when after an infarct to the tissue fibrotic material came in to infiltrate that which was dead or dying. This scarring fibrous band of tissue does contract like the rest of the tissue around it and with some time it begins to billow out and form an aneurysm.
Why are aneurysms in the tissue of the heart wall (e.g. the LV) such a problem? What kind of pharmacologic therapy must patients with a condition like this be put on?
In addition to the abnormal motion of the heart and flow of blood, there can be areas of stasis and this becomes prone to clot formation which can be thrown anywhere in the body from the left ventricle; these patients must be put on anticoagulant therapy
How long does it take for LV aneursm to show up following an infarct?
3-6 weeks
Why is the remodeling of heart tissue that follows an infarct a bad thing?
Following infarct, infarcted heart tissue becomes fibrotic and does not contract. Increased work and remodeling of this tissue lead to dilation of the chamber where this has occurred. The ejection fraction is lowered and signs and symptoms of heart failure are seen.
What medications are given to patients post MI to deal with heart failure that may occur as a result of tissue remodeling and to try and prevent further remodeling? Why?
Beta blockers to lessen the work load of the heart and prevent dilation and hypertrophy; ACE inhibitors because as the ejection fraction is lowered the kidney senses less perfusion and initiates the RAAS system, which helps retain salt and fluid. This creates more problems as the already weakened heart tries to pump out bigger volumes of blood against increased pressures. ACE inhibitors try to protect against this.
What medication are all patients post-MI indicated to be started on and why?
Beta blockers because they decrease the chance for reinfarction and decrease myocardial work
Explain the physical properties behind what is going on when we hear crackles in the lungs due to pulmonary edema.
This is the sound of alveoli popping open upon inspiration. The negative intrathoracic pressure that is generated by taking a deep breath overcomes the hydrostatic pressure that is holding the alveolar membranes together
Patients with what condition are at the highest risk of sudden cardiac death?
Patients with a low ejection fraction
How long do patients with a low ejection fraction do to heart failure generally survive after this diagnosis?
~ 6 months, they have a high 6 month mortality
What is the only treatment that has been shown to improve survival in patients with a low ejection fraction due to heart failure?
Implantation of an Automatic Implantable Cardiac Defibrillator (AICD); they can detect electrical abnormalities and correct heart rhythms
What feature do you see on an EKG when you have ventricular septal damage and are experiencing a bundle branch block?
A wide QRS complex
What does a wide QRS complex mean on an EKG? What can produce this?
That there is a bundle branch block in conduction; ischemic heart disease can produce this and so can fibrosis with old age.
What is a favorite medication found on crash carts to be used in the event of bradycardia that affects vagal tone?
Atropine
SA and AV nodal complications are found most commonly to be involved with Inferior Wall infarcts and which coronary vessel?
The Right Coronary artery, because 65% of people have an SA nodal branch that comes off of the RCA, 90% of people have an AV nodal branch that comes off of the RCA
We use Exercise stress testing on patients with what level of risk for MI? Why only them?
This testing is used on patients with an intermediate level of risk for MI. The test is not sensitive enough to pick up those who are at low level risk, and does not provide any new information about those who are high risk
What are we looking for in a treadmill stress test by raising the HR and BP? What artificial condition are we inducing?
We are looking for any presence of ST depression indicating ischemia; We are artificially inducing a mild subendocardial infarction
Reversibility of a radionuclide enhancement (cintagraphic view) of EST is sina qon non for what result of the EST (elevated stress test)? What are the pictures showing? What if there is poor perfusion in the stress stage, but the rest stage looks just like it?
A positive stress test; the pictures are showing how well perfused the heart tissue is at many levels and slices; if the stress stage looks like poorly perfused, but the rest stage looks just like it this indicates that there was poor perfusion to begin with and it is likely an old area of dead tissue
What are the medications that we give to patients suspected of having an MI? What is the magic quartet Post confirmed-MI?
MONHAS (morphine, oxygen, nitro, heparin, aspirin, statin); ACE inhibitor, aspirin, Beta Blocker, Statin
What is the time frame of development when developmental congenital cardiac defects can take place?
They take place at 3-8 weeks of gestation.
What is the most common congenital arrhythmia that we see?
Bradycardia.
Explain how an untreated left to right heart shunt can progress to Cyanosis Tardi and Cor pulmonale.
Right heart has to work harder and you can end up with pulmonary hypertension. This results in RVH, which can be so severe that the pressure in the right heart is greater than the pressure in the left heart and so the shunt is reversed. This results in cyanosis which is occuring later in life (Cyanosis Tardi) and RCHF due to pulmonary hypertension (Cor pulmonale)
What is the most common congenital heart defect that we are likely to see (30%)? What other conditions is it most commonly seen with?
Ventricular Septal Defect (VSD); commonly associated with Trisomy 21 and also possible problems with the conducting system
What is the second most common congenital heart defect that we are likely to see (20%)? What can happen if this is left untreated?
Patent Ductus Arteriosis (PDA); most commonly seen in children born before 36 weeks gestation. There is a left to right shunt and if it is left untreated the patient can develop pulmonary hypertension
What is the third most common congenital heart defect that we are likely to see (15%)? What area of the heart is this most commonly seen in? What hemodynamic complications are often seen associated with this?
Atrial septal defect; this is most commonly seen in the area of the foramen ovale; clot and thrombus formation due to hypercoagulatbility syndromes
Are you usually going to hear a murmur associated with an atrial/septal defect? Why or why not?
No, because there is usually not high enough pressure in the atria to cause enough turbulence to hear a murmur with the heart beat
What is the most common congenital cyanotic heart disease that we will see?
Tetralogy of Fallot
What are the four defects associated with Tetralogy of Fallot?
Overriding aorta, VSD in the endocardial cushion, pulmonic stenosis, RVH
What is the deciding factor of the severity of disease in Tetralogy of Fallot?
The degree of pulmonic stenosis
Describe the two types of Aortic Coarctation that we see.
There is Child Coarctation (coarctation above the Ductus areteriosis) and Adult Coarctation (coarctation below the Ductus arteriosis)
Explain the phenomenon observed in Adult Aortic Coarctation that is seen regarding to tissue perfusion? Why do we see notching of the ribs?
Because we see coarctation occurring below the joining of the upper extremity vessels to the aorta, we find that there is adequate perfusion of the tissues in the upper body, but there is cyanosis in the lower body and lower extremities; we see notching of the ribs because the collateral circulation of the superior epigastric and intercostal arteries is greatly dilated and the pressure that comes through them notches the ribs
What condition do we see in newborns with Coarctation of the Aorta (normally occurs above the vessels to the upper extremity)?
Here we see LVH and CHF with a very poor prognosis
What physical findings are indicative of Diastolic heart failure?
Only slightly displaced PMI, reverse splitting (on expiration) of the second heart sound, which is called S4, due to a fibrotic ventricle that has become stiff, hypertrophied and non-compliant. This is detected at the end of diastole when the "atrial kick" occurs and the ventricle does not comply to the blood that is presented to it
What heart sound is the hallmark of diastolic dysfunction? At what point in the heart sounds does it occur? What kinda of splitting is it correlated with?
This is S4 and this sound serves as a marker for decreased compliance. This occurs right before S1 at the end of diastole. It is correlated with reverse splitting
What is physiological splitting of the second heart sound and why does it occur?
Physiological splitting is a splitting of the second heart sound upon inspiration. Normally S1 is the sound of M/T valves closing and S2 is the sound of A/P valves. When you inspire there is more blood returned to the heart and so when the right ventricle contracts there is more blood that must be pushed through the Pulmonic valve and into the lungs. This delays its closing slightly, thus S1 is the M/T valves as usual, S2 is just the A valve, and S3 is the delayed pulmonic valve
What is the mechanical cause of paradoxical splitting of the second heart sound (splitting on expiration)? What are the three things that will present with paradoxical splitting?
The splitting indicates delayed closure of the Aortic Valve due to existing hypertension and increased intrathoracic pressure upon expiration ; 1) Severe systemic Hypertension 2) Aortic stenosis 3) Left bundle branch block
What change feature of the heart chamber is much more indicative of systolic heart failure rather than diastolic heart failure?
Dilatation
What valve feature is considered a "hallmark" of a dilated heart? What sound is heard?
Mitral regurgitation; there is a murmur heard at the apex of the heart and there is no increase in the intensity of the murmur upon expiration
When do you hear and S3 gallop? What is the physical feature that is producing the classical S3 gallop early in diastole?
You hear an S3 gallop early in diastole when the ventricle has not ejected all of the blood that had been presented to it in the previous diastolic systolic cycle. Now when the left atrium empties, the blood "splashes" into the blood left in the left ventricle from poor systolic emptying
What conditions can be classically associated with Cardiac Tamponade? What is the description that will be in a question stem that will be the key indicator to this problem?
SLE (serositis), history of malignant metastasis (breast cancer and lung cancer); the description will be that the "heart tones are hard to hear
Explain what Beck's triad is indicative of and what signs or symptoms make up the triad.
It describes Cardiac tamponade; the triad is elevated neck veins, low blood pressure, and decreased heart sounds (quiet heart)
What is the most common cause of death associated with Aortic dissection?
Cardiac tamponade
What is unique about blood that comes from the pericardium when it is drawn off?
The blood that comes off of the pericardium is non-clotting and will not clot in the syringe.
What is electric alterans or pulsis alterans associated with?
Pericardial tamponade
Explain how sickle cell disease can cause Right-sided heart failure
This can develop because sickle cell can cause pulmonary arteriole hypertension, which then leads to Cor pulmonale
When you hear "wide splitting of S2" what should you think?
Pulmonary hypertension
What are the correlate causes of a "wide splitting of the second heart sound" when compared with those of Paradoxical splitting?
wide splitting occurs because of problems with the left side of the heart and things that make the aortic valve close more slowly (i.e. severe systemic hypertension,aortic stenosis, and LBBB). The problems associated with wide splitting are affecting the right side of the heart and are Pulmonary hypertension, pulmonic stenosis, and RBBB.
How would you treat someone who has pulmonary hypertension due to sickle cell anemia?
Endothelial recedptor antagonists and Suldenofil (Viagra)
What kind of murmur would you hear with mitral regurgitation?
You would most likely hear a lloud holosystolic murmur
Which coronary artery has most likely been involved if you observe papillary muscle rupture following an acute MI?
The Right coronary artery
Which coronary artery has most likely been involved if you observe free wall or ventricular septal rupture following an acute MI?
The Left coronary artery
If you see a mural thrombus on an echocardiogram, what is normally the underlying cause?
Poor contractility of the heart
What types of conditions might cause someone to have both pericardial and pleural effusion?
Lung cancer- invasion and disruption of the lymphatics in the pericardial and pleural space leading to exudate. Also, Endstage Renal Disease- leading to low serum albumin and decreased colloid oncotic pressure in blood
What is the main risk associated with proximal aortic dissections?
Pericardial tamponade, due blood leaking and filling in the pericardium; this results in death from hemopericardium in 24-48hrs
Which imaging method can help you visualize valvular endocarditis: TTE or TEE?
TEE
How do we do a pharmacologic stress test?
We add radionucleide marker and adenosine. Adenosine preferentially vasodilates those arteries that are not stenotically lesioned. This uses the logic based on the STEAL phenomenon of stealing blood from one area of the heart and delivering it to another
What is the gold standard imaging study for getting a map of coronary artery disease?
Coronoary angiography
In the 18 y/o to 30 y/o age group what are the #1 and #2 causes of Sudden Cardiac Death?
#1) Hypertrophic Cardiac Myopathy

#2) Anomalous Coronary artery
What diseases can cause constrictive pericarditis? What is the treatment?
TB and HIV; strip away the restrictive tissue and material by pericardiectomy
What imaging study of the heart is used to determine both perfusion and viability of heart tissue? (detects stunned or hibernating myocardium)
These parameters can be defined using PET scan.
What medication do patients take that might give a false positive EKG on a stress test? What is a condition that might do the same thing?
Digoxin; LVH
What constitutes a positive stress test and scintographic study?
An EKG showing 1mm horizontal or downsloping ST depression during exercise or the recovery period; scintographic study shows reversibility and delineates which segments of the myocardium are at risk
In addition to adenosine, what Beta agonist pharmacologic agent can be used in a pharmacologic stress test? What functional characteristic can it be used to asses in the heart?
Dobutamine (B1 agonist); it can be used to assess wall motion when heart rate is increased
TEE is specifically good for visualizing what conditions in the heart?
TEE is specifically good for Aortic dissections and small vegetations!!!
Where do left atrial myxomas almost always attach to?
Left atrial myomas almost always attach to the interatrial septum.
What is the most common cause for Tricuspid valve regurgitation?
The most common cause of Tricuspid regurg is left heart failure leading to right heart failure and incompetent valves
What are two examples of valvular abnormalities that might lead to tricuspid regurgitation?
Carcinoid!!! and Vegitations
What pulmonary artery pressure is normal and what is considered to be elevated?
PA pressure of 25 mmHg is normal; above that is elevated
What are the pearls to consider with a patient presenting with Aortic Dissection? (i.e. when do we suspect Aortic dissection?)
You suspect aortic dissection if the patient presents with sudden chest pain, atypical heart movement, or a tearing sensation, this all clasically occurs suddenly. Can be found with hypertension and chest pain, a wide mediastinum on CXR, and the patient looks and feels terrible, they feel like they are "going to die", EKG is usually non-specific, and you can give beta blockers to help contain the dissection by lowering shear stress
What are the differences in treatment of proximal aortic dissection versus distal aortic dissection?
Proximal aortic dissection is managed surgically and distal aortic dissection is managed medically.
What are two pearls that a patient will present with when they have Left Atrial Myxoma?
They will present with recurrent episodes of syncope and a plopping sound heard on auscultation
What are some of the immunologically generated phenomena associated with infective endocarditis?
Osler's nodes (on the finger tips, palms and soles, tender), Janeway lesions (palms and soles, non-tender), Roth spots, rheumatoid factor, glomerulonephritis, petechia formation
Of patients in the hospital, who are at the highest risk of developing endocarditis?
Those with central lines in place
Of patients who are not in the hospital, who are at the highest risk of developing endocarditis?
Those with prosthetic valves, those who have had previous episodes of infective endocarditis, and those who have complex congenital heart disease (e.g. Tetralogy of Fallot patients)
What is the primary organism responsible for bacterial endocarditis?
Streptococcus viridans
What is the primary organism responsible for bacterial endocarditis for those who inject foreign bodies into their systems? (i.e. I.V. drug users) What is the most likely valve to be affected?
Staph aureus; the Tricuspid valve
Is TTE or TEE more sensitive for detecting vegetations due to Infective Endocarditis? What if you use TTE and get a negative result? Which is the preferred test for evaluation of prosthetic valves?
TEE is much more sensitive; If TTE is negative, consider using TEE; TEE is preferred for evaluating prosthetic valves.
When you hear the pearls of a murmur increasing with Valsalva and decreasing with squatting, what do you think is causing the murmur?
Hypertrophic Cardio Myopathy; there are two components associated with this 1) Everyday component of outflow obstruction 2) Subgroup of patients who have a tachyarrhythmia associated with this who are very prone to sudden cardiac death
What is the genetic mutation most associated with HCM (hypertrophic cardio myopathy)?
Beta-myosin heavy chain defect. If this is encoded improperly it tends to be most associated with cardiac death.
How do you treat someone for HCM (hypertrophic cardio myopathy)?
Beta blockers, or alcohol septal ablation and myomectomy for others; AICD for a small number of patients who have additions malignant arrhythmias (Beta myosin heavy chain defect)
What are the three clinically relevant intervals for the EKG reading?
PR interval, QRS duration and the QT interval
What does a flattened T-wave and a prominent U wave seen on an EKG indicate?
These two indications mean Hypokalemia
What does the PR interval on an EKG represent and about how long is normal?
The PR interval is the amount of time it takes to depolarize the atria, the His perkinje system and the bundle branches; it usually takes less than 0.2 sec
On an EKG what does a PR greater than or equal to 0.20 sec indicate?
A PR interval greater than or equal to 0.20s indicates a First Degree AV Block
What are some likely causes of a First Degree AV block?
Ischemic heart disease (Right coronary arteries supplying the conduction system), Drugs (Digoxin, Verapamil, Diltiazem), Old Age, Infiltrative and inflammatory disorders (Lupus, Lyme disease, Chagas, Amyloid, Sarcoid)
What does the QRS duration on an EKG represent and about how long is normal?
Ventricular depolaorization; it should last less than .12 sec
On an EKG what does a QRS duration greater than or equal to 0.12 sec (three tiny EKG boxes) indicate/ what is this most likely due to?
Bundle branch block, Hyperkalemia, Infarct, Drugs (Amiodarone), Inflammation/Infiltration
In the hospitalized population who is at highest risk for Hyperkalemia?
Those patients with Chronic Renal Dysfunction.
What is T-wave peaking on an EKG due to?
This is due to Hyperkalemia
What does the QT interval measure?
This measures the time it takes for ventricular depolarization and ventricular repolarization.
Is there an absolute normal value for the QT interval on an EKG reading like there is for the PR interval and the QRS duration? Why or why not? What is the rule for how ling it should take?
No there is no absolute value for the length of the QT interval like there is for the PR and QRS duratio because QT is a function of Hear Rate. The faster the heart rate, the shorter the QT interval. The general rule is that the QT interval should NOT be LONGER than HALF of the R-R interval.
What defines a long QT interval on an EKG?
A QT interval that is greater than Half of the R-R interval is considered to be a long QT.
What are some things that can cause a long QT interval?
Ischemia, Drugs (Anything that causes hypokalemia, hypomagnesia, hypocalcemia; also Class 1A antiarrhythmic agents- Quinidine; many psychotropic agents, and those drugs associated with inhibiting CYP3A4 taken with a drug that effects QT), Hypometabolic states; anything that effects the hearts access to its energy source, or its ability to repolarize
What is it thought that the U wave (seldom seen) on the EKG represents?
It is thought that the U wave represents the repolarization of the perkinje fibers and it is usually only seen during profound bradycardia
What EKG abnormality can lead to a long Torsades de Pointes?
Long QT
If someone is on a drug that prolongs a QT what drug interactions must you be careful about prescribing? Why
You should be careful about prescribing Quinolone antibiotics and Macrolide antibiotics if someone has a taken a drug that creates long QT and/or is on antiarrhythmics because those antibiotics inhibit CYP3A4 that is responsible for metabolizing many long QT producing drugs, and left unopposed, those drugs can lead to Torsades de Pointes!!!!
In an ideal world what heart feature does the electrical voltage represent?
It represents myocardial mass. The bigger the voltage, the bigger the myocardial mass. But this is affected by body habitus.
Explain how a patient with nephrotic syndrome coul have pulsis alterans and low voltage on an EKG?
This could happen because a patient with nephrotic syndrom, by definition has greater than 3.5 grams/day proteinura coupled with hypertension, and edema. Losing this much protein a day could lead to low serum protein and low oncotic pressure. Thus pericardial effusion could form and cause pericardial tampenade that would be responsible for and EKG with findings of pulsis alterans and low voltage.
What would low voltage and bradycardia on an EKG most likely be associated with?
Low voltage and bradycardia on an EKG would most likely be associated with a Hypometabolic state.
How many types of Ca++ channels are found in cardiac tissue?
Two types: L and T
Where are the L-type Calcium Channels found in the heart?
L-type channels are found in both ventricular cells and atrial cells
Were are the T-type Calcium Channels found in the heart?
T-type channels are found mainly in atrial cells (including the SAN)
Which therapeutic agents block L-type Calcium Channels in the heart?
Verapamil and Diltiazem
On an EKG, what does a peaked T wave indicate?
Hyperkalemia
On an EKG, what does a flattened T wave indicate?
Hypokalemia
On an EKG, what does an inverted T wave indicate?
Ischemic Heart Disease
What are the two EKG findings that Hyperkalemia can cause? Which one will occur first?
QRS complex widening, and T- wave Peaking; the T-wave peaking will happen first and the effects on the QRS complex happen with prolonged exposure to high [K+]
What do both P wave enlargement and a notched P wave indicate on an EKG?
They both indicate atrial hypertrophy