Cardio Winter Break

Sodium Channel Blockers (class I)

Class IA
Quinidine, Procainamide, Disopyramide
MOA: Increase action potential duration, increase effective refractory period,
increase QT interval
Clinical use: Atrial and ventricular arrhythmias, especially re-entrant and ectopic
SVT and VT
Toxicity
Thrombocytopenia, torsades de pointes due to increase QT interval
Quinidine - Cinchonism (headache and tinnitus)
Procainamide - Reversible SLE-like sydrome
Disopyramide - heart failure
Class IA antiarrhythmics, such as procainamide, affect both atrial and ventricular
arrhythmias. They block sodium channels and thus slow conduction velocity in
the atria, ventricles, and Purkinje fibers. This decreased conduction velocity
slows phase 0 of the action potential (AP) and is manifested as an increased
QRS duration on the ECG. In addition to blocking sodium channels, class IA
antiarrhythmics also block potassium channels and thus increase the AP duration
by proloning the effective refractory period.
Class IB
Lidocaine, Mexiletine
MOA: Decreased AP duration; Preferentially affect ischemic or depolarized
Purkinje and ventricular tissue
Clincial Use: Acute ventricular arrhythmias (especially post-MI), digitalis-induced
arrhythmias
Lidocaine is used in treatment of acute ventricular arrhythmias such as postmyocardial infarction arrhythmias
Toxicity: CNS stimulation/depression, cardiovascular depression
Slow phase 0 of the action potential, but decrease the AP duration. These
antiarrhythmics affect ischemic or depolarized Purkinje and ventricular tissues.
These antiarrhythmics have no effect on ERP.
Class IC
Flecainide, Propafenone
MOA: Prolongs ERP in AV node; no effect on ERP in Purkinje and ventricular
duration

Clinical Use: SVTs, including atrial fibrillation; last resort in VT

Toxicity: Proarrhythmic, especially post-MI (contraindicated)
Slow phase 0 of the action potential, but have no effect on the AP duration
Potassium Channel Blockers (class III)
Amiodarone, Ibutilide, Dofetilide, Sotalol (AIDS)
MOA: Increase action potential duration, increase effective refractory period,
increase QT interval
Clinical Use: Atrial fibrillation, atrial flutter; ventricular tachycardia (amiodarone
and sotalol)
Sotalol is used when other antiarrhythmics fail (also a beta-blocker - class II)
Toxicity
Sotalol - Torsades de pointes
Ibutilide - Torsades de pointes
Amiodarone - Pulmonary fibrosis, hepatotoxicity,
hypothyroidism/hyperthyroidism > weight loss, hyperreflexia, palpitations
(amiodarone is 40% iodine), corneal deposits, blue/gray skin resulting in
photodermatitis, neurological effects, constipation, cardiovascular effects
(bradycardia, heart block, HF)
Tests to monitor: Thyroid, liver, and pulmonary function tests
Pulmonary fibrosis is a restrictive lung disease (low FEV1 and low FVC but
FEV1:FVC > 80%); Decreased diffusing capacity; increased A-a gradient;
decreased lung volume, decreased FVC and TLC
Bretylium - used when other antiarrhythmics fail
Calcium-Channel Blockers (class IV)
Amlodipine, clevidipine, nicardipine, nifedipine, nimodipine (dihydropyridines, act
on vascular smooth muscle)
Diltiazem, verapamil (non-dihydropyridines, act on heart)
Vascular smooth muscle - amlodipine = nifedipine > diltiazem > verapamil
Heart - Verapamil > diltiazem> amlodipine = nifedipine
MOA:
Dihydropyridines (except nimodipine): hypertension, anginal (including
Prinzmental), Raynaud phenomenon
Nimodipine: subarachnoid hemorrhage (prevents cerebral vasospasm)
Clevidipine: hypertensive urgency or emergency
Non-dihydropyridines: hypertension, angina, atrial fibrillation/flutter

Toxicity:
Cardiac depression, AV block (non-dihydropyridines), peripheral edema, flushing,
dizziness, hyperprolactinemia (verapamil), gingival hyperplasia, constipation
Verapamil can cause constipation and abdominal pain.
RANDOM
Estrogen containing medications such as oral contraceptives can cause the
blood to clot more readily
EDEMA
In right sided heart failure (most often from left-sided heart failure), venous
hydrostatic pressure increases, leading to transudation of fluid to the
extravascular space, secondary to poor cardiac output. Physical findings include
ascites, peripheral edema, and elevated jugular venous distantion. Causes can
be any mechanism of heart failure like cardiac sarcoidosis (granulomas formed
in heart tissue) or pulmonary hypertension.
Increased capillary permeability occurs in sepsis and anaphylaxis, where the
inflammatory cytokine cascade results in the flow of fluid to the extracellular
space (toxins, infections, burns)
Albumin plays an important role in increasing intravascular oncotic pressure and
drawing water intravascularly. When a patient is hypoalbuminemic, the oncotic
pressure of the intravascular space is decreased and water tends to flow out of
the blood vessels into the extravascular space. (also due to liver failure)
Nephrotic syndrome leads to anascara (generalized edema), through loss of
albumin in the urine, leading to decreased capillary oncotic pressure
Increased interstitial oncotic pressure is the mechanism causing edema in
patients with metastatic cancer (lymphatic blockage).
Digoxin and diuretics are often given to increase cardiac output and reduce
edema. Diuretics such as thiazides, furosemide (acts on Na+/K+/2Cl- of the thick
ascending limb of loop of Henle), or ethacrynic acid (just like furosemide but used
in patients with a sulfonamide allergy) can cause hypokalemia, and hypokalemia
can worsen digoxin toxicity. Digoxin competes with potassium for binding to
Na+/K+ ATPase. In hypokalemia, digoxin binds more readily to its target, leading
to possible toxicity.
TUMOR MARKERS
alpha-fetoprotein - tumor marker used to detect hepatocellular carcinoma and
gonadal germ cell tumors (such as yolk sac carcinoma)
Cancer antigen-125 - tumor marker used to monitor the response to treatment

and to detect recurrence of ovarian cancer

Carbohydrate antigen 19-9 - tumor marker used to monitor the progress of
pancreatic adenocarcinoma
Carcinoembryogenic antigen (CEA) - produced in ~70% of colorectal and
pancreatic cancers
Serotonin is secreted by carcinoid tumors and causes symptoms of flushing,
watery diarrhea, and right-sided valvular dyfunction. 5-hydroxyindoleacetic acid
(5-HIAA) is a metabolite of serotonin that can be measured in a 24-hr urine
collection.
DRUGS
Mild sedation and depression are common adverse effects of beta-blockers.
Diarrhea, pruritis, impotence, disturbance of sleep cycle, exercise tolerance, and
a diminished hypoglycemic response can also occur with the use of betablockers.
Furosemide is a loop diuretic and thus can cause electrolyte abnormalities such
as hypokalemia and metabolic alkalosis.
Hydrochlorthiazide and the other thiazide diuretics inhibit sodium chloride
reabsorption in the early distal tubule. Unlike the loop diuretics, they lead to
decreased calcium excretion. Other adverse effects of the thiazide diuretics
include sulfa allergy, hyperglycemia, hyperlipidemia, hyperuricemia,
hypercalcemia, and hypokalemia. In diabetics, HCTZ can cause significant
hyperglycemia.
Losartan is an angiotensin receptor blocker. Its use can result in hyperkalemia.
Nifedipine is a calcium channel blocker that acts primarily on the vasculature. It
can be associated with edema, flushing, and dizziness.
Prazosin, an alpha-antagonist, can be associated with dizziness, headache, and
orthostasis. Alpha-1 receptor inhibitors, including prazosin and terazosin, are
prescribed mainly as a treatment of urinary retention in benign prostatic
hyperplasia. These drugs slightly lower systemic blood pressure by relaxing
arteriolar smooth muscle in the periphery, which lowers peripheral vascular
resistance.
Adenosine - extremely useful in abolishing atrioventricular (AV) nodal
arrhythmias when given in a high-dose intravenous boluses. Adenosine works by
hyperpolarizing AV node tissue by increasing the conductance of potassium and
by reducing calcium current. As a result, the conduction through the AV node is
markedly reduced. In addition to this, adenosines extremely short duration of
action (15 seoconds) limits the occurrence of toxicities.

Epinephrine is an agonist of alpha and beta adrenergic receptors. Epinephrine

has a slight preference for beta over alpha. Administering a large dose of
epinephrine causes an increase in blood pressure via an increased heart rate
and in contractility through stimulation of beta-1 receptors (increased inotropy
and chronotropy). The net increase in systemic vascular resistance is caused by
alpha-1 mediated vasoconstriction, especially at higher doses of drug (the beta-2
mediated vasodilation is negligible compared with alpha-1 effects).
Phenoxybenzamine is a nonselective and irreversible alpha-antagonist, and
blocks the alpha-1 effects of epinephrine
Isoproterenol is a non-selective agonist of beta-adrenergic receptors, leading to
vasodilation through beta-2 stimulation, and increased inotropic/chronotropic
effects through beta-1 stimulation. Isoproterenol tends to cause a net decrease in
pressure through beta-2 mediated vasodilation
Clonidine is an alpha-2 agonist. Among anti-hypertensive agents, the only
widely available transdermal (or patch) medication for lowering blood pressure
is clonidine. It is typically prescribed as a last resort medication for refractory
hypertension. The patch is placed on the skin and is typically replaced every few
days. Clonidine is a centrally acting agonist of presynaptic alpha-2
adrenoreceptors in sympathetic neurons in the brainstem. Agonsim of alpha-2
adrenoreceptors in the brain results in a decrease in sympathetic outflow from the
central nervous system. Inhibition of the sympathetic nervous system leads to a
decrease in peripheral vascular resistance, heart rate, and blood pressure.
Adverse effects of clonidine include dry mouth, sedation, and sexual dysfunction.
Sudden discontinuation of clonidine can result in rebound hypertension as a
result of a sudden increase in sympathetic outflow; as result, patient compliance
is critical, and patients who are discontinuing a clonidine need to be tapered off
the medication slowly.
Propanolol is a non-specific beta-blocker
Norepinephrine is an agonist mainly at alpha-adrenergic receptors but also has
some beta-1 activity; it does not stimulate beta-2 or dopamine-1 receptors
Phenylephrine is an alpha-1 agonist that would cause an increase in pressure
through alpha-1 stimulated vasoconstriction
Metoprolol is a beta-1 blocker
Furosemide and the loop diuretics inhibit the Na+-K+-2Cl- cotransport in the
thick ascending limb of the loop of Henle, which decreases the reabsoprtion of
calcium and other cations. Thus, long-term furosemide therapy may worsen
osteoporosis. Adverse effects of the sulfonamide loop diuretics include sulfa

allergy, ototoxicity, hypokalemia, nephritis, hyperuricemia, hypocalcemia,

hypomagnesemia, and dehydration.
Acetazolamide is a carbonic anhydrase inhibitor that causes a very mild diuresis
by inhibiting sodium bicarbonate reabsorption in the proximal tubule. Carbonic
anhydrase inhibitors are used in patients with metabolic alkalosis, or to alkalinize
the urine in cases of drug toxicity. Adverse effects of acetazolamide include sulfa
allergy, metabolic acidosis, and neuropathy.
Amiloride is a potassium-sparing diuretic that blocks sodium reabsorption in the
cortical collecting tubule of the distal nephron. It is used to prevent hypokalemia
when using a loop or thiazide diuretic, but does not affect calcium excretion.
Metoprolol is a selective beta-1 blocker that decreases both heart rate and
contractility (negatively chonotropic and inotropic, respectively). It is a mainstay
treatment for CHF. Adverse effects for metoprolol include impotence, sedation,
bradycardia, and an acute exacerbation of heart failure if cardiac output is
severely compromised. It can cause bradycardia and mask signs of
hypoglycemia due to its beta-1 blocking mechanism.
Mirtazapine is an example of an alpha-2 adrenergic receptor antagonist, used
primarily to treat depression.
Torsades de pointes - Polymorphic ventricular tachycardia characterized by
shifting sinusoidal waveforms that can progress to ventricular fibrillation; long QT
interval; Caused by drugs (antiarrhythmics (IA and III), antibiotics
(macrolides), antipsychotics (haldoperidol), antidepressants (TCA), and
antiemetics (odansetron)), decreased K+, decreased Mg2+
Right-sided Valve Pathology - Suspect carcinoid tumor or Intravenous drug
abuse
Ruptured abdominal aortic aneurysm - Abdominal or back pain, hypotension,
lightheadedness, and pulsatile mass constitute the typical presentation. An AAA
is a dilation in the aorta usually due to weakness of the wall. The most common
site of an arterial aneurysm is the abdominal aorta. In contrast to dissecting
aneurysms, AAAs affect all layers of the aorta and thus do not form a false
lumen. Treatment for a ruptured aneurysm is emergent surgical repair. However,
if AAA is found that is not ruptured, treatment usually consists of medical
management, with surgery reserved for aneurysms > 5.5 cm in diameter.

Aortic Dissection - A tear in the wall of the aorta involves severe and sharp
chest or back pain, which may radiate anywhere in the thorax or abdomen.
Depending on the location of the dissection, it may be associated with syncope,
cerebrovascular accident, myocardial infarction, or heart failure.
Thoracic aortic dissection is predisposed by malignant hypertension. Symptoms
are similar to myocardial infarction except they are not recognized on ECG and
cardiac enzymes are not elevated. It can result in sudden death.
GERD may also mimic the symptoms of MI but does not result in sudden death
Diverticulitis - Results from perforation of a diverticulum and typically occurs in
the LLQ. Common presenting features include abdominal pain that has lasted for
several days, fevers, nausea, vomiting, and constipation or diarrhea
Acute mesenteric ischemia - Nonspecific symptoms that involve abrupt onset of
severe periumbilical pain, nausea, vomiting. The index of suspicion should be
higher with patients who possess the following risk factors: atrial fibrillation,
congestive heart failure, peripheral vascular disease, history of hypercoagulability
Pancreatitis - Epigastric abdominal pain radiating to the back, nausea and
vomiting, abdominal distention (if ileus has developed), relief on bending forward,
fever, and tachycardia. Symptoms become severe within 30 minutes of onset and
may last for hours to days. Pancreatitis is often a clinical diagnosis and may or
may not show up on CT.
Coarctation of the Aorta - Congenital narrowing of the aorta near the site of the
ligamentum arteriosum. Can be either preductal or postductal, which occur
proximal or distal to the ligamentum arteriosum, respectively. The mechanical
obstruction leads to a higher blood pressure to maintain constant flow through
the coarcted segment, causing severe hypertensive disease in the head, upper
torso, and upper extremities. The decrease in flow also causes hypotension in
the lower extremities. An ascending aortic dissection is most closely associated
with isolated systemic hypertension. Dissection is also associated with some
congenital conditions, such as Marfan syndrome, Ehlers-Danlos syndrome, and
syphilis. Increased workload on the left ventricle resulting from coarctationrelated hypertension can lead to hypertensive cardiomyopathy and left-sided
heart failure. This in turn can lead to secondary pulmonary hypertension and
right-sided heart failure.

Neuropathy of lower extremities - Common complication of diabetes mellitus

related to microvascular disease caused by chronically high blood sugar levels
Hypertrophic obstructive cardiomyopathy - AKA Idiopathic hypertrophic
subaortic stenosis > disorder follows an autosomal dominant mode of
inheritance in more than 50% of cases. Microscopic pathology shows myofiber
hypertrophy and disarray. It is a common cause of sudden death in young
athletes
Myocardial Infarction - Extensive neutrophilic infiltrate is present with necrotic
myofibers
Viral myocarditis - Lymphocytic infiltration
Amyloidosis - Restrictive cardiomyopathy involving infiltration; leads to
ventricular stiffening and impaired cardiac filling during diastole; Congo red
staining that turns green under polarized light indicates the presence of amyloid
within the myocardium
Rheumatic fever - fever, pleuritic chest pain, joint pain, rash (erythema
marginatum). If left untreated rheumatic fever can evolve into rheumatic heart
disease, which typically presents with mitral valve stenosis.

Rheumatic Heart Disease - A consequence of pharyngeal infection with group A

beta-hemolytic streptococci. Late sequelae include rheumatic heart disease
which affects heart valves mitral > aortic >> tricuspid (high-pressure valves
affected most). Early lesion is mitral valve regurgitation; late lesion is mitral
stenosis. Associated with Aschoff bodies (granulomas with giant cells),
Anitschkow cells (enlarge macrophages with ovoid, wavy rod-like nucleus),
increased anti-streptolysin O titers. Immune mediated (type II hypersensitivity);
not a direct effect of bacteria. Antibodies to M protein cross-react with self
antigens (molecular mimicry). Treatment/prophylaxis: penicillin
Joint (migratory polyarthritis)
Carditis
Nodules in skin (subcutaneous)
Erythema marginatum

Syndenham chorea
Stable Angina Pectoris - Transient chest pain that is brought on by situations
that increase myocardial oxygen demands, such as exercise, cold, or emotional
stress, and is relieved by rest. In stable angina, the coronary blood flow through
atherosclerotic vessels is sufficient to meet the demands of the heart at rest;
however, during exertion blood flow through the coronary vessels is not able to
increase enough to meet the increased myocardial oxygen demands in the areas
of the heart supplied by these vessels leading to ischemia and chest pain.
Sublingual nitroglycerin tablets are a mainstay of both the diagnosis and
treatment of angina pectoris. At low doses, the organic nitrates affect veins more
than arterioles, and the increased compliance of the veins decreases the venous
return to the heart, causing a decrease in preload, thus decreasing the
myocardial oxygen demands to a level that can be met by the narrowed coronary
vessels. Nitroglycerin also dilates the coronary arterioles directly, and this
increased coronary blood flow may be of particular importance in cases of angina
due to coronary vasospasm. At higher doses the organic nitrates cause
widespread arteriolar dilation in addition to venous dilation, which can decrease
afterload by decreasing blood pressure, but can also lead to hypotension and
reflex tachycardia.
Myxoma - Most common primary cardiac neoplasm and are characterized by
amorphous extracellular matrix. Approximately 35% of myxomas are friable, and
these often present with emboli. Findings include symptoms of mitral valve
obstruction and auscultatory abnormalities such as the classic tumor plop.
Rhabdomyoma - most frequent primary cardiac tumor in children (associated
with tuberous sclerosis)
Patent ductus arteriosus - a left-to-right shunt that rarely causes cyanosis. PDA
is associated with maternal rubella infection during pregnancy. During fetal
development, the ductus arteriosus remains patent through the action of PGE2.
PDA at birth is closed with indomethacin, a NSAID that inhibits PGE2.
Indomethacin also decreased thromboxane formation by inhibiting
cyclooxygenase 1 and 2 enzymes.
Dressler syndrome is an autoimmune phenomenon that results in fibrinous

pericarditis. This delayed pericarditis typically develops 2-10 weeks postmyocardial infarction (MI) and presents clinically as chest pain and a pericardial
friction rub. It is generally treated with aspirin, nonsteroidal anti-inflammatory
agents, or corticosteroids. On auscultation, the heart sound is usually continuous
and is heard diffusely over the chest. It typically has three components, one
systolic and two diastolic, and is accentuated when the patient leans forward.
Fibrinous pericarditis is both an early and a late complication of MI.

Post-MI complications:
Dressler Syndrome - autoimmune fibrinopericarditis (within weeks)
Cardiac arrhythmia is a common cause of post-MI death, typically occurring the
first few days following the event.
Left ventricular failure occurs in 60% of people who suffer MI and can present as
CHF, which can cause chest pain, dyspnea, and an elevated jugular venous
pressure.
Ventricular rupture typically 4-10 days after MI. It can present with persistent
chest pain, syncope, distended veins, but most frequently, sudden death.
Postinfarction fibrinous pericarditis (within days)

Congestive Heart failure is associated with interstitial and alveolar edema. in

CHF, there is a decrease in effective arterial blood volume due to the inability of
the heart to effectively pump blood, which stimulates the renin-angiotensinaldosterone axis to increase the tubular absorption of Na+ to help increase
intravascular volume. Sympathetic outflow would be increased to counteract the
diminished cardiac output of the failing heart. Norepinephrine stimulates beta-1
receptors on myocardial cells to raise the heart rate and increase contractility so
more blood is ejected with each beat. The venous pressure would actually be
increased due to the inability of the heart to effectively pump blood into the
arterial system. The blood backs up and leads to passive congestion of the
venous circulation. Increased venous pressure leads to increased intracapillary
pressure causing fluid to leak out into the interstitial tissue space. The transudate
collects in dependent areas and manifests clinically as pitting ankle edema. The
effective arterial blood volume would be decreased. Glomerular filtration rate
would be decreased because the ineffective pump leads to lowered effective
arterial blood volume, resulting in a reduction of renal blood flow. Aldosterone
would lead to a constriction of the efferent arteriole, but GFR overall is reduced.
Symptoms include dyspnea, orthopnea, fatigue, rales, JVD, pitting edema

Systolic dysfunction: reduced EF, increased end-diastolic volume; decreased

contractility often secondary to ischemia/MI or dilated cardiomyopathy
Diastolic dysfunction: preserved EF, normal EDV, decreased compliance often
secondary to myocardial hypertrophy
HEART SOUNDS
Low-pitched early to mid-diastolic murmur (low-frequency decrescendo diastolic
murmur best heard over the apex) , and maybe an high-pitched opening
click/snap that follows S2, S3 - Mitral stenosis
Could be heard with rheumatic fever
Left arial pressure increases leading to a relative decrease in left ventricular
pressure
Continous, machine-like murmur - Patent ductus arteriosus
S4 - commonly called the atrial kick is not normally present in adults. Its
presence suggests a decrease in ventricular compliance, such as occurs in
ventricular hypertrophy resulting from chronic hypertension. S4 is thought to
result from vibration of a stiff, noncompliant ventricular wall as blood is rapidly
ejected into the ventricle from the atrium (near the end of diastole)
S3 - may be heard during mitral stenosis at the beginning of diastole; S3 is due to
the vibration of the distended ventricular wall during rapid filling and is usually
soft and low in frequency. While the presence of S3 is normal in children, in
adults it usually suggests volume overload, such as occurs in CHF
S1 - mitral and tricuspid valves close at the end of diastole
Ejection click - aortic stenosis
S2 - aortic and pulmonic valves closing
Fluroescent treponemal antibody-absorption test (FTA-ABS) is a test used to
detect antibodies directed against the species Treponema pallidum. Tertiary
syphilis disrupts the vaso vasorum of the aorta, consequently dilating the aortic
root and aortic valve ring. This leads to aortic aneurysm and thus aortic
insufficiency. Additionally, the ascending arch of the aorta is often calcified and
atherosclerotic. Tertiary syphilis can lead to tree-barking, irregular wrinkling of
the tunica intima of the aorta.
Antistreptolysin O titers would be helpful in diagnosing streptococcal infection.
Rheumatic fever is known to occur after a streptococcal infection, typically
pharyngeal. Rheumatic fever can cause valvular damage (mitral > aortic >>

tricuspid), but not aortitis.

Bacterial cultures could be helpful in diagnosing endocarditis. Endocarditis of the
aortic valve could contribute to aortic insufficiency, but vegetations would likely be
seen on echocardiogram. In addition, endocarditis is usually accompanied by
systemic symptoms of malaise, low-grade fever, weight loss, and splinter
hemorrhages.
Substances such as cocaine and alcohol are known to cause dilated
cardiomyopathy.

During exercise, increased sympathetic outflow causes increased systemic

arteriolar vasoconstriction by way of alpha-1 adrenergic receptors. In the
circulation of the skin, splanchnic regions, kidney, and inactive muscles, this
vasoconstriction results in increased resistance and decreased blood flow to
these organs. However, selective vasodilation of active musculature is achieved
because metabolic factors such as lactate, potassium, and adenosine overcome
the sympathetic effect in these areas. This mechanism results in a cumulative
decrease in total peripheral resistance, whereas sympathetic activation alone
would cause an increase.
Heart rate and stroke volume act in concert to increase cardiac output. Increased
cardiac output ensures that necessary oxygen and nutrients are delivered to the
active skeletal muscles.
Increased cardiac contractility would cause a decrease in systemic oxygen level
as a result of increased cardiac oxygen consumption.
During exercise, pulmonary resistance decreases in order to accommodate
greater pulmonary flow. Decreased resistance also improves gas exchange and
allows an even distribution of blood throughout the lungs. These changes occur
in order to meet the bodys increased oxygen requirement during exercise.
During exercise, there would be a decrease in venous oxygen pressure as the
maximum amount of oxygen is unloaded to the tissues.
Clinically, cardiac tamponade and constrictive pericarditis have similar
presentations, although cardiac tamponade typically presents acutely and with
hemodynamic instability. Constrictive pericarditis is associated with postradiation, which leads to thickening of the pericardium. Constrictive pericarditis
can also occur due to viral illness, trauma, neoplastic disease, and other chronic

diseases. Additionally, diastolic volumes are reduced in cardiac tamponade and

constrictive pericarditis. Constrictive pericarditis is marked by proliferation of
fibrous tissue, with occasional small foci of calcification, that causes loss of
elasticity of pericardial tissues. It can mimic the signs of right heart failure, and
can be caused by a variety of disease processes and infections such as SLE,
rheumatic fever, postradiation changes, and viral and bacterial infections.
Cardiac tamponade presents with Becks triad (distant heart sounds, jugular
venous distention, and hypotension), and pulsus paradoxus (a decrease in
systolic pressure by 10 mmHg during inspiration). These symptoms are typically
the first signs of tamponade.
In dilated cardiomyopathy, end-diastolic volumes are increased.
Breast and lung carcinomas, lymphomas, and melanomas are the most common
metastases to the pericardium.
Systolic CHF produces signs and symptoms of weight gain and fatigue, but not
fever. Also, systolic CHF will present with increased left ventricular end-diastolic
volume.