cardiology2 Flashcards
Quinidine
class 1a Na channel blocker, also blocks K particularly well, thereby prolonging action potential duration and it is a vagal inhibitor (anti-cholinergic) as it is a alpha-adrenergic receptor.
Procainamide
class 1a Na channel blocker
Disopryamide
class 1a Na channel blocker
Lidocaine
most important class 1b Na channel blocker in treating arrhythmias, shortens phase 2, increases refractory period.
Mexiletine
class 1b Na channel blocker, shortens phase 2, increases refractory period.
Phenytoin
class 1b Na channel blocker, shortens phase 2, increases refractory period.
Propafenone
class Ic Na channel blockers
Flecainide
class Ic Na channel blockers
Encainide
class Ic Na channel blockers, no longer marketed
Propranolol
beta blocker (class II), reduces L-type Ca current and K current.
Metoprolol
beta blocker (class II), reduces L-type Ca current and K current.
Esmolol
beta blocker (class II), reduces L-type Ca current and K current.
Ibutilide
K channel blockers (class III)
Dofetillide
K channel blockers (class III)
Amiodarone
K channel blockers (class III), also markedly reduces conduction velocity and increases refractory period by blocking Na channels. Also decreases the rate of diastolic depolarization (phase 4) in automatic cells, thus reducing firing rate
Sotalol
K channel blockers (class III), is also a beta blocker
Bretylium
K channel blockers (class III)
Verapamil
use dependent blockers of L-type Ca channels.
Ditiazem
use dependent blockers of L-type Ca channels.
Lisinopril
ACEI
Enalapril
ACEI
Benazepril
ACEI
Valsartan
ARB
Candesartan
ARB
Losartan
ARB
Spironolactone
aldosterone receptor blocker
Eplerenone
aldosterone receptor blocker
Carcedilol
beta blocker (class II), reduces L-type Ca current and K current.
Bisoprolol
beta blocker (class II), reduces L-type Ca current and K current.
Spironolactone
mineralocorticoid receptor
Eplerenone
mineralocorticoid receptor
Digoxin
Digoxin’s primary mechanism of action involves inhibition of the Na+/K+ ATPase, mainly in the myocardium. This inhibition causes an increase in intracellular sodium levels, resulting in a reversal of the action of the sodium-calcium exchanger, which normally imports three extracellular sodium ions into the cell and transports one intracellular calcium ion out of the cell. The reversal of this exchange causes an increase in the intracellular calcium concentration that is available to the contractile proteins. Increased intracellular calcium lengthens phase 4 and phase 0 of the cardiac action potential, which leads to a decrease in heart rate. Increased amounts of Ca2+ also leads to increased storage of calcium in the sarcoplasmic reticulum, causing a corresponding increase in the release of calcium during each action potential. This leads to increased contractility (the force of contraction) of the heart without increasing heart energy expenditure.
Furosemide
diuretic
Bumetanide
diuretic
Torsemide
diuretic
Nesirtide
vasodilator
Diuretics
Furosemide. Often used first to reverse sodium and fluid retention and relieve signs or symptoms of volume overload (dyspnea and peripheral edema). Loop diuretics preferred because of efficacy, but can augment with a thiazide diuretic. Can be used chronically and acutely. Most commonly used is furosemide, but some patients respond better to torsemide or bumetanide due to better and more reliable absorption
Angiotensin Converting Enzyme Inhibitors (ACEIs)
Lisinopril. Started during or after the optimization of diuretic therapy – low doses-> titrated to goal. Produce vasodilation and decreased aldosterone activation plus antiremodeling effect. Angiotensin II Receptor Blockers (AT-1) (ARBs) can be used in patients intolerant to ACEIs (most often due to cough), but NO apparent benefit from dual therapy with ACEI and ARB
Aldosterone Antagonists
Spironolactone. Added to therapy for NYHA class II with LVEF < 30% optimized on ACEI/ARB and beta-blocker therapy or NYHA class III-IV with LVEF < 35%. Must be carefully monitored for serum potassium (< 5.0) and renal function (GFR > 30 ml/min). Blocks aldosterone effect on kidney producing additional sodium loss (since ACEI and/or ARB block of aldosterone action is incomplete) plus antiremodeling effect. If endocrine side effects occur with spironolactone, can use Eplerenone.
Introduction to diurectics
Diuretic agents are best understood in relation to their site of action in the nephron and the normal physiology of that particular segment. Nearly all diuretic agents exert their effects at luminal (urine) surface of renal tubule cells.
Mechanisms include: Interactions with membrane transport proteins (thiazides, furosemide, triamterene), Specific interactions with enzymes (acetazolamide) or hormone receptors (spironolactone), and Osmotic effects preventing water reabsorption (mannitol). Na+ is the major extracellular cation and its movement between compartments is controlled by regulated active transport via Na+-K+-ATPase activity at the interstitial (blood) surface. This enzyme produces the gradient necessary for Na+ reabsorption from the urine back into the blood. However, no diuretics act via inhibition of Na+-K+-ATPase. The diuretic agents decrease Na+ reabsorption at the indicated sites in the nephron below and, as a result, increased amounts of Na+ (and other ions) enter the urine along with H2O entering passively to maintain osmotic equilibrium.
Sites of Acetazolamide Diuretic Action
acts on proximal convoluted tubule in the cortex
Sites of Aldosterone antagonists Diuretic Action
acts on the collecting tubule in the cortex
Sites of ADH antagonists Diuretic Action
acts on the collecting duct in the medulla
Proximal Convoluted Tubules
Almost all of glucose, amino acids, NaHCO3, and other metabolites are reabsorbed here. 60-70% of Na+ reabsorbed (Cl- and H2O follow passively). Presence of H+ ion and the enzyme carbonic anhydrase (CA) on luminal surface allows for reabsorption of HCO3- (and exchange of H+ for Na+). Inhibition of CA by acetazolamide results in retention of HCO3- in lumen (urine) with mild alkaline diuresis. Site of organic acid (diuretics, antibiotics) and base (procainamide) secretion. Important site for delivery of diuretics to their specific site of action in nephron and for potential drug-drug interactions.
Carbonic Anhydrase Inhibitors
Acetazolamide (Diamox), Dorzolamide, Brinzolamide
Pharmacodynamics of carbonic anhydrase inhibitors
Inhibition of carbonic anhydrase enzyme depresses NaHCO3 reabsorption in proximal tubule. Also inhibits formation of aqueous humor and CSF that is dependent on HCO3- transport
Pharmacokinetics of carbonic anhydrase inhibitors
Well absorbed orally; effects within 30 min that persist for 12 hrs; secreted into proximal tubule
Clinical Uses of carbonic anhydrase inhibitors
Major use is NOT as diuretic agent and NOT used in heart failure. Glaucoma: Topical administration for chronic open angle glaucoma. Acute mountain sickness. Systemic administration slows progression of pulmonary or cerebral
edema via decrease in formation and pH of cerebrospinal fluid
Adverse Reactions / Toxicities of carbonic anhydrase inhibitors
Minor: Loss of appetite, drowsiness, confusion, tingling in extremities, hypersensitivity rxns. Hyperchloremic metabolic acidosis, renal stones (via increase in urinary pH), K+ wasting
Loop of Henle (thick ascending limb)
Water removal (from lumen) occurs in descending limb as a result of hypertonic osmotic forces generated in interstitial spaces. H2O removal opposed if impermeable solutes present (HCO3-, glucose, osmotic diuretics). Ascending limb is impermeable to H2O, but active NaCl reabsorption occurs in ascending limb via Na+-K+-2Cl- cotransporter (NKCC2 on the luminal side). Although cotransporter itself is electrically neutral, action leads to excess intracellular K+ which then back diffuses into lumen creating a lumen positive potential. This potential then drives the reabsorption of cations Mg++ and Ca++.
Pharmacodynamics of Loop of Henle Agents (High Ceiling Diuretics)
Inhibit NaCl transport (Na+-K+-2Cl–transporter) in thick ascending limb of loop of Henle. Loop diuretics have greatest diuretic effect because of large capacity of this segment. Associated with increase in Mg++, Ca++ excretion (diminish lumen-positive potential). Increase renal blood flow (via effect on renin-angiotensin and prostaglandin systems). Retain substantial diuretic effect even if renal function is compromised.
Pharmacokinetics of Loop of Henle Agents (High Ceiling Diuretics)
Rapidly absorbed orally; extremely rapid IV diuretic response. Handled by renal secretion and filtration. Duration of effect 2-3 hrs for furosemide, 4-6 hrs for torsemide, 6 hours for bumetanide
Clinical Uses of Loop of Henle Agents (High Ceiling Diuretics)
Congestive heart failure - Preferred diuretic class because of greater efficacy. Used in HF patients with volume overload - goal of eliminating signs of fluid retention (pulmonary congestion - peripheral edema). Efficacy of diuretics is enhanced with salt restriction (< 2 g/day). Furosemide is most commonly used. If lack of response can increase dose of furosemide or can switch to bumetanide or torsemide (more reliable bioavailability with both and longer duration of activity with torsemide). IV administration may be required initially in some patients due to congestion-related interference with oral absorption. Patients with HF have reduced diuretic response related to decreased drug delivery to kidney due to decreased RBF and hypoperfusion activation of RAAS and SNS. Refractory edema– A thiazide (metolazone) can be added to therapy if a loop diuretic produces insufficient diuresis. Thiazide action to block distal tubule Na+ reabsorption can counter loop-induced increases in Na+ delivery and reabsorption at that segment. Note that thiazides can add to loop-induced hypokalemia so careful monitoring of serum potassium is warranted with initiation of therapy. An aldosterone antagonist (spironolactone) is recommended in some patients with systolic HF to improve survival. Its actions at the collecting tubule will also enhance diuresis and ameliorate the potassium wasting. Acute pulmonary edema. Rapid reduction of extracellular fluid and venous return (extra-renal hemodynamic response via decrease in RV output and pulmonary vascular pressure). Refractory edema. Loop diuretics used if no response to Na+ restriction or thiazide diuretic; especially useful if renal disease and fluid overload present. Hypercalcemia. Given with saline infusion to prevent extracellular fluid (ECF) volume depletion
Adverse Reactions / Toxicities of Loop of Henle Agents (High Ceiling Diuretics)
Hypokalemic metabolic alkalosis via enhanced secretion of K+ and H+. More pronounced than with thiazides. Hypokalemia predisposes patients to ectopic pacemakers and arrhythmias. Ototoxicity. Especially for ethacrynic acid (also higher incidence with concomitant use of aminoglycoside antibiotics) and if diminished renal function present; usually reversible. Hyperuricemia / hyperglycemia. Hypomagnesemia. Overdose. Rapid blood volume depletion -> dizziness, headache, orthostatic hypotension
Distal Convoluted Tubules
Segment is relatively impermeable to H2O. NaCl reabsorption occurs via an electrically neutral Na+/Cl- cotransporter (pharmacologically distinct from Loop cotransporter). Site of active Ca++ reabsorption via a Na+/Ca++ exchanger. This process is regulated by parathyroid hormone (PTH). This exchanger is not present at the loop of Henle and results in important differences in calcium excretion effects between diuretic classes.
Pharmacodynamics of Thiazide Diuretics
Thiazide diuretics act by inhibiting the Na+/Cl- cotransporter and increasing urinary excretion of NaCl (modest diuretic effect, only 5-10% of filtered Na+ is reabsorbed here). In contrast to loop diuretics, thiazides increase reabsorption of Ca++ (lowering of intracellular Na+ drives Ca++ exchanger or decreased blood volume increases absorption at PCT)
Pharmacokinetics of Thiazide Diuretics
All absorbed well orally (if GI upset, can take with food or milk); best to take early in day. Differences in metabolism / excretion: Hydrochlorothiazide (Hydrodiuril): Prototype thiazide, twice daily dose. Chlorthalidone - Metolazone: longer durations-> once daily dosing. All secreted by organic acid secretory system; competition with uric acid secretion may precipitate a gout attack
Clinical Uses of Thiazide Diuretics
Congestive heart failure. Higher doses needed than in hypertension and more efficacious diuretics are usually required (i.e., loop diuretics). True synergistic diuretic effect with loop diuretics (esp. metolazone) may be useful in refractory edema. Hypertension: First line for mild hypertension (esp., blacks, elderly, obese). Hypercalcuria: Reduced urinary excretion of Ca++ decreases incidence of kidney stones
Adverse Reactions / Toxicities of Thiazide Diuretics
Hypokalemia, can result in weakness, paresthesias, cardiac sensitization (predisposition to ectopic pacemakers), thus use not advisable in patients with arrhythmias, history of myocardial infarction, pre-infarction angina. Volume contraction may lead to secondary hyperaldosteronism. Impaired carbohydrate tolerance (dose-related): hyperglycemia, glucosuria [(?) via impaired pancreatic insulin release (opens K+ channel) or decreased peripheral utilization]. Hyperuricemia. Avoid in patients with gout. Hyperlipidemia. Complicating factor if used long-term for hypertension. Allergic reactions. Skin rashes occasionally, related to sulfonamide component; some cross- allergenicity with sulfonamides
Collecting Tubules
Site of regulation by the mineralocorticoid aldosterone. Only 2-5% of NaCl reabsorption occurs at this site (thus only weak diuretic action possible), but as the most distal site it has important role in determining final urinary Na+ (and ultimately K+ and H+) concentration. Na+ (and H2O) and K+ transport occurs in principal cells via separate channels that exclude anions. The driving force for Na+ entry into cell exceeds that for K+ exit so lumen becomes negative, driving Cl- into cells and K+ into urine. Thus, K+ excretion is coupled to Na+ reabsorption and ALL diuretics that cause a greater delivery of Na+ (and greater tubular flow) to this site will enhance K+ excretion. Aldosterone, through effects on gene transcription, increases the number and activity of both Na+ (ENaC) and K+ membrane channels and the Na+-K+-ATPase. Diuretics that block the Na+ channel (triamterene and amiloride) or antagonize the aldosterone receptor (spironolactone - eplerenone) will decrease Na+ reabsorption and decrease K+ excretion (known as “potassium-sparing” diuretics)
Pharmacodynamics Potassium-Sparing Diuretics - Aldosterone Antagonists and Na+-channel Blockers
Spironolactone / Eplerenone. Only mild diuresis possible if used alone. Competitive antagonist at aldosterone receptor, binds to cytosolic receptor preventing enhancement of protein synthesis. Eplerenone reported to have lower affinity for androgen and progesterone receptors. Blocks aldosterone effect at collecting tubule, thus Na+ is not reabsorbed, lumen- potential becomes more positive, thus less K+ and H+ ions move into urine. Promotes only moderate increase in Na+ excretion. Triamterene / Amiloride: Direct effect to block the Na+-channels on collecting duct lumen to decrease Na+ reabsorption (and thus decreases coupled K+ secretion)
Pharmacokinetics of Potassium-Sparing Diuretics - Aldosterone Antagonists and Na+-channel Blockers
Spironolactone (Aldactone): 1-2 doses/day; poor oral absorption. Slow onset of action. Eplerenone (Inspra): Dosed 1-2 times/day orally, metabolized by CYP3A4. Triamterene (Dyrenium) / Amiloride (Midamor): Triamterene metabolized in liver, amiloride excreted unchanged thus given less frequently. Effect within 2-4 hrs, but 1-3 days to maximal effect.
Clinical Uses of Potassium-Sparing Diuretics - Aldosterone Antagonists and Na+-channel Blockers
Congestive Heart Failure: Survival benefits seen with aldosterone antagonists. Most important action is block of aldosterone receptors on heart rather than kidney. Anti-remodeling action - block of deleterious effect of aldosterone on heart-> cardiac hypertrophy and fibrosis. Additional benefits from raising serum potassium to counter risk of hypokalemia- induced arrhythmias resulting from use K+-wasting diuretics (loop and thiazides). Primary hyperaldosteronism (spironolactone and eplerenone). Hirsutism of polycystic ovary syndrome via block of androgen receptor (spironolactone). Hypertension (in combination with thiazides). Spironolactone-HCTZ (Aldactazide), Triamterene-HCTZ (Dyazide)
Adverse Reactions of Potassium-Sparing Diuretics - Aldosterone Antagonists and Na+-channel Blockers
Hyperkalemia-> EKG changes, conduction abnormalities, arrhythmias. Risk increased by: increasing age, underlying renal dysfunction, higher doses, combined use of ACEI or ARB, use of NSAID analgesics. Endocrine abnormalities (gynecomastia) with spironolactone via block of androgen receptor (∼ 10%). NOT seen with eplerenone which is more selective for aldosterone receptors. Mild effects: GI upset, drowsiness
Angiotensin-Converting Enzyme Inhibitors [ACEIs]
Lisinopril (Zestril, Prinivil), Captopril (Capoten), Enalapril (Vasotec), Ramipril (Altace), Quinapril (Accupril), Moexipril (Univasc), Benazepril (Lotensin)
Mechanism of Action in Heart Failure of Angiotensin-Converting Enzyme Inhibitors [ACEIs]
Inhibits ACE conversion of Ang I to Ang II, blocking Ang II-induced vasoconstriction. This results in decreased preload and afterload. However, other vasodilators have less survival benefits than ACEIs suggesting that ACEIs work by other mechanisms. Primary mechanism may be ACEI decrease of Ang II-induced release of aldosterone which moderates the myocardial hypertrophy and remodeling response to aldosterone. Decreases bradykinin inactivation, increasing its vasodilator action. Improve endothelial function via enhancement of nitric oxide action. Reduce sympathetic activity.
Other Uses: Hypertension - first-line therapy and Delay progression of diabetic nephropathy
Pharmacokinetics and Dosing Considerations of of Angiotensin-Converting Enzyme Inhibitors [ACEIs]
All are well absorbed orally; most have reduced absorption if taken with food. All ACEIs, except lisinopril and captopril, are prodrugs that are converted to the active metabolite by de-esterification in the liver. The active metabolites are primarily eliminated by the kidneys (exceptions: moexipril and fosinopril) requiring dosage reduction in patients with renal insufficiency. Duration of action generally sufficient to allow once-daily dosing for most agents.
Side Effects of Angiotensin-Converting Enzyme Inhibitors [ACEIs]
Contraindicated in pregnancy (Category C/D in 2nd and 3rd trimester). Dry cough. Hyperkalemia. Severe hypotension (if hypovolemic), acute renal failure (esp. with renal artery stenosis), angioedema. Neutropenia and proteinuria seen with high doses of captopril – rare with newer agents. Minor effects include altered taste sense, skin rashes
Angiotensin II Receptor (AT1) Antagonists [ARBs]
Losartan (Cozaar), Valsartan (Diovan), Irbesartan (Avapro), Olmesartan (Benicar), Candesartan (Atacand)
Mechanism of Action in Heart Failure of Angiotensin II Receptor (AT1) Antagonists [ARBs]
Selective inhibition of Angiotensin II receptor AT1. Similar to ACEIs, ARBs prevent remodeling and reduce sympathetic activity. Advantage vs ACEIs: Potential for more complete inhibition of angiotensin action since alternative pathways (chymase) exist to form Angiotensin II that are NOT blocked by ACEIs and No side effects mediated by increased bradykinin levels-> cough, angioedema. Disadvantage vs ACEIs: Loss of increased bradykinin actions (vasodilation) that result from ACE inhibition and Block only Ang II actions at AT-1 receptors while decreased Ang II synthesis by ACEIs will block actions mediated by both AT-1 and AT-2 receptors. Other Uses: Alternative in conditions that respond to ACE inhibitors, but ACEIs not tolerated
Dosing Considerations of Angiotensin II Receptor (AT1) Antagonists [ARBs]
All agents are effective orally with once daily dosing except for losartan (twice daily). Decreased losartan dose necessary in hepatic dysfunction.
Side Effects of Angiotensin II Receptor (AT1) Antagonists [ARBs]
Similar to ACEI, contraindicated in pregnancy, but NO angioedema or cough
atrial kick
Atrial systole Cardiology The contraction of the atrium, which accounts for 5-30% of cardiac output; it appears as an abrupt notch in the pressure curve in the ventricular outflow tract, and is typical of hypertrophic cardiomyopathy–formerly idiopathic hypertrophic subaortic stenosis
amyloidosis of the heart
Amyloid deposition in the heart can cause both diastolic and systolic heart failure. EKG changes may be present, showing low voltage and conduction abnormalities like atrioventricular block or sinus node dysfunction. On echocardiography the heart shows restrictive filling pattern, with normal to mildly reduced systolic function.[4] AA amyloidosis usually spares the heart.
Acute myocarditis
Myocarditis is defined as inflammation of the myocardium accompanied by myocellular necrosis. Acute myocarditis must be considered in patients who present with recent onset of cardiac failure or arrhythmia. Fulminant myocarditis is a distinct entity characterized by sudden onset of severe congestive heart failure or cardiogenic shock, usually following a flu-like illness, parvovirus B19, human herpesvirus 6, coxsackievirus and adenovirus being the most frequently viruses responsible for the disease. Treatment of myocarditis remains largely supportive, since immunosuppression has not been proven to be beneficial for acute lymphocytic myocarditis. An inflammatory disease of the myocardium that usually attacks a healthy child or adult and is often viral in origin. There is a wide range of presentations. Myocarditis often presents within 2 weeks following development of an upper respiratory infection or a flu-like syndrome with fever and chills or gastrointestinal symptoms. If concurrent pericarditis is present patients may have chest pain as well. Adult cases often present with heart failure with or without cardiogenic shock. Arrhythmias with palpitations or syncope are sometimes the presenting symptoms and may cause sudden death. Acute inflammation of the cardiac muscle that is usually viral in etiology. May be focal or diffuse. Often seen in relatively young adults and children. 50% have preceding respiratory of GI symptoms. Common presentations include fever, chest pain with ECG changes, arrhythmia, and heart failure. The ECG findings most commonly seen in myocarditis are diffuse T wave inversions; saddle-shaped ST-segment elevations may be present (these are also seen in pericarditis). Low ejection fraction and heart failure have high mortality but some recover and others develop a chronic dilated cardiomyopathy.
Causes of myocarditis
Many viruses may cause myocarditis. Hypersensitivity to drugs (anthracyclines and other chemotherapeutic agents most common); Systemic inflammatory diseases (such as systemic lupus erythematosus); and certain bacterial, fungal or other infectious diseases are among less common causes. Peripartum cardiomyopathy which begins the last month of pregnancy or within 5 months after pregnancy is a poorly understood myocarditis that often resolves but may proceed to a serious cardiomyopathy. In cases of viral etiology an immune-related process rather than direct damage from the actual pathogen may be the major mechanism of injury. Certain viruses such as Coxsackie B have a relatively high incidence of myocarditis. However, in any viral epidemic only a very small percentage of victims are afflicted by clinically detectable myocarditis and the reason for this is unknown. One theory is that a genetic predisposition is a major factor enabling the immune-related process. Myocarditis is often an autoimmune reaction. Certain viruses such as coxsackie B have regions (epitopes) that are immunologically similar to cardiac myosin.
Physical findings with myocarditis
Physical findings include a third heart sound (S3), pulmonary congestion or peripheral edema, or if cardiac dilation is present mitral or tricuspid insufficiency murmurs. Increased troponins resembling findings in acute myocardial infarcts may be present. A variety of nonspecific ECG changes may occur including patterns suggestive of pericarditis or acute myocardial infarction. Echocardiograms often demonstrate global or diffuse ventricular dysfunction and are very useful in confirming that a myocardial process is present. Biopsies are rarely done but if obtained show focal or diffuse necrosis and myocyte swelling with inflammatory changes. A large percentage of cases of myocarditis with minimal or absent symptoms other than evidence of an acute viral infection probably go unrecognized. Some such cases may eventually develop a dilated cardiomyopathy. Cases presenting with heart failure may resolve without apparent injury, may proceed rapidly down hill to death or may evolve into a chronic dilated cardiomyopathy.
Treatment of myocarditis with heart failure
If heart failure is present usual methods for this condition are applicable, particularly diuresis, low dose beta blockade and angiotensin converting enzyme (ACE) inhibitors. Occasionally inotropic agents may be a consideration. In nonviral infections appropriate antimicrobial agents are used. In diseases in which steroids are known to effective, such as systemic lupus, they are useful. However, in viral or idiopathic cases steroids are controversial.
Types of cardiomyopathy
There are three types of cardiomyopathy. By far the commonest is a dilated cardiomyopathy. The left ventricle is always involved but in many cases all four chambers of the heart are markedly dilated. Mild hypertrophy with increased cardiac mass is usual. The other two types are rare. In hypertrophic cardiomyopathy the left ventricle is hypertrophied but not dilated, and there often is disproportionate hypertrophy of the septum. In restrictive cardiomyopathy there is infiltration or fibrosis of the ventricles, usually without dilatation.
Causes of dilated cardiomyopathy
There are many causes of dilated cardiomyopathy. Clinically a distinction is often made between “ischemic”, due to coronary artery disease and “nonischemic” dilated cardiomyopathy. Dilation may be present without development of heart failure in mild cases or early stages of the disease. It is usually idiopathic. Can also be caused due to genetics or a virus.
Clinical manifestations of dilated cardiomyopathy
It is commonest to detect this condition when severe heart failure is present. In the presence of heart failure, demonstration by echocardiography of dilation and impaired systolic function of both ventricles (dilated and more spherical, diffuse poor wall motion, low ejection fraction) and chest film show cardiomegaly confirm the diagnosis. Arrhythmia injury fibrosis, and dilation) and thromboembolism (dilation, porr contraction and abnormal surface) are common complications. Sudden death from ventricular arrhythmias may occur. Spherical diffuse poor wall motion, low ejection fraction. BNP is slightly elevated with asymptomatic LV dysfunction and greatly elevated with patients with CHF.
Presentation of dilated cardiomyopathy
Heart failure with a large silent heart with impaired systolic function. Congested lung fields. Dilated poorly contractile LV that is hypokinetic.
Etiology of dilated cardiomyopathy
Usually idiopathic, Ischemic, Familial, Viral, and Other
Treatment of dilated cardiomyopathy
treat heart failure with drugs such as Digoxin, Diuretics, ACE Inhibitors, Beta blockers, Spironolactone, Vasodilators, Inotropes, Biventricular pacing if ventricular asynchrony present. May also need to treat anticoagulation, anti-arrhythmic agents (drugs or implantable defibrillators), or heart transplant. Use of drugs to treat heart failure is needed. Diuretics, beta blockers and ACE inhibitors are usually effective. If ventricular asynchrony is present, often due to left bundle branch block, biventricular pacing may be helpful in refractory cases. Anticoagulation to prevent emboli, particularly if atrial fibrillation is present, is usually advisable. Appropriate antiarrhythmic agents may be needed or in some cases implantable defibrillators to prevent sudden death. As a last resort implantable left ventricular assist devices (LVADs) or heart transplant may be a consideration. Neurohumoral activation to development and reversal of remolding. Myocyte dysfuction and structural alterations are propagated by cardiac adrenergic and RAAS signaling. Improved function and reverse remodeling can by propagated by ACE inhibitors and beta blocker therapy
Hypertrophic cardiomyopathy
Hypertrophy which is often eccentric, predominantly involving the septum, without dilation. Predominant diastolic dysfunction. Normal or enhanced systolic function. Dynamic out flow obstruction may be present. Usually familial. There is a strong genetic component in this relatively rare disease. The left ventricle is hypertrophied but not dilated. The muscle fibers and collagen matrix are disorganized, particularly in the septum which tends to be disproportionately thickened. In some cases the disproportionate intraventricular septal thickening and a hyperdynamic contraction may cause aortic outflow tract obstruction. Especially if obstruction is present, sudden death may occur with exertion. Autosomal dominant inheritance occurs.
Treatment of hypertrophic cardiomyopathy
decrease contractility- beta/calcium channel blockade, surgical resection, avoid extreme exertion, and ventricular pacing. If an obstructive component is present several steps should be taken. Decreasing contractility may decrease the outflow tract obstruction. If drugs are ineffective, surgical resection or percutaneous alcohol septal ablation in the outflow tract often relieves obstruction. Avoiding extreme exertion may prevent sudden death. Ventricular pacing may occasionally be useful for relief of obstruction or arrhythmia control.
Hypertrophic cardiomyopathy without aortic outflow obstruction
diastolic dysfunction due to impaired diastolic relaxation and increased stiffness. Elevated LV diastolic pressure causes increased pulmonary venous and capillary pressure. Dyspnea on exertion usual symptom. No risk for sudden death.
Hypertrophic obstructive cardiomyopathy
asymmetric myocardial hypertrophy, diastolic dysfuction, enhanced systolic dysfunction, dynamic left ventricular outflow obstruction, and propensity for syncope and sudden death. Vasodukator decrease ventricular volume and increases outflow obstruction.
Clinical manifestation of hypertrophic obstructive cardiomyopathy
variable, can be asymptomatic to severe symptoms. dyspnea due to increased LV filling pressure, angina due to hypertophic LV and increased systolic LV pressure, and sudden death due to arrhythmia may also occur. It is by far the main cause of sudden death in athletes from ages 12-35. Sudden death is also the main cause of death in patients with HCM 45 years of age and younger. Later on in life HCM can degrade into HF, which is the main cause of death in older patients. There is also an increased risk in stroke at old age.
Hypertrophic obstructive cardiomyopathy treatment
Avoid competitive sports and other extreme exertion. Decrease contractility–Beta blockers/ Verapamil. Surgical myomectomy or Alcohol ablation. Automatic Implantable Cardiac Defibrillator
Arrhythmogenic myocardial substrate in patients with HCM
disorganized myocytes, remodeled coronary arteriole, and replacement fibrosis
Systolic Anterior Motion of the Mitral Valve
Systolic anterior motion of the mitral valve (SAM) is a paradoxical motion of the anterior, and occasionally posterior, mitral valve leaflet towards the left ventricular outflow tract (LVOT) during systole. The exact mechanism of SAM in hypertrophic cardiomyopathy (HCM) is debated, with some investigators postulating that it is a Venturi effect, while others believe that it is secondary to anatomical differences in the positions of the papillary muscles and valve leaflets. According to the Venturi effect, fluid pressure decreases and velocity increases as fluid flows through a region of reduced cross sectional area. Septal hypertrophy in HCM creates the Venturi effect through reduction in the LVOT diameter, which leads to an increased velocity and reduced pressure of the ejected blood in the LVOT. This pressure differential between the left atrium and the outflow tract is thought to lead to deviation of the mitral valve towards the septum. SAM may alternatively be caused by the more anterior and inward location of the papillary muscles which alters chordal tension, resulting in a push of the leaflets towards the ventricular septum at the beginning of systole. The pathogenesis of SAM is likely a combination of these two mechanisms and varies depending on the underlying associated condition. SAM is most commonly seen in the asymmetric septal form of HCM but has also been described in hypertensive heart disease, diabetes mellitus, acute myocardial infarction, after mitral valve repair, and even in asymptomatic patients during pharmacologic stress with dobutamine.4 Approximately 25% of patients with HCM have dynamic subaortic outflow obstruction occurring at rest caused by SAM contacting the hypertrophied interventricular septum. Current therapies aim to reduce the risk of congestive heart failure through reduction of the LVOT pressure gradient. The hallmarks of therapy are medications (eg, β-blockers and calcium channel blockers), septal myectomy, and transcatheter alcohol ablation of the interventricular septum. The effectiveness of alcohol ablation is evaluated with delayed gadolinium hyperenhancement and VENC phase contrast sequences.9 Reduced septal thickness, resolution of SAM, and reduced pressure gradient across the LVOT indicate a response to treatment. It is important to consider a diagnosis of HCM when SAM is identified in conjunction with asymmetric septal hypertrophy and mitral regurgitation.
Restrictive cardiomyopathy
Most commonly infiltrative: amyloidosis and sarcoidosis. Impaired ventricular filling due to stiff (noncompliant) ventricles. Systolic function often normal and ventricles usually not dilated. Diagnosed by echocardiography with Doppler assessment of ventricular filling. This rare entity has a poor prognosis. Intractable failure and fatal arrhythmias may occur.
Introduction to the ECG
The initial deflection is the P wave, which is due to atrial depolarization. The next deflection is the QRS which is due to ventricular depolarization. The Q is negative, the R is positive and the S is a late negative deflection. One, two, or all of these deflections may be present in a given lead. Normally the duration of the QRS is 0.06-0.10 seconds. The T wave is due to ventricular repolarization. U waves are inconstant. The paper speed is 25 mm/second. Thin vertical lines (small squares) are 0.04 seconds apart and thick vertical lines (large squares) are 0.2 seconds apart. The PR interval from the onset of the P wave to the onset of the QRS is a measure of atrioventricular node conduction time, since most of the interval reflects delay in traversing the node. A normal PR interval is 0.12-0.20 seconds. The QT interval represents the total duration of depolarization and repolarization. Abnormalities in the QT interval and t wave due to drugs, abnormal electrolytes, or other causes predispose to arrhythmias usually through alterations in repolarization
Heart rate and ECG
Paper speed 25mm/sec. Light lines (1mm) 0.04 sec. Heavy lines (5mm) 0.2 sec. HR = 300 ÷ # heavy lines between 2 QRS’s. HR= 1500 ÷ # mm between 2 QRS’s
EKG leads
Leads are electrodes which measure the difference in electrical potential between either: 1. Two different points on the body (bipolar leads). 2. One point on the body and a virtual reference point with zero electrical potential, located in the center of the heart (unipolar leads). Polarity of leads depends on whether the depolarization is moving toward (positive) or away from (negative) the electrode. QRS will be upright (+) in left and lateral leads. And downward (-) in right-sided leads
RA lead
placement is on the right arm, avoiding thick muscle.
LA lead
placement is in the same location as RA but on the left arm
RL lead
placement is on the right leg, lateral calf muscle
LL lead
placement is in the same location as RL but on the left leg
V1 lead
placement is in the fourth intercostal space (between ribs 4 and 5) just to the right of the sternum (breastbone).
V2 lead
placement is in the fourth intercostal space (between ribs 4 and 5) just to the left of the sternum.
V3 lead
placement is between leads V2 and V4.
V4 lead
placement is in the fifth intercostal space (between ribs 5 and 6) in the mid-clavicular line.
V5 lead
placement is horizontally even with V4, in the left anterion axillary line
V6 lead
placement is horizontally even with V4 and V5 in the midaxillary line
Inferior leads
Leads II, III and aVF. Look at electrical activity from the vantage point of the inferior surface (diaphragmatic surface of heart)
Lateral leads
leads I, aVL, V5 and V6. Look at the electrical activity from the vantage point of the lateral wall of left ventricle
Septal leads
leads V1and V2. Look at electrical activity from the vantage point of the septal surface of the heart (interventricular septum)
Anterior leads
leads V3 and V4. Look at electrical activity from the vantage point of the anterior wall of the right and left ventricles (Sternocostal surface of heart)
Axis on ECG
The heart’s electrical axis is the general direction of the ventricular depolarization wavefront (or mean electrical vector) in the sagittal plane (the plane of the limb leads and augmented limb leads). The QRS axis can be determined by looking for the limb lead or augmented limb lead with the greatest positive amplitude of its R wave. A lead can only detect changes in voltage that are aligned with that lead; therefore the lead that is best aligned with the axis of ventricular depolarization will have the tallest positive QRS complex. The normal QRS axis is generally down and to the left, following the anatomical orientation of the heart within the chest. An abnormal axis suggests a change in the physical shape and orientation of the heart, or a defect in its conduction system that causes the ventricles to depolarize in an abnormal way. Left axis deviation may indicate left ventricular hypertrophy, left anterior fascicular block, or an old inferior q-wave myocardial infarction. Right axis deviation may indicate right ventricular hypertrophy, left posterior fascicular block, or an old lateral q-wave myocardial infarction.
ECG of patient with a fixed stenosis of a coronary artery
The resting ST segment is normal but during exercise there is ST depression due to transient ischemia.
P-wave feature
The p-wave represents depolarization of the atria. Atrial depolarization spreads from the SA node towards the AV node, and from the right atrium to the left atrium. The p-wave is typically upright in most leads except for aVR; an unusual p-wave axis (inverted in other leads) can indicate an ectopic atrial pacemaker. If the p wave is of unusually long duration, it may represent atrial enlargement. Typically a large right atrium gives a tall, peaked p-wave while a large left atrium gives a two-humped bifid p-wave. Duration is less than 80 ms.
PR interval
The PR interval is measured from the beginning of the P wave to the beginning of the QRS complex. This interval reflects the time the electrical impulse takes to travel from the sinus node through the AV node. A PR interval shorter than 120 ms suggests that the electrical impulse is bypassing the AV node, as in Wolf-Parkinson-White syndrome. A PR interval consistently longer than 200 ms diagnoses first degree atrioventricular block. The PR segment (the portion of the tracing after the p-wave and before the QRS complex) is typically completely flat, but may be depressed in pericarditis. Duration is 120 to 200 ms.
QRS complex
The QRS complex represents the rapid depolarization of the right and left ventricles. The ventricles have a large muscle mass compared to the atria, so the QRS complex usually has a much larger amplitude than the P-wave. If the QRS complex is wide (longer than 120 ms) it suggests disruption of the heart’s conduction system, such as in LBBB, RBBB, or ventricular rhythms such as ventricular tachycardia. Metabolic issues such as severe hyperkalemia, or TCA overdose can also widen the QRS complex. An unusually tall QRS complex may represent left ventricular hypertrophy while a very low-amplitude QRS complex may represent a pericardial effusion or infiltrative myocardial disease. Duration is 80 to 100 ms.
ST segment
The ST segment connects the QRS complex and the T wave; it represents the period when the ventricles are depolarized. It is usually isoelectric, but may be depressed or elevated with myocardial infarction or ischemia. ST depression can also be caused by LVH or digoxin. ST elevation can also be caused by pericarditis, Brugada syndrome, or can be a normal variant (J-point elevation).
T wave
The T wave represents the repolarization of the ventricles. It is generally upright in all leads except aVR and lead V1. Inverted T waves can be a sign of myocardial ischemia, LVH, high intracranial pressure, or metabolic abnormalities. Peaked T waves can be a sign of hyperkalemia or very early myocardial infarction. Duration is 160ms.
Corrected QT interval
The QT interval is measured from the beginning of the QRS complex to the end of the T wave. Acceptable ranges vary with heart rate, so it must be corrected by dividing by the square root of the RR interval. A prolonged QTc interval is a risk factor for ventricular tachyarrhythmias and sudden death. Long QT can arise as a genetic syndrome, or as a side effect of certain medications. An unusually short QTc can be seen in severe hypercalcemia. Duration is less than 440 ms.
U wave
The U wave is hypothesized to be caused by the repolarization of the interventricular septum. It normally has a low amplitude, and even more often is completely absent. If the U wave is very prominent, suspect hypokalemia, hypercalcemia or hyperthyroidism.
ECG of a patient with an acute clot in a coronary artery
Normally T waves and the QRS go in the same direction. Here the T wave is inverted, a sign of ischemia. This could be transient or result ultimately in tissue injury.
ST elevation
is a sign of transmural injury in an acute coronary syndrome, usually with a clot due to platelet aggregation obstructing a coronary artery. Most commonly the injury is associated with an acute myocardial infarction. However, if the obstructed artery is quickly opened with angioplasty or a thrombolytic agent the ST elevation may partially or entirely reverse and much, or rarely all, injury avoided.
Small Q wave
Although very small Q waves may not be pathological, in general development of a sizable Q wave is due to transmural necrosis. Typically sizable means at least one small box wide (≥0.04 seconds). Infarcts usually involve only the left ventricle. When Q waves develop in leads which would normally be positive they give information on localization of the infarct. Q waves in inferior leads (II,III, aVF) are due to inferior infarcts. Q waves in leads V1-V4 are due to anterior wall infarcts. Leads I, aVL and the anterolateral leads (V5,V6) are associated with lateral wall infarcts.
Transmural acute myocardial infarct
Typically a transmural acute myocardial infarct evolves over time as shown on the left. There is an early stage that is rarely seen, because it often lasts only a few minutes in which there are giant, upright “hyperacute” T waves. Subsequently the T wave inverts (“ischemia”) and the ST segments then rise (“current of injury”). Sometimes the ST elevation precedes or occurs simultaneously with the T inversion. Q waves are usually the last ECG findings to develop.
Transmural infarct
Transmural infarcts involve the full thickness of the left ventricular wall and tend to be large. Smaller infarcts may be localized to the inner layer of the left ventricular wall, the subendocardium. Subendocardial infarcts do not have Q waves or ST elevation. They do have persistent ST depression. Whereas ST depression may reflect transient ischemia without necrosis, ST depression lasting two or three days probably reflects a subendocardial infarct.
Prolonged QT interval and ECG
When the QT interval is altered susceptibilities to arrhythmias increase. This is especially likely with QT prolongation. There are congenital QT prolongation syndromes associated with serious, sometimes fatal arrhythmias. More commonly QT prolongation is acquired due to electrolyte abnormalities or drugs. A nl. QT depends on heart rate but the rule of thumb here is easier to remember than specific time intervals.
Serum calcium abnormalities ECG changes
Both hypercalemia and hypocalcemia can predispose to arrhythmias. Hypercalcemia shortens the QT interval. The commonest cause is hyperparathyroidism. Hypocalcemia lengthens the QT interval, is more commonly encountered, has many causes, and may be associated with life threatening ventricular arrhythmias.
Hypokalemia and ECG changes
Hypokalemia is extremely common. Common causes are overuse of diuretics and vomiting or diarrhea. Alkalosis, potassium losing nephropathies and excess aldosterone are among other causes. The QT interval is generally prolonged, prominent U waves are frequent and T waves may be inverted . Hypokalemia is a common cause of arrhythmias. The ECG changes are not specific and serum potassium levels should be checked to confirm the diagnosis.
Changes induced by excess potassium are distinctive
Mild elevations cause increased T wave voltages with a distinctive peaked, symmetrical appearance. At higher levels the P waves may flatten and the QRS & T waves widen. A broad S wave often appears. At very high levels a sinusoidal pattern appears without P or R waves. Renal failure is the commonest cause. If unrecognized hyperkalemia often causes fatal arrhythmias.
Types of bradyarrhythmias
sinus node dysfunction, atrioventricular block
Sinus node dysfunction
the sinus node is composed of a finite amount of myocytes, which can be replaced over time du to the normal aging process or as a result of an underlying process, such as an infiltrative cardiomyopathy or heart failure. Eventually, everyone will manifest some evidence of sinus node dysfunction. In those individuals that are symptomatic, a pacemaker can be useful for improving symptoms. There is a very limited role for medications, except for withdrawal of potentially causative agents such as beta-blockers or most anti-arrhythmic drugs.
Sinus arrest
occurs when there is a pause in the rate at which the SA node fires. With sinus arrest there is no relationship between the pause and the basic cycle length. Failure of sinus node discharge resulting in the absence of atrial depolarization and periods of ventricular asystole. Rate = 75 bpm. PR interval = 180 ms (.18 seconds). 2.8-second arrest
Atrioventricular block
can occur as a result of disease in the AV node or at a level below the AV node (His-Purkinje system). The distinction is important because of the urgency that treatment is required. AV block is either incomplete with either occasional or frequent drop beats, or complete, with no association between atrial and ventricular depolarizations. Incomplete AV block is further delineated into Mobitz I and Mobitz II varieties.
Mobitz I AV block
is characterized by progressive prolongation of the PR interval on the ECG until a blocked beat is encountered. The underlying PR interval is usually prolonged at the beginning of the cycle, indicating underlying AV nodal disease.
Mobitz II AV block
usually results from disease below the level of the AV node in the His-Purkinje system. This type of block is much more unpredictable and urgent action is required to avoid potential asystole.
Complete heart block (3rd degree AV block)
is seen when there is no association between the atrial and ventricular depolarizations. Usually block in the AV node will permit for a reliable excape rhythm from the AV junction. This rhythm is usually identified with a regular (53-45 bpm), narrow QRS complex indicating its origination from the junction. Infranodal AV block is much more unreliable with escape rhythm from the AV junction. This rhythm is usually identified with a regular (35-45 bpm), narrow QRS complex indicating its origination from the junction. Infranodal AV block is much more unreliable with escape rhythms originating from the purkinje system or ventricular myocardium. It is identified by a wide QRS complex with a very low and often irregular heart rate (15-30 bpm).
Treatment for AV block
pacemaker implantation. For potentially reversible causes, drugs that exhibit a chronotropic effect on the AV junction (i.e. isoproterenol, dopamine) can be useful to temporarily relieve symptoms in AV block involving the AV node. Patients with infranodal AV block may have symptoms exacerbated by increasing AV nodal conduction and underlying heart rate, causing block to worsen.
Cardiac pacemakers
a pacemaker is an implantable device which acts to restore normal cardiac rhythm. They can be single (atrial or ventricular) or dual chamber and usually consist of a pulse generator implanted over the pectoral muscle and one or more leads implanted via a transvenous approach. The device acts as a timer, which senses electrical activity in one chamber and either delivers or withholds an electrical impulse. The simplest pacemaker is a single chamber device set to a back up pacing mode. If an impulse is not sensed above a baseline pacing rate, then the device will send an electrical impulse to the chamber causing it to depolarize. The timing for the devices are set in milliseconds, such as 1000 msec (equivalent of 60 beats/min). The timer resets and inhibits pacing if there is an impulse within 1000 msec of the prior impulse, and acts if nothing is sensed in the 1000 msec window.
Types of tachyarrhythmias
sinus tachycardia, atrial flutter, atrial fibrillation, atrial tachycardia, AV nodal reentrant tachycardia, AV reentrant tachycardia, and ventricular tachycardia.
Sinus tachycardia
is an arrhythmia itself, but can be an abnormal finding. It is important to not ignore this if discovered clinically. It is often a manifestation of an important underlying process, such as poor pain control, volume depletion, anemia, bacteremia or sepsis, hypoxia and hypercarbia, to name a few. There are unusual and infrequently encountered variants of sinus tachycardia, which are not due to an underlying cause and are pathologic unto themselves. These include inappropriate sinus tachycardia and postural orthostatic tachycardia syndrome.
Atrial flutter
is the prototypical reentrant arrhythmia and best illustrates the concept of reentry as a tachycardia mechanism. Typical right atrial flutter involves unidirectional electrical conduction around the tricuspid valve utilizing an area of slow conduction (critical isthmus). A critical isthmus is an area of slow conduction between two electrically unexcitable structures (myocardial scar, valves, and viens).
Mechanism of tachycardia with atrial flutter
in sinus rhythm, activation around the valve takes place in both clockwise and counterclockwise directions. Eventually the two wavefronts collide and extinguish each other. If a premature atrial stimulus arrives at the lateral or septal aspect of the valve, the cavotricuspid isthmus (region of slow conduction, or critical isthmus) may be refractory and unable to propagate the impulse. Conduction will simultaneously proceed around the tricuspid valve, allowing time for the critical isthmus to recover. Once the wavefront reaches the critical isthmus, it can be conducted in a unidirectional manner and one cycle of the tachycardia circuit has been completed this process is called reentry. The rate of the tachycardia is governed by the ability of tissue to conduct the impulse; the slow link in the chain is the cavotricuspid isthmus (small rim of tissue between the tricuspid valve and inferior vena cava).
Diagnosis of atrial flutter
usually diagnosed on the basis of the surface 12-lead ECG or monitor showing characteristic “sawtooth” pattern in the inferior leads for the first half of the cycle (positive deflection), then away for the second half of the cycle (negative deflection). The rate is usually around 200 milliseconds (300 beats/minute), but may be longer depending on the presence of right atrial dilation or scar. If the right atrium is dilated from a variety of conditions (pressure overload- pulmonary embolism, pulmonary hypertension; volume overload- septal defect with left to right shunt; anatomic defect- tricuspid atresia, Ebstein’s anomaly), then the tricuspid valve is necessarily stretched and the circuit is physically longer. Also, conditions that predispose to right atrial disease tend to cause a myopathic process which affects tissue conduction of electrical signals. In the absence of rate-controlling agents (which affect conduction through the AV node), the ventricular rate is typically 150 beats/minute and conduction takes place in a 2:1 manner from the atrium to the ventricle.
Treatment of atrial flutter
controlling the heart rate is difficult in the absence of very high doses of AV nodal blockers, and nearly impossible during exertion unless there is underlying AV nodal disease. Anti-arrhythmic drugs may be useful to minimize the premature atrial beats, which initiate tachycardia. Once tachycardia has been initiated and established, using anti-arrhythmic drugs (class I or class III) may be helpful (terminate tachycardia) or harmful (helping maintain the arrhythmia). If depolarization/recovery along the leading edge is slowed by a drug more than the trailing edge, conduction will catch up and tachycardia will be terminated because the excitable gap is bridged. If depolarization/ recovery is affected more along the trailing edge, then the excitable gap is widened and tachycardia is more likely to continue. Administration of AADs in atrial flutter may slow conduction enough (280-300 msec; 200-220 beats/ minute) to facilitate 1:1 AV conduction at a rate causing significant symptoms such as syncope; important that patients receiving these drugs are also on an AV nodal blocker such as a beta-blocker or calcium channel blocker. Long term success rates of pharmacologic atrial flutter treatment are less than 50%. Electrical cardioversion is almost always initially successful, but is associated with a relatively high recurrence rate (up to 50% in twelve months). Cardioversion is the application of DC energy in a single rapid shock across the precordium. Ablation of the arrhythmia is associated with a 93-98% long-term success rate; accomplished by applying radiofrequency energy, transferred to the tissue in the form of heat, which destroys the myocytes and causes scar. Area that is targeted is the cavotricupsid isthmus between the IVC and tricuspid valve. If this tissue cannot conduct, the electrical wavefront cannot continue to propagate around the valve.
Atrial fibrillation
is the most common arrhythmia experienced in the US. It is due to chaotic electrical activity in the atria with multiple microreentrant wavelets existing simultaneously. This gives an effective atrial rate of > 300 beats/minute. Often there is a trigger which initiates the tachycardia and the underlying substrate to maintain the arrhythmia. Atrial fibrillation is referred to as paroxysmal (occurring intermittently and terminating spontaneously), persistent (recurrence without spontaneous conversion), and permanent (inability to restore sinus rhythm).
The tree tenets of treatment of atrial fibrillation
are rate control, rhythm control, and anticoagulation. Rate control is accomplished with AV nodal blockade or, in refractory cases, ablation of the AV node. Rhythm control is accomplished with either pharmacologic agents, cardioversion, or ablation. Individuals that are symptomatic should have attempts at rhythm control. Pharmacologic agents consist primarily of class I and class III antiarrhythmics. Cardioversion is almost always successful acutely, with carrying degrees of recurrence depending depending on underlying substrate. Ablation has been recently described and refined, initially in 1998. Triggers for atrial fibrillation have been discovered to emanate from within the pulmonary veins in the majority of cases. An approach to electrically isolating the pulmonary veins and ablation in the left atrium for “substrate modification” reduces the recurrence of atrial fib. Success rates are 70-75% in paroxysmal patients and 40-50 % in permanent patients. The risk of the procedure, including stroke precludes its recommendation as a first line strategy. Anticoagulation is important to minimize the risk of stroke and overall morbidity from atrial fibrillation. A risk stratification for embolic events has been established called CHADS scoring system (congestive heart failure, hypertension, age greater than 75, diabetes, stroke- counts as 2 point). Daily aspirinis given for zero points, aspirin or warfarin for one point and warfarin for two points or more. Regular supraventricular tachcardias with predominant 1:1 AV association are often grouped together. Primary diagnostic possibilities are atrial tachycardia (AVRT), and AV reentrant tachycardia (AVRT) mediated by an accessory pathway. In general population, AVNRT accounts for 655 of the overall, AVRT for 25% and atrial tachycardia for 10%.
Atrial tachycardia
an arrhythmia that is analogous to sinus tachycardia. There is usually 1:1 AV conduction unless the arrhythmia is very fast or there is underlying AV nodal conduction disease. In atrial tachycardia, there is an abnormal focus of atrial tissue which possesses its own automaticity and ability to generate atrial beats. There is usually a rapid onset and offset which distinguishes this arrhythmia from sinus tachycardia. Atrial tachycardia often occurs in the setting of a trigger, such as a catecholamine surge, caffeine, or heart failure. It can be seen in the setting of structurally normal hearts or underlying cardiac disease. Treatment options include antiarrhythmics are 30% at one year. Ablation targets the abnormal focus and destroys this tissue with a controlled lesion. The success rates for ablation are between 70-90%.
AV nodal reentrant tachycardia
this arrhythmia involves a reentrant circuit around the AV node. About 10-20% of individuals possess two distinct pathways within the AV node. These are termed the fast and slow pathways (FP and SP). The pathways are electrically connected at their proximal and distal ends. During sinus rhythm, conduction is propagated down both the fast and slow pathways, but faster (obviously) through the FP. Once it reaches the His, the electrical activation proceeds both down the ventricle, and returns up the SP which collides with and extinguishes the electrical wavefront already traveling down the slow pathway. If an early beat from the atrium (an atrial premature depolarization, or APD) conducts to the AV node and finds the FP unable to conduct because it has not recovered from its prior activation (refractory), conduction may proceed solely down the SP. The slow pathway, while conducting slower the FP, is able to recover down the SP and activate the His and ventricle. It can simultaneously return up the FP and conduction again down the SP in a reentrant manner. Continued electrical activation leads to AVRT. AVNRT is treated differently acutely and chronically. During the acute presentation, strategies to break the arrhythmia focus on slowing conduction through one or both of the pathways or halting conduction temporarily altogether. AV nodal blockers such as beta blockers or calcium channel blockers can be administered but usually only slow the rate. Administration of adenosine, often in escalating doses, will lead to transient AV nodal blockade and almost always terminate the arrhythmia. Patients can also perform maneuvers that increase the endogenous level of adenosine, termed vegal maneuvers. These include carotid sinus message, clenching the abdominal muscle by bearing down, and cold water immersion. The chronic treatment for AVNRT can be minimal to invasive. Because the arrhythmia is very low risk, long term treatment should be pursued if there are relatively frequent episodes. For very infrequent episodes, demonstration of vagal manuvers can be helpful. Individuals with more frequens episodes can be prescribed daily AV nodal blockers, which significantly reduce or eliminate symptoms about 50%of the time. Because many patients with AVNRT are young, side effects such as fatigue and reduced exercise tolerance can make these medications intolerable. Invasive treatment of AVRNT is performed with catheter ablation for individuals with frequent symptoms who fail, cannot tolerate, or do not want to take medications. The approach involves ablation of the slow pathways; ablation of the fast pathway is associated with a higher risk of heart block. The long-term success rates for AVNRT ablation are 95-98% with less than 1% risk.
AV reentrant tachycardia
AVRT is mediated via conduction through accessory pathway (AP). An AP is an abnormal electrical connection between the atrium and ventricle. They either conduct both antegrade (atrium to ventricle) and retrograde (ventricle to atrium) or only retrograde. There are rare cases of Aps which conduct only antegrade and possess AV nodal-like properties. Antegrade conduction down an AP is termed the Wolff-Parkinson-white syndrome when associated with tachycardia. On the surface activation, the AP conduction can be seen by the delta wave, which represents activation of the ventricle through the AP prior to ventricular activation via the AV node. This is termed ventricular preexcitation. The WPW syndrome is generally the only SVT, which is associated with sudden cardiac death.
Different mechanisms that lead to tachycardia in patients with AP conduction
there are three different mechanisms. Conduction can occur down the AV node to the ventricule, back to the atrium via the AP, and repeat the cycle to continue tachycardia. This is called orthodromic reciprocating tachycardia (ORT) because ventricular activation proceeds in the normal manner via the AV node. The majority of regular SVTs using an AP utilize this mechanism. Activation down the AP and retrograde through the AV node is called antidromic reciprocating tachycardia. In comparison to ORT, which demonstrates a narrow QRS complex, antidromic tachycardia is the characterized by a wide QRS complex due to activation of the ventricles via the myocardium, and not the normal conduction system. The third and most dangerous tachycardia involving Aps is atrial fibrillation in the presence of an antegrde conducting AP. The AV node has a maximum rate at which it can conduct, depending on age. Some Aps can conduct much faster and activate the ventricular fibrillation can result leading to sudden cardiac death. For this reason, some recommend screening for and ablation of all APs, which can conduct faster than a certain rate (greater than 240bpm) in order to eliminate this already relatively low risk of sudden death.
Treatment for AVRT and APs
is similar to that for AVNRT. Acutely, adenosine should be withheld if an AP is known to be present. Administration of this medication can lead to both 1) AV nodal block and conduction solely down the AP, which is not usually affected by adenosine, and 2) risk of atrial fibrillation with adenosine and rapid AP conduction. Procainamide can be used safely as it also affects conduction down the AP, and cardioversion is used for unstable tachycardia. In general, individuals with known antegrade AP conduction faster than 240 bpm should undergo ablation.
Ventricular tachycardia
in contrast to SVT, relies entirely on the ventricle for arrhythmia, especially in patients with structural heart disease (heart failure, coronary disease, etc). the mechanisms for VT are either a reentrant arrhythmia using prior scar or an automatic or triggered focus. Usually the QRS during VT has a single morphology, but can occasionally have alternating morphologies due to drugs (digoxin) or alternating reentry circuits.
Acute therapy for VT
The acute therapy for VT depends on the patient’s status and underlying heart function/ heart disease if known. For patients that are awake, and hypotensive, medications can be administered. Amiodarone is usually administered first as a bolus and then an IV drip because there are few contraindications for short term administration. For individuals that are not hemodynamically stable, cardioversion is then relied upon for restoration of normal rhythm.
Long term therapy for VT
The long term therapy for VT depends on the presence or absence of underlying heart disease. For patients with structurally normal hearts, two main types of VT are seen. The first, and most common, are ventricular outflow tract tachycardias. About 90% of these originate from the right ventricular outflow tract, usually right below the pulmonic valve, and 10% from the left ventricular outflow tract, including the aortic cusps. The other type of VT seen in patients with structurally normal hearts is termed idiopathic VT, also called verapamil-sensitive VT. This is a reentrant rhythm utilizing the left posterior fascicle and has a characteristic ECG pattern. The long term therapy for these patients depends on symptoms. Infrequent episodes which are not poorly tolerated requires as needed treatment. For frequent episodes of outflow tract tachycardia, beta blockers or calcium channel blockers can be used, as well as either Class or Class III anti-arrhythmics. Alternatively, ablation is about 90% curative with a 1-2% risk of complications. The therapy for idiopathic VT is either a calcium channel blocker, both acutely and long-term, such as verapamil or diltiazem or catheter ablation.
VT in patients with structural heart disease or coronary artery disease
is considered life-threatening and can result in sudden death. 90% of these episodes result from reentry, and the other 10% are triggered or automatic foci. Acutely, treatment is determined by the hemodynamic status can deteriorate quickly. The long term therapy for VT (and all ventricular arrhythmias) is these patients focuses on both reduction of mortality and reduction in symptomatic events. The only therapy that has been shown to improve mortality in patients with VT and structural heart disease is the implantable cardioverter-defibrillator (ICD). This device is similar to a pacemaker but instead detects rapid heart rates. Via detection algorithms designed to discriminate rapid, normal heart rhythms (sinus tachycardia with exercise) from ventricular arrhythmias, including VT, the ICD can recognize ventricular arrhythmias and treat with either a shock or rapid pacing designed to suppress and terminate the arrhythmia. Several trials have been completed who survived a ventricular arrhythmia outside of the setting of a myocardial infarction has a significant mortality benefit with ICD implantation. Individuals with left ventricular ejection fractions less than 35% also have a benefit, although more modest, and in both of these patient groups ICDs are strongly considered. The role for antiarrhythmic medications in the treatment of VT with structural heart disease focuses on minimizing symptoms from the arrhythmia, especially ICD shocks. Because of the underlying cardiac disease, treatment options are limited. Usually amiodarone and sortalol are used as first-line agents. Beta blockers have been shown to reduce ventricular ectopy and are also associated with improved mortality in most varieties of cardiac disease. Beta blockers may function as antiarrhythmics in this case by minimizing the ventricular ectopy which serves to initiate ventricular arrhythmias.
Where in the conduction system can problems develop leading bradyarrhythmias?
Sinus node, AV node, and below the AV node. Sinus node dysnfuction can produce sinus bradycardia, sinus arrest/ pause, tachy-brady syndrome, chronotropic incompetence (inability to mount age-appropriate HR with exercise). AV node problems include first degree AV block and mobitz 2nd degree AV block (wenkebach). Problems below the AV node (infranodal/His Purkinje system) include MobitzII 2nd degree AV block and complete heart block. You should be concerned when the patient is symptomatic, no matter what part of the conduction system is affected and when the rhythm is infranodal (below the AV node).
Where does problems leading tachyarrhythmias
Tacharrhythmias fall into one of two major categories, depending on the origin of the tachycardia. If it’s above the ventricle, it’s a supraventricular tachycardia. Or, it’s coming from the ventricle (includes ventricular tachycardia and ventricular fibrillation).
Bradycardia-Tachycardia (Brady-Tachy) Syndrome
Brady-tachy syndrome occurs when the SA node has alternating periods of firing too slowly (< 60 bpm) and too fast (> 100 bpm). Brady-tachy syndrome often manifests itself in periods of atrial tachycardia, flutter, or fibrillation. Cessation of the tacycardia is often followed by long pauses from the SA node.
Chronotropic Incompetence
the inability of the heart to increase its rate commensurate with increased activity or demand, is common in patients with cardiovascular disease, produces exercise intolerance which impairs quality-of-life, and is an independent predictor of major adverse cardiovascular events and overall mortality.
Take home points of bradyarrhythmia
Determine level of block responsible for bradycardia: sinus node, AV node, infranodal. Symptoms and infranodal disease, which can progress to unreliable heart rhythms, should dictate treatment. Treat potential reversible causes. Acutely stabilize patients. Only long-term treatment is a permanent pacemaker.
Ventricular hypertrophy ECG
more muscle=more volts=greater amplitude of QRS. Also inverted s wave. Left ventricular hypertrophy big R waves in left-sided leads I, aVL, V5, V6. Right ventricular hypertrophy big R waves in right sided leads V1 and V2.
Ischemia
occurs when blood supply is insufficient to meet oxygen demand in the ventricles. Ischemic changes in the EKG alter ventricular repolarization and affect the ST segment and the T wave. Ischemia due to sudden high oxygen demand in the presence of fixed coronary obstruction causes depression of the ST segment. Ischemia due to acute coronary artery obstruction during low oxygen demand causes T wave inversion. Stress induved myocardial ischemia is due to increased oxygen consumption with inability to increase coronary flow appropriately and can be seen on an ECG with ST depression. Ischemia can also be due to acute coronary syndrome and results in decreased coronary flow without increased oxygen consumption. Can be seen in ECG as inverted T wave.
Transmural current of injury
When acute ischemia is transmural (whether caused by diastolic and/or systolic injury currents), the overall ST vector is usually shifted in the direction of the outer (epicardial) layers, and ST elevation and sometimes tall positive (hyperacute) T waves are produced over the ischemic zone. Reciprocal ST depressions can appear in leads reflecting the contralateral surface of the heart. (Occasionally, the reciprocal changes can be more apparent than the primary ST elevations.)When ischemia is confined primarily to the subendocardium, the overall ST vector typically shifts toward the inner ventricular layer and the ventricular cavity such that the overlying (e.g., anterior precordial) leads show ST segment depression with ST elevation in lead aVr. This subendocardial ischemic pattern is the typical finding during spontaneous episodes of angina pectoris or during symptomatic or asymptomatic (“silent”) ischemia induced by exercise or pharmacological stress tests. Absence of normal transmural vector produces a negative deflection in leads over infarcted myocardium leading to Q-wave.
A significant Q wave
- is ≥ one fourth the amplitude of the R wave. 2. is ≥ one small box (0.04 seconds) wide. 3. is usually in at least 2 leads reflecting the same region of the left ventricle.
Evolving transmural myocardial infarct
acutely causes peaked T-wave-> T-wave inversion-> ST elevation-> Q-wave, ST-elevation, and T-inversion.
Subendocardial myocardial infarct
ST depression and no Q wave
Prolonged QT interval
the QT interval is more than half the RR interval. Causes: Hypocalcemia, hypokalemia, hypomagnesemia, Class 1A or 3 anti-arrhythmic drugs, Hypothermia, and Congenital Long QT syndrome.
Hyperkalemia and ECG
K+ 5.5-7.5mmol/l= tall T waves that are peaked and symmetrical. K+ 7.5-9 mmol/l= P and R waves flatten, QRS and T broaden, big S waves develop. K+>9.0 mmol/l= P and R waves gone, S and T waves broaden in a sine wave pattern.
Atrial fibrillation
irregularly irregular ventricular rhythm, and no P waves. Can be due to MI subjects (lone A fib), aging, post-operative, heart disease, and hyperthyroidism. Problems related to a fib include rapid heart rate (leading to syncope, ischemia or heart failure), loss of atrial kick (leading to heart failure), atrial thrombi (leading to emboli stroke. Treatments include anticoagulation, rate control with drugs, cardioversion (electrical or drugs), and ablation. Because of the increased risk of embolic stroke, nearly all patients are treated with anticoagulation, usually with coumadin (warfarin). Aspirin is less effective but can be used in low risk cases. Rate control is usually possible with beta blockers, some calcium channel blockers (diltiazem or verapamil) or digoxin -either singly or in combination. Because atrial fibrillation has a very high recurrence rate, most patients are managed with anticoagulation and rate control. Conversion to sinus rhythm can be achieved with electrical cardioversion drugs or with drugs. However, maintenance of sinus rhythm often requires drugs with high toxic potential. As result this is generally reserved for patients in whom rate is poorly controlled, there are intolerable palpitations, or who need their “atrial kick” to maintain cardiac output. Patients without underlying heart disease or patients who have minimal evidence of pathology may also be cardioverted for AF because of better results in maintaining sinus rhythm.
Reentry
Arrhythmias may rarely arise from a single ectopic pacemaker. However, most ectopic rhythms arise from reentry. In a normal heart arrhythmias are self- terminating because depolarization at a junction usually meets tissue which has already been depolarized and is therefore refractory to reentry. However, if chamber dilation and/or islands of fibrosis create a long and circuitous path, the depolarization can continue to find non-refractory myocardium and be sustained. Abnormal reentry pathways can be present in the atria, ventricles, or the junctional tissue.
Atrial tachycardia
rapid heart rate, narrow QRS complexes, and P waves are present, but abnormal. Quite uncomfortable and disturbing. They are easily terminated by adenosine infusion. They are frequently a recurrent problem. Recurrence is usually prevented by ablation of the reentry pathway.
Junctional rhythm
ECG is regular, narrow (normal) QRS, and no antecedent P waves. The region surrounding the atrioventricular node is often termed “the junction” and rhythms originating there are called “junctional rhythms”. They may be either slow or fast. They are a regular rhythm usually with narrow QRSs. P waves are often not seen because they are buried within the QRS complex or they may occur very shortly before or after the QRS. They are often inverted because they are conducted upward from the AV node rather than downward from the sinus node.
Arrhythmia
can be due to premature atrial contraction leading to premature, beats, preceded by abnormal P wave, and narrow QRS. Can also be due to premature ventricular contraction which show up as wide abnormal QRS, no P wave, ectopic ventricular focus conducted by slow myocardium (not purkinje), and short path length blocks re-entry. Both of these are common in healthy persons and are experienced as single-beat palpitations. They are most commonly noticed at rest when low heart rates permit occurrence of premature ‘skipped beats’ and when distractions are reduced allowing awareness. Premature atrial complexes are preceded by P waves usually of different shape than those of the regular complexes and the QRS is normal. Premature ventricular complexes have no P waves and the QRS is widened and of abnormal shape.
Life threatening arrhythmias
Rapid ventricular tachycardia or VF require emergency defibrillation. There is typically abnormal ventricular contraction in VT and there is no contraction in VF. In asystole only a straight line is seen on the ECG and prognosis is dismal. Ventricular tachycardia can be seen on the ECG as repetitive wide abnormal QRS, no P wave, ectopic ventricular focus conducted by slow myocardium (not purkinje), and long path length permits re-entry.
Larry’s awesome algorithm
a simple way to identify common cardiac rhythms. 1. Look for the P wave.
A normal P wave is inverted in lead aVR and upright in aVF . 2. Does each P wave precede a QRS? Normal sinus rhythm (rate 60-100 b/min),
Sinus bradycardia (rate 100 b/min). 3. Is atrioventricular heart block present? 1st degree block (sinus rhythm with PR interval longer than 0.2 secs). 2nd degree block (sinus rhythm but QRS rate slower than P rate because some P waves do not conduct to the QRS). 3rd degree block (sinus rhythm but QRS slower than P rate because none of the P waves conduct to the QRS). 4. Are occasional early QRS complexes present? Atrial premature beats (QRS is usually narrow and preceded by an abnormal P wave). Ventricular premature beats (QRS is wide without a preceding P wave). 5. Are very fast, abnormal P waves present? Atrial flutter (P waves extremely fast 240-320/min - typically P:QRS ratio 2:1 or 3:1 or 4:1). Atrial tachycardia (abnormal P waves fast 160-220/min with an abnormal P wave before each QRS). 6. No P waves but QRS complexes present. Atrial fibrillation (irregularly irregular QRS beats often with an undulating baseline. QRS may be narrow or wide.). Junctional rhythm (regular rhythm with flat baseline). Ventricular tachycardia (Wide, regular, usually fast QRS). 7. No P wave and no QRS? Ventricular fibrillation (wavy baseline). Asystole (flat baseline). 8. Are there P wave abnormalities in sinus rhythm? Tall P (>2.5 mm in an inferior lead =Rt. atrial enlargement). Wide notched P wave with late negativity in V1= (Lt. atrial enlargement) Nl. P is inverted in aVR and positive in inferior leads. 9. Are there QRS abnormalities? Is the QRS axis normal, left, or right? (Use leads I and II) Is the QRS wide? ( ≥ .12 secs usually right or left bundle branch block) Is there an axis shift? (Right axis - think RVH or posterior hemiblock) (Left axis - think LVH or anterior hemiblock) Is there high voltage? (Ventricular hypertrophy if no bundle block). Are there Q waves? (usually infarct if localized in ≥2 leads. 10. Are there ST segment or T wave abnormalities? ST elevation (ischemic injury if localized, pericarditis if diffuse or nl earlyrepolarization) ST depression (often ischemia or subendocardial infarct). T inversion (often ischemia or secondary to hypertrophy). Tall peaked T waves (possible hyperkalemia). Long QT (consider electrolyte imbalance, drug effect)
Sinus tachycardia
(also colloquially known as sinus tach or sinus tachy) is a heart rhythm originating from the sinoatrial node with an elevated rate of impulses, defined as a rate greater than 100 beats/min (bpm) in an average adult. Tachycardia is often asymptomatic. If the heart rate is too high, cardiac output may fall due to the markedly reduced ventricular filling time.[2] Rapid rates, though they may be compensating for ischemia elsewhere, increase myocardial oxygen demand and reduce coronary blood flow, thus precipitating an ischemic heart or valvular disease[citation needed]. Sinus tachycardia accompanying a myocardial infarction may be indicative of cardiogenic shock.
Causes of sinus tachycardia
Sinus tachycardia is usually a response to normal physiological situations, such as exercise and an increased sympathetic tone with increased catecholamine release—stress, fright, flight, anger. Other causes include: sympathetic activation due Pain, Fever, Anxiety, hypotension, response to acute lung or abdomical pathology, and thyrotoxicosis. May also be due to Dehydration, Malignant hyperthermia, Hypovolemia with hypotension and shock, Anemia, Heart failure, Hyperthyroidism, Mercury poisoning, Kawasaki disease, Pheochromocytoma, Sepsis, Pulmonary embolism, Acute coronary ischemia and myocardial infarction, Chronic pulmonary disease, Hypoxia, Intake of stimulants such as caffeine, nicotine, cocaine, or amphetamines, Hyperdynamic circulation, Electric shock, and Drug withdrawal.
Diagnosis of sinus tachycardia
Usually apparent on the ECG, but if heart rate is above 140 bpm the P wave may be difficult to distinguish from the previous T wave and one may confuse it with a paroxysmal supraventricular tachycardia or atrial flutter with a 2:1 block. Ways to distinguish the three are: Vagal maneuvers (such as carotid sinus massage or Valsalva’s maneuver) to slow the rate and identification of P waves. Administer AV blockers (e.g., adenosine, verapamil) to identify atrial flutter with 2:1 block
ECG characteristics of sinus tachycardia
Rate: Greater than or equal to 100. Rhythm: Regular. P waves: Upright, consistent, and normal in morphology (if no atrial disease). P–R interval: Between 0.12–0.20 seconds and shortens with increasing heart rate. QRS complex: Less than 0.12 seconds, consistent, and normal in morphology.
Treatment of sinus tachycardia
Not required for physiologic sinus tachycardia. Underlying causes are treated if present. Acute myocardial infarction. Sinus tachycardia can present in more than a third of the patients with AMI but this usually decreases over time. Patients with sustained sinus tachycardia reflects a larger infarct that are more anterior with prominent left ventricular dysfunction, associated with high mortality and morbidity. Tachycardia in the presence of AMI can reduce coronary blood flow and increase myocardial oxygen demand, aggravating the situation. Beta blockers can be used to slow the rate, but most patients are usually already treated with beta blockers as a routine regimen for AMI. Practically, many studies showed that there is no need for any treatment. IST and POTS. Beta blockers are useful if the cause is sympathetic overactivity. If the cause is due to decreased vagal activity, it is usually hard to treat and one may consider radiofrequency catheter ablation. Must also treat thyrotoxicosis if present.
Sinus bradycardia
Sinus bradycardia is a heart rhythm that originates from the sinus node and has a rate that is lower than normal. In humans, bradycardia is generally defined to be a rate of under 60 beats per minute.
Sinus bradycardia signs and symptoms
The decreased heart rate can cause a decreased cardiac output resulting in symptoms such as lightheadedness, dizziness, hypotension, vertigo, and syncope. The slow heart rate may also lead to atrial, junctional, or ventricular ectopic rhythms.
Causes sinus bradycardia
This rhythm may be caused by one of the following: vagotonic states can be seen asIncreased vagal tone, sick sinus syndrome, or inferior infarct. Can also be due to Sleep, Hypothermia, Hypothyroidism, Intrinsic disease of the SA node (E.g. sick sinus syndrome), An effect of drugs, such as the use of digitalis, beta-blockers, quinidine, Adenosine, Calcium channel blocker, Seizure, It could also be a normal finding in a healthy, well-conditioned person, It may be secondary to infections like Diphtheria, acute rheumatic fever, viral myocarditis, Increased intracranial pressure, Rhodotoxin poisoning, and As a result of an eating disorder, such as Anorexia Nervosa.
Diagnosis of sinus bradycardia
ECG Characteristics. Rate: Less than 60 beats per minute. Rhythm: Regular. P waves: Upright, consistent, and normal in morphology and duration. P-R Interval: Between 0.12-0.20 seconds in duration. QRS Complex: Less than 0.12 seconds in width, and consistent in morphology.
Treatment of sinus bradycardia
usually none, atropine, pacemaker if symptoms.
First degree AV block
PR intercal is prolonged due to increased junctional delay. Causes include dug induced (beta blockers, some calcium blockers, digitalis) and conduction system disease. It is usually benign.
Third degree heart block
causes include severe conduction system disease, rarely due to drugs. The P waves with a regular P to P interval represents the first rhythm. The QRS complexes with a regular R to R interval represent the second rhythm. The PR interval will be variable, as the hallmark of complete heart block is no apparent relationship between P waves and QRS complexes. Treatment includes pacing if ventricular rate or BP are too low.
Atrial flutter (AFL)
an abnormal heart rhythm that occurs in the atria of the heart. When it first occurs, it is usually associated with a fast heart rate or tachycardia (beats over 100 per minute), and falls into the category of supra-ventricular tachycardias. While this rhythm occurs most often in individuals with cardiovascular disease (e.g. hypertension, coronary artery disease, and cardiomyopathy) and diabetes, it may occur spontaneously in people with otherwise normal hearts. It is typically not a stable rhythm, and frequently degenerates into atrial fibrillation (AF). However, it does rarely persist for months to years. While atrial flutter can sometimes go unnoticed, its onset is often marked by characteristic sensations of regular palpitations. Such sensations usually last until the episode resolves, or until the heart rate is controlled. Atrial flutter is caused by a reentrant rhythm in either the right or left atrium. Typically initiated by a premature electrical impulse arising in the atria, atrial flutter is propagated due to differences in refractory periods of atrial tissue. This creates electrical activity that moves in a localized self-perpetuating loop. For each cycle around the loop, there results an electric impulse that propagates through the atria. P waves (flutter waves) at rate of 240-320 beats/min. Pulse may be regular or irregular. Ventricular rate vary widely, typically rapid if untreated. Treatments include anticoagulation, rate control with drugs, cardioversion, and ablation
Atrial tachycardia
a type of atrial arrhythmia in which the heart’s electrical impulse comes from ectopic atrial pacemaker, that is to say an abnormal site in the upper chambers of the heart or atria, rather than from the SA node which is the normal site of origin of the heart’s electrical activity. Atrial tachycardias can exhibit very regular rates ranging typically from 140–220bpm. As any other form of tachycardia, the underlying mechanism can be either the rapid discharge of an abnormal focus, the presence of a ring of cardiac tissue that gives rise to a circle movement - reentry - or a triggered rapid rhythm due to other pathological circumstances as would be the case with some drug toxicities - digoxin toxicity. There is also a narrow QRS complexes and p waves are present but abnormal. Treatments include adenosine, vagal maneuver, beta blocker, verapamil or diltiazem.
Ventricular tachycardia
a type of tachycardia, or a rapid heart beat that arises from improper electrical activity of the heart presenting as a rapid heart rhythm, that starts in the bottom chambers of the heart, called the ventricles. The ventricles are the main pumping chambers of the heart. This is a potentially life-threatening arrhythmia because it may lead to ventricular fibrillation, asystole, and sudden death. ECG has usually regular, wide complexes 100-200 b/min. In most cases no P waves visible. Termed “sustained” if equal to or greater than 30 seconds duration. Often life threatening. Treated with amiodarone, lidocaine, and cardioversion.
Multifocal (or multiform) atrial tachycardia (MAT)
a cardiac arrhythmia,[1] specifically a type of supraventricular tachycardia, that is particularly common in older people and is associated with exacerbations of chronic obstructive pulmonary disease (COPD). Normally, the heart rate is controlled by a cluster of cells called the sinoatrial node (SA node). When a number of different clusters of cells outside of the SA node take over control of the heart rate, and the rate exceeds 100 beats per minute, this is called multifocal atrial tachycardia (if the heart rate is ≤100, this is technically not a tachycardia and it is then termed multifocal atrial rhythm). ‘Multiform’ simply describes the variable P wave shapes and is an observation, ‘multifocal’ is an inference about the underlying cause. Although these are interchangeable terms, some purists prefer the former nomenclature since it does not presume any underlying mechanism. It is characterized by an electrocardiogram (ECG) strip with 3 or more P-waves of variable morphology and varying P–R intervals, plus tachycardia, which is a heart rate exceeding 100 beats per minute. Narrow QRS complexes are visible as well. The P-waves and P–R intervals are variable due to a phenomenon called wandering atrial pacemaker (WAP). The electrical impulse is generated at a different focus within the atria of the heart each time. WAP is positive once the heart generates at least three different P-wave formations from the same ECG lead. Then, if the heart rate exceeds 100 beats per minute, the phenomenon is called multifocal atrial tachycardia.
Cardiac sarcoidosis
Sarcoidosis is a heterogeneous, non-caseating, granulomatous disorder of unknown etiology that can involve any organ within the body. Cardiac involvement may be detected alone and may precede, follow, or occur concurrently with other organ (eg, lung) involvement. Clinical manifestations include conduction abnormalities (atrioventricular block or bundle-branch block), tachyarrhythmias, cardiomyopathy, congestive cardiac failure, and sudden cardiac death.
Histone acetlytransferase
turns gene on through lysine acetylation
Histone deacetylase
turns gene off
Histone tail modifications
Histone tails extend beyond the nucleosome, and are sites of (mostly) reversible post-translational modification. Methylation turns gene off. Acetylation turns gene on.
Epigenetic Regulation of Hypertrophy by HDAC9
The attachment of an acetyl group to lysine residues neutralizes the basic charge of the residue. Hence, his- tone acetylation by HATs disrupts intra- and internucleosomal interactions, which in turn “relaxes” chromatin structure and activates transcription. In contrast, deacetylation of histones by HDACs removes acetyl groups and consequently increases histone-DNA contacts, resulting in condensation of chromatin and gene repression. This phosphorylation event increases chromatin accessibility and is required for chromatin-mediated transcription of the Mef2 transcription factor
Epigenetic Regulation of Hypertrophy by HDACl/2
Recent studies also demonstrated that HDAC2 (a class I HDAC), unlike HDACs of class II, is involved in a pro-hypertrophy pathway. Hdac2-deficient mice are resistant to pro-hypertrophy stimulation; in contrast, mice overexpressing HDAC2 are over-sensitive to these stimuli. The pro-hypertrophy activity of HDAC2 is linked to its ability to repress the expression of Inpp5f, which encodes phosphatidylinositol-3,4,5-trisphosphate (PIP3) phosphatase, a negative regulator of the pro-hypertrophy PI3K–Akt–Gsk3β pathway
Mean QRS axis calculation
- Inspect limb leads I and II. If the QRS is primarily upward in both, then the axis is normal and you are done. If not, then proceed to the next step. 2. Inspect the six limb leads and determine which one contains the QRS that is most isoelectric. The mean axis is perpendicular to that lead. 3. Inspect the lead that is perpendicular to the lead containing the isoelectric complex. If the QRS in that perpendicular lead is primarily upward, then the mean axis points to the (+) pole of that lead. If primarily negative then the mean QRS points to the (-) pole of that lead.
5 c’s of atrial fibrillation
reverse cause, control rate, anticoagulation, control rhythm, cure (ablation)
causes of AF
common: Hypertension 14%, IHD, Mitral valve Disease, Alcohol, Cardiomyopathies, Hyperthyroidism, Lone AF 14%. Other causes: Congenital Ht disease, Pulmonary embolism, Infection, Hypoxia, Cardiac surgery, Carditis, Ca Bronchus
Mitral valve anatomy
has two cusps, or leaflets, (the anteromedial leaflet and the posterolateral leaflet) that guard the opening. The opening is surrounded by a fibrous ring known as the mitral valve annulus. The anterior cusp protects approximately two-thirds of the valve (imagine a crescent moon within the circle, where the crescent represents the posterior cusp). Note that although the anterior leaflet takes up a larger part of the ring and rises higher, the posterior leaflet has a larger surface area. These valve leaflets are prevented from prolapsing into the left atrium by the action of tendons attached to the posterior surface of the valve, chordae tendineae. The inelastic chordae tendineae are attached at one end to the papillary muscles and the other to the valve cusps. Papillary muscles are fingerlike projections from the wall of the left ventricle. Chordae tendineae from each muscle are attached to both leaflets of the mitral valve. Thus, when the left ventricle contracts, the intraventricular pressure forces the valve to close, while the tendons keep the leaflets coapting together and prevent the valve from opening in the wrong direction (thus preventing blood to flow back to the left atrium). Mitral valve opens in diastole, allowing blood to flow from the left atrium to the left ventricle. Closes in systole preventing blood from flowing backwards from the LV to the LA.
Mitral stenosis
decreased mitral valve opening, which causes obstruction of flow from the LA to the LV during diastole. Leads to increased pressure within the LA, pulmonary vasculature and right heart. Causes inlucude rheumatic, calcific, obstruction (tumor), prosthetic valve (thrombosis, degeneration, congenital).
Rheumatic mitral stenosis
80% of MS are rheumatic. Only 50% patients report a history of rheumatic fever. Inflammatory condition involving the heart, skin and connective tissues. Complication of URI caused by group A strep. ARF occurs 2-3 weeks after the initial throat infection. Symptoms include chills, fever, migratory arthralgias, fatigue. Inflammation of the heart occurs inflammation of the valvular endocardium leads to chronic rheumatic heart disease. Symptoms of valve dysfunction typically do not manifest for 10-30 years after initial infection.
Clinical presentation of mitral stenosis
dyspnea, due to increase left atrial pressure-> increased pulmonary venous and capillary pressure -> pulmonary edema. Hemoptysis- high pulmonary vascular pressures -> rupture of a bronchial vein into lung parenchyma. Pulmonary hypertension. Right sided heart failure (edema, ascites)- due to the RV working chronically against increased resistance of pulmonary hypertension. Atrial fibrillation- chronically elevated LA pressures lead to LA dilation. Thromboembolic event (i.e. stroke)- stagnant blood flow in the LA may lead to blood colt formation.
Physical exam of mitral stenosis
cardiac auscultation: loud S1 due to the high A-V pressure gradient keeps the MV open until ventricular systole forcefully closes the valve. Opening snap, which follows S2, due to the opening of the stenotic leaflets. The severity of the MS, inversely proportional to the interval between S2 and the 0S. higher LA pressure forces the valve open ealier. Diastolic rumble is a low frequency decrescendo murmur due to turbulent flow across the stenosis valve during diastole. The duration but not the intensity correlates with the intensity of mitral stenosis. EKG shows left atrial enlargement. RVH if pulmonary hypertension has developed. Atrial fibrillation may be see. Echocardiography show left atrial enlargement, restricted opening of MV during diastole, thickened mitral valve leaflets, fusion of commissures (rheumatic mitral stenosis), and MS severity can be estimated by measuring pressure gradients with Doppler or by direct visualization (planimetry).
Mitral stenosis treatment
medications include beta blockers to slow heart rate (slowing heart rate allows more time for blood to cross the mitral valve in diastole), diuretics to treat CHF symptoms, and anticoagulants if afib is present (MS can cause stasis of blood flow in the left atrium, which can lead to thrombus formation and stroke). Mitral valve replacement with either bioprosthetic valves and mechanical valves. Percutaneous balloow mitral valvuloplasty.
Indications for intervention for mitral stenosis
symptoms, atrial fib, and pulmonary hypertension.
Mitral regurgitation
inadequate mitral valve closure such that blood flows backwards, from the ventricle to the left atrium, during systole. May be caused by an abnormality of any component of the mitral valve apparatus (annulus, leaflets, chordae, papillary muscles). Myxomatous degeneration (pathological weakening of connective tissue), which can lead to mitral valve prolapse. Ischemic heart disease can cause papillary muscle dysfunction or rupture. Endocarditis can cause valve deformity or perforation. Rheumatic valve disease. LV enlargement, stretches mitral annulus and/ or papillary muscles. Physical exam shows a holosystolic murmur best heard at the apex with radiation to the axilla. Secondary MR most commonly occurs in patients with severe LV dysfunction and dilation.
Mitral valve prolapse
most often asymptomatic and found on routine physical exam. Clinical course is typically benign with good prognosis. The primary concern is the development of progressive mitral regurgitation over time. Physical exam has midsystolic click due to the sudden tensing of the chordae tendineae and mitral leaflet, followed by a late systolic murmur. Mitral valve prolapse is the most common cause of primary MR.
Hemodynamics of mitral regurgitation
part of the LV stroke volume is ejected backwards into the left atrium. Elevated left atrial colume and pressure causing pulmonary edema and pulmonary hypertension. Decreased forward cardiac output. Volume related stress on the LV (the regurgitated blood returns to the LV along with normal pulmonary blood flow). This may lead to LV dysfunction over time.
Clinical presentation of mitral regurgitation
congestive heart failure presenting as dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea, and edema).
Treatment of mitral regurgitation
medications include diuretics for CHF and afterload reduction (ACE inhibitors, ARBs). Surgery including valve repair (preferred if possible) and mitral valve replacement (bioprosthetic versus mechanical). Mitraclip. Surgical indications for chronic severe MR including symptoms, LV dilation, decreased LV systolic function, new onset atrial fibrillation, and pulmonary hypertension.
Tricuspid valve
opens in diastole to allow blood to flow from the RA to the RV. Closes in systole to prevent blood in the RV from flowing backwards into the RA. The normal tricuspid valve usually has three leaflets and three papillary muscles. They are connected to the papillary muscles by the chordae tendineae, which lie in the right ventricle. Tricuspid valves will not always consist of three leaflets and may also occur with two or four leaflets; the number may change during one’s lifetime.
Tricuspid regurgitation
during systole, the tricuspid valve does not close adequately and blood flows backwards into the RA. Elevated RA pressure leads to increased venous pressure. LE edema, ascites, and hepatic congestion. 80% of cases of significant TR are functional. This is secondary to annular dilation and leaflet tethering in the setting of RV dilation from volume and or pressure overload. Other causes include rheumatic disease, congenital disease (Ebstein’s), endocarditis, radiation, carcinoid, trauma from endomyocardil biopsy, and pacemaker leads.
Causes of tricuspid regurgitation
structural abnormality of the TV including congenital, ebstein anomaly, TV dysplasia, TV hypoplasia, TV cleft, double orifice TV, and unguarded TV orifice. Acquired causes include endocarditis, trauma, carcinoid heart disease, rheumatic heart disease, TV prolapse, and latorgenic (radiation, drugs, biopsy, device lead). Functional (morphologically normal leaflets with annular dilatation) causes include idiopathic tricuspid annular dilation, RV dysplasia, endomyocardial fibrosis, primary PHT, secondary PHT, atrial septal defect, and anomalous pulmonary venous drainage. Most common cause of TR is functional valve disease related to RV pressure/ volume overload.
Physical exam findings with tricuspid regurgitation
jugular venous distention with a visible systolic “v” wave in 35-75% of patients. Hepatomegaly is present in 90% of patients, but systolic pulsation of the liver is noted inconsistently. Classically the holosystolic murmur of tricuspid regurgitation is heard along the sternal boarder and increases in intensity with inspiration.
Tricuspid regurgitation symptoms
fatigue from low cardiac output, abdominal fullness, edema, palpitations (if atrial arrhythmias are present), and hepatic congestion/ dysfunction may occur due to elevated RA pressure.
Treatment of tricuspid regurgitation
if functional TR, treat the underlying cause of RV pressure/ overload. Medications include diuretics. Surgery including tricuspid repair and tricuspid replacement.
Indications for surgery for tricuspid regurgitation
severe TR in patients undergoing left-sided valve surgery. TV repair in patients with less severe TR with tricuspid annular dilation or evidence of right heart failure. Symptomatic severe TR unresponsive to medical therapy. Asymptomatic severe TR and progressive RV dilation or dysfunction.
Tricuspid stenosis
rare. Usually from rheumatic heart disease. Murmur is similar to that of mitral stenosis, but is heard closer to the sternum and intensifies with inspiration. Symptoms include dyspnea and edema. Often occurs simultaneously with mitral stenosis. Causes include rheumatic heart disease, congenital TS, RA tumors, carcinoid heart disease, endomyocardial fibrosis, valvular vegetations, extracardiac tumors. Treatment includes diuretic and TV surgery (severe TS at the time of operation for left-sided valve disease) for isolated, symptomatic severe TR.
Aortic stenosis
Once thought a degenerative disease, the mechanism by which a healthy tricuspid aortic valve becomes stenotic is now believed to be similar to that of atherosclerosis. The tricuspid aortic valves become stenotic in the sixth, seventh, and eighth decades of life, mainly caused by calcium deposits in the valve cusps and not by fusion of the commissures. In developed countries, rheumatic fever has become a very rare cause of aortic stenosis. When the aortic valve is affected by rheumatic heart disease the mitral valve is almost always affected as well. The echocardiogram with Doppler interrogation of the aortic valve serves as the mainstay of diagnosis. Valve replacement is recommended for individuals with symptomatic severe aortic stenosis. Such patients have a dire outlook, with 75% dying within 3 years of symptom onset. The cardinal symptoms of severe aortic stenosis are angina, syncope and shortness of breath
Bicuspid aortic valve
The bicuspid aortic valve is the most common congenital cardiac malformation, occurring in 1% to 2% of the population. The majority of BAV patients develop complications eventually requiring treatment.
Embryology of bicuspid aortic valve
BAVs are the result of abnormal aortic cusp formation during valvulogenesis. Adjacent cusps fuse to form a single aberrant cusp, larger than its counterpart yet smaller than 2 normal cusps combined. BAVs are likely the result of a complex developmental process, not simply the fusion of 2 normal cusps.
Aortic Root in Bicuspid Aortic Valve
After development, BAV is associated with aortic dilation, aneurysms, and dissection . In light of this, the BAVs should be considered a disease of the entire aortic root.
The elastic laminae of the aortic media
In patients with BAV (B), deficient microfibrillar elements result in smooth muscle cell detachment, matrix metalloproteinases (MMPs) release, matrix disruption, cell death, and a loss of structural support and elasticity.
Heredity of Bicuspid Aortic Valve
BAV occurs in 1% to 2% of the population. Familial clustering is compatible with autosomal dominant inheritance with reduced penetrance. Males are affected 4:1. Echocardiographic screening of first-degree relatives is warranted.
Complications of bicuspid aortic valve
valvular complications include Aortic stenosis (Most frequent valvulopathy, AS age 15-65= BAV, AS more rapid in asymetric valves or antero-posterior), Aortic Insufficiency (Cusp prolapse and More complications), and Endocarditis (In 30% of patients, specially the young and with AI). Vascular complications include aortic dilation, aneurysm formation, aortic dissention. It is also associated with coarctaction, PDA, and coronary anomalies.
Management of Bicuspid Aortic Valve
Serial assessment of the aortic valve by echocardiography is a valuable tool to evaluate the functional state of the valve as well as to measure the aortic diameter, chamber dimensions, and ventricular function. Patients with mild-to-moderate valvular dysfunction and normal left ventricular (LV) dimensions and function should be monitored by echocardiography at regular intervals.
Other Forms of Aortic Stenosis
Subvalvular disease: thin membrane (the most common lesion), thick fibromuscular ridge, diffuse tunnel-like obstruction, Hypertrophic Obstructive Cardiomyopathy, abnormal mitral valve attachments, and ccessory endocardial cushion tissue
Key points about bicuspid aortic valve disease
Bicuspid aortic valve disease is the most common congenital cardiac defect (1-2% of babies) . While it can be found in isolation, it is often associated with dilation of the proximal ascending aorta secondary to abnormalities of the aortic media.
Aortic regurgitation
can be caused by valve disease including rheumatic, degenerative, endocarditis, and congenital (bicuspid and quadricuspid). Can also be caused by disease of the aorta including dissection, marfan’s, atherosclerosis, annulo-aortic ectasia, syphilis, ankylosing spondylitis, and osteogenesis imperfecta. Stenosis of the pulmonic valve is one of the more common forms of congenital heart disease. Most of the patients are children however patients with congenital pulmonic stenosis may come to medical attention during adolescence or adulthood. In recent years percutaneous balloon valvuloplasty has largely replaced surgical valvotomy except in patients with dysplastic valves. Huge pulse pressure
Signs of aortic regurgitation
corrigan’s pulse is rapid forceful carotid upstroke followed by rapid decline. Quincke’s pulse is diastolic blanching in nail bed when slightly compressed. De musset’s sign is bobbing of head. Durozie’z sign is systolic and diastolic femoral bruits when compressed with stethoscope. Hill’s sign is systolic BP in legs > 30 mmhg than in arms.
pulmonary wedge pressure or PWP
or cross-sectional pressure (also called the pulmonary arterial wedge pressure or PAWP, pulmonary capillary wedge pressure or PCWP, pulmonary venous wedge pressure or PVWP, or pulmonary artery occlusion pressure or PAOP), is the pressure measured by wedging a pulmonary catheter with an inflated balloon into a small pulmonary arterial branch. Physiologically, distinctions can be drawn among pulmonary artery pressure, pulmonary capillary wedge pressure, pulmonary venous pressure and left atrial pressure, but not all of these can be measured in a clinical context. Because of the large compliance of the pulmonary circulation, it provides an indirect measure of the left atrial pressure. For example, it is considered the gold standard for determining the cause of acute pulmonary edema; this is likely to be present at a PWP of >20mmHg. It has also been used to diagnose severity of left ventricular failure and mitral stenosis, given that elevated pulmonary capillary wedge pressure strongly suggests failure of left ventricular output. Traditionally, it was believed that pulmonary edema with normal PWP suggested a diagnosis of acute respiratory distress syndrome (ARDS) or non cardiogenic pulmonary edema (as in opiate poisoning). However, since capillary hydrostatic pressure exceeds wedge pressure once the balloon is deflated (to promote a gradient for forward flow), a normal wedge pressure cannot conclusively differentiate between hydrostatic pulmonary edema and ARDS. Physiological pressure: 6–12mm Hg.
Consistently high values pulse pressure
If the usual resting pulse pressure is consistently greater than 100 mmHg, the most likely basis is stiffness of the major arteries, aortic regurgitation (a leak in the aortic valve), arteriovenous malformation (an extra path for blood to travel from a high pressure artery to a low pressure vein without the gradient of a capillary bed), hyperthyroidism or some combination. (A chronically increased stroke volume is also a technical possibility, but very rare in practice.) While some drugs for hypertension have the side effect of increasing resting pulse pressure irreversibly, other hypertension drugs, such as ACE Inhibitors, have been shown to lower pulse pressure. A high resting pulse pressure is harmful and tends to accelerate the normal aging of body organs, particularly the heart, the brain and kidneys. A high pulse pressure combined with bradycardia and an irregular breathing pattern is associated with increased intracranial pressure and should be reported to a physician immediately. This is known as Cushing’s triad and can be seen in patients after head trauma related to intracranial hemorrhage or edema.
Low (Narrow) Pulse Pressure
A pulse pressure is considered abnormally low if it is less than 25% of the systolic value. The most common cause of a low (narrow) pulse pressure is a drop in left ventricular stroke volume. In trauma a low or narrow pulse pressure suggests significant blood loss (insufficient preload leading to reduced cardiac output). If the pulse pressure is extremely low, i.e. 25 mmHg or less, the cause may be low stroke volume, as in Congestive Heart Failure and/or shock. A narrow pulse pressure is also caused by aortic valve stenosis and cardiac tamponade.
pulsus tardus et parvus
also pulsus parvus et tardus, slow-rising pulse and anacrotic pulse, is a sign where, upon palpation, the pulse is weak/small (parvus), and late (tardus) relative to its usually expected character. It is seen in aortic valve stenosis. Typical findings in aortic stenosis include a narrow pulse pressure, left ventricular hypertrophy, a harsh late-peaking crescendo-decrescendo ejection systolic murmur heard best at the right second intercostal space with radiation to the carotid arteries, and a delayed slow-rising carotid upstroke (pulsus parvus et tardus). A weak S2 and/or an S4 may also be noted.
Cardiac myxoma
Benign Neoplasm. Most common primary tumor of heart in teens and adults. Frequency: Rare. Location: Left atrium»_space; right atrium and other sites - Structure: pedunculated or sessile; Ball-valve obstruction and damage (mitral valve most commonly involved). Fragments can embolize into systemic circulation and lodge in brain, kidneys or other organs. Can cause syncope or sudden death. Small uniform cells-> not malignant. Tend to have gelatinous look.
Other primary neoplasms found in heart
Lipoma (benign). Rhabdomyoma (benign), made of skeletal muscle cells
and is the most common primary cardiac tumor of infancy/childhood. It is a hematoma or congenital malformation made of skeletal muscle. Angiosarcoma (malignant), tumor of blood vessels, poor prognosis. Thrombus (blood clot), not really a neoplasm but often presents as a “mass” in the heart
Neoplastic: metastatic/ hematopietic
Woman with a history of ductal carcinoma
of the breast. Can have metastasis to the inside of the heart (can lead to conduction problems) or the pericardium (restrictive pericarditis). Metastatic poorly differentiated carcinoma, consistent with breast primary. These tend to sit on the outside of heart, preventing relaxation. Even small tumors can cause death because it can interrupt normal function such as electric conduction.
Causes of inflammatory/ infectious myocarditis
infectious causes include viral (coxsackievirus), bacterial ( chlamydiae, ricketssiae), fungal (candida), parasitic (protozoa, ehlminths). Immune mediated reacterions causes include postviral, poststreptococcal (rheumatic fever), SLE, drug hypersensitivity (methldopa, sulfonamides), transplant rejection. Unknown causes include sarcoidosis and giant cell myocarditis.
Viral myocarditis
Inflammation (mostly lymphocytes) with injury to the myocardium. Typical viral causes are Coxsackievirus A or B or other enteroviruses.
Autoimmune diseases of the heart
also called Collagen Vascular Diseases (CVD) / Connective Tissue Disease (CTD). Systemic “auto-immune diseases” : variable organ system involvement (i.e., (systemic lupus erythematosus, Scleroderma / Systemic Sclerosis, Rheumatoid Arthritis). Distinguished from Organ-Specific Autoimmune Disease (Lung and Kidney: Goodpasture Disease, Red Blood Cells: autoimmune hemolytic anemia, Thyroid: Graves Disease). Heart involvement as part of systemic disease process: Variable involvement of pericardium, myocardium, endocardium and can have heart blood vessel-focused attack: vasculitis leading to small infarcts
Lipofuscin
the name given to finely granular yellow-brown pigment granules composed of lipid-containing residues of lysosomal digestion. It is considered to be one of the aging or “wear-and-tear” pigments, found in the liver, kidney, heart muscle, retina, adrenals, nerve cells, and ganglion cells.
Toxic-Metabolic Diseases of the heart
toxic effects due to some agents have toxic effects on muscle; mechanism is often not known. Can vary among patients: some sensitive, some not (idiosyncratic). Can be caused by medications such as Adriamycin (chemotherapeutic drug with cumulative dose dependent toxicity). Exogenous substances such as ethanol (or metabolite acetaldehyde) +/- associated nutritional deficiencies. Cobalt from artificial joint prostheses.
Amyloidosis
Proteins deposited: deposition as “beta-pleated sheets”. Plasma Cell Neoplasm/Dyscrasia: e.g. “multiple myeloma” are pumping out immunoglobulin light chain: κ, λ light chain, leading to chronic disease: Amyloid P, and Other: transthyretin / prealbumin. There are also genetics causes: Most cases sporadic, Rare familial amyloidosis. Organs Involved, +/ -Symptomatic: Wax-like consistency: Heart, Kidneys, Nerves, Liver, Spleen. Amorphous desposits are cardiomyocytes separated by fibrosis and amorphous material. Congo red stain shows deposits as salmon orange. If polarized deposits show up as granny apple green.
Developmental/ degenerative heart disease
metabolic/systemic diseases include any diseases that affects muscle
(multiple types of inherited glycogen storage disease or multiple types of muscular dystrophy)
can also affect the heart muscle
Hemochromatosis
a hereditary disease characterized by excessive intestinal absorption of dietary iron resulting in a pathological increase in total body iron stores. The most susceptible organs include the liver, adrenal glands, heart, skin, gonads, joints, and the pancreas; patients can present with cirrhosis, polyarthropathy, adrenal insufficiency, heart failure or diabetes. Heart problems include congestive heart failure, arrhythmias or pericarditis
Cardiomyopathy
heart disease resulting from a primary abnormality in myocardium. Primary myofiber abnormality that can be anatomic or metabolic. Generally excluded (secondary cardiomyopathy) are ischemic disease (ischemic cardiomyopathy), hypertensive disease, and valve-associated abnormality. Clinical significance is that it can lead to mechanical dysfunction and electrical dysfunction.
Cardiomyopathy classification
dilated is impairment of contractility (systolic dysfunction). Hypertrophic is impairment of compliance (diastolic dysfunction). Restrictive is impairment of compliance (diastolic dysfunction.
Dilated cardiomyopathy
Mechanism: Impaired contractility, low ejection fraction. Microscopic myocardial Pathologic Changes are Non-specific; cant diagnose under a microscope. Complications include mural thrombus formation-> systemic embolization. Also because the heart is so large they can develope arrhythmia. Hearts are BIG and dilated (walls may be thick or thin). 30-40% of cases have associated genetic mutations, more yet to be discovered.
Familial forms of dilated and hypertrophic cardiomyopathies
proteins leading to dilated cardiomyopathy desmin, dystrophin, sarcoglycans and lamin a/c (nuclear membrane proteins). Hypertrophic cardiomyopathy 70-80% are cause by three mutations including myosin binding protein C, beta myosin heavy chain and cardiac troponin T
Hypertrophic cardiomyopathy
100% due to genetic mutations. Often due to mutations in the carcomere. Thickened interventricular septum bulges into the left ventricle outflow tract during early systole. Outflow obstruction through aortic valve (~25%) / ejection murmur. Anterior leaflet of the mitral valve may also impinge on septal wall during systole. Complications: sudden death (young athletes). Pathologic Changes: Hypertrophy & disarray of fibers. Cannot relax in diastole (impaired compliance)
Restrictive cardiomyopathy
Cannot relax during diastole (impaired compliance). Typically acquired (not really genetically linked). Amyloid deposition and radiation‐induced fibrosis (are not seen as much anymore) are good examples.
Myosin heavy chain mutation
(MYH7). No treatment available per se. High rate of sudden death noted in literature. Cardiology consultation is critical. Genetic counseling for family.
Hypertension
Left Heart effected by Systemic Hypertension: BP >140/90 Essential (first degree) - “90%”. Usually idiopathic but rule out other possible causes (medication, etc.). Secondary causes include Renal disease (i.e., diabetes, renal artery stenosis), Endocrine (i.e., adrenal neoplasm, steroid medication), and Cardiovascular: e.g. coarctation. Pathogenesis is Sustained pressure overload on the left ventricle leads to concentric hypertrophy of myofibers. Additional sarcomeres / myofibrils added to existing cardiomyocytes
Systemic hypertension
Clinical Manifestations is that it is often silent, so treatment doesn't effect noticeable change for most individuals. Can manifest with headache, dizziness. Complications include Atherosclerosis (turbulent blood flow) and aneurysm, Cerebral vascular disease (blockage or rupture of vessel in the brain), and Ischemic (arteriolosclerosis), Hemorrhage. Kidney is the key cause of "chronic renal disease"; often along with diabetic renal disease. The small vessels in the kidney can also have arteriolosclerosis and glomerulosclerosis. Kidney shrink down due to scaring. Congestive heart failure starts on left side and can lead to pulmonary edema and eventual right heart failure.
Septal myectomy
a cardiac surgery treatment for hypertrophic cardiomyopathy (HCM). The surgery entails removing a portion of the septum that is obstructing the flow of blood from the left ventricle to the aorta. Septal myectomies have been successfully performed for more than 25 years. The alternatives to septal myectomies are treatment with medication (usually beta or calcium blockers) or non-surgical removal of tissue with alcohol ablation.
Normal weight and thickness of heart
Weight: Normal Man 275 – 340 g / Normal Woman 230 – 290 g. Ventricular Thickness-Left: up to 1.5 cm- Right Ventricle: up to 0.4 cm.
Pulsus paradoxus (PP)
also paradoxic pulse or paradoxical pulse, is an abnormally large decrease in systolic blood pressure and pulse wave amplitude during inspiration. The normal fall in pressure is less than 10 mm Hg. When the drop is more than 10 mm Hg, it is referred to as pulsus paradoxus. Pulsus paradoxus is not related to pulse rate or heart rate. The normal variation of blood pressure during breathing/respiration is a decline in blood pressure during inhalation and an increase during exhalation. Pulsus paradoxus is a sign that is indicative of several conditions, including cardiac tamponade, pericarditis, chronic sleep apnea, croup, and obstructive lung disease (e.g. asthma, COPD).
Microscopic evaluation of hypertrophy
car box nucli, much larger. Same number of myocytes but increased number of sarcomeres.
Pulmonary hypertension
Left Heart
problems can cause right heart failure. Also congenital heart disease (ventricular septal defect) and Left heart failure. Pulmonary and Thoracic Causes (Cor Pulmonale) include Pulmonary Parenchyma Disease, (Emphysema, Interstitial lung disease, Bronchiectasis), Pulmonary Vessel Disease (Pulmonary Emboli, Primary pulmonary hypertension, Sleep apnea), and Chest Movement Alterations (Kyphoscoliosis, Morbid obesity, Neuromuscular: myasthenia gravis, muscular dystrophy, ALS). Passive congestion of liver appears as nutmeg liver, swollen with or without necrosis, which can lead to ascites and lower leg edema.
Developmental/ congenital problems with valves
Types that might not be recognized in the neonatal / childhood period include Hypoplastic valve, Unicuspid aortic valve, and Bicuspid aortic valve. Problem are related to reduced outflow, leading to ventricular hypertrophy and increased turbulence, leading to valve thickening and stenosis. Developmental abnormalities include bicuspid aortic valve.
Acquired valve diseases
Degenerative disease can be “Toxic-Metabolic”, Developmental, or Traumatic. A variety of diseases may damage the cardiac valves and impair their function by causing stenosis and/or regurgitation/ insufficiency resulting in myocardial hypertrophy / dilatation in the cardiac chambers proximal to the abnormal valve. The aortic and mitral valves are the predominant valves involved. The abnormal valves show increased susceptibility to nodular calcification and fibrosis, vegetation formation, and infection. Such changes further complicate the already compromised function of the valve.
Acquired valve diseases
include myxomatous degeneration (mitral valve prolapse) and calcification aortic stenosis.
Myxomatous degeneration
(mitral valve prolapse). Names for valves changes include ballooning, tenting, myxomatous degeneration, and hooding. Most common cause of isolated mitral regurgitation (occurs in ~5% of the population). In most cases, pathogenesis is uncertain. Defect in the metabolism of extracellular matrix. Accumulation of myxomatous extracellular material. Leads to softening / enlargement including ballooning of leaflet(s) (especially of the posterior leaflet) into the left atrium during systole and elongation / fibrosis of the chordae tendinea. Marfan syndrome is a fibrillin defect due to elastic fiber problems. Heart and Aorta have life threatening changes including mitral valve prolapse, aortic ring dilation, and aneurysm of aorta – with possibility of dissection. Asymptomatic in the majority of patients. Complications include regurgitation
and infective endocarditis is a potential complication.
Calcific Aortic Stenosis
can be due to trauma/ response to injury. Degenerative calcific aortic stenosis is most often seen in the elderly, which is called “Senile Calcific Stenosis” or “Degenerative Aortic Stenosis”. Can also be due to underlying valve abnormality. Can lead to left ventricle outflow deficits and to left ventricle hypertrophy. Clinical Correlations: myocardial oxygen demand is increased in the hypertrophied ventricle, blood flow to myocardium via coronaries (limited by the pressure drop across the valve and reduced outflow leading to angina), blood flow to systemic circulation leading to syncope, dizziness. Under a microscope, connective tissue is separated by bluish myxoid material, leading to a thickened valve and possible calcification.
Post-Infectious heart disease
Antibody mediated. Can be due to rheumatic fever, vegetations, non-infectious endocarditis
Rheumatic Fever
is due to group A Streptococcus (Strep. pyogenes). Antibodies against M protein of Group A Streptococcus cross-react with body’s own glycoproteins. Systemic Effects: Criteria for Diagnosis of Acute Rheumatic Fever (by Jones Criteria). The major Criteria include “Pancarditis” in the heart, “Migratory polyarthritis” in the joints, “Erythema marginatum and subcutaneous nodules in the skin, “Sydenham chorea” (involuntary movement) in the CNS. Minor criteria
include fever, arthralgias, elevated “acute phase reactant“. Evidence of Streptococcal infection (positive throat culture or antibodies against antistreptolysin O). “Pancarditis” occurs 10 days - 6 weeks after pharyngitis episode (~3% of patients) and can have chronic effects of myocardial damage. Endocardium: Endocarditis: Valve damage / necrosis leading to fibrosis and increases susceptible to “vegetation“ formation on valves. Myocardium: Myocarditis: “Aschoff bodies” = collection of mononuclear cells. Pericardium: Fibrinous pericarditis leading to fibrosis / adhesions Symptoms: Acute: arrhythmia, tachycardia, pericardial friction rub- may be mostly “asymptomatic,” lost in the prodrome of “rheumatic fever“. Chronic: major manifestation is mitral and aortic valve disease. Over time findings include valve leaflets and cusps (fibrosis, fusion, calcification) and chordea tendinea (including fibrosis, fusion, and shortening). Complications include valves that can’t open (stenosis) or close (regurgitation) normally, which can progress to heart failure and susceptibility to infective endocarditis
Time line of rheumatic heart disease
initial group A strep. 2-6 weeks later acute rheumatic fever. Many years or decades later rheumatic heart disease.
Vegetations on valves
can be Sterile / Marantic / Non-Bacterial Thrombotic Endocarditis. Definition is thrombus (clot) formation on valve and is sterile = no organism. Etiology - in Damaged Valve, can be due to rheumatic heart disease or lupus (causing “Libman-Sachs Endocarditis”) or in normal Valve can be due to Hypercoagulable state. Complications include Embolism, Valve function deficits – especially when large, and Potential to become infected: fertile culture medium
Infective Endocarditis
Definition: Primary infection of normal valve or damaged valve. Blood culture key in attempt to identify causative organism (the organism is not identified in some cases). Bacteria – most common: sources include skin/oral flora/GI tract. Normal Valves are more commonly infected by virulent organisms (i.e., Staph aureus). Abnormal “vulnerable” valves: even relatively “benign” bacteria can be implicated (Strep. viridans 50 - 60% of cases). Virulent organisms can attack diseased valves too. Fungal organisms can occur but considerably less common than bacterial organisms
Risk factors for endocarditis
Bacteremic episodes allow organisms to be implanted on the valve / endocardial surfaces such as Dental procedures (and brushing one’s teeth too), Surgical procedures, Venous access for interventional and catheterization purposes (indwelling access lines), Venous access for intravenous drug abuse passing through non- decontaminated skin. Mucosal injuries (anywhere in the GI system): e.g. Diverticulitis and Skin injuries. Acute Endocarditis has acute onset / high mortality. Highly virulent organisms (Staph aureus), which can destroy the valve leaflets resulting in perforation and incompetence with acute onset congestive heart failure (often seen in IV drug users). Can infect normal and abnormal valves. Subacute Endocarditis has insidious onset (fever, weight loss). Complications include “Septic Emboli” – to heart, various organs, skin (“Janeway lesions”). Compromised valve function due to damage by bacteria and inflammatory response
Bipolar limb leads
Lead I is bipolar with the positive electrode at the left arm and the negative electrode at the right arm. Lead II is positive in the left leg and negative in the right arm. Lead III is positive in left leg and negative in left arm.
The unipolar augmented leads
share the frontal plane of the heart with the bipolar leads. aVR is positive in the right arm, aVL is positive in the left arm and aVF is positive in the left leg.
Chest leads
The chest leads are placed on the front of the chest at the locations shown above. The leads are unipolar and reflect changes in the horizontal plane, Leads V1 & V2 are close to the right ventricle. Increased voltage from right ventricular hypertrophy is seen there. In addition V1 and V2 are close to the septum. Septal infarcts are most evident in these leads. Leads V5 and V6 are close to the left ventricle, especially its anterolateral portion. Increased voltage from left ventricular hypertrophy and changes from anterolateral infarcts are most evident in V5 and V6
The QRS axis
Because of its greater muscle mass the dominant producer of voltage is the left ventricle. Normal depolarization of the ventricles goes from right to left and downward from the right arm towards the left leg. Lead aVR which has its positive electrode to the upper right (right arm) is negative since all forces are away from it leftward and downward. Leads I and II are positive because forces are going towards their positive electrodes on the left arm and left leg respectively. V1 and V2 are mostly negative because predominant forces are away from the right ventricle. By near-consensus, the normal QRS axis is defined as ranging from -30° to +90. -30 to -90 is referred to as a left axis deviation (LAD). +90 to +180 is referred to as a right axis deviation (RAD). Normal axis is positive in both leads I and II. Left axis is positive in lead I and negative in lead II. Right axis is negative in lead I and positive in lead II. Indeterminate axis is negative in both leads I and II.
Causes of widened QRS
When the right bundle or left bundle is blocked or there is an ectopic ventricular beat, conduction of the QRS is outside the specialized conduction system and the QRS is wide. If the right bundle is blocked there are late forces to the right ventricle. This results in a tall late positive deflection (an R prime) in V1 and V2 (rt sided leads) and a negative deflection, a wide S wave in I and V6 (away from these left sided leads). When the left bundle is blocked there is high voltage generated in the left ventricle. The QRS is widened and all forces are away from the rt. sided leads (V1) and towards the left sided leads (V6).
Hemiblocks cause axis shifts without widening the QRS
Distal blocks in the left bundle cause axis shifts. Blocks in the anterior fascicle cause left axis deviation. Posterior fascicle block causes right axis deviation. The QRS is not prolonged significantly.
Ventricular hypertrophy and ECG
Left ventricular hypertrophy causes large positive deflections (R waves in V5 & V6 (lt. sided leads) and large negative
deflections (S waves) in V1 (rt. sided lead). In right ventricular hypertrophy there is high voltage in V1 and V2.
Ischemia and EKG
ischemia occurs when blood supply is insufficient to meet oxygen demand in the ventricles. Ischemic changes in the EKG alter ventricular repolarization and affect the ST segment and the T wave. Ischemia due to sudden high oxygen demand in the presence of fixed coronary obstruction causes depression of the ST segment. Ischemia due to acute coronary artery obstruction during low oxygen demand causes T wave inversion.
Stress-induced myocardial ischemia
The resting ST segment is normal but during exercise there is ST depression due to transient ischemia.
ECG of acute coronary syndrome
Normally T waves and the QRS go in the same direction. Here the T wave is inverted, a sign of ischemia. This could be transient or result ultimately in tissue injury.
Transmural current of injury
ST elevation is the classical sign of transmural injury in an acute coronary syndrome, usually with a clot due to platelet aggregation obstructing a coronary artery. Most commonly the injury is associated with an acute myocardial infarction. However, if the obstructed artery is quickly opened with angioplasty or a thrombolytic agent the ST elevation may partially or entirely reverse and much, or rarely all, injury avoided.
Q waves
Although very small Q waves may not be pathological, usually development of a sizable Q wave in at least two adjacent leads is due to transmural necrosis. Typically sizable means at least one small box wide (≥0.04 seconds). Infarcts usually involve only the left ventricle. When Q waves develop in leads which would normally be positive they give information on localization of the infarct. Q waves in inferior leads (II,III, aVF) are due to inferior infarcts. Q waves in leads V1-V4 are due to anterior wall infarcts. Leads I, aVL and the anterolateral leads (V5,V6) are associated with lateral wall infarcts.
Evolving transmural myocardial infarct ECG
Typically a transmural acute myocardial infarct evolves over time as shown on the left. There is an early stage that is rarely seen, because it often lasts only a few minutes in which there are giant, upright “hyperacute” T waves. Subsequently the T wave inverts (“ischemia”) and the ST segments then rise (“current of injury”). Sometimes the ST elevation precedes or occurs simultaneously with the T inversion. Q waves are usually the last ECG findings to develop.
Mechanical effects of inspiration on heart functions
Left ventricular stroke volume decreases during inspiratory efforts whether lung volume is actually increasing as in normal inspiration or whether it remains constant as in a Mueller Maneuver (M.M.). Explanations have included phase lag between lung volume changes and left ventricular volume changes during inspiration as well as increased capacity of pulmonary vessels due to inflation. The capacitance changes could not be used to explain stroke volume (SV) fall in Mueller Maneuvers where lung volume is constant. The increased negative pleural pressure may be responsible for increases in right heart volume due to increased venous return. This mechanism has also been suggested as one of the causes of the fall in left ventricular stroke volume by ventricular interdependence due to changes in left ventricular pressure/volume (P/V) relations, i.e., compliance. In all these explanations a decrease in left ventricular diastolic filling and decreased diastolic pressure is assumed. The fact that decreases in pleural pressure may also act like an increase in left ventricular afterload and impede outflow, thereby decreasing stroke volume, has not been generally considered. We found that left ventricular stroke volume can still decrease without a decrease in left ventricular filling and even when increases in venous return have been prevented (right-heart bypass, i.e., constant pulmonary inflow). Thus the fall in stroke volume during inspiratory effort appears to be caused by a variety of factors, among which increased left ventricular afterload must be considered of primary importance. In addition, decreased left ventricular diastolic compliance due to increased right ventricular (RV) volume also has to be considered (interdependence).
Transmural vs subendocardial myocardial infarct ECG
Transmural infarcts involve the full thickness of the left ventricular wall and tend to be large. Smaller infarcts may be localized to the inner layer of the left ventricular wall, the subendocardium. Subendocardial infarcts do not have Q waves or ST elevation. They do have persistent ST depression. Whereas ST depression may reflect transient ischemia without necrosis, ST depression lasting two or three days probably reflects a subendocardial infarct.
Pericardial disease
The pericardium is a fibroelastic sac with visceral and parietal layers. The visceral layer dirtectly abuts the epicardium, the outer portion of the myocardium. A very small quantity of fluid is normally present between the two layers. However, in certain diseases large quantities of fluid may accumulate in theis pericardial space. There are four types of pericardial disease: Acute Pericarditis. Pericardial Effusion without hemodynamic compromise. Cardiac tamponade in which excessive pericardial fluid compresses the heart and reduces cardiac output. This is an acute emergency. Constrictive Pericarditis, a chronic process in which the pericardium thickens to the point where it compresses the heart to the point where it limits cardiac output.
Dressler’s syndrome
a secondary form of pericarditis that occurs in the setting of injury to the heart or the pericardium (the outer lining of the heart). It consists of fever, pleuritic pain, pericarditis and/or a pericardial effusion.
Beck’s triad
is a collection of three medical signs associated with acute cardiac tamponade, an emergency condition wherein fluid accumulates around the heart and impairs its ability to pump blood. The signs are low arterial blood pressure, distended neck veins, and distant, muffled heart sounds.
Acute pericarditis
commonest causes: Viral illness, Connective tissue or autoimmune diseases, Uremia, and Metastatic tumors. Commonest presentation: Sudden onset chest pain - often severe Chest pain varies with position and breathing. Diagnosis is made based on chest pain varies with position and breathing, pericardial rub on cardiac exam, EKG shows diffuse ST elevation, ECHO shows pericardial fluid, and response to anti-inflammatory agents. RX includes Ibuprofen 300-800 mg p.o. every 6 to 8 hours. Ibuprofen is the nonsteroidal anti-inflammatory drug of choice but others may be effective as well. Aspirin 325-650 mg is an alternative. Acute pericarditis of ECG shows ST segment elevation (injury) involving most of the heart (diffuse).
Pericardial effusion
common causes include viral or acute idiopathic pericarditis, metastatic malignancy, uremia, autoimmune disease, and hypothyroidis. It is best diagnosed by xray or echocardiogram. Small effusions without high intrapericardial pressure may be asymptomatic. Large effusions with high intrapericardial pressures cause cardiac tamponade where myocardial compression impairs diastolic filling.
Pericardial effusion
The key point about pericardial tamponade is that because of the high intrapericardial pressure there is impaired filling of the right side of the heart. This decreases right ventricular output. Therefore, the lungs are not congested. This contrasts with dilated cardiomyopathy where the dilated heart is associated with pulmonary venous congestion in the lungs. With inspiration there is increased filling of the right ventricle but this impinges on the left ventricle lowering stroke volume. Paradoxical pulse with a fall in systolic pressure >10 mmHg during inspiration occurs. Electrical alternans on the ECG reflects movement of the heart back and forth within a sea of fluid with each beat.
Constrictive pericarditis
cause is often scarring and loss of elasticity of the pericardium. It is a chronic disease that usually takes considerable time to develop. Cardiac silhouette usually normal size but encased by thickened pericardium. Lungs not congested because constriction selectively impairs filling of right ventricle. Often mistaken for liver disease because prolonged high venous pressure causes hepatic enlargement and ascites. Filling occurs very abruptly only in early diastole. Unlike the normal filling curve there is little or no further filling later in diastole. In addition the diastolic filling pressures are very high and equalized between the right and left ventricles. Normally during diastole the RV pressure is much lower than the LV. Common etiologies includes idiopathic, after cardiac surgery, radiation, and infection. Pathophysiology is impaired diastolic filling with normal systolic function. Presentation is elevated jugular venous pressure, hepatomegaly, edema, ascites, and tachycardia. Diagnosis is based on echocardiogram, xray (thickened or calcified pericardium). Treatment is surgical stripping of the pericardium. Catherization in constrictive pericarditis shows a dip and plateau (square root sign) during diastole and equalization of diastolic pressures between LV and RV.
Distinguishing Pericardial pain from Other Causes of Chest Pain
The distinguishing symptomatic feature of pericardial pain is that it is “pleuritic” i.e. aggravated by deep breathing and “positional” i.e. relieved by sitting up or other postural changes. Pain from acute coronary syndromes is not altered by breathing, cough or positional changes. Pain from acute pulmonary embolus may be pleuritic but lacks the electrocardiographic changes of pericarditis or a pericardial rub and often occurs in conjunction with recent surgery or after long automobile or plane travel in which deep vein thrombosis, often with localized tenderness, occurs in the lower extremities. Pneumonias may also present with pleuritic pain but there are generally localized rales in the ling fields and sputum production.
Distinguishing Pericardial Tamponade from Congestive Heart Failure
In tamponade the major impairment is in right heart filling during diastole. In congestive heart failure there is usually no impairment in right heart filling but diminished myocardial function causes pulmonary and systemic congestion. In common features - tamponade and CHF: Distended neck veins, tachycardia, low blood pressure, large cardiac silhouette on xray.
Differences between pericardial tamponade and congested heart failure
In tamponade the lungs are usually clear on physical exam and xray but in CHF the lungs are congested with presence of rales on exam and redistribution of blood flow to the upper lobes along with other xray findings. Pulsus paradoxus is expected in tamponade and rare in CHF. In tamponade heart sounds tend to be distant and the apex may not be palpable, whereas in CHF it is more common to have normal heart sounds often with murmurs and an S3, and presence of ventricular lifts. Low voltage and pulsus alternans are common in tamponade and infrequent in CHF. Echocardiograms are distinctly different. In tamponade a large pericardial effusion, right atrial collapse, and lack of normal decrease in inferior vena cava diameter are present. In CHF poor contractile function and dilation of the ventricles are typical but the distinctive findings of tamponade are absent.
Common Features between Pericardial Tamponade and Constrictive Pericarditis
Reduced diastolic function with preserved systolic function. Jugular venous distention Tachycardia and tendency to low blood pressure
Differences between Pericardial Tamponade and Constrictive Pericarditis
Tamponade has a large cardiac silhouette on xray whereas the silhouette is often normal and may have pericardial calcification in constriction. Pulsus paradoxus is present in tamponade and uncommon in constriction. Constrictive pericarditis typically develops very slowly over considerable time and is often accompanied by hepatic congestion, ascites and marked pedal edema whereas these findings are uncommon in tamponade which tends to develop more quickly. The echocardiogram demonstrates pericardial fluid, and right atrial collapse with inspiration in tamponade but these are absent in constriction.
S4
when audible in an adult is called a presystolic gallop or atrial gallop. This gallop is produced by the sound of blood being forced into a stiff or hypertrophic ventricle. “ta-lub-dub” or “a-stiff-wall”. It is a sign of a pathologic state, usually a failing or hypertrophic left ventricle, as in systemic hypertension, severe valvular aortic stenosis, and hypertrophic cardiomyopathy. The sound occurs just after atrial contraction at the end of diastole and immediately before S1, producing a rhythm sometimes referred to as the “Tennessee” gallop where S4 represents the “Ten-“ syllable. It is best heard at the cardiac apex with the patient in the left lateral decubitus position and holding his breath. The combined presence of S3 and S4 is a quadruple gallop, also known as the “Hello-Goodbye” gallop. At rapid heart rates, S3 and S4 may merge to produce a summation gallop, sometimes referred to as S7. Atrial contraction must be present for production of an S4. It is absent in atrial fibrillation and in other rhythms in which atrial contraction does not precede ventricular contraction. Rarely, there may be a third heart sound also called a protodiastolic gallop, ventricular gallop, or informally the “Kentucky” gallop as an onomatopoeic reference to the rhythm and stress of S1 followed by S2 and S3 together (S1=Ken; S2=tuck; S3=y). “lub-dub-ta” or “slosh-ing-in” If new, indicates heart failure or volume overload.
S3
It occurs at the beginning of diastole after S2 and is lower in pitch than S1 or S2 as it is not of valvular origin. The third heart sound is benign in youth, some trained athletes, and sometimes in pregnancy but if it re-emerges later in life it may signal cardiac problems, such as a failing left ventricle as in dilated congestive heart failure (CHF). S3 is thought to be caused by the oscillation of blood back and forth between the walls of the ventricles initiated by blood rushing in from the atria. The reason the third heart sound does not occur until the middle third of diastole is probably that during the early part of diastole, the ventricles are not filled sufficiently to create enough tension for reverberation. It may also be a result of tensing of the chordae tendineae during rapid filling and expansion of the ventricle. In other words, an S3 heart sound indicates increased volume of blood within the ventricle. An S3 heart sound is best heard with the bell-side of the stethoscope (used for lower frequency sounds). A left-sided S3 is best heard in the left lateral decubitus position and at the apex of the heart, which is normally located in the 5th left intercostal space at the midclavicular line. A right-sided S3 is best heard at the lower-left sternal border. The way to distinguish between a left and right-sided S3 is to observe whether it increases in intensity with inspiration or expiration. A right-sided S3 will increase on inspiration, while a left-sided S3 will increase on expiration.
Kussmaul sign
a paradoxical rise in jugular venous pressure (JVP) on inspiration. It can be seen in some forms of heart disease and is usually indicative of limited right ventricular filling due to right heart failure. The differential diagnosis generally associated with Kussmaul sign is constrictive pericarditis, as well as with restrictive cardiomyopathy. With cardiac tamponade, jugular veins are distended and typically show a prominent x descent and an absent y descent as opposed to patients with constrictive pericarditis (prominent x and y descent), see Beck’s triad
