CLINICAL PATHOPHYSIOLOGY made ridiculously simple™ / Клинична патофизиология направена изключително лесна: CHAPTER 1. THE CARDIOVASCULAR SYSTEM

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regurgitation of blood into the right atrium and ele­ vated right atrial pressure, the JVP can be elevated, as in tricuspid stenosis. The systolic murmur of tricus­ pid regurgitation is best heard at the left lower ster­ nal border and increases with inspiration.

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Pulmonary Valve

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Pulmonic Stenosis. Unlike aortic stenosis, which typ­

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ically arises from calcification with age, pulmonic steno­ sis is almost always the result of a congenital anomaly of the valve. Since blood passes across this valve during systole, the murmur is systolic (as in aortic stenosis). The murmur of pulmonic stenosis can be heard more prominently over the patient's left upper sternal border.

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Pulmonic Regurgitation. In pulmonary hyperten­ sion, the normally low-pressure system in the lungs de­ velops high pressure. Due to the high pressure, the pulmonary artery may dilate, and this can lead to a separation of the leaflets of the pulmonic valve, result­ ing in pulmonic regurgitation. The murmur occurs dur­ ing diastole, as with aortic regurgitation, though it occurs over the pulmonic valve region (on the patient's left). Pulmonic regurgitation lacks the changes in pulses and blood pressure seen with aortic regurgita­ tion, since the right heart ejects into the lungs, and is thus not responsible for what is measured in the pe­ ripheral pulses.

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Review of Valves 1: Review by Pathology

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Fig. 1-11. Summary of valvular pathology.

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There are four valves, any of which can be regurgi­ tant or stenotic. (A stenotic valve can also be regur­

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gitant. Stenotic valves are hard to open and can also be hard to shut. Thus, a stenotic valve can per­ mit some regurgitation.)

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Aortic stenosis greatly increases the work of the left heart, which can cause hypertrophy (and thus dias­

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tolic dysfunction, associated with S4) and can lead to syncope, angina/infarction, and congestive heart failure. Since blood normally passes forward across the aortic valve during systole, aortic stenosis causes a systolic murmur.

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Aortic regurgitation allows blood to flow back into the heart after systole, thus decreasing systemic

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blood pressure during diastole, resulting in a widened pulse pressure. Increased volume demand on the heart can lead to left ventricular dilatation (and thus systolic dysfunction, associated with S3

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and heart failure symptoms). Since the blood is flowing back after systole, aortic regurgitation causes a diastolic murmur.

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Mitral stenosis increases the pressure in the left atrium, causing it to enlarge. Since blood passes

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across the mitral valve into the left ventricle during diastole, mitral stenosis causes a diastolic murmur.

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Mitraldoes notregurgitationfully preventoccursbackflowwhen acrossthe mitralthe valvevalve

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during systole. This leads to a systolic murmur.

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In both mitral pathologies, increased left atrial pressure leads to increased pulmonary pressure,

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which can cause dyspnea. Also, both mitral patholo­ gies can lead to left atrial dilatation, which can cause atrial fibrillation.

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Though tricuspid and pulmonic valve pathologies do occur, they are rarer than left-sided valvular disease.

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Murmurs can mimic the counterparts on the left, but right heart failure signs/symptoms (elevated JVP, edema) would be predominant (if pathology is severe enough to cause signs/symptoms).

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Review of Valves II: Review by Murmur

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Fig. 1-12. Summary of murmurs.

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Systolic Murmurs occur between Sl and S2. During systole, blood flows across the aortic and pulmonic valves, so stenosis of either of these valves can lead to a systolic murmur. The closed mitral (on the left) and tricuspid (on the right) valves prevent backflow dur­ ing systole (their closure is Sl). If they are incompe­ tent, allowing for regurgitation, this too will create a systolic murmur. The only other direction blood could go during systole would be through a ventricular sep­ tal defect. Thus, causes of a systolic murmur include aortic stenosis, pulmonic stenosis, mitral regurgita­ tion, tricuspid regurgitation, and a ventricular septal defect. Note that a systolic aortic flow murmur can also occur in normal individuals, in pregnant women, or in cases of pathologically increased flow (e.g., in a patient with anemia or a fever).

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Diastolic Murmurs occur between S2 and Sl. Dur­ ing diastole, blood flows across the mitral and tricus­ pid valves, so if either of these is stenotic, this would lead to a diastolic murmur. The closure of the aortic and pulmonic valves (S2) ends systole and begins di­ astole. If this closure is incomplete, blood will leak back during diastole, so aortic and pulmonic regur­ gitation can also lead to diastolic murmurs. Thus, causes of a diastolic murmur include mitral stenosis, tricuspid stenosis, aortic regurgitation, and pul­ monic regurgitation.

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Notice that stenotic valves produce murmurs when blood is flowing in the fo rward I normal direction across them, whereas regurgitant valves produce murmurs when blood is flowing backward/the wrong way across them.

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Diseases of the Electrical System: Arrhythmias

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The electrical system of the heart conducts impulses

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to the cardiac muscle, causing it to contract in an or­ ganized, rhythmic way. An arrhythmia is an abnormal heart rhythm: a rhythm that is too slow, too fast, and/or irregular. If the electrical activity of the heart is uncoordinated, then muscular contraction will be uncoordinated. A ventricular arrhythmia can thus lead to inefficient ventricular contraction, leading to an immediate drop in forward flow. This can cause hy­ potension, syncope, or, in some cases, sudden death.

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Fig. 1-13. The cardiac conduction system. Each cardiac muscle cell (myocyte) spontaneously depolarizes at some intrinsic rate. Cells from different parts of the heart depolarize at different rates. The fastest cells are in the atria. As one moves down the heart, there is a decreasing rate of spontaneous depolarization (i.e., the slowest spontaneous firing rate occurs in ventricular cells). The cardiac myocytes are connected, so the heart beats at the rate of whichever cells are depolarizing the fa stest. The cardiac myocytes that depolarize fastest are those that make up the sinoatrial (SA) node. Sinoatrial node impulses travel to the myocytes of the atria, resulting in their synchronized depolarization and con­ traction. The electrical impulse then travels to the atri­ oventricular (AV) node, where it is held up by a built-in delay before proceeding to the bundle of His and bundle branches. Finally, the electrical signal spreads across the ventricles by way of the Purkinje fibers. This causes the ventricles to contract as a unit.

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Fig. 1-14. Components of the EKG. The P wave repre­ sents the electrical depolarization that occurs just prior to atrial contraction. The flat interval until the next spike represents the time where the impulse is held up in the AV (atrioventricular) node before passing to

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the ventricles (this is called the PR interval). The QRS

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complex represents ventricular depolarization and the T wave represents ventricular repolarization.

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The U wave can sometimes be seen in normal pa­ tients following the T wave, but it is not always visi­ ble. When seen, the U wave may represent further depolarization in the ventricle or repolarization of the Purkinje system. The U wave can become more promi­ nent in bradycardia (slow heart rates) or electrolyte

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abnormalities (e.g., hypokalemia). Fig. 1-15. Bradyarrhythmia (bradycardia) vs. tachy­ arrhythmia (tachycardia). Arrhythmias are first classi­ fied as either too slow (bradyarrhythmia or bradycardia) or too fa st (tachyarrhythmia or tachycardia). The next level of classification is where the aberration is coming from in the conduction pathway (atria vs. ventricles).

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The term arrhythmia can be confusing to musi­ cians, because some of the arrhythmias are in fact perfectly rhythmic, just faster or slower than normal. A heart rate can be regular (i.e., a normal rhythm), regularly irregular (i.e., an abnormal rhythm which is repeated over and over), or irregularly irregular (i.e., a totally random pattern).

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Bradyarrhythmia (Bradycardia)

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Fig. 1-16. Causes of bradycardia. Bradyarrhythmia

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(bradycardia) is usually defined as a heart rate less than 60 beats per minute. For a slow heart rate to oc­ cur, there must either be a problem with the SA node (such that the impulses it is generating are at a slower rate) or there must be a block somewhere in the con­ duction system. Slower heart rates can also occur in normal people (e.g., trained athletes).

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Slow SA Node. Why would the SA node fire more slowly than usual? A decrease in SA node firing rate can be a normal physiological response (e.g., during sleep) or the result of ischemia, certain drugs, or increased vagal tone. Increased vagal tone refers to increased activity of the vagus nerve (cranial nerve X), which provides the parasympathetic input to the heart. The parasympathetic nervous system slows heart rate ("rest and digest"), while the sym­ pathetic nervous system increases heart rate ("fight or flight").

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Fig. 1-15B. Sinus bradycardia rhythm strip. How would bradycardia secondary to a slow SA node look on EKG? The P wave should appear normal and the PR interval (which indicates the conduction of the im­ pulse) should also appear normal. The difference in si­ nus bradycardia would be that the rate would be slowed: the number of P and QRS complexes per unit time will be decreased, but they will appear normal in configuration.

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Abnormal Conduction (Heart Block). In heart block, the sinus node pulses away at its normal rate, but the conduction is blocked somewhere along the route to the ventricles. The block can occur in the AV node, in the bundle of His, or in the bundle branches (Fig. 1-13). There are four types of heart block: First-degree, Second-degree Mobitz type I (also known as Wenckebach), Second-degree Mobitz type II, and Third-degree (also known as complete heart block). Each cell of the heart has its own intrinsic rate. If the pace generated by the SA node slows below the intrinsic rate of cells in the AV node, those cells can escape the pacemaker's rhythm and generate junc­ tional escape beats. If there is heart block at the AV node or below, the ventricular cells can generate es­ cape beats.

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