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

Английски оригинал Перевод на български



Fig. 1-1. Basic circulatory circuit. Deoxygenated blood from the right side of the body travels to the right heart by way of the venous system. The right hearts pumps this blood to the lungs via the pul­ monary artery. The lungs oxygenate this blood and send it to the left heart by way of the pulmonary veins. This oxygenated blood is pumped by the left heart through the aorta to the body.


Фиг. 1-1. Основна кръвоносна верига. Деоксигенираната кръв от дясната страна на тялото преминава към дясното сърце по венозната система. Дясното сърце изпомпва тази кръв към белите дробове чрез белодробната артерия. Белите дробове окисляват тази кръв и я изпращат в лявото сърце чрез белодробните вени. Тази оксигенирана кръв се изпомпва от лявото сърце през аортата към тялото.

thegreenmarker 24.09.20 в 1:10

Fig. 1-2. Heart chambers and valves. There are four heart valves. The two atrioventricular valves (mitral and tricuspid) lie between the atria and the ventricles, and the aortic and pulmonic valves lie between the ventricles and their outflow vessels (aorta and pul­ monary artery). During systole, the ventricles con­ tract, fo rcefully expelling blood into the outflow vessels; while this occurs, the atrioventricular valves prevent backflow of this blood from the ventricles to the atria. During diastole, the ventricles relax and fill with blood from the atria; while this occurs, the aortic and pulmonary valves prevent backflow of the blood that has just been ej ected during systole. Mnemonic for the atrioventricular (AV) valves: The tricuspid is on the right. The mitral is on the left.


Фиг. 1-2. Сърдечни камери и клапани. Има четири сърдечни клапи. Двете предсърдно-камерни клапи (митрална и трикуспидална) лежат между предсърдията и камерите, а аортната и пулмоналната клапа се намират между камерите и техните изходящи съдове (аорта и белодробната артерия). По време на систола камерите се съкращават, като изхвърлят кръвта в изходящите съдове; докато това се случва, предсърдно-камерните клапи предотвратяват обратния поток на кръв от камерите към предсърдията. По време на диастола камерите се отпускат и се пълнят с кръв от предсърдията; докато това се случва, аортните и белодробните клапи предотвратяват обратния поток на кръвта, която току-що е била изведена по време на систолата. Мнемоника за запомняне на предсърдно-камерните (AV) клапи: ТрикуспиДалната е вДясно. МитраЛът е вЛяво.

thegreenmarker 24.09.20 в 1:17



We will first discuss the manifestations and treat­ ment of heart failure as a means of reviewing cardiac physiology. Following this, we will examine the four components of the heart (muscle, valves, electrical system, and blood supply), how each can be affected by disease, and the pathophysiological and clinical man­ ifestations of such diseases.


Left Heart Failure


Fig. 1-3A. Left heart failure. Consider a patient who gets short of breath with activity. Shortness of breath means that the lungs are somehow affected. The lungs may be affected directly (by pulmonary disease) or in­ directly (e.g., by cardiac disease). How could cardiac disease affect the lungs? Imagine that a patient's left ventricle cannot pump as well as it should (the causes of such pumping problems comprise the bulk of this chapter). This would decrease the flow from the left heart to the body, which in turn would cause blood to back up into the pulmonary vasculature (Fig. 1-3A). This backup increases pressure in the pulmonary veins, causing transudation of fluid into the lungs. This results in pulmonary edema, which causes short­ ness of breath (dyspnea). The name congestive heart failure comes from the congestion in the lungs caused by backup of flow from a failing left heart. On physical exam, you might hear crackles in the bases of the lungs as a result of this ex­ cess fluid. The worse the failure and the more fluid in the lungs, the higher up in the lung fields these crack­ les will be heard (as the lungs fill with fluid from the bottom up).


Right Heart Failure


Fig. 1-3B. Left heart failure as a cause of right heart failure. The right ventricle is not nearly as strong as the left ventricle, since it only squeezes into the low-pres­ sure pulmonary system, whereas the left ventricle must squeeze into the higher-resistance systemic vascula­ ture. The right ventricular walls are thus thinner than the walls of the more muscular left ventricle. Any dis­ ease process that increases resistance in the pulmonary vasculature (pulmonary hypertension) can cause the right heart's job to be increasingly difficult for this thin­ ner-walled ventricle. Because backup of flow in left heart failure can increase pressure in the pulmonary vasculature, left heart failure can cause pulmonary hy­ pertension and subsequent right heart failure.


Fig. 1-3C. Right heart failure. If the right heart fails, now where does the blood back up? Where does the blood in the right heart come from? The simple answer is the body; more specifically, the venous return from the body via the superior and inferior venae cavae. What would you expect to see on physical exam if the venous return backs up? An elevated jugular venous pressure (JVP). The jugular veins in the neck are a straight shot to the superior vena cava, which is a straight shot to the right heart. The JVP thus serves as a sort of barometer of right heart pressure. Where else would the blood back up? Backup can reach the liver, the abdomen, and the rest of the body via the in­ ferior vena cava. Thus, ascites (fluid in the abdomen), hepatic congestion, and peripheral edema (fluid in the ankles, legs, etc.) can be signs of right heart failure.


Symptoms and Signs of Heart Failure


We have been discussing how a failing heart causes blood to back up . A failing heart also has trouble main­


taining fo rward flow - this was the whole reason for


this backup in the first place. What symptoms might be caused by decreased forward flow? Decreased blood flow to the muscles and the rest of the body can result in fatigue, weakness, and shortness of breath. De­ creased blood flow to the brain may cause drowsiness or changes in mental status.


Fig. 1-4. Symptoms and signs of heart failure. Orthop­ nea and paroxysmal nocturnal dyspnea are two addi­ tional symptoms that can appear in heart failure. Orthopnea: The classic story is that a patient gets very short of breath upon lying down. Why? What changes physiologically when one lies down? When one is standing, gravity causes venous blood to pool in the feet. When one lies down, all of this blood can find its way back to the heart more easily, suddenly increas­ ing the heart's work. Normally, the heart can handle it, but a weak and failing heart cannot, and the blood backs up into the lungs, causing shortness of breath. You can ask the patient, "How many pillows do you sleep on?" Of course, some people just like to sleep on a lot of pillows, but if you ask, ''What would happen if you were to lie flat?'', a patient with heart failure may tell the classic story that s/he cannot breathe as easily when lying flat.


A related symptom is paroxysmal nocturnal dysp­ nea. The pathophysiology is the same, though the end result is that the patient wakes up in the middle ofthe night coughing and short of breath, classically resolv­ ing when the patient gets up and goes to the window for air.


Preload, Afterload, and Treatment of Heart Failure


Preload is the pressure that fills the ventricles during diastole, and afterload is the resistance that the heart faces during systole. More specifically, preload is the blood pressure in the left ventricle at the end of dias­ tole, right before the ventricles contract. Where does this come from? Originally, the preload comes to the heart from the venous system. Afterload is the sys­ temic vascular resistance, or the resistance to flow in the arterial tree against which the heart must work (afterload is created by the arteries).


Fig. 1-5. Treatment of heart failure. In heart fail­ ure, there is decreased forward flow and increased backup of flow. The goals of therapies are thus to increase fo rward flow and decrease backup of flow. To increase forward flow, cardiac output must be increased. To decrease backup, the workload on the heart must be decreased.



Increasing forward flow by increasing car­ diac output can be accomplished by one of two ba­


sic mechanisms:


- Increase the fo rce of ventricular contraction (in­


otropes, e.g., digoxin/digitalis, dopamine/dobuta­ mine, amrinone/milrinone)


Decrease the rate of contraction to increase filling time (beta-blockers, e.g., propranolol, metopro­ lol). The increase in filling time allows more blood to accumulate in the ventricles before con­ traction, leading to a subsequent increase in car­ diac output.



Decreasingwork. The heart'sbackupworkby decreasingis to pump thethe heart's preload (грешно!!!)


against the after load. In heart failure, what could be done to preload and afterload to make the heart's job easier? Therapies should decrease pre­ load and decrease afterload. How can preload be reduced? One can decrease venous return by dilating veins, which slows the return of blood from the veins to the heart (nitrates have this action). Also, one can use diuretics, which cause the patient to urinate more, reducing the intra­ vascular fluid volume. Success of diuretic ther­ apy can be monitored by observing the decrease in symptoms/signs related to excess fluid, such as shortness of breath and edema. Arterial dilators decrease afterload (e.g., ACE inhibitors, hydralazine). The Kidneys in Heart Failure


Fig. 1-6. The kidneys in heart failure. Since cardiac output is weak in heart failure, the perfusion pressure in the kidneys decreases. The blood volume itself is not changed, but the pressure at which this volume reaches the kidneys decreases, hence the term effec­ tive blood volume decrease. Effective volume depletion also occurs in cirrhosis.1 When the kidneys sense decreased perfusion pressure, they try to increase this pressure by increasing blood volume. How can the kid­ neys increase blood volume in response to decreased perfusion pressure? Through the renin-angiotensin­ aldosterone system. This system senses decreased re­ nal perfusion and releases renin, which increases conversion of angiotensinogen to angiotensin I. An­ giotensin I is in turn converted to angiotensin II by an­ giotensin converting enzyme (ACE). Angiotensin II causes vasoconstriction, which raises the blood pres­ sure. Angiotensin II also stimulates aldosterone re­ lease from the adrenal gland. This leads to increased sodium reabsorption by the kidneys, which causes wa­ ter to follow it, which increases intravascular volume. The increased vasoconstriction and increased blood volume raise the blood pressure. Additionally, the per­ ceived low volume status causes release of antidiuretic hormone (ADH) from the posterior pituitary. ADH increases water reabsorption in the kidneys, fur­ ther contributing to increased volume and increased blood pressure.


If the heart is already having trouble handling the existing blood volume, are the kidneys and ADH help­ ing by increasing plasma volume in heart failure? No. This increased intravascular volume further aggra­ vates the backup into the lungs and body as discussed above. ACE inhibitors (Fig.l-6) decrease the conversion of angiotensin I to angiotensin II. Reducing angioten­ sin II production decreases both aldosterone release and angiotensin II-induced vasoconstriction, thus in­ hibiting further increase in blood volume and blood pressure. Angiotensin II receptor blockers (ARBs) block the angiotensin II receptor, leading to a similar effect.


Aldosterone itself can be blocked at its receptor by al­ dosterone antagonists such as spironolactone.






We have just discussed the physiologic basis of the clini­


cal manifestations of heart failure, but why does the heart fail? The heart has four components that help it to pump blood: muscle, values, an electrical conduction system, and the heart's own blood supply. If any of these four elements is not working properly, this impedes the heart's ability to pump blood to the tissues, which can lead to both "decreased forward flow'' symptoms/signs (fatigue, weakness, shortness of breath) and increased "backup of flow" symptoms/signs (shortness of breath,


paroxysmal nocturnal dyspnea, orthopnea, edema, ele­ vated JVP). Be it disease of the muscle, valves, electri­ cal system, or coronary vasculature, if the heart is not functioning optimally, these are the sorts of symptoms that can occur. Ischemic heart disease (e.g., angina, my­ ocardial infarction) and inflammation of the heart can also cause chest pain in addition to these symptoms. Although the above symptoms are characteristic of cardiac disease of some sort, they are certainly not exclusive to cardiac disease. For example, shortness of breath can also be due to pulmonary disease, anemia, or anxiety; chest pain can also arise from esophageal, musculoskeletal, or pulmonary disease.


Diseases of the Heart Muscle


The ventricular muscles relax during diastole, accept­ ing blood; they contract during systole, ej ecting this blood. If the musculature thickens (hypertrophy), the ventricle cannot relax as well, and the ventricle cham­ ber size is reduced, decreasing how much blood it can receive (diastolic dysfunction). If the musculature thins and weakens (dilatation), the strength of the ventricular muscle decreases, and it cannot contract as forcefully (systolic dysfunction).


Cardiac Hypertrophy


Fig.l-7A. Cardiac Hypertrophy. Hypertrophy means in­


creased growth. Hypertrophy of cardiac muscle can be caused by genetic disease (hypertrophic cardiomyopa­ thy) or by certain pathophysiologic circumstances. What circumstances make any group of muscles grow big and strong? Hard work. What would cause the heart to have to work hard? Let's take it one side at a time. The left heart squeezes blood to the body, namely to the entire systemic vascular tree via the aorta. This resistance is the afterload: what the heart works against. Thus, one cause of increased strain on the left heart is increased blood pressure in the arteries (hypertension). What else might cause the left ventricle to have to work extra hard? Reviewing figure 1-2, note that blood goes from the left ventricle through the aortic valve to the aorta. In aortic stenosis, the left ventricle has to squeeze hard against the resistance posed by the stenotic aortic valve. Over time, this can cause left ventricular hypertrophy.


What causes right ventricular hypertrophy? Using the same logic, what site of increased resistance would cause the right heart to have to work harder? Since the right heart ejects into the lungs, any process that increases resistance in the pulmonary vasculature (pulmonary hypertension) can lead to right ventricu­ lar hypertrophy and eventual failure. Examples in­ clude left heart failure (Fig. l-3B), pulmonic valve stenosis, and pulmonary causes (Fig. 2-5). Right heart failure secondary to a pulmonary cause is called cor pulmonale.


If any process increases the resistance that the heart must pump against, the heart will have to work harder to squeeze, and can eventually grow big and thick. Although this growth may initially be compen­ satory, it eventually reaches diminishing returns.


Consequences of Cardiac Hypertrophy. First, the increased thickness of the hypertrophied ventricular wall also makes it more difficult to adequately per­ fu se. As the cardiac muscle outgrows its blood supply, ischemia (decreased blood flow/oxygen supply) can oc­ cur, which can result in angina, and/or infarction. Sec­ ond, what does the hypertrophied heart do better than the normal heart, and what does it do worse? The hypertrophy allows the heart to squeeze better, but its thick walls do not relax as well. In addition, the muscle can get so thick that the chamber becomes quite small. Poor relaxation and small chamber size lead to decreased filling ofthe ventricles, which results in decreased cardiac output. Ventricular relaxation occurs during diastole, so since the hypertrophied heart cannot relax as well, cardiac hypertrophy causes diastolic dysfunction. If the heart cannot relax opti­ mally, it cannot fill optimally; thus, forward flow de­ creases and backup of flow occurs. Hypertrophy of the left ventricle can eventually lead to left heart failure symptoms and signs, and right ventricular hypertro­ phy can lead to right heart failure symptoms and signs (Fig. 1-4).


Treatment of Cardiac Hypertrophy. If the hyper­ trophied heart has a smaller chamber size, and does not fill optimally, the treatment(s) of choice should de­ crease heart rate and contractile force, allowing for in­ creased filling and increased cardiac output. Beta blockers and calcium channel blockers accomplish these goals.


Restrictive Cardiomyopathy


In infiltrative diseases, substances can accumulate in


the heart muscle, such as amyloid (which can occur from amyloidosis or multiple myeloma) or iron in he­ mochromatosis. Rarer diseases, such as sarcoid and Pompe's disease, can also lead to infiltration, causing a restrictive cardiomyopathy. The pathophysiology in restrictive heart disease is essentially the same as in cardiac hypertrophy: the heart is stiff and does not re­ lax well (diastolic dysfunction).


Treatment of Restrictive Cardiomyopathy. One treats the underlying cause if possible. Otherwise, the treatment is the same as that for heart failure, aiming to increase forward flow and decrease backup of flow (Fig.l-5).


Cardiac Dilatation


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