nursing:cardiac class

Question 1

What is the Bernheim effect and the reverse Bernheim effect?

Question 2

Kindly explain why the left side of the heart is more prone to disease.

Question 3

1. Is it always necessary to examine the cardiovascular system of a

patient in the 45° incline of the head end? Other than convenience for

examining the jugular venous pressure (JVP), does this position have

any other advantage?

2. If the JVP is not visible when the patient is in the upright position, can

one presume it is not raised?

Question 4

The mitral area (of auscultation) normally corresponds with the apex

beat. When the heart is dilated and the apex beat is shifted laterally, will

the mitral area follow the apex beat to its new location or remain at the

place where the apex beat is normally situated?

Question 5

Please explain in detail how to measure the pulsus paradoxus using

a sphygmomanometer.

Question 6

What is the difference between dicrotic pulse and pulsus bisferiens?

Question 7

1. Why does the radial pulse become more prominent when the hand is

lifted overhead?

 

2. Please explain the mechanism of a collapsing pulse. Which is the best

artery to elicit it: radial, brachial or carotid?

Question 8

What is the mechanism of Durozier's sign?

Question 9

What effects o aortic stenosis, aortic regurgitation and coarctation of the

aorta have on systolic and diastolic blood pressure, and why do they

produce these effects?

1. 

• The reverse Bernheim effect occurs when there is right ventricular pressure and volume overload that results in the interventricular septum bulging toward the left ventricle causing left ventricular diastolic impairment. This can cause symptoms of left heart failure and is actually due to right heart failure.
• The Bernheim effect occurs when left heart failure and left ventricular hypertrophy causes the interventricular septum to bulge towards the right ventricle causing right heart failure that sometimes precedes left heart failure. This classically occurs in aortic valve stenosis.

2. Your heart muscle cells may get larger in response to some factor that causes the left ventricle to work harder, such as high blood pressure or a heart condition. As the left ventricle's workload increases, the muscle tissue in the chamber wall thickens. Sometimes, the size of the chamber itself also increases.

Factors that can cause your heart to work harder include:

• High blood pressure (hypertension). This is the most common cause of left ventricular hypertrophy. More than one-third of people show evidence of left ventricular hypertrophy at the time of their diagnosis with hypertension.
• Aortic valve stenosis. This disease is a narrowing of the aortic valve that separates the left ventricle from the large blood vessel leaving your heart (aorta). The narrowing of the aortic valve requires the left ventricle to work harder to pump blood into the aorta.
• Athletic training. Intense, prolonged endurance and strength training can cause the heart to adapt to handle the extra workload. It's unclear whether this athletic type of left ventricle hypertrophy can lead to stiffening of the heart muscle and disease.

Abnormalities in heart muscle cell structure that result in increased heart wall thickness include:

• Hypertrophic cardiomyopathy. This genetic disease occurs when the heart muscle becomes abnormally thick, even with completely normal blood pressure, making it harder for the heart to pump blood.
• Amyloidosis. A condition that causes abnormal protein deposits around the organs, including the heart

3. A thorough cardiovascular assessment will help to identify significant factors that can influence cardiovascular health such as high blood cholesterol, cigarette use, diabetes, or hypertension (CDC, 2011). Therefore, a cardiovascular exam should be a part of every abbreviated and complete assessment. The cardiac examination consists of evaluation of (1) the carotid arterial pulse and auscultation for carotid bruits; (2) the jugular venous pulse and auscultation for cervical venous hums; (3) the precordial impulses and palpation for heart sounds and murmurs; and (4) auscultation of the heart. 

• The position of the patient is extremely important for the examination of the jugular veins. Relax the neck muscles by placing a small pillow behind the neck. The head should not be rotated more than a few degrees, since rotation may tense the SCM muscle and obscure the transmission of venous pulsations. The trunk of the body should be elevated until maximal venous pulsations are noted. The degree of trunk elevation varies from subject to subject and must be established for each person. In most normal individuals, the maximum pulsation of the internal jugular vein is usually observed when the trunk is inclined to about 15 to 30 degrees. In patients with elevated venous pressure, it may be necessary to elevate the trunk more than 45 degrees to visualize the maximum venous pulsation. At times there is venous distention without visible waves and the pulsations are only seen with the patient upright at 90 degrees. Jugular venous pressure (JVP) provides an indirect measure of central venous pressure. The internal jugular vein connects to the right atrium without any intervening valves - thus acting as a column for the blood in the right atrium.

• First, the patient must be positioned in a manner so that the physician can observe the venous pulse. Thus, the neck and chest must be bared to permit an unobstructed view from the midportion of the sternum to the antihelix of the ears. This requires that the dressing gown (preferrably opening to the patient's back) be positioned at the level of the nipples. Moreover, a woman's long hair should be tucked out of the way behind her head. Second, the patient should be reclining in a comfortable position. Except for patient comfort, the exact angle of inclination from horizontal is relatively unimportant. Indeed, this angle does not even need to be reported in the physical examination, since the mean venous pressure can be given in units of "centimeters of water," which is an absolute number. In general, patients who are dyspneic will not tolerate reclining at angles of less than 45 to 60 degrees from horizontal, and thus this should be the initial position of the head of the bed. Third, the examining table (or hospital bed) should be raised to a comfortable height for the physician. The cardiac examination—if performed properly—is time-consuming and must not be hurried; physical discomfort on the physician's part will detract from the adeptness of his bedside skills. Fourth, an adequate light source with a strong beam must be readily available. This source may be either a pocket flashlight (with a strong battery) or a bedside lamp that the physician can direct. Ambient room or window lighting is not usually as good as directed artificial lighting. If I am still uncertain as to whether or not I am observing the venous pulse, I try to obliterate the venous pulse by placing my right thumb or index finger across the base of the patient's right neck. By compressing this area with a force of approximately 10 to 20 mm Hg, the venous pulse can be obliterated. Movement that remains will then be observed to have the characteristic monophasic contour of the carotid pulse. During this maneuver, it is important to continue to cast a tangential light across the right side of the neck in order to observe the contour of the various pulses.

4. The apex beat or apical impulse is the palpable cardiac impulse farthest away from the sternum and farthest down on the chest wall, usually caused by the LV and located near the midclavicular line (MCL) in the fifth intercostal space. Lateral and/or inferior displacement of the apex beat usually indicates enlargement of the heart, called cardiomegaly. The apex beat may also be displaced by other conditions: Pleural or pulmonary diseases. Deformities of the chest wall or the thoracic vertebrae. If the ventricle becomes dilated, most commonly as the result of past infarcts and always associated with ventricular dysfunction, the PMI is displaced laterally. In cases of significant enlargement, the PMI will be located near the axilla.

5. ulsus paradoxus is traditionally measured using a sphygmomanometer. The brachial cuff must be inflated above the presumed value of systolic arterial pressure and then deflated slowly to find the highest pressure at which the first Korotkoff sound is heard, normally during expiration. The cuff must be further deflated to the pressure at which the Korotkoff sounds are heard during both inspiration and expiration. Pulsus paradoxus is present if the difference between the latter and the former pressures is >10 mmHg. In general, the procedure is repeated two or three times to improve accuracy. However, this method is cumbersome and time-consuming (2-5 min) 44. In addition, in some patients, audibility of sounds is poor because of tachypnoea and a noisy clinical environment (emergency room). In a great number of cases, experienced physicians have failed to measure reliably the amplitude of pulsus paradoxus 45.

Because of all these drawbacks, >98% of care providers do not use the manual measurement at the bedside in acute asthma 46. Alternative methods have been proposed to measure pulsus paradoxus, in particular methods allowing automatic and real-time measurements, such as noninvasive blood pressure monitors 47 and pulse oximetry 48. In a series of 26 patients with COPD, respiratory waveform variation of pulse oximetry closely correlated with pulsus paradoxus measured using sphygomanometry 48. In an intensive care context, invasive monitoring of blood pressure using an arterial catheter provides an accurate real-time assessment of pulsus paradoxus.

6. The main distinguishing feature of pulsus bisferiens is that two peaks are seen in systole whereas, the dicrotic pulse is characterized by one peak in systole and other in diastole. Pulsus bisferiens is Latin for 'beat twice'. This describes the pulse where two systolic beats are palpated each cardiac cycle with an interposed mid-systolic dip. The dicrotic pulse is an abnormal carotid pulse found in conjunction with certain conditions characterised by low cardiac output. It is distinguished by two palpable pulsations, the second of which is diastolic and immediately follows the second heart sound.

7. 

• Compression of tissues and vessels is involved in this position. Artificially induced vascular turgescence of the lower limbs in the sitting or standing, but not in the horizontal, position is attended by increase in pulse?rate. Your radial pulse can be taken on either wrist. Use the tip of the index and third fingers of your other hand to feel the pulse in your radial artery between your wrist bone and the tendon on the thumb side of your wrist. Apply just enough pressure so you can feel each beat.
• The collapsing or sudden down stroke may be partly due to a sudden fall in the diastolic pressure in the aorta due to regurgitation of blood into the left ventricle through a leaky valve and partly due to the rapid emptying of the arterial system due to the marked increase in the velocity of the bloodstream. An increased stroke volume filling the relatively empty arterial vessels causes the rapid upstroke when feeling the water hammer pulse. This increased stroke volume is secondary to an increase in end-diastolic volume from the retrograde blood flow from the aorta into the left ventricle during ventricular diastole, or relaxation. The rapid downstroke is partly due to two causes. The first cause is the sudden fall in diastolic pressure in the aorta, which is due to regurgitation of blood from the aorta, or "aortic run-off," into the left ventricle through the leaky valve. The second cause is the rapid emptying of the arterial system.

8. Mechanism of Durozier's - The murmur is produced when firm pressure from the bell of the stethoscope is applied to the artery then altering the pressure proximally and distally. The diastolic component often becomes louder with pressure applied distal to the stethoscope.

9.

• Aortic stenosis (AS) is the most common valvular lesion that affects 2-7% of the population age >65 years worldwide (1). Increased afterload caused by the stenotic valve inevitably leads to systolic and diastolic dysfunction. Aortic stenosis is a narrowing of the aortic valve opening. Aortic stenosis restricts the blood flow from the left ventricle to the aorta and may also affect the pressure in the left atrium. In aortic stenosis, there is a narrowing of the aortic valve, which interferes with the ejection of blood from the left ventricle into the aorta, which results in a decrease in stroke volume and subsequent decrease in pulse pressure.
• In the majority of these cases, systolic pressures increase while diastolic pressures remain near normal. In aortic regurgitation, the aortic valve insufficiency results in a backward, or regurgitant flow of blood from the aorta back into the left ventricle, so that blood ejected during systole returns during diastole. This increased pressure is automatically transmitted to the pulmonary vasculature, leading to severe symptoms of left heart failure, including flash pulmonary edema. As aortic regurgitation worsens, allowing larger volumes of blood to be regurgitated during diastole, aortic diastolic pressures drop significantly. This elevates aortic systolic pressure (160 mmHg in this example); however, the aortic diastolic pressure (60 mmHg in this example) is much lower than normal because blood more rapidly leaves the aorta due to regurgitation back into the ventricle.
• With coarctation of the aorta, the lower left heart chamber (left ventricle) of your heart works harder to pump blood through the narrowed aorta, and blood pressure increases in the left ventricle. This may cause the wall of the left ventricle to thicken (hypertrophy). Blood pressure in both arms and one leg must be determined; a pressure difference of more than 20 mm Hg in favor of the arms may be considered evidence of coarctation of the aorta.