Pulsus paradoxus , also paradoxic pulse or paradoxical pulse , is a large decrease in stroke volume, systolic blood pressure and pulse wave amplitude during inspiration. The fall of normal pressure is less than 10 mmHg. When the drop is more than 10 mmHg, it is referred to as the pulsus paradoxus. Pulsus paradoxus is not associated with pulse or heart rate and not an increase in paradoxical systolic pressure. Normal variation of blood pressure during respiration/breathing is decreased blood pressure during inhalation and increase during respiration. Pulsus paradoxus is a sign that shows several conditions, including cardiac tamponade, chronic sleep apnea, croup, and obstructive pulmonary disease (eg, asthma, COPD).
The paradox in pulsus paradoxus is that, on physical examination, one can detect the pulse on cardiac auscultation during unpassable inspiration on the radial pulse. This results from a drop in blood pressure, which causes the pulse (radial) is not palpable and may be accompanied by an increase in jugular venous pressure (Kussmaul's sign). As always with inspiration, the heart rate increased slightly, due to decreased left ventricular output.
Video Pulsus paradoxus
Mekanisme
NB During Inspiration negative intra-thoracic pressure produces right venous increase, increased blood volume enlarges the right atrium reduces left atrium adherence (overrides the left atrium) this reduces left venous atrium rejection and as a consequence of left ventricular preload reduction, this results in a decrease in left ventricular stroke volume, and will be recorded as a decrease in systolic blood pressure in inspiration. Therefore, pulses paradoxus is excessive or an increase in the fall of systolic blood pressure exceeding 10 mmHG during inspiration. It is caused by restrictive heart disease such as Heart Tamponade, constrictive pericarditis or severe asthma.
Usually during inspiration, one's systolic blood pressure decreases by <= 10 mmHg and the pulse rate slightly increases. This is because inspiration reduces intra-thoracic pressure relative to atmospheric pressure, which increases blood flow (systemic venous return) to the right atrium of the heart by reducing the pressure on the veins, especially the cavae vein. However, the decrease in intra-thoracic pressure and stretching of the lungs during inhalation also extends the compliant pulmonary blood vessels so that blood flows in the lungs and reduces the pulmonary vein back into the left atrium. Also, increased venous return of the systemic veins to the right side of the heart extends the right heart and directly compromises the left side filling of the heart with slightly bulging the septum to the left, reducing the maximum volume. Reducing left heart filling causes a reduced volume of stroke that manifests as a decrease in systolic blood pressure, which causes a faster heart rate due to baroreceptor reflex, which stimulates sympathetic flow to the heart.
Under normal physiological conditions, a large pressure gradient between the right and left ventricles prevents the septum from inflating dramatically into the left ventricle during inspiration. However, such bulges occur during cardiac tamponade where pressure equals between all chambers of the heart. Following the principle of zero-sum game, when the right ventricle receives more volume, it can push the septum into the left ventricle to reduce its volume interchangeably. An additional loss of left ventricular volume that only occurs with equalization of pressure (as in the tamponade) allows further volume reduction, resulting in reduced cardiac output, leading to a further decrease in blood pressure.. However, in situations where left ventricular pressure remains higher than the pericardial sac (most often of the disease together with high left ventricular diastolic pressure), there is no pulsus paradoxus.
Although one or both of these mechanisms may occur, one-third may contribute additional. A large negative intra-thoracic pressure increases pressure on the left ventricular wall (increased transmural pressure, equivalent to [ventricular pressure] - [pressure outside the ventricle]). This pressure gradient, withstand left ventricular contraction, causes increased afterload. This results in a decrease in stroke volume, contributing to a decrease in pulse pressure and an increase in heart rate as described above.
Pulsus paradoxus occurs not only with severe cardiac tamponade but also with asthma, obstructive sleep apnea and croup. This mechanism, at least with severe tamponade, is likely to be very similar to hypertrophic and restrictive cardiomyopathy (diastolic dysfunction), where the left ventricular filling (LV) decrease corresponds to a reduced stroke volume. In other words, with this cardiomyopathy, as LV filling decreases, ejection fraction decreases directly, but not linearly and with negative basins (first and second negative derivatives). Similarly with tamponade, the degree of diastolic dysfunction is inversely proportional to the end-diastolic volume of LV. Thus during inspiration, since LV filling is relatively lower than during expiration, diastolic dysfunction is also greater proportionately, resulting in systolic pressure down & gt; 10 mmHg. This mechanism is also possible with pericarditis, where diastolic function is hurt.
Maps Pulsus paradoxus
Measurement
PP was quantified using blood pressure and stethoscope (Korotkoff sound), by measuring the systolic pressure variation during expiration and inspiration. Inflate cuff until no sound (as is usually done when taking BP) slowly lowers the cuff pressure until the first systolic sound is heard during expired but not during inspiration, (note this reading), slowly decrease pressure cuffs until the sound is heard during the breathing cycle, (inspiration and expiration) (note this second reading). If the pressure difference between the two readings is & gt; 10mmHg, it can be classified as pulsus paradoxus.
Cause
Pulsus paradoxus can be caused by several physiological mechanisms. Anatomically, these can be grouped into:
- heart cause ,
- cause of pulmonary and
- non-pulmonary and non-cardiac causes .
Considered physiologically, PP is caused by:
- reduces the right heart function reserve, e.g. myocardial infarction and tamponade,
- right ventricular flow or outflow obstruction, ie. superior vena cava obstruction and pulmonary embolism, and
- lowers blood to the left heart due to hyperinflation of the lungs (eg asthma, COPD) and anaphylactic shock.
List of causes
Kardiak:
- constrictive pericarditis. One study found that pulsus paradoxus occurs in less than 20% of patients with constrictive pericarditis.
- pericardial effusion, including cardiac tamponade
- cardiogenic shock
Lung:
- pulmonary embolism
- tension pneumothorax
- asthma (especially with severe asthma exacerbations)
- chronic obstructive pulmonary disease
Non-pulmonary and non-cardiac:
- anaphylactic shock
- hypovolemia
- superior vena cava obstruction
- pregnancy
- overweight
PP has been shown to predict the severity of cardiac tamponade. Pulsus paradoxus may not be seen with cardiac tamponade if a significant atrophic septal defect or aortic regurgitation is present.
See also
- Paradox list
- Prehistoric exam
- Alternative pulsus
References
External links
- Clinical signs in medicine: pulsus paradoxus - Mechanism, pathophysiology, detection and management of patients with pulsus paradoxus.
- Another definition of Pulsus Paradoxus
- Hamzaoui, O; Monnet, X; Teboul, JL (December 6, 2012). "Pulsus paradoxus". European respiratory journal . 42 (6): 1696-705. doi: 10.1183/09031936.00138912. PMID 23222878.
Source of the article : Wikipedia
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