Respiratory Arrhythmia
also called Sinus Arrhythmia is a variation of the Heart Rate with respiration. Heart rate increases with inspiration and decreases with expiration, it's a physiological phenomenon and perhaps useful for the body as you don't want to wast heart beats when you have less alveolar ventilation

Pulsus Paradoxus
is decreased Systolic Pressure [hence pulse amplitude] during inspiration,
--if the decrease is less than 10 mmHg then it's physiological [it happens because at inspiration your lung vessels expand pooling more blood and so less venous return to the LEFT atrium so decreased systolic pressure another proposed mechanism of pulsus paradoxus is that during inspiration the right heart is filled with blood and if there no space for it to expand because of restrictive heart or an overinflated lungs then it will push on the left ventricle decreasing its end diastolic volume and thereby decreasing systolic blood pressure]
--if more than 10 then look for the following conditions:
Cardiac temponade or pericarditis, Asthma Croup and COPD, also Obstructive sleep apnea

You may want to know about

• Pulsus Alternans [beat to beat variation in pulse pressure seen in systolic dysfunction],
• Pulsus Parvus [weak upstroke seen in hypovolemia],
• Pulsus Bisferiens [double pulsation during systole seen in LV dysfunction],
• Pulsus Tardus [delayed upstroke, seen in AS]

 

Bainbridge reflex is the name of that explanation in respiratory arrhythmia!

Respiratory Arrhythmia
also called Sinus Arrhythmia is a variation of the Heart Rate with respiration. Heart rate increases with inspiration and decreases with expiration it's a physiological phenomenon and perhaps useful for the body as you don't want to wast heart beats when you have less alveolar ventilation Bain

Pulsus Paradoxus
is decreased Systolic Pressure [hence pulse amplitude] during inspiration,
--if the decrease is less than 10 mmHg then it's physiological [it happens because at inspiration your lung vessels expand pooling more blood and so less venous return to the LEFT atrium so decreased systolic pressure another proposed mechanism of pulsus paradoxus is that during inspiration the right heart is filled with blood and if there no space for it to expand because of restrictive heart or an overinflated lungs then it will push on the left ventricle decreasing its end diastolic volume and thereby decreasing systolic blood pressure]
--if more than 10 then look for the following conditions:
Cardiac temponade or pericarditis, Asthma Croup and COPD, also Obstructive sleep apnea

You may want to know about

• Pulsus Alternans [beat to beat variation in pulse pressure seen in systolic dysfunction],
• Pulsus Parvus [weak upstroke seen in hypovolemia],
• Pulsus Bisferiens [double pulsation during systole seen in LV dysfunction],
• Pulsus Tardus [delayed upstroke, seen in AS]

(((Bainbridge Reflex))) Inspiration increase HR and vice versa.

 

Finally I understood what is pulsus paradoxus

 

Differential Diagnosis of Cardiac Temponade and Right Ventricular Infarction

I'd like to add here that pulsus paradoxus is a very important differentiating clinical sign between cardiac temponade and right ventricular infarction.
Both conditions can present post-MI with hypotension, tachycardia, distended jugular veins, and clear lungs.
However, pulsus paradoxus is seen in cardiac temponade but not in right ventricular infarct.
In temponade there's no place for the right ventricle to expand when blood returns in inspiration and so it pushes on the neighboring left verntricle decreasing systolic pressure. That's not the case in right ventricular infarction where the right ventricle can still expand upon increased return in inspiration.
The distinction is crucial is treatment of temponade involves emergency pericardiocentesis while in RV infarct you give fluids to override the failure (Starling law, when the ventricle has more volume it contracts better).

 

Increase preload ????

RV infarct you give fluids to override the failure (Starling law, when the ventricle has more volume it contracts better).

Aren't we supposed to reduce preload in case of Heart failure ?
Giving fluids will raise blood volume thus raise preload, increased preload will add more workload on the already failing heart. What I remember is we tend to give venodilators to reduce preload and reduce venous return !!!

Correct me please!!!!!:sorry::sorry::sorry::sorry:

 

Thanks....

This video is also helpful

 

hey damn good video

 

pathophysiology

How does the pathophysiology of pulsus paradoxus differ in cardiac tamponade from constrictive pericarditis from asthma.

I understood that of normal systolic pressure decrease in normal inspiration and tamponade but not of asthma and pericarditis