That’s normal . . . what happens during pathological states ?
There are important diseases that restricts entry of blood into right heart chambers. They can occur either in an acute (Tamponade) or in chronic fashion like constrictive pericarditis and restrictive cardiomyopathy.These entities show distinctive impact on JVP and systemic pulse.
The two pathognomonic signs are Kussmaul sign and pulsus paradoxus* that go hand in hand in most situations.Inappropriate elevation of JVP with inspiration is termed as Kussmaul sign , while exaggerated fall in systemic BP with inspiration is called Pulsus paradoxus.The later is the arterial counter part of Kussmaul sign in JVP .However, there can be dissociation between these two signs occasionally.
* Pulsus paradoxus is a term originally used by Kussmaul when he noted heart sounds were retained while pulse dissappeared in patients with cardiac tamponade .Later we realised the loss of pulse was linked to inspiratory cycle of respiration. To make this sign objective sphygmomanometery criteria was formulated which measured the difference between inspiratory and expiratory korotkoff’s sounds .
Coming up next
Why Kussmaul sign is often absent in Tamponade while its arterial counterpart pulsus paradoxus may still be conspicuous ?
We know aortic regurgitation causes a deluge of hugely popular peripheral signs of aortic run off , which are taught right from 2nd year medical school.
When the aorta leaks it reflects in the entire vascular tree .How is that a leak in the remote aortic valve cause a quincke’s to and fro pulsations in the finger pulp ?
Is the blood in the finger trying to follow the regurgitant jet that go back into left ventricle ? Does the to and fro murmur of Duroziez over the femoral artery imply there is reversal of blood flow in femoral artery ?
Things are little complex than it appears
It is true the initiating event of collapsing pulse is the regurgitant jet , however the mechanism that amplifies and sustains it , lies in the altered peripheral hemodynamics.
The systemic arteriolar resistance is dramatically low in chronic severe AR by a reflex phenomenon , as cardiac out put is increased and vascular tree adopt to it. So, with each beat when blood is ejected two things happen in diastole .While a small fraction runs back into LV , the rest of blood runs off , as if it goes in a free way making all peripheral pulses dynamic , bounding and collapsible.
Hence as the name suggest all the peripheral signs of AR are due to the peripheral mechanisms rather than primary event of aortic run off into left ventricle.
Why carotid pulse does not show the collapsible nature of pulse in AR ?
If aortic leak into LV is the dominant mechanism , carotid artery should obviously manifest a collapse ,but it doesn’t ,as carotid has no direct continuity with the peripheral low resistance circuit
What is the hemo-dynamic correlates of descending aortic flow reversal in severe AR ?
The central vascular tree manifest some reversal till the regurgitant velocity fades off . This can occur in severe AR, extending into certain length of aorta. This can be picked up by Doppler probe. Please realise it is only the wave form that get reversed not the actual blood stream.( The momentum gained in systole continues to push forward in-spite of the pulling back forces of regurgitation)
Why peripheral signs are absent in acute AR ?
Acute AR even if it’s significant does not cause a collapsing pulse because it takes time for the peripheral vascular tree to go for vasodilatory mode.Further ,LV is also less compliant keeping the LVEDP high and regurgitant fraction low.
Answering the title question ,the mechanism of Aortic run off in AR is both central and peripheral. However clinical signs are largely due to high cardiac out put and the resultant adaptive response of the vascular tree due to low systemic vascular resistance triggered by reflex dilatation of small arteriolesof the peripheral vascular bed.
When a patient comes with angina at rest , it could mean two things .Either a STEMI or an NSTEMI .This , we can diagnose only after seeing the ECG .
Can we differentiate these two by the character of chest pain alone ?
Very tough task isn’t ? But there are some definite clues .
Is mostly sudden .
Likely to be crescendo , lasts more than 20-30 minutes .
Fails to get relived by rest or even Nitrites.
Sweating due to sympathetic activation is more pronounced.
Is rarely sudden .Often has a pro-drome.
UA is mostly precipitated by an increased demand situation or a stress.
It has a typical waxing and waning pattern . Rarely assume a true crescendo character as myocytes does not necrose (Just threaten to die !)
The chest pain radiation to shoulder is less conspicuous , instead it tends to reach the jaw area .(* An observation,Is it something to do with multi-vessel CAD in UA ?)
Mechanism of the difference : Epicardial vs Endocardial angina
The pain of UA is due to subtotal occlusion and endocardial ischemia , while STEMI is sudden total occlusion and the resultant transmural ischemia . In STEMI epicardial surface is always involved (Which lifts the ST segment in ECG .).We know epicardium is same as visceral layer of pericardium which is well innervated .Hence pain of STEMI acquires more of somatic character than a predominately visceral type pain that occurs with UA/NSTEMI where epicardial ischemia is absent.
The demarcation between unstable angina and Infarct pain becomes vital when we calculate the time window for thrombolysing STEMI .Many of them have a phase of pre infarction angina which is a type of unstable angina. If we mistake it for Infarct pain then one may falsely calculate a prolonged time window and deny re-perfusion therapy.
It is tricky issue to differentiate the chest pain of STEMI and NSTEMI .A significant overlap can occur in real coronary care scenario . We know chest pain that occurs in both pre and post infarct phase is considered as unstable angina .(With infarct pain sandwiched between them!) Hence differentiating them may even be termed as futile.
Still,clinical cardiology can be made fascinating by indulging in such exercise !
This query often evokes confusion among fellows and General physicians .
The answer is simple .Yes , you can.(With few conditions)
Thrombolysis or PCI is done with reference to the presence or absence of ST elevation and chest pain.
If there is ongoing chest pain and significant new onset ST elevation thrombolysis or PCI is indicated whether there is associated q waves or not.
Ischemic q waves: Q wave can occur with transmural ischemia which result in electrical stunning and loss of R waves . (Many of them regenerate this R within few days after STEMI , indicating the q waves can be ischemic in origin)
Reinfarction : Patients with old MI can develop fresh ST elevation in q leads due to tachycardia and dyskinetic infarct segment .This group of patients should be carefully evaluated before labeling them as re-infarction
* q RBBB in early hours of anterior STEMI is fairly common which may revert later. qRBBB is not a contraindication for re-perfusion .
Presence of q waves does not imply one should not entertain thrombolysis or PCI .The decision to reperfuse , rather goes with presence of chest pain , ST elevation and of course within the acceptable time window!
The right ventricle is considered as a docilecardiac chamber with passive filling and emptying properties .
This belief was reinforced when Fontan in early 1970s suggested a principle in the management of cyanotic heart disease when the right side of the heart is underdeveloped. He proved RV can be by-passed safely , with great veins (IVC/SVC) by themselves take care of filling the pulmonary circulation without the need of RV pumping function.
While it is true for few complex cyanotic heart disease, largely this a misleading concept. In clinical cardiology practice ,sudden or non sudden RV deaths happen every day in the form of . . .
Acute RV dysfunction in massive pulmonary embolism
COPD with RV dysfunction
Most cases dilated cardiomypathy the terminal event is due to RV failure.
So , RV function can never be dispensable in day to day cardiac hemodynamics.
RV has some unique properties in terms of shape , size and hemodynamics . We are getting more insights from modern blood pool imaging by MRI , about how the RV handles the blood volume .
I stumbled upon this excellent work by Alexandru G.Fredriksson published in APS (American physiology society ) This MRI study have documented RV fucntion in a dramatic fashion.
We know RV has a unique shape triangular ( partially pyramidal ) . It can be inferred the RV cavity is formed by fusion of many eccentric spacial planes. We have always believed RV handles the blood it receives from right atrium in a unique way .Now we are beginning to understand it .It is now documented the RV segregates the blood it receives into 4 components.
It is curious to know RV inflow is connected to the outflow by an invisible physiologic Bridge . About 44% of blood traverse the RV in this fashion.
Which is the most important part in RV ? (Among Inflow, Body, Apex, Out flow)
After reading this article it seems to me , the mechanical function of RVOT could be most vital. If it fails to handle the first increment which comes directly from RV inflow, stasis is likely in RV body and apex , elevating RVEDP and later promoting stasis leading to clinical events.
Clinical implication of this study
Differential dilatation RV chambers to pressure or volume overload is observed .
We need to analyse why RV dilates in some but goes for hypertrophyin others when confronted with pressure overload (VPS vs PAH)
RV apical clot in restrictive cardiomyopathy is a direct consequence of stasis of blood in RV apical zone .
RVOT pacing may have a hemodynamic advantage over RV apical pacing . However , for anatomical reasons RV apical pacing is far safer than RVOT pacing where the lead is subjected to constant life long strain due to this busy RV inflow to outflow express high way !
Traditionally we have labeled RV as a passive venous chamber .It is clearly a misnomer.It has to handle both the venous and pumping function beat to beat with precision without back log .Obviously , RV has to think and work more than it’s big brother !
I wonder , if there is any other site other than APS . . . to find crucial answers in cardiac physiology !
There is huge gap between physiologists who work in research labs and the physicians at bed side .
I appeal all young cardiologists to visit APS once in a while ,between your busy cath lab schedule and help narrow this gap.
Without understanding the physiology properly how are we going to intervene the pathology ?
Can we close an ASD in a 25 year old women severe pulmonary hypertension ?
Volumes of literature has been written on the subject.Dedicated cath studies have been done with multiple parameters .
Still , there is a lingering doubt !
Here is a 3 minute practical* solution based on 5 easily available parameters. (*Also referred to as unscientific in medical parlance !)
1. O2 saturation
2. Pulmonary artery diastolic and pulse pressure
3. RV function,
4 .Systemic pressure
5. Functional class
If O2 saturation is > 90 % consistently there is likely to be significant left to right shunt .Closure is to strongly considered
If 02 saturation is near 95 % there is absolutely no contraindication at any level of PVR.
Systolic pulmonary artery pressure derived by TR jet is least useful index.Pulmonary artery diastolic pressure reflects true vascular reactivity of the pulmonary circulation.A wide swinging pulmonary arterial pulse indicates dynamism in circulation and hence operablity.
If pulmonary artery pulse pressure is wide (>50) , or PA diastolic BP is < 30 one can safely presume irreversible damage to pulmonary vasculature has not occurred and these patients would benefit from surgical closure .
RV function should be assessed carefully in every patient.This is as important as PVR .Significant RV dysfunction is an absolute contraindication.
Never close the shunt in patients who is in class 4 symptoms.
Never close a shunt if the systemic blood pressure is low( 90mmhg)
Some believe PDA may be closed at any given PVR , while worst outcomes occur with ASD as supra-systemic pulmonary pressure is possible.
Always monitor these patients meticulously especially in the initial days following surgery for deterioration .Most patients will do well if they cross the first 30 days. The RV learns to adopts with new pulmonary hemodynamics !
Unfortunately, there is a strong bias towards raw basic science when it is given in the filed of medicine.Do you know ,there is no Nobel prize exclusive for medical science ? It shares with human physiology the only field included for Nobel prize in medicine.
Evolution of human history reveals it is not the stunning scientific discoveries that impact the mankind . It is largely dependent on how we use them . It is true and natural ,invention of sub atomic particles , decoding quantum mechanics and trans-cellular signals always generate great interest than others.
In medical science, time and again we have seen problems arise in applying fruits of scientific research into practical usage in the patient domain in the bedside.
What is use of rewarding inventor of nitric oxide with a Nobel prize , when billion-dollar nitrate industry is thriving on a non existing life long indication of stable angina .
It is surprising to note , Nobel committee does give credit to wisdom & intellect while awarding prize in peace, literary or economic sciences. For some reason it lacks such a vision when it comes to medical sciences !
We have seen Nobel prize being awarded to organization that strive for peace and welfare of society and community like UN ,EU etc.The world health organization is the premier power supposed to provide and regulate the health in this planet.I do not recall any time WHO was close to considered for the Noble prize in medicine !
Nobel committee rewards economists who point out lacunae in vital world macro and micro economics theories.
Dubious men(Heads of state ) are decorated with Noble peace prizes for preventing a war in one geographical area while doing exactly the opposite elsewhere !
In this modern millennium where scientific pursuits are contaminated and many of the research questions are misdirected or irrelevant , Nobel committee needs a through rejig in the manner in which medical Nobel prize is being awarded. We know ,Noble’s death wish was to award the brightest mind with highest scientific breakthroughs in those world . . . but
I guess Alfred Nobel if alive would have changed his rules .He wouldn’t have imagined modern science would systematically devalue common sense and reinventing it would also deserve an award equivalent to Nobel !
Some of the medical discoveries that deserve noble medical prize
States which excel in school health nutrition and other basic health programs for the downtrodden
Doctors who promote bed side clinical skills
Tobacco eradication networks
Organisations like medicine san-frontiers which strives for basic life saving medication for all
Journal houses that specialise on Medical ethics and clinical sciences
Medical professionals and institutions provide value education
Medical economists who expose the wasted financial resources that widen the gap between sick and rich
How about Nobel prize in cardiology for preventive cardiologist who successfully terminates a million statin prescription and restoring natural exercise directed lipid regulation in them ?
How about Noble prize for a noble physician sitting in corporate hospital infested with all commercial ingredients who could resist and argue successfully against inappropriate tonsillectomies and appendectomies ?
I am sure , such a man will be a laughing stock for most of us !
An appeal to Nobel committee
It is a wish , Noble prize in medicine is to be included for people who do yeomen services in preventive and clinical care and professional who carry forward the legacy of caring for the sick with clinical application of available scientific wisdom !
In this scientifically obsessed world , It will be a new beginning in the way future medical research will be directed and nurtured ! Only then the true power of Noble prize in medicine will be realised !