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 ?
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!
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 !
What happens to diastolic blood pressure in severe Aortic stenosis ?
Traditional answer: The diastolic BP remain unchanged. Only systolic BP falls as it is related to LV stroke volume .(What we refer to as systolic decapitation of BP )
Reasoning :Diastolic BP is related to peripheral vascular resistance , hence aortic stenosis has little impact on diastolic BP .
If we assume only the systolic blood pressure is bound to decrease in AS , at one critical point of time* systolic BP should approach the diastolic pressure and pulse pressure should approach zero .This can not happen , hence at that point diastolic pressure will also fall.
*What is that point ?
No one really knows !
In severe aortic stenosis both systolic and diastolic pressure falls , but the fall in systolic BP is more striking .
* Though it is customary for clinicians to discuss them in isolation both systolic and diastolic blood pressure are closely coupled parameters..In the absence of peripheral run off one of the strong determinant of diastolic BP is . . . systolic BP !
1. What happens in combined aortic stenosis and regurgitation ?
In combined AS and AR we get pulsus bisferiens. implying AR will elevate the systolic blood pressure in spite of obstruction.
2.What happens in associated systemic Hypertension and aortic stenosis . (Which is very common combo in elderly )
Since HT will increase the aortic pressure , the LV-Aorta gradient tend to fall.
However ,this does not happen always as if the original cause for HT was dependent more on the stroke volume rather than peripheral mechanisms .
3. Aortic stenosis with aortic atherosclerosis .
A stiff aorta augments the percussion wave amplifying the symbolic BP and blunting the classical anacrotic pulse of AS.
4.What happens to BP during exercise in severe AS ?
Exercise demands raise in systolic BP and temporary reduction in diastolic BP due to peripheral vaso dilatation in exercising muscles.
If a fixed crtical AS does not allow the systolic BP to raise as required , diastolic continue to fall pulse pressure should still become wide .
Excercise testing is a tricky business in AS. Some have attempted it to assess the functional capacity.(Read below)