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Posts Tagged ‘mechanism of dyspnea’

Exertional dyspnea disproportional to the effort is the most common (cardinal)symptom of heart disease. Whenever we discuss the mechanism of cardiac dyspnea , we primarily attribute it to left heart disease, elevated LVEDP and the resultant pulmonary congestion.Conventional teaching in the past (may be in the present too !) doesn’t implicate raised RVEDP in the genesis of dyspnea.

It’s good to recall , the sensation of dyspnea is felt at the peri -Amygdala nuclear zone after complex processing with various cortical and sub-cortical level .It is subjected to as many afferent triggers other than J receptors in pulmonary micro circulation. (Eg Exercising skeletal muscle). It is believed, mechanical stretch receptors exist within the walls of heart along  the sub-endocardial aspects of chamber.

(Muscle spindles which are the sensors of muscle tension are extensively noted in skeletal muscle that contribute to the origin of dyspnea .We are not yet accruing enough evidence  whether cardiac muscle do have the same muscle spindle or it’s equivalents to cause dyspnea when stretched. However, we clearly witness in the practice of clinical cardiology , isolated elevation of RVEDP ( also RVSP ) to cause significant dyspnea in specific clinical situations.

Potential causes for Isolated Right ventricular dyspnea

  • Pulmonary hypertension  (COPD included* where in it could be a combination of lung and cardiac dyspnea)
  • Acute pulmonary embolism
  • RV Infarction
  • Acute rupture of sinus of Valsalva aneurysm (RSOV) Here RVEDP is often > LVEDP and dyspnea is due to the acute stretch of RV
  • Isolated normal pressure TR(RVEDP is low still cause dyspnea  due to volume related RV triggers)
  • Any RVOT obstruction (Classically valvular pulmonary stenosis)
  • Does RV dilatation without elevated RVEDP cause dyspnea ?  Though right ventricle is developmentally and hemo-dynamically better suited to handle volume , still, it  struggles to manage sudden increase in volume .(Another clinical example is seen in patients who are on dialysis)

*RV diastolic dysfunction is still a Infantile hemo-dynamic concept .Whether it can raise RVEDP significantly during exercise and Independently contribute to dyspnea is at best a hypo-science.

Role of muscle spindle and mechno-receptors

 

Muscle spindle

structure of skeletal muscle spindle. Though we don’t have a highly developed spindles in smooth muscle and cardiac muscle we have evidence to suggest cardiac neural ending do have mechano-receptors with afferent connection through visceral neural plexus that can trigger both heart rate and respiratory centers Further reading : Neuroscience. 2nd edition. Show details Purves D, Augustine GJ, Fitzpatrick D, et al., editors. Sunderland (MA): Sinauer Associates; 2001.

Bain-Bridge reflex: The hidden link in right heart dyspnea

Bain-Bridge reflex is a 100 year old concept. still helping us to understand the basics of right heart hemodynamics and how adjustments with acute volume loading take place.He proposed that  veno-atrial stretch receptors are located  primarily in great veins as it enter ,right atrium (RV as well).

This gets activated through vagus and stimulates  in brain-stem sympathetic system and increase the heart rate to handle the excess blood reaching the heart. How often we feel the symptom of palpitation  whether due to this reflex ( when it is operating) is not really tested. But, what we can infer is , the surge in sympathetic tone perceived can be perceived as  dyspnea.

*Clinical Relevance of the Bezold–Jarisch Reflex and its possible interactions with Bain Bridge reflex is a different topic.

It is interesting to note many of these reflexes cause hypo-tension, bradycardia and hypopnea (Even near Apnea.) The word dyspnea is surprisingly not used .It is highly plausible many of the unexplained dyspnea we see in otherwise healthy population is attributed to acute or chronic volume overloading or under-loading of right heart.

Role of PFO in right heart dyspnea

PFO is a natural decompressing orifice in the IAS guarded by a flip-flap safety valve which is a remnant of septum primum .Though it can flow either way , since the flap of the valve is larger in LA side,  it gets closed when  LA pressure raises but opens up , if RA pressure raises making it more often a right to left shunt at times of elevated RA mean pressure. In isolated right heat pathology , this communication shunts  right to left and  adds a new dimension to cardiac dyspnea (Now, It becomes a hypoxic /biochemical dyspnea over and above the right heart stretch related dyspnea )

Other mechanisms in right heart dyspnea

Pulmonary arterial stretch and altered QP : Role of ventilation perfusion mismatch should also be considered as a cause for dyspnea in isolated RV pathology. The term V/Q mismatch is a poorly understood term fro me. My Inference is, since RV contraction  provides the Q in the equation V/Q .Whenever Q falls V has to fall to maintain neutrality causing net hypoxia and dyspnea.

Final message

Dear fellows, never hesitate to attribute the origin of dyspnea,  to elevated RA mean pressure /RVEDP. It is due to RA/RV stretch secondary to volume and pressure overloading with a perfectly normal pulmonary capillary wedge pressure or LVEDP. As in the left heart ,this occurs both in pathological as well as perfectly exaggerated physiological times.

Reference 

1.Bainbridge FA. The influence of venous filling upon the rate of the heart. J Physiol. 1915 Dec 24;50(2):65–84. [PMC free article] [PubMed[]

2..A J Crisp, R Hainsworth, and S M Tutt  The absence of cardiovascular and respiratory responses to changes in right ventricular pressure in anaesthetized dogs. J Physiol. 1988 Dec; 407: 1–13(This paper actually undermines the importance of RV receptors. It is still perplexing to note both the inflow into RV (ie RA  and the out flow  pulmonary artery circuit has richly innervated by receptors , its difficult to accept why we  have failed to get much evidence for RV stretch receptors) Its potentially great area of research for cardiac physiologists. That will be a tribute to the greats like  Bain Bridge and Bazolds Jarich.)

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No  body wouldn’t  ever have  differentiated   dyspnea with reference to  systolic and diastolic dysfunction .I have made some  observations  in certain group  of patients  during EST  . I do not know how far one would agree  with this .

For  the same amount of  stress or work load persons with  systolic dysfunction  behave differently . However ,both will complete the activity but the onset and perception of dyspnea is slightly different in patients with predominant diastolic dysfunction.

Diastolic dyspnea (Dyspnea due to predominant diastolic dysfunction / HFPEF)

  • Delayed dyspnea .  It manifest  well after the exertion is completed.
  • It is more off a struggle to handle the venous return .The forward flow (Arterial circuit )  is relatively well toned and  tuned  and hence fatigue is rare .
  • Typically it has a prolonged recovery time .(? > 1-2 minutes )
  • Is it  less harmful  in terms of longevity ?  May be . . . since it is more related to physical  de-conditioning. Most of the physiological  episodes of dyspnea are probably  diastolic dysfunction  mediated .
  • Dyspnea that is triggered  in diastole is also dependent very much  on the  heart rate .If the heart rate fail to reach the baseline the recovery of dyspnea is also delayed
  • Some believe , physiological dyspnea should disappear within 30-60 seconds after termination of activity  .(Highly  arbitrary!)

The pressure volume loop in various forms of heart disease will determine the degree of myocardial stretch and the resultant dyspnea .Image source : http://www.1cro.com/medicalphysiology/chapter10/chap_10.htm

Systolic dyspnea (Dyspnea due to predominant systolic dysfunction )

  • Patients with primary systolic pump failure experience dyspnea very early into exercise  .
  • Much of dyspnea  occur during activity itself .
  • Exercising muscles show hypoxia  and hence  fatigue is conspicuous .
  • Recovery  of dyspnea is relatively immediate as the activity is stopped .Demand from exercising  muscle is  significantly dropped.
  • If the venous return is well handled by the ventricles the  recovery phase is more comfortable .

Summary

In primary diastolic dysfunction  ,the maximum stress  to ventricle occurs  when  the venous return peaks that usually happen in the exercising muscles , as they shed  vaso-dilatory  property  in post exertion phase .

Management Implication

 Fluid overload ,  Tachycardia   are more  related to diastolic dysfunction .(Beta blockers by prolonging  the diastole can , provide important relief of dyspnea in diastolic dysfunction (In HOCM patients   this action could be  more important that  the much hyped negative inotropism !)

Final message

Dyspnea is  a complex cortical  perception , influenced by filling pressure of heart, stretch receptor in lungs , respiratory and   exercise muscle . It is further impacted by number of biochemical parameters (Lactate/ O2 etc )

Of-course  , it could be a  far fetched  imagination to  to split dyspnea  mechanism with reference to cardiac cycle. Combinations  of both  systolic and diastolic dysfunction is the norm in many  cardiac conditions . Hence the issue may be redundant .

However  , I believe  we need   more insight in the  pathogenesis of  this ,  “most important  symptom”   that emanate  from the heart .

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Angina and dyspnea are the  two cardinal ( classic ) symptoms of cardiac disease . While dyspnea is a manifestation of raised LV filling pressure ,  angina  implies reduction in blood supply to heart .

In other words dyspnea is related to excess blood in the  lungs and angina is due to less  blood in  the coronaries  !

So , it is obvious  even though these  two  symptoms are closely knit entities , patho- physiologically  they are  distinctly different  in real time , when an actual  cardiac event unfolds in the bed side .

This also partially explains  , why simultaneous  presentation   of  angina and dyspnea is  relatively  uncommon in CCUs  , than one would expect .(In a given patient , one of them will be dominant)

Why and how our patients (and also  physicians !)  get confused  with dyspnea and angina ?

When William Heberden described  angina over a century ago ,  he was  so meticulous in his description and observation. In fact , it was,  as if  he felt the angina  himself  and wrote it .One can rarely  expect such a  description from any of our patients .  So , it is not at all a surprise  for mistaking  any mid sternal discomfort as dyspnea instead of  angina . (This error in describing angina  is the commonest cause  for dyspnea  playing this  dubious dual role !)

When to suspect  dyspnea  as an Anginal equivalent ?

Here  are some real situations ( and clues )  where  dyspnea  may be  considered as  anginal equivalent.

  • Diabetics
  • In elderly with autonomic dysfunction
  • Patients with chronic beta blocker and other anti anginal drugs.
  • Post PCI/CABG patients (Normal LV function but dyspnea : Denerved heart blocks pain  ?)
  • Exertional dyspnea that stops immediately could be anginal equivalent.
  • Dyspnea with palpitation is  rarely be anginal  equivalent as palpitation indicate good LV /mitral valve function.
  • Dyspnea on  isometric  exercise rather than isotonic exercise .

Mechanism of anginal equivalence

While the trigger for dyspnea is elevated LVEDP  which   stimulates the  stretch receptors in lung .For angina ,  it is the free nerve ending in myocytes that gets irritated and generate pain signals.

When ischemia  presents as dyspnea  two mechanisms are considered. One is myocardial , other is purely neurogenic.

  1. It is  believed critical   ischemia  of myocardium  ( Defective Ca ++ uptake  into sarcoplasmic reticulum) induce  “a wide area  diastolic dysfunction” of LV  that   raises  PCWP  to generate  dyspnea. Further , ischemia induced regional LV dysfunction  that  subtends the pap muscle could  result  in ischemic  MR and severe dyspnea. (Exertional Mitral regurgitation is getting major attention now  )
  2.  In many patients with diabetes or autonomic dysfunction the velocity of  pain signals  become sluggish  or  blocked  en-route  to brain stem . Often they change track to travel in the nerves  meant  for  carrying somatic siganls  ,  J receptors  , intercostal spindle etc . This spill over and cross talk  creates a  false sense of dyspnea , whenever ischemia  occurs. This is attributed to the  wide and complex  neural network of thoracic sympathetic ganglions.

Some of the known  associations with Angina equivalent .

  • Diastolic dysfunction
  • Ischemic MR
  • Small rigid  left atrium
  • Atrial fibrillation

How to  investigate a patient who is  suspected to have  angina equivalent dyspnea ?

  • ECG
  • X ray chest
  • Echocardiogram will settle the issue most times.

Nuclear scan and angiogram in deserving patients

When can  angina and   dyspnea occur together  ?

Angina and dyspnea  if   truely  occur together causes  grave concern for the physician.

This indicates two things .

  1. The myocardium is ischemic  and generates  pain (And possibly ongoing necrosis) .
  2. Simultaneously its  pumping or receiving function is also compromised resulting in  entry block from the lung resulting in acute dyspnea.

Both are ominous signals . This situation occurs  most often in  STEMI with LV failure .

If  dyspnea occur in NSTEMI/UA ,  it is a worst possible complication . GRACE  registry quotes  maximum  mortality for unstable angina with cardiac failure .The reason being the cardiac failure in UA is due to non necrotic global ischemic stunning of LV myocardium with or with out acute  mitral valve failure.(Flash pulmonary edema)

Why angina is rare  in  chronic congestive  cardiac failure ?

The main reason being  , a severely dysfunctional heart  contracts  poorly .In reality , it is never thirsty for blood  . Even if it  is  perfused  well  , there is no good muscle  mass  to burn the ATPs from it .A failed myocardium is  more or less a  sleeping  myocardium .It does not even have the  energy   to cry with pain at times of ischemia ! .However significant the ischemia  is ,   it can often  evoke only  a gasping sensation .

The other explanation  is more imaginative . In cardiac failure heart  dilates .The end diastolic and end systolic  volume is high. The cardiac chamber is always filled with  excess residual blood .This , some how tend to perfuse the myocardium directly and provide a good reserve .This may be  more important in  RV perfusion  .( Trans myocardial laser revascularization is based on this concept – direct myocardial perfusion from the chambers)

While angina is  rare in chronic cardiac failure,   it should also be realised ,dyspnea  is  rare in  uncomplicated acute coronary  syndromes. We know ACS  primarily present with angina.  Exceptions are always there.

In elderly, diabetic , with co morbid   patients ,    ACS  may  present without  angina . Instead  they present with vague dyspnea and shortness of breath . It is here ,  physicians  face a tough task to identify  dyspnea  behaving like   angina  equivalent.  Of course , the  good old  ECG bails us out most of the time.

Therapeutic importance of recognising anginal  equivalents ?

The revascularisation  procedures (CABG/PCI)  are too good  in  relieving  angina , but least effective in providing relief from dyspnea.So  real anginal equivalents if recognised properly can be subjected to early revascularisation .

Can we consider  exertional dyspnea as evidence for ongoing ischemia  in a post MI patient ?

This is tricky question . We do not have answers to it. Readers can try to  answer . The commonest cause of dyspnea following MI is due to physical deconditioning and associated LV dysfunction.

Final message

Coming back to the basic question  , Is  this dyspnea  . . .  an angina equivalent  doctor ?   No simple answer is available .

The first and foremost investigation to do  is ECG .This will settle the issue many times.  Next is the reassessment of  history  clinical  presentation and past history.  Every patient with unexplained dyspnea must undergo a minimum of three investigations (ECG,  X ray chest and Echocardiogram )  If any of these  suggest a cardiac compromise   further evaluation is   indicated.

So, the message here is ,  clinical findings  are insufficient  to rule out ischemic etiology for dyspnea.

References

Nil . Every thing is my random thoughts !

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Thorax is a rigid bony  box  with a fixed space.The intra thoracic organs are snugly  arranged  within the cavity.The two lungs on either side with the heart in the middle fill the major volume of the mediastinum .In  physiological conditions the volume of mediastinum remain almost constant , except for the respiratory swings.

heart lungs pulmonary function test dyspnea cardiomegaly ct ratio

It is to be noted the two major organs inside the thorax has a distinct behavioral pattern.  Lung  a very pressure sensitive  structure tend to collapse   whenever confronted  with external pressure .This is evident in all cases of large pleural effusion (Note :The heart collapses only in a fraction of patients with  large pericardial effusion -ie tamponade) . Similarly in any mediastinal syndromes , first  the lung function is affected , logics then dictate ,  the  low pressure venous system to get compressed resulting in SVC /IVC syndrome.Finally the   right  heart chambers may get interfered with .This is due the  dynamic  intracardiac  pressures   that resists any compression from exterior.

So, it is obvious  ,  lung function is affected with raised intrathoracic volume or pressure .The increase in intrathoracic volume can be due to any thing .

cardiomegaly massive dyspnea mechanism lvedp

The volume of heart in cardiac failure can  increase very significantly .For a fraction  raise of CT ratio there is many fold raise in it’s volume.A CT ratio of 75% can cause a huge ” housing & accommodation ” problem for the lungs on either side . As we have discussed , the lung is  passive organ  has absolutely  no other option  but to bow down like a touch me not plant . The  lung , reduces it’s ventilatory   function impairing  the already poor exercise capacity .The terminal respiratory units collapse  significantly. This collapse is not visible in x rays as there is no intrinsic obstruction within the airways as happens in lung pathology.

The course of events in progressive cardiomegaly is often  silent and heart successfully encroaches the the human breathing space  until the heart failure is corrected and normal heart  size is restored. Complete reversal of heart size may not be possible always !

A new unrecognized mechanism for cardiac dyspnea ?

Yes,the mechanism of cardiac dyspnea always been  centered around elevated LVEDP , lung congestion etc and the resultant stimulation of lung receptors.

Now we realise  a reduction in the lung ventilatory  capacity  may also  contribute significantly in every patient with cardiac  failure and cardiomegaly.

When a person with single pnemonectomy lead a comfortable life what is the big issue of heart compressing few respiratory segments of a patient ?

It is true a single normally functioning lungs is sufficient for living but what we are dealing here is patients with compromised cardiac function.Recruitment or non recruitment  of even few  respiratory bronchooles may have a bearing on  patients symptoms and exercise capacity.

Final  message

Cardiomegaly  is not an  inert  consequence  of cardiac  failure. It can have important functional  impact on the pulmonary ventilatory  and perfusion capacity .It should be emphasised  this mechanical encroachment on the lung space is over and above the hemodynamic effects on pulmonary capillary circulation .

Youngsters  should recognise  this fact  as this offers  one more explanation for cardiac dyspnea. This is not often discussed in the clinical  classes.

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