HEART RATE

•Pulse rate represents heart rate.

 

•With each stroke output, blood is ejected into circulation which produces arterial pulsation

 

•Arterial pulse rate coincides with ventricular ejection rate.

NORMAL HEART RATE 

• Normal heart rate is 60-100 beats per minute in adults.

 

•HR less than 60 bpm is called bradycardia.

 

•HR more than 100 bpm is called tachycardia.

 

•HR is the rate of discharge of SA node.

PHYSIOLOGICAL VARIATIONS OF HEART RATE 

•Age 

HR is more in infants and children .

HR is less after sixty years age.

 

•Gender 

Its less in females due to their high parasympathetic tone and less basal metabolism.

 

•Diurnal variation 

More in the day time and less in sleep due to less physical activity and less stress.

 

•Respiration 

HR is more during inspiration and less during expiration (sinus arythmia)

 

•Body temperature 

Higher temperature favours higher heart rate.

 

•Environment 

HR is more in summer

 

•Food intake 

It increases HR by increasing body metabolism.

•Posture 

On standing from supine , heart rate increases due to decreased stimulation of baroreceptors.

 

•Exercise

HR increases with exercise due to sympathetic stimulation.

 

REGULATION OF HEART RATE (HR)

•HR is primarily controlled by autonomic nervous system.

 

•Vagus nerve (Parasympathetic-PNS) inhibits and sympathetic nerves (SNS) stimulates HR.

 

•HR is primarily a vagal function.

 

•Neural and humoral mechanisms are involved in regulation of HR.

AUTONOMIC REGULATION  (medullary CV center)

 

Receives input from higher brain centers and variety of sensory receptors.

       •Proprioreceptors

       •Chemoreceptors

       •Baroreceptors

 

•Sympathetic output increases HR and contractility.

 

•Parasympathetic impulses decreases HR.

•PNS has little effect on contractility ( because

 it does not innervate ventricular myocardium)

•Several factors contribute to regulation of heart rate:

CHEMICAL REGULATION 

•Cardiac activity is depressed by.    

       •Hypoxia

       •Acidosis

       •Alkalosis

PARASYMPATHETIC NERVOUS SYSTEM 

•Vagus nerve (via ACh) decreases HR by decreasing or slowing down the inflow of Na+ and Ca++ and by increasing the subsequent outflow of potassium (K+).

 

•Acts at SA and AV nodes.

 

•May treat SNS-driven heart attack by gagging or massage of carotid arteries and activates vagal reflexes. 

PNS counteracts SNS.

CARDIVASCULAR RESPONSE TO STRESS 

•It leads to increase in heart rate which is due to increase in SNS tone and decrease in PNS tone

 

•Norepinephrine (NE) and epinephrine (Epi) increases which leads to increase in inflow of Na+ and Ca++

Which increase rate of re-excitation in SA node.

 

•This increase in intracellular  Ca++ also increases contractility.

 

•SNS terminals also excite AV node and whole myocardium therefore enhances contractility everywhere.

REFLEX CONTROL 

•Cardiovascular reflexes that regulate BP also control HR , which is part of integrated control mechanisms.

 

• Reflexed includes -

        •Baroreceptor reflex

        •Chemoreceptor reflex

        •Bainbridge reflex

        •Cushing’s reflex

BARORECEPTOR REFLEX 

•Baroreceptors are located in the carotid sinus and aortic arch.

 

•They are stimulated when BP rises and this stimulates Nucleus Tractus Solitarius(NTS) in medulla via 9th and 10th cranial nerves

 

•NTS inhibits Vasomotor center(VMC)

BAINBRIDGE REFLEX 

•The receptors are present in the atria at the venoatrial junction . They are known as tachycardia producing receptors.

 

•This reflex accounts for tachycardia produced following saline infusion or blood transfusion.

 

•It is more observable when initial HR is low.

CHEMORECEPTOR REFLEX 

•Chemoreceptors responds to hypoxia, hypercapnia and acidosis.

 

•Activation of chemoreceptors primarily produces bradycardia.

CUSHING'S REFLEX 

• Activated in gross hypotension that decreases blood flow to the VMC .

 

•Direct stimulation of VMC  produces vasoconstriction and tachycardia.

 

 REGULATION OF HEART RATE BY HIGHER CENTRES 

•Stimulation of motor cortex, frontal lobe, and thalamus increases HR.

 

•Increase in HR in emotional states, anxiety and excitement is due to stimulation of limbic system.

HUMORAL AND CHEMICAL CONTROL OF HR 

It is mediated by .

    •Hormones

•Catecholamines and thyroid hormones increase HR and contractility

     •Cations

•Alterations in balance of K+, Na+ and Ca2+ alter HR and contractility

 

MAREY'S LAW 

•Muscular exercise and anxiety are exception for Marey’s law. Both BP and HR increases

HEART RATE VARIABILITY 

•Heart rate variability is the physiological phenomenon of variation in the time interval between heartbeats.

 

• It is measured by the variation in the beat-to-beat interval

 

•Other terms used include: "cycle length variability", "RR variability", and "heart period variability"

Heart rate variability or HRV is the physiological phenomenon of the variation in the time interval between consecutive heartbeats in milliseconds.

PHYSIO LOGICAL IMPORTANCE OF HEAR RATE VARIABILITY ( HRV)

•HRV is regulated by the autonomic nervous system (ANS), and its sympathetic and parasympathetic branches.

 

• It is commonly accepted as a non-invasive marker of autonomic nervous system activity.

•The sympathetic branch activates stress hormone production and increases the heart’s contraction rate and force (cardiac output) and decreases HRV.

 

• It  is needed during exercise and mentally or physically stressful situations.

•The parasympathetic branch slows the heart rate and increases HRV to restore homeostasis after the stress passes.

 

• This natural interplay between the two systems allows the heart to quickly respond to different situations and needs.

Study of HRV in time and frequency domain

•The HRV was evaluated by both time domain and frequency domain analysis.

 

•Mean heart rate, standard deviation of all R–R intervals (SDNN) and root-mean-square of successive differences (RMSSD) were measured in the time domain analysis of HRV.

 

•Done with holter monitoring for 24 hrs

EFFECT OF RESPIRATION ON HEART RATE

•While breathing normally, heart rates usually increase during inhalation and decrease during exhalation.

 

•This cyclic change in heart rate, that is driven by breathing, is known as Respiratory Sinus Arrhythmia (RSA).

RESPIRATORY SINUS ARRHYTHMIA (RSA)

Clinical importance of RSA

•Sinus arrhythmia is a commonly encountered variation of normal sinus rhythm.

 

•Sinus arrhythmia characteristically presents with an irregular rate in which the variation in the R-R interval is greater than 0.12 seconds.

 

•Additionally, P waves are typically monoform and in a pattern consistent with atrial activation originating from the sinus node.

 

•During respiration, the intermittent vagus nerve activation occurs, which results in beat to beat variations in the resting heart rate.

 

•When present, sinus arrhythmia typically indicates good cardiovascular health.

•Sinus arrhythmia is a common rhythm variation. It is seen more often in children and young adults.

 

•Respirations lead to vagal stimuli resulting in R-R interval variations.

 

•Typically its presence is an indicator of good cardiovascular health.

 

• Loss of sinus arrhythmia may indicate underlying heart failure or structural heart disease.

JUGULAR VENOUS PRESSURE(JVP)

•The jugular venous pressure (JVP, sometimes referred to as jugular venous pulse) is the indirectly observed pressure over the venous system via visualization of the internal jugular vein.

 

•It can be useful in the differentiation of different forms of heart and lung disease.

•Classically three upward deflections and two downward deflections have been described.

 

•The upward deflections are the "a" (atrial contraction), "c" (ventricular contraction and resulting bulging of tricuspid into the right atrium during isovolumetric systole) and "v" = venous filling.

 

•The downward deflections of the wave are the "x" (the atrium relaxes and the tricuspid valve moves downward) and the "y" descent (filling of ventricle after tricuspid opening) .

VISUALISATION OF JVP

 

•The veins of the neck, are viewed from in front.

 

•The patient is positioned at a 45° incline, and the filling level of the external jugular vein determined.

 

•Visualize the internal jugular vein when looking for the pulsation.

 

•In healthy people, the filling level of the jugular vein should be less than 3 centimeters vertical height above the sternal angle.

 

•A pen-light can aid in discerning the jugular filling level by providing tangential light.

 

 •The JVP is easiest to observe if one looks along the surface of the sternocleidomastoid muscle  as it is easier to appreciate the movement relative to the neck when looking from the side (as opposed to looking at the surface at a 90 degree angle).

 

•Pulses in the JVP are rather hard to observe, but trained cardiologists do try to discern these as signs of the state of the right atrium.

 

DIFFERENCES BETWEEN JVP AND CAROTID PULSE 

 

•The JVP and carotid pulse can be differentiated in several ways:

•Multiphasic - the JVP "beats" twice (in quick succession) in the cardiac cycle. In other words, there are two waves in the JVP for each contraction-relaxation cycle by the heart.

 

•The first beat represents that atrial contraction (termed a) and second beat represents venous filling of the right atrium against a closed tricuspid valve (termed v) and not the commonly mistaken 'ventricular contraction'.

 

• The carotid artery only has one beat in the cardiac cycle.

 

•Varies with respiration - the JVP usually decreases with deep inspiration.

 

•Physiologically, this is a consequence of the Frank–Starling mechanism as inspiration decreases the thoracic pressure and increases blood movement into the heart (venous return), which a healthy heart moves into the pulmonary circulation.

 

JVP RECORD

•There is no valve at the junction of superior venacava and right atrium.

 

•Hence right atrial pressure changes are transmitted to the jugular vein in the neck , producing 3 characteristic waves.

 

•“a” wave – due to atrial systole. Some blood regurgitates into the great veins when atria contracts , even though the orifices of ‘IVC’ and ‘SVC’ are constricted.

 

•In addition, venous inflow stops , causing rise in venous pressure , contributing to the

a wave’.

 

•‘ c wave’ – it is the transmitted manifestation of the rise in atrial pressure produced by the bulging of the tricuspid valve into the right atrium during isovolumetric ventricular contraction phase.

 

•‘v wave’ – it is due to rise in atrial pressure before the tricuspid valve opens during diastole.

JVP WAVE FORM

 

•The jugular venous pulsation has a biphasic waveform.

 

•The " a " wave corresponds to right Atrial contraction and ends synchronously with the carotid artery pulse. The peak of the 'a' wave demarcates the end of atrial systole.

 

•The " c " wave corresponds to right ventricular Contraction causing the triCuspid valve to bulge towards the right atrium.

 

 •The " x' " (x prime) descent follows the 'c' wave and occurs as a result of the right ventricle pulling the tricuspid valve downward during ventricular systole.

 

•(As stroke volume is ejected, the ventricle takes up less space in pericardium ,  allowing relaXed atrium to enlarge).

 

•The x' (x prime) descent can be used as a measure of right ventricle contractility.

 

•The " x " descent follows the 'a' wave and corresponds to atrial relaXation and rapid atrial filling due to low pressure.

 

•The " v " wave corresponds to Venous filling when the tricuspid valve is closed and venous pressure increases from venous return - this occurs during and following the carotid pulse.

 

•The " y " descent corresponds to the rapid emptYing of the atrium into the ventricle following the opening of the tricuspid valve.

 

INTERPRETATION

 

•Certain wave form abnormalities, include Cannon a-waves - increased amplitude 'a' waves, are associated with AV dissociation (third degree heart block),when the atrium is contracting against a closed tricuspid valve, or even in ventricular tachycardia.

 

•Another abnormality, "c-v waves", can be a sign of tricuspid regurgitation. The absence of 'a' waves may be seen in atrial fibrillation.

 •An elevated JVP is the classic sign of venous hypertension (e.g. right-sided heart failure). JVP elevation can be visualized as jugular venous distention, whereby the JVP is visualized at a level of the neck that is higher than normal.

 

•Kussmaul sign - paradoxical increase of the JVP with inspiration (instead of the expected decrease).

•It indicates impaired filling of the right ventricle.

 

•Differential diagnosis of Kussmaul's sign includes constrictive pericarditis , restrictive cardiomyopathy , pericardial effusion,  and severe right-sided heart failure.

 

•An exaggerated "x" wave or diastolic collapse of the neck veins from constrictive pericarditis is referred to as Friedreich's sign

 

•Parodoxical JVP (Kussmaul's sign): JVP rises with inspiration, drops with expiration) occurs in the following conditions

        •Pericardial effusion

        •Constrictive pericarditis

        •Pericardial tamponade

 

•Raised JVP, normal waveform occurs when their is one of the following 

       •Bradycardia

       •Fluid overload

       •Heart Failure

       •Raised JVP, absent pulsation

       •Superior vena cava syndrome

 

•Large 'a' wave (increased atrial contraction pressure) occurs in following conditions 

       •tricuspid stenosis

       •Right heart failure

       •Pulmonary hypertension

 

•Cannon 'a' wave (atria contracting against closed tricuspid valve) can be seen in the following conditions 

        •Atrial flutter

        •Premature atrial rhythm (or tachycardia)

        •third degree heart block

        •Ventricular ectopics

        •Ventricular tachycardia

 

CARDIAC MURMURS 

•A number of different adventitious sounds or heart murmurs , may also be detected.

 

•These abnormal sounds are usually associated with turbulence of blood generated as blood passes through the leaking valves or a valve that has a narrowed orifice resulting from a disease.

 

•HS3 and HS4 are less important , being normally inaudible.