End-systolic pressure volume relationship by E.S.Prakash is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported License.
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Download a copy – Updated 2014
During ventricular filling, the papillary muscles are relaxed and the AV valves are opened by the pressure gradient between the atrium and the respective ventricle.
This illustration may be helpful: http://www.youtube.com/watch?v=rgY7Ic_9K0M
At the start of ventricular systole, contraction of the papillary muscles tenses the chordae tendineae, and causes the AV valves to shut (S1). This minimizes regurgitation of blood into the atrium during ventricular contraction.
When both papillary muscles are damaged in the left ventricle (such as by papillary muscle infarction), the clinical consequence is typically mitral regurgitation.
Poorly contracting papillary muscles (in the left ventricle) may allow the cusps of the mitral valve to prolapse into the left atrium during left ventricular systole. When the leaflets of the valve prolapse into the atrium, the inner margins of the cusps are further separated making regurgitation more likely.
Of course, additional factors may contribute to mitral regurgitation depending on the presence of other predisposing factors. For example, an abnormally dilated left ventricle may widen the mitral valve annulus, and regurgitation can occur in the absence of pathology in the mitral (or tricuspid) valve per se. This phenomenon is called “functional” regurgitation.
Potassium efflux is the major mechanism of repolarization of ventricular myocytes. This current is sensitive to extracellular potassium level, and in hyperkalemia, potassium conductance is increased so that more potassium leaves the myocyte in any given time period. This leads to an increase in the slope of phases 2 and 3 of the action potential and a shortening of the repolarization time. This is thought to be the mechanism responsible for some of the early electrocardiographic manifestations of hyperkalemia, such as ST-T segment depression, peaked T waves, and Q-T interval shortening.
Jose and Collison (1970) defined <strong>“intrinsic heart rate (IHR)”</strong>, as the heart rate under the simultaneous presence of the nonselective β-adrenoceptor antagonist propranolol (0.2 mg/kg) and the muscarinic receptor blocker atropine (0.04 mg/kg) 5 min after these injections, and this definition continues to be used in mainstream cardiology literature. In their study of over 400 apparently healthy human subjects age (ranging from 18-60 yr) intrinsic heart rate of the SA node in humans ranged from 80-120 (mean 104) beats per minute. Another important observation they made was a reduction in intrinsic heart rate with age. Based on their data, the relationship between age and IHR was as follows:
IHR = 118 – (age * 0.57); even for someone 60 years old, IHR would be 80 bpm.
If resting HR is lower (as it is in most healthy individuals) than an individual’s intrinsic HR, it means that, at rest, vagal influences dominate over sympathetic influences on the SA node’s intrinsic firing rate.
Sick sinus syndrome (or sinus node dysfunction) is by definition an abnormally low “intrinsic heart rate”. Someone with an intrinsic sinus rate of 60 bpm would likely be very prone to the consequences of bradycardia (low cardiac output and hypotension and its consequences).
The “intrinsic rate” of the AV node or the Purkinje system is not as easily determined in healthy humans and indirect electrophysiologic methods are used, but it is true that even with autonomic support AV nodal firing frequency is significantly lower than that of the SA node. That is why the SA node normally is the pacemaker. Similarly, even with sympathetic stimulation, an infranodal rhythm originating in the Purkinje system may result in a ventricular rate as low as 20 bpm (but this rate is not to be called intrinsic rate of the Purkinje system).
If you encounter someone with a resting heart rate of say 40-50 bpm, there are only two broad possibilities:
– Increase in vagal tone;
– Abnormally low intrinsic heart rate (and or disease of the cardiac conduction system);
Individuals whose low resting HR is as low as 40 bpm because of heightened vagal tone at rest may be going about their work as usual (example, well trained athletes), because they have a larger stroke volume. On the other hand someone whose resting HR is 40 bpm because of sinus node dysfunction or disease of the conduction system will be very vulnerable to hypotension from low cardiac output.
Dissecting these two possibilities in an individual with bradycardia (HR < 60 bpm) is usually achieved clinically by asking the question: HR is low – so what? Is there any evidence of cerebral hypoperfusion because the HR is as low, and with an EKG. Someone with bradycardia due to sinus node dysfunction is less likely to demonstrate significant sinus arrhythmia (one can assess this by checking the ECG during deep breathing); normally, during deep inspiration, cardiac acceleration is apparent, and the heart rate decreases during deep expiration. On the other hand an athlete with sinus bradycardia will have profound respiratory sinus arrhythmia (and this is a normal phenomenon brought about by fluctuations in vagal nerve traffic to the heart with breathing).
If further evidence is needed, the response to an intravenous bolus of atropine will provide the answer. If the resting bradycardia is due to high vagal tone, the response to atropine will consist of a profound increase in HR 20 bpm or greater. On the other hand if bradycardia were due to SA nodal dysfunction, the heart rate increment with atropine will be negligible (not exceed 5 bpm).
See this video clip http://www.nature.com/gimo/contents/pt1/images/gimo19-v3.mov
It is a videofluoroscopic study of the oropharyngeal phase of swallowing that shows aspiration of barium sulfate into the trachea. Patients with strokes affecting the medulla, myasthenia gravis, or motor neuron disease may have defects in swallowing that increase the likelihood of aspiration pneumonia.