What is the Significance of Heart Rate

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What is the significance of Heart Rate?
The heart rate is a fundamental element of hypotension both in terms of cause (tachyarrhythmias / bradyarrhythmias) and compensation – hypotension should be accompanied by a tachycardia. The amount of blood pumped from the heart per minute is the cardiac output. It is determined by the volume pumped in each cycle, the stroke volume (end diastolic volume minus the end systolic volume) and the frequency of the cycles, the heart rate. The ability of the heart to both receive and eject blood is a fundamental function of heart rate. Firstly if the rate is excessive, then the heart is unable to either fill or eject efficiently. If, for any reason the stroke volume falls, the heart is able to compensate by increasing the heart rate. The filling of the left ventricle is not just determined by the venous return, 30% of filling is derived from the “atrial kick”, which is lost in atrial fibrillation. In some circumstances, the stroke volume is fixed, such as in mitral and aortic stenosis and in infancy, the cardiac output is rate dependent. If baby’s, who normally have a fast heart rate, become bradycardic, then their cardiac output (and thus their blood pressure) falls. Patients who have permanent pacemakers behave in an opposite manner: if their stroke volume falls, they are unable to increase their heart rate to compensate. Hypotension and bradycardia is characteristic of excessive vagal activity. Cholinergic agents (particularly anticholinesterases such as neostigmine) will mimic vagotonicity. Other drugs may excessively slow nodal conduction - beta blockers, calcium channel blockers, digoxin etc. Hypotension may be the “egg, not the chicken” - it follow an excessively slow or fast heart rate. Complete heart block may cause hypotension, particularly in the non compliant left ventricle. Tachyarrhythmias will reduce filling time and curtail stroke volume

What is the significance of Stroke Volume
Low Stroke volume is caused by a problem with reception or a problem with ejection or inadequate blood volume. The heart’s normal tasks are to receive and eject blood. The stroke volume is the amount of blood ejected per cycle. If there is a problem with the stroke volume, it must involve either reception or ejection. Throughout this tutorial series we will separate out stroke volume and heart rate from the cardiac output.

What causes inadequate blood volume? Hypovolemia may be absolute or relative. Relative hypovolemia occurs when there is an increase in the size of the vascular tree, and there is inadequate blood volume available to fill this space. Absolute hypovolemia is caused by 1. inadequate intake of fluids relative to losses (dehydration), 2. Increased losses due to bleeding, diarrhea, diuresis (including diabetes insipidis), excessive sweating. The body compensates for volume loss in three ways. 1. Macrovascular compensation, 2. Renal adjustment, 3. Microciurulatory compensation.

Low Stroke Volume Problems with Reception (filling)
Problems with reception are: Inadequate venous return diastolic dysfunction & cardiac inflow obstruction

Fluid loss is caused by either absolute hypovolemia (e.g.blood loss) or relative hypovolemia (“third spacing”).

1) Inadequate venous return: due to hypovolemia. Inadequate preload or filling pressure occurs as a result of intravascular fluid depletion, which may be due to volume loss, such as bleeding or dehydration, or fluid redistribution – third space losses, such as occurs in bowel obstruction or capillary leak syndrome. Often severe fluid depletion exists before patients become hypotensive, due to the potency of the compensatory mechanism. In this state patients are vulnerable to interventions which may unmask fluid depletion, such as the administration of vasodilators, including anesthetic agents, and aggressive manual ventilation. Patients admitted to intensive care in compensated shock may become severely hypotensive following the administration of even very small doses of propofol or thiopental. There are many warning signs of under-resuscitation: a lingering tachycardia, cold peripheries or a pulse oximeter that is not reading, oliguria, low CVP, a large base excess on blood gas analysis, a lactic acidosis. Diastolic Dysfunction = stiff heart, requiring higher filling pressure to achieve normal volume. 2) Diastolic Dysfunction: loss of left ventricular compliance impairs it’s ability to receive blood. This disorder most commonly results from systolic dysfunction, and as a consequence of myocardial fibrosis – for example due to ischemia or hypertension. Diastolic dysfunction is characterized by the requirement of higher filling pressures to achieve normal filling volumes, while the heart is less compliant and receptive to blood. Aggressive volume loading of patients with diastolic dysfunction frequently results in backward heart failure, causing acute pulmonary edema. Cardiac inflow obstruction is caused by a pericardial (tamponade) or intrathoracic process (PEEP), or a lesion within the heart itself (mitral stenosis). 3) Cardiac inflow obstruction: occurs either due to a constriction around the heart, a pericardial or intrathoracic process, or a lesion within the heart itself. Pericardial injuries include pericardial effusion or hematoma constrictive pericarditis – an acute crisis associated with a pericardial injury is called tamponade. Tamponade is diagnosed as a tetrad of shock, clear lung fields, inaudible or muffled heart sounds, and an increase in the jugular venous pulse waveform on inspiration. An often forgotten but extremely common cause of hypotension is excessive intrathoracic pressure. This can be transmitted from within the alveolar space – as with positive end expiratory pressure (PEEP) and gas trapping in airway obstruction (autoPEEP), or within the pleural space – Pneumothorax, hemothorax or, if the patient is in extremis, tension Pneumothorax. Intracardiac lesions may also cause inflow obstruction; these include mitral and tricuspid stenosis or thrombosis, and atrial myxoma.

Low Stroke Volume Problems with Ejection (emptying)

Problems with ejection (systolic dysfunction) include pump failure and outflow obstruction Pump failure is caused by ischemia, overload, contusion, inflammation 1. Problems with the pump itself: the heart is a muscle, and if there is damage to the muscle it will not pump effectively. This may be due to inadequate functioning muscle mass, as occurs with ischemia, contusion (bruising in trauma), inflammation (myocarditis) and fibrosis, or to excessive stretch, with excessive fluid administration or valvular incompetence (e.g. aortic regurgitation). With each of these, confirmatory evidence may be available, electro-cardiographic or echocardiographic evidence of acute ischemia. The patient may give a good history of chest pain or trauma, cardiac enzymes may be positive, and murmurs may be audible. Do not forget the right ventricle: right ventricular contusion or infarction may be much more difficult to diagnose and the treatment is almost the polar opposite of that of left ventricular failure. The pump may be overwhelmed by excessive volume administration, or valvular (aortic or pulmonary) regurgitation. Cardiac outflow obstruction is caused by pulmonary embolism, aortic stenosis, aortic crossclamps 2. Outflow obstruction: there are two major sites that cardiac outflow may be blocked: at the level of the aortic valve (aortic stenosis) or within the low pressure (at thus easily occluded) pulmonary circulation – pulmonary embolism. The former can be diagnosed on the basis of history, ECG and classic murmur. The latter may be more difficult to diagnose. Useful information includes risk (cancer, immobility, deep venous thrombosis, lack of prophylaxis, pelvic and hip surgery), ECG changes (right sided – RVH, sinus tachycardia, atrial fibrillation, right bundle branch block), occasional chest x-ray findings, and definitive diagnosis on ventilation-perfusion scanning, spiral CT or pulmonary angiography.

Problems with Peripheral Resistance (distributive shock)
Shock caused by low peripheral vascular resistance is caused by loss of tonic vasoconstriction (vasoplegia), due to sympathectomy, anaphylaxis or sepsis, leading to relative hypovolemia. Distributive shock is a problem with the peripheral vascular resistance. Blood vessels are normally kept in a state of tonic vasoconstriction, maintained by the interaction between the baroreceptors and sympathetic nervous system. Under certain circumstances, injuries may reverse this process, blood vessels dilate, and the patient becomes hypotensive. An example of this situation occurs with spinal shock, due to high transection of the spinal cord, or spinal anesthesia, which causes a sympathetic

blockade. The patient develops a “relative hypovolemia” – the amount of fluid is the same, but the tubing is bigger. A similar picture occurs in anaphylactic shock: there is extensive mast cell degranulation in response to an allergen, and the histamine release causes vasodilatation. In sepsis, there are three fundamental physiologic upsets: increased synthesis of nitric oxide, activation of ATP-sensitive potassium channels in vascular smooth muscle, and deficiency of vasopressin. The plasma concentration of nitric oxide is markedly increased in septic shock. The production of this endogenous vasodilator appears to occur due to the expression of inducible nitric oxide synthetase by cytokines. This agent appears to be responsible for the end organ resistance to catecholamines and endothelin in sepsis. Tissue hypoxemia, acidosis and nitric oxide cause the activation of ATP sensitive potassium channels, which facilitates entry of potassium into smooth muscle cells and causes hyperpolarization of the membrane: the cells become resistant to depolarization and contraction. Vasopressin functions normally as part of the water conservation reflex system. However, this hormone is an effective vasoconstrictor in shock. In patients with vasodilated septic shock there appears to be an absolute deficiency of vasopressin, the reason for which is not clear. Administration of exogenous vasopressin appears to be very effective at reversing hypotension, even in very small doses. Vasopressin appears to enhance the effect of norepinephrine, and interfere with nitric oxide.

Shock Key Points
1. Blood 2. Cardiac Pressure Output is Cardiac is Output Heart multiplied Rate by times Peripheral Stroke Resistance. Volume.

3. Hypotension is caused by either inadequate Cardiac Output or inadequate Peripheral Resistance 4. Heart Rate, Stroke Volume and Total Peripheral Resistance exist in dynamic equilibrium: these interactions maintain blood pressure. If one of the three becomes abnormal, the other two compensate. This represents the cardiovascular physiologic reserve. 5. Hypotension is an indication of 1) an abnormality of Heart Rate, Stroke Volume or Peripheral Resistance, & 2) failure of the others to compensate. 6. Shock is acute circulatory failure leading to inadequate tissue perfusion and end organ injury: it classified as being due to malfunction of 1) the Pump (cardiogenic), 2 ) the Tubing (distributive), or 3) the Fluid (hypovolemic). 7. The heart rate is a fundamental element of hypotension both in terms of cause (tachyarrhythmias / bradyarrhythmias) and compensation – hypotension should be

accompanied

by

a

tachycardia.

8. Low Stroke volume is caused by a problem with reception or a problem with ejection.
9. Problems with reception are: inadequate venous return or cardiac inflow obstruction. 10. Fluid loss is caused by either absolute hypovolemia (e.g. blood loss) or relative hypovolemia (“third spacing”). 11. Cardiac inflow obstruction is caused by a pericardial (tamponade) or intrathoracic process (PEEP), or a lesion within the heart itself (mitral stenosis). 12. Problems with ejection include pump failure (ischemia, overload, contusion, inflammation) and outflow obstruction (embolism, aortic stenosis, aortic crossclamps). 13. Shock caused by low peripheral vascular resistance is caused by loss of tonic vasoconstriction (vasoplegia), due to sympathectomy, anaphylaxis or sepsis, leading to relative hypovolemia. 14. Vasodilation associated with septic shock occurs due to increased synthesis of nitric oxide, activation of ATP-sensitive potassium channels in vascular smooth muscle, and deficiency of vasopressin.

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