Coronary perfusion pressure

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Coronary Vasculature Coronary vessels, with annotated arteries.svg
Coronary Vasculature

Coronary perfusion pressure (CPP) refers to the pressure gradient that drives coronary blood pressure. The heart's function is to perfuse blood to the body, however the heart's myocardium must, itself, be supplied for its own muscle function. The heart is supplied by coronary vessels and therefore CPP is the pressure within those vessels. If pressures are too low in the coronary vasculature, then the myocardium risks ischemia with subsequent myocardial infarction and/or cardiogenic shock.

Contents

Physiology

The coronary arteries originate off of the ascending aorta and continue onto the surface of the heart (the epicardium). When the heart contracts during systole, the contraction compresses the coronary arteries which prevents perfusion. Therefore, it is only when the heart relaxes, during diastole, that the coronary vessels open up and allow for perfusion; thus CPP is highest during diastole, unlike most other arteries which experience higher perfusion pressures under systole. CPP can be measured by calculating the difference between the aortic pressure and the left ventricular end diastolic pressure:

Coronary Perfusion Pressure (CPP) = Aortic Diastolic Pressure – Left Ventricular end-diastolic Pressure (LVEDP)

In the research setting, the absolute CPP can be measured using coronary and aortic pressure transducers, however, CPP is not regularly measured in human clinical practice. During cardiac surgery, when a patient is placed on cardiopulmonary bypass, and blood is passed through the coronary vessels in a retrograde direction, CPP can be approximated by using the measured right atrial pressure in place of LVEDP because the coronary sinus drains into the right atrium.

CPP is not the sole determinant of coronary blood flow (CBF). CBF is also determined mainly by metabolic autoregulation; sympathetic regulation plays some role in coronary dilation/constriction but less so than in other vascular systems. That is, when the ventricular myocardium is working, it extracts oxygen from the coronary blood and produces adenosine as a by product of ATP use. Hypoxia and adenosine both contribute to coronary vasodilation, which increase CBF. Both higher CPP and greater vasodilation will result in higher CBF. [1]

Clinical Relevance

Cardiac Arrest

The concept of CPP, while relevant to overall cardiovascular physiology, is acutely important in cardiac arrest care. Cardiac arrests are fundamentally treated with CPR which includes chest compressions. These compressions serve two goals. First, the compressions circulate blood to the brain and other tissues which helps reduce their ischemia and attenuates later post-cardiac arrest syndrome. This goal is accomplished during the compression phase of the CPR cycle as it creates systole-like hemodynamics .

The second goal, is to perfuse the heart itself. Perfusion of the heart is necessary for successful defibrillation (if the arrest type is shockable) and ROSC. [2] This is accomplished during the relaxation phase of CPR as it creates diastole-like conditions. [3]

During cardiac arrest, CPP is one of the most important variables associated with the likelihood of return of spontaneous circulation (ROSC), the restoration of a pulse. A CPP of at least 15 mmHg is thought to be necessary for ROSC. [4] Epinephrine, administered as part of ACLS for cardiac arrest care seems to increase CPP due to its combined effects of inotropy and vasoconstriction. [5]

Myocardial Infarction

Type 2 myocardial Infarctions (T2MI) result any time coronary flow is reduced secondary to a non-thrombotic cause. Because coronary flow is determined partly by coronary perfusion pressure, a reduction in CPP increases the risk of T2MI. Reduced CPP can be the result of a multitude of pathologies including cardiogenic shock and tachyarrythmia. Patients who are CPP dependent, such as those with CAD and heart failure, are particularly susceptible to T2MI when insulted with a further reduced CPP. [6]

Coronary Artery Disease (CAD)

CPP becomes relevant in coronary artery disease as atherosclerosis causes stenosis of the coronary arteries. The arteries initially respond by vasodilating to maintain coronary blood flow. However once the vasodilatory capacity is maximized, the coronary arteries become solely dependent on high enough CPP to perfuse past the atherosclerotic lesion. If CPP can not be maintained at a high enough pressure, the coronary arteries and underlying myocardium become ischemic. [6]

Heart Failure

Heart failure, both with and without preserved ejection fraction, though though different mechanisms, result in an increase in left ventricular end-diastolic pressure (LVEDP). [7] Because CPP is measured by the difference in aortic and LVEDP pressures, an increase in LVEDP will decrease CPP. The heart may compensate for this reduction in CPP by increasing contractility and subsequent aortic pressure. However, this process requires greater oxygen consumption and will promote ventricular remodeling. While this process may acutely compensate for the initial reduction in CPP, the overall process of hypertrophic remodeling is deleterious and leaves the heart susceptible to ischemia. [6]

See also

Related Research Articles

Cardiac arrest Sudden stop in effective blood flow due to the failure of the heart to contract effectively

Cardiac arrest is the sudden loss of blood flow throughout the body resulting from the heart not being able to pump blood efficiently. It is a rapidly fatal medical emergency requiring immediate intervention with cardiopulmonary resuscitation (CPR) until further treatment can be provided. Cardiac arrest results in rapid loss of consciousness and breathing may be abnormal or absent. While cardiac arrest may be caused by heart attack or heart failure, these are not the same, and in 15 to 25% of cases there is a non-cardiac cause. Some individuals may experience chest pain, shortness of breath or nausea immediately before entering cardiac arrest. Additionally, an elevated heart rate and feelings of light-headedness may occur before the episode. If not intervened by CPR and defibrillation, cardiac arrest typically leads to death within minutes.

Coronary circulation Circulation of blood in the blood vessels of the heart muscle (myocardium)

Coronary circulation is the circulation of blood in the blood vessels that supply the heart muscle (myocardium). Coronary arteries supply oxygenated blood to the heart muscle. Cardiac veins then drain away the blood after it has been deoxygenated. Because the rest of the body, and most especially the brain, needs a steady supply of oxygenated blood that is free of all but the slightest interruptions, the heart is required to function continuously. Therefore its circulation is of major importance not only to its own tissues but to the entire body and even the level of consciousness of the brain from moment to moment. Interruptions of coronary circulation quickly cause heart attacks, in which the heart muscle is damaged by oxygen starvation. Such interruptions are usually caused by coronary ischemia linked to coronary artery disease, and sometimes to embolism from other causes like obstruction in blood flow through vessels.

Ventricular fibrillation Rapid quivering of the ventricles of the heart

Ventricular fibrillation is an abnormal heart rhythm in which the ventricles of the heart quiver. It is due to disorganized electrical activity. Ventricular fibrillation results in cardiac arrest with loss of consciousness and no pulse. This is followed by death in the absence of treatment. Ventricular fibrillation is initially found in about 10% of people with cardiac arrest.

Aortic valve Valve in the human heart between the left ventricle and the aorta

The aortic valve is a valve in the heart of humans and most other animals, located between the left ventricle and the aorta. It is one of the four valves of the heart and one of the two semilunar valves, the other being the pulmonary valve. The aortic valve normally has three cusps or leaflets, although in 1–2% of the population it is found to congenitally have two leaflets. The aortic valve is the last structure in the heart the blood travels through before stopping the flow through the systemic circulation.

Systole Part of the cardiac cycle when a heart chamber contracts

The systole is the part of the cardiac cycle during which some chambers of the heart muscle contract after refilling with blood. The term originates, via New Latin, from Ancient Greek συστολή (sustolē), from συστέλλειν, and is similar to the use of the English term to squeeze.

Ventricle (heart) Chamber of the heart

A ventricle is one of two large chambers toward the bottom of the heart that collect and expel blood towards the peripheral beds within the body and lungs. The blood pumped by a ventricle is supplied by an atrium, an adjacent chamber in the upper heart that is smaller than a ventricle. Interventricular means between the ventricles, while intraventricular means within one ventricle.

Diastole

Diastole is the part of the cardiac cycle during which the heart refills with blood after the emptying is done during systole (contraction). Ventricular diastole is the period during which the two ventricles are relaxing from the contortions/wringing of contraction, then dilating and filling; atrial diastole is the period during which the two atria likewise are relaxing under suction, dilating, and filling. The term originates from the Greek word διαστολή (diastolē), meaning "dilation", from διά + στέλλειν.

Cardiac cycle Performance of the heart from the end of one heartbeat to the beginning of the next

The cardiac cycle is the performance of the human heart from the beginning of one heartbeat to the beginning of the next. It consists of two periods: one during which the heart muscle relaxes and refills with blood, called diastole, following a period of robust contraction and pumping of blood, called systole. After emptying, the heart immediately relaxes and expands to receive another influx of blood returning from the lungs and other systems of the body, before again contracting to pump blood to the lungs and those systems. A normally performing heart must be fully expanded before it can efficiently pump again. Assuming a healthy heart and a typical rate of 70 to 75 beats per minute, each cardiac cycle, or heartbeat, takes about 0.8 seconds to complete the cycle. There are two atrial and two ventricle chambers of the heart; they are paired as the left heart and the right heart—that is, the left atrium with the left ventricle, the right atrium with the right ventricle—and they work in concert to repeat the cardiac cycle continuously,. At the start of the cycle, during ventricular diastole–early, the heart relaxes and expands while receiving blood into both ventricles through both atria; then, near the end of ventricular diastole–late, the two atria begin to contract, and each atrium pumps blood into the ventricle below it. During ventricular systole the ventricles are contracting and vigorously pulsing two separated blood supplies from the heart—one to the lungs and one to all other body organs and systems—while the two atria are relaxed. This precise coordination ensures that blood is efficiently collected and circulated throughout the body.

The intra-aortic balloon pump(IABP) is a mechanical device that increases myocardial oxygen perfusion and indirectly increases cardiac output through afterload reduction. It consists of a cylindrical polyurethane balloon that sits in the aorta, approximately 2 centimeters (0.79 in) from the left subclavian artery. The balloon inflates and deflates via counter pulsation, meaning it actively deflates in systole and inflates in diastole. Systolic deflation decreases afterload through a vacuum effect and indirectly increases forward flow from the heart. Diastolic inflation increases blood flow to the coronary arteries via retrograde flow. These actions combine to decrease myocardial oxygen demand and increase myocardial oxygen supply.

Cardioplegia is intentional and temporary cessation of cardiac activity, primarily for cardiac surgery.

Coronary artery anomalies are variations of the coronary circulation, affecting <1% of the general population. Symptoms include chest pain, shortness of breath and syncope, although cardiac arrest may be the first clinical presentation. Several varieties are identified, with a different potential to cause sudden cardiac death.

The following outline is provided as an overview of and topical guide to cardiology, the branch of medicine dealing with disorders of the human heart. The field includes medical diagnosis and treatment of congenital heart defects, coronary artery disease, heart failure, valvular heart disease and electrophysiology. Physicians who specialize in cardiology are called cardiologists.

Myocardial bridge Medical condition

A myocardial bridge (MB) is a congenital heart defect in which one of the coronary arteries tunnels through the heart muscle itself (myocardium). In normal patients, the coronary arteries rest on top of the heart muscle and feed blood down into smaller vessels which then take blood into the heart muscle itself. However, if a band of muscle forms around one of the coronary arteries during the fetal stage of development, then a myocardial bridge is formed - a "bridge" of heart muscle over the artery. Each time the heart squeezes to pump blood, the band of muscle exerts pressure and constricts the artery, reducing blood flow to the heart. This defect is present from birth. It is important to note that even a very thin ex. < 1 mm and/or short ex. 20 mm MB can cause significant symptoms. MBs can range from a few mm in length to 10 cm or more. The overall prevalence of myocardial bridge is 19%, although its prevalence found by autopsy is much higher (42%).

Cardiac physiology or heart function is the study of healthy, unimpaired function of the heart: involving blood flow; myocardium structure; the electrical conduction system of the heart; the cardiac cycle and cardiac output and how these interact and depend on one another.

Return of spontaneous circulation (ROSC) is the resumption of a sustained heart rhythm that perfuses the body after cardiac arrest. It is commonly associated with significant respiratory effort. Signs of return of spontaneous circulation include breathing, coughing, or movement and a palpable pulse or a measurable blood pressure. Someone is considered to have sustained return of spontaneous circulation when circulation persists and cardiopulmonary resuscitation has ceased for at least 20 consecutive minutes.

Impella is a family of medical devices used for temporary ventricular support in patients with depressed heart function. Some versions of the device can provide left heart support during other forms of mechanical circulatory support including ECMO and Centrimag.

Heart failure with preserved ejection fraction Medical condition

Heart failure with preserved ejection fraction (HFpEF) is a form of heart failure in which the ejection fraction – the percentage of the volume of blood ejected from the left ventricle with each heartbeat divided by the volume of blood when the left ventricle is maximally filled – is normal, defined as greater than 50%; this may be measured by echocardiography or cardiac catheterization. Approximately half of people with heart failure have preserved ejection fraction, while the other half have a reduction in ejection fraction, called heart failure with reduced ejection fraction (HFrEF).

Rearrest

Rearrest is a phenomenon that involves the resumption of a lethal cardiac dysrhythmia after successful return of spontaneous circulation (ROSC) has been achieved during the course of resuscitation. Survival to hospital discharge rates are as low as 7% for cardiac arrest in general and although treatable, rearrest may worsen these survival chances. Rearrest commonly occurs in the out-of-hospital setting under the treatment of health care providers.

Extracorporeal cardiopulmonary resuscitation is a method of cardiopulmonary resuscitation (CPR) that passes the patient's blood through a machine in a process to oxygenate the blood supply. A portable extracorporeal membrane oxygenation (ECMO) device is used as an adjunct to standard CPR. A patient who is deemed to be in cardiac arrest refractory to CPR has percutaneous catheters inserted into the femoral vein and artery. Theoretically, the application of ECPR allows for the return of cerebral perfusion in a more sustainable manner than with external compressions alone. By attaching an ECMO device to a person who has acutely undergone cardiovascular collapse, practitioners can maintain end-organ perfusion whilst assessing the potential reversal of causal pathology, with the goal of improving long-term survival and neurological outcomes.

Pathophysiology of heart failure

The main pathophysiology of heart failure is a reduction in the efficiency of the heart muscle, through damage or overloading. As such, it can be caused by a wide number of conditions, including myocardial infarction, hypertension and amyloidosis. Over time these increases in workload will produce changes to the heart itself:

References

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