Coronary Perfusion Pressure

Issues of Concern

Coronary Perfusion Pressure and Coronary Blood Flow

It is important to note that CPP is not the only determinant of coronary blood flow. While CPP provides the pressure that drives coronary perfusion, coronary autoregulation describes the process that allows coronary blood flow to match myocardial demand over a range of CPP between 60 to 180 mmHg.[6] Coronary vasoconstriction and vasodilation are responsible for autoregulation; when CPP is reduced, vasodilation will improve flow, and the opposite is true when CPP becomes elevated.[1] These combined processes can be explained by Ohm’s Law[6][1]:

Flow = Difference in pressure across a vessel/resistance

Therefore, CPP represents the pressure gradient across the coronary vasculature, while resistance is mediated by autoregulation to deliver the required flow rates.[7] Multiple factors are responsible for the coronary vasoconstriction and vasodilation that occurs in autoregulation. These can categorize into neurohormonal, endocrine, metabolic, and endothelial-derived (Table 1). The combination of CPP and coronary autoregulation are crucial in ensuring adequate myocardial oxygen delivery because cardiac oxygen extraction is the highest of any organ at approximately 70 to 80% under resting conditions.[2] Clinically, systemic hypoxia and decreased coronary perfusion can cause myocardial ischemia; increasing coronary blood flow by increasing CPP and inducing coronary vasodilation are the predominant means by which myocardial oxygen delivery can increase in such circumstances. Finally, it bears mentioning that because left ventricular perfusion occurs in diastole, tachycardia decreases the relative proportion of time spent in diastole and therefore reduces myocardial perfusion.[8] Alterations in CPP and autoregulation in cardiovascular disease will be discussed before type 2 myocardial infarction, infarction resulting from decreased CPP.[7][2][8] Coronary autoregulation is under the control of neurohormonal, endocrine, metabolic, and endothelial-derived systems, which induce either coronary vasoconstriction or vasodilation (see Table. Coronary Autoregulation).

Clinical Significance

Coronary Perfusion Pressure in Cardiovascular Disease

CPP becomes reduced in common cardiac conditions, including heart failure and coronary artery disease; patients with these conditions are more prone to myocardial ischemia.

The impaired ejection of blood from the left ventricle defines systolic heart failure; this increases LVEDP, and thus CPP and left ventricular perfusion are reduced.[9] LVEDP also increases in diastolic heart failure.[10] Compensatory increases in sympathetic drive initially increase myocardial contractility and blood pressure, which increases aortic diastolic pressure to maintain systemic and coronary blood flow.[11] However, increases in systolic blood pressure also increase cardiac afterload and promote cardiac remodeling. Therefore, myocardial oxygen demand increases due to hypertrophy of the myocardium and increased afterload on a background of raised LVEDP; the myocardium will be vulnerable to ischemia.[9][10][11]

Atherosclerotic plaques causing stenosis of coronary vessel lumens characterize coronary artery disease. Plaques impede flow through coronary circulation, necessitating compensatory coronary vasodilation distal to the plaque to maintain coronary flow and myocardial oxygen delivery. As stenosis progresses, the coronary flow becomes dependent on CPP. Myocardial ischemia occurs when CPP is unable to sustain coronary perfusion as autoregulation fails.[7][12] Myocardial infarction resulting from reduced coronary perfusion will be a topic of discussion below.[7][12]

Coronary Perfusion Pressure in Type 2 Myocardial Infarction

Type 1 myocardial infarction implies the rupture of a coronary atherosclerotic plaque with subsequent thrombus formation and stenosis of the arterial lumen.[13] Type 2 myocardial infarction occurs independently from coronary atherosclerotic plaque rupture instead of resulting from an imbalance in myocardial oxygen supply and demand. Decreased myocardial oxygen delivery may be caused by hypotension with reduced CPP, systemic hypoxia, or anemia. Increased myocardial oxygen demand may result from increased afterload or tachyarrhythmia. Type 2 myocardial infarction may be multifactorial; for example, tachyarrhythmia may increase oxygen demand and reduce stroke volume with subsequent hypotension and reduced CPP. According to the physiologic principles discussed above, patients with pre-existing cardiac disease, including coronary artery disease and myocardial hypertrophy, are reliant on CPP, so are less tolerant of reduced CPP and decreased myocardial oxygen delivery.[13]

Type 1 and 2 myocardial infarctions are associated with similar mortality rates [14]. However, while protocolized management of type 1 myocardial infarction has improved outcomes in recent decades, difficulties exist regarding the management of type 2 myocardial due to a lack of accepted definitions and treatment. Acute management involves the restoration of blood pressure and, thus re-establishment of CPP. This article will discuss the therapeutic modification of CPP by pharmacological and mechanical therapies will be discussed below.[14]

Therapeutic Modification of Coronary Perfusion Pressure

Two examples of therapies that modify CPP are glyceryl trinitrate and the intra-aortic balloon pump (IABP).

• Glyceryl Trinitrate

Glyceryl trinitrate is an agent used in the acute management of type 1 myocardial infarction. Studies have shown that low-dose glyceryl trinitrate administration reduces LVEDP without reducing aortic diastolic pressure, thus increasing CPP.[15] The predominant action of Glyceryl trinitrate is central venous dilatation, which reduces cardiac preload; this reduces stroke volume according to the Frank-Starling law, and therefore, myocardial oxygen demand decreases.[16][15]

• Intra-Aortic Balloon Pump

The IABP is the most commonly used form of mechanical support in the acutely failing heart.[17] It is placed percutaneously and sits in the descending aorta distal to the aortic arch. Inflation occurs during diastole, which increases aortic diastolic blood pressure to increase CPP and augment myocardial oxygen delivery. LVEDP and cardiac afterload are reduced, which decreases myocardial oxygen demand. IABPs, therefore, simultaneously increase myocardial oxygen supply and decreased oxygen demand.[17] 

Pearls

• Left ventricular myocardial perfusion occurs in diastole rather than systole due to the arrangement of the coronary anatomy.
• Coronary perfusion pressure is a significant determinant of myocardial oxygen supply; local factors regulate coronary flow across a range of coronary perfusion pressures.
• If coronary perfusion pressure becomes acutely reduced in patients with circulatory shock, type 2 myocardial infarction may occur; this has a different etiology from the widely known type 1 myocardial infarction.

Nursing, Allied Health, and Interprofessional Team Interventions

Coronary Perfusion Pressure and Interprofessional Team Monitoring

Blood pressure is a common measurement in both hospital and community healthcare settings. Adequate blood pressure is required to drive blood flow to organs. Coronary perfusion pressure (CPP) is the term used to measure the flow through coronary arteries.[1] This section will introduce CPP and its effect on myocardial infarction, cardiopulmonary resuscitation (CPR), and hypotension.[1]

Coronary Perfusion Pressure

Blood pressure is a vital determinant of coronary blood flow. Interestingly, while the non-cardiac organs get perfused during systole (cardiac contraction) and diastole (cardiac relaxation), the high pressures generated in the heart during contraction impede coronary blood flow.[1] Therefore, coronary blood flow occurs during cardiac relaxation, and diastolic blood pressure is a major determinant of CPP. Both excessively high and low blood pressure can be hazardous to patients in hospital and community settings.[1]

Myocardial Infarction

Myocardial infarction due to inadequate blood supply to the heart is a common cause of mortality in the United States, with 790000 cases per year. Therapeutic advances and improvements in care have led to improvements in long-term survival post-myocardial infarction.[18] The involvement of interprofessional team members, including nursing staff and physical therapists, is crucial in ensuring optimal patient outcomes post-myocardial infarction. Invasive or frequent non-invasive blood pressure monitoring is undertaken in these patients to ensure blood pressure is optimally managed, as both hypotension and hypertension can be harmful in cardiac patients and should be escalated to the treating physician as either can be detrimental to patient outcomes. Hypotension reduces CPP and can worsen myocardial ischemia, while hypertension will increase myocardial oxygen demand because cardiac contraction will have a greater force against which to pump.[18]

Many patients will be treated with glyceryl trinitrate sublingual spray or intravenous infusion after myocardial infarction. At high doses, glyceryl trinitrate infusions decrease blood pressure.[19] Although a decrease in systolic blood pressure is desirable to reduce cardiac oxygen requirement, excessive decreases in diastolic blood pressure decrease CPP and worsen myocardial ischemia. Targets for blood pressure should, therefore, be established by the clinical team on commencement of therapy, and infusions titrated accordingly.[19]

Cardio-Pulmonary Resuscitation

Cardiac arrest describes a state where cardiac output ceases due to an array of potential underlying causes. CPR is necessary for patients who have had cardiac arrest to temporarily replace the oxygenation function of the lungs and the pumping function of the heart while rendering treatment to return the patient’s spontaneous circulation. It is important to maintain CPP during CPR because, due to the absence of cardiac output, these patients are unable to maintain coronary or cerebral perfusion. Studies in humans have shown that greater CPP is associated with higher rates of patient survival.[20][21] Chest compressions are a key component of effective CPR. Their use temporarily replaces the pumping function of the heart to generate CPP. Adrenaline is used in CPR protocols; its action is to increase diastolic blood pressure to increase CPP.[21] These factors illustrate the importance of protocolized, high-quality CPR delivery by the interprofessional team.[20][21] 

Hypotension

Hypotension is a common clinical finding in hospital inpatients and arises from a wide array of causes. Hypotension and circulatory shock, when blood pressure is unable to ensure organ perfusion, most commonly result from hypovolemia (low circulating blood volume) and sepsis (abnormal immune response to infection). When hypotension occurs to the extent that CPP is not maintained, a myocardial infarction occurs. This type of myocardial infarction results from low blood pressure rather than the presence of a thrombus in the coronary arteries. Patients who suffer from this type of myocardial infarction have a similar mortality rate compared to patients with myocardial infarction resulting from a coronary artery thrombus.[22] Protocols exist for the management of major hemorrhage while the Surviving Sepsis Campaign has produced a range of recommendations to improve recognition and management of sepsis to prevent complications, including type 2 myocardial infarction [23]. Aggressive resuscitation with intravenous fluids in sepsis and blood products in major hemorrhage is the recommended strategy to maintain target blood pressure and prevent consequences of hypotension, including myocardial infarction. Early detection through observation of vital signs and escalation is crucial in ensuring optimal patient outcomes.[22][23]

Nursing, Allied Health, and Interprofessional Team Monitoring

Frequent observation of vital signs is crucial to identify changes in the patient's condition, which may require changes in clinical management. The above examples highlight the importance of this monitoring and the physiology which underlies these conditions.