Hypertensive emergency: an overview of heart as target organ damage

Hypertension is currently still a global problem in the cardiology and vascular fields with an increasing trend. One of the emergency conditions related to an increase in blood pressure is emergency hypertension. Emergency hypertension is a condition where blood pressure rises rapidly and severely, resulting in new or progressive organ damage. Symptoms can range from chest pain, shortness of breath to delirium. The heart is one of the organs that can be damaged by hypertensive emergencies. The availability and demand for oxygen from the coronary blood vessels to the heart muscle cells will experience an imbalance due to a sudden increase in blood pressure. Lack of oxygen that occurs can cause heart muscle cells’ death affected heart structure and its function. The symptoms that appear can be in the form of acute coronary syndrome or acute heart failure. Some modalities can detect heart structure changes, like electrocardiography for general and echocardiography for specific examination. Hypertensive emergencies can be treated by several rapid-acting antihypertensive agents, which can be selected based on the clinical manifestations. As the symptoms related to heart damage are acute coronary syndrome and acute heart failure, so the treatment will be specific, respectively. Good knowledge related to emergency hypertension management and early treatment will reduce patient morbidity.


BACKGROUND
Hypertension is still a global health problem, including in Indonesia, because of its high prevalence. Nearly 1 billion people in the world experience hypertension and this number will continue to increase every year, especially in the elderly population. 1-3 Results of primary health research (Riskesdas) Indonesia from year to year, there is a significant increase in hypertension sufferers. In 2018 amounting to 34.1%. 4 Hypertension emergencies is a condition of a sudden increase in blood pressure by one or more target organ damage. 1,2,4- 15 One of the target organs that can be damaged is the heart. 4- 15 The heart's damage will cause an imbalance in demand and oxygen availability from the coronary vessels to the heart muscle cells. This imbalance will result in heart muscle cells' death resulting in acute coronary syndrome and acute heart failure. 1,2 Attention is needed in pathomechanism and management of a hypertensive emergency, especially on heart organ damage.

OVERVIEW OF HYPERTENSIVE EMER-GENCY Definition and Risk Factor
Emergency hypertension is defined as a sudden increase in systolic blood pressure >180mmHg and diastolic blood pressure >120 mmHg accompanied by target organ damage. The organ damage that is often affected is the brain, eyes, heart, kidneys and blood vessels. 2,4-15 Hypertension that is chronic with irregular or inadequate treatment has the potential to become hypertensive emergencies. Part of the hypertensive crisis, where blood pressure increases suddenly, must be managed as soon as possible so that further damage does not occur. 2

Sign and Symptoms
Emergency hypertension is characterized by acute organ damage accompanied by blood pressure above 180/120 mmHg. Some of the signs and symptoms that need to be considered in hypertensive emergencies are chest pain (location, quality, radiation and duration), shortness of breath, acute changes in mental status, headache, nausea, vomiting, and blurry eyes. Stroke and hypertensive encephalopathy can be obtained in the cerebrovascular. Also, acute heart failure symptoms (leg edema, hepatojugular reflex, murmur) and aortic dissection (different blood pressure reading). 6, 8 Physical examination should look for acute signs of hypertensive emergencies, including increased jugular venous pressure, rhonchi sound, gallops,

ORIGINAL ARTICLE
of the hypertensive crisis. 8 This sudden increase can cause vascular damage, resulting in platelet activation and the coagulation cascade, deposits of fibrin, and induction of oxidative stress and proinflammatory cytokines. Production of NO is interrupted. That results in tissue ischemia and vascular lesions from fibrinoid necrosis of the arterioles and other small arteries. The vascular damage will then result in low perfusion, extravasation of fluids and tissue ischemia. The cascade of these events is caused by tissue ischemia, which stimulates the release of vasoactive substances, which results in worsening hypertension. 2,7, 8 Organ damage in hypertensive crises occurs due to sudden changes in blood pressure that the target organs cannot compensate for those changes. On the other hand, a chronic increase in blood pressure protects the organs from sudden increases in transmitted pressure due to chronic hypertensioninduced arterioles hypertrophy. 6 The organs most commonly affected are the brain, heart, eyes, large arteries and kidneys. With proper treatment, the vasoconstriction-ischemia-vasoconstriction cycle can be stopped. 2,8, 9 Due to hypertensive emergencies, sudden damage to the heart will cause an imbalance in the supply and demand for oxygen from the coronary blood vessels to the heart muscle cells. Those imbalances can result in the heart muscle cells' death, leading to the acute coronary syndrome. Suppose a sudden increase in blood pressure occurs in the aorta. In that case, it can result in a tear in the lining of the aortic intima, allowing shear forces from the bloodstream to tear off the intima from the tunica media and spread along the aorta. In some cases, this can result in bleeding from the aorta. According to the Stanford system, aortic dissections involving the ascending aorta are classified as type A. Those that do not involve the ascending aorta are classified as type B. 1, 2 The heart muscle's compensatory mechanism against excess pressure by hypertrophy of the myocardial muscles resulted in several changes in the heart muscles' structure and function. Hypertrophy of the heart muscles can be divided into two general parts, namely concentric hypertrophy, where there is an increase in the width of the myocardial muscles and eccentric hypertrophy, where there is an increase in the length of the myocardial muscles. 2, 10 The cardiac muscle response to this compensation is explained by Laplace's law (Figure 2). 10 Several diagnostic modalities can be used to detect changes in the structure of the heart. The easiest and cheapest examination that can be done is the examination of heart records or electrocardiography (EKG). 2 A more specific

General Treatment
Several rapid-acting antihypertensive agents are available to treat hypertensive emergencies. The choice of these drugs is selected based on the clinical manifestations of target organ damage. Clinicians must know about frequently used drugs, potential clinical scenarios in which they can be used most effectively, and a side effect/risk profile for each of these drugs to initiate therapy successfully. 7 In general, the target of lowering blood pressure is based on the principle of autoregulation, namely a decrease in the mean arterial blood pressure of no more than 20-25% in the first 1 hour, then from 160/100 to 110 mmHg in 2 -6 hours later. If the patient's condition is stable, the target of lowering blood pressure to normal can be achieved within 24-48 hours. 12

Pathomechanism of Hypertensive Emergency on Heart
A prolonged increase in blood pressure can precede a sudden increase in blood pressure in hypertensive emergencies. An increase in blood pressure that reaches a critical level stimulates a vascular response increasing the resistance. 8 Myogenic vascular response provoked by increased intravascular pressure is vasoconstriction. The periphery's relative hypoperfusion exacerbates this situation by stimulating the release of vasoactive hormones such as angiotensin-II, norepinephrine, endothelin, and antidiuretic hormone. The sudden increase in systemic vascular resistance is the cause systolic blood pressure below 140 mmHg within 1 hour, and the diastolic blood pressure maintained at 60 mmHg. Administration of oxygen and morphine can be used according to clinical needs and assessment. The drugs of choice for acute coronary syndrome can be seen in Table 1. Avoid using hydralazine in these patients because it can cause a "rebound" hypertensive effect. Administration of the drug sodium nitroprusside can cause a "stealing" mechanism of coronary flow caused by coronary vasodilation and should be avoided. 7,8,11,12 Patients with acute heart failure need to lower their systolic blood pressure below 140 mmHg in the first 1 hour with the choice of nitroglycerin and nitroprusside (Table 1). In most cases of acute heart failure, loop diuretics, enalaprilat or hydralazine may still be useful and must avoid the use of betablocking drugs. The use of nitroglycerin or other nitrate groups is still widely used today. Side effects that must be considered when giving nitrate group drugs are hypotension, reflex tachycardia, dizziness and redness. 11

CONCLUSION
The hypertensive emergency will usually be followed by organ damage. The symptoms of acute coronary syndrome or acute heart failure are the symptoms that resulted from heart damage due to hypertensive emergency. Early and appropriate acute coronary syndrome or acute heart failure management in the hypertensive emergency condition will reduce patient morbidity.  examination is echocardiography. This examination can see the function and structure of the muscle mass of the heart. 1,5,6 Criteria in echocardiography examination uses a reference to the mass of the left ventricular muscle. 17, 18 In addition to changes in the heart structure, long-term hypertension can also trigger several severe conditions cardiac emergencies such as acute heart failure, acute coronary syndrome and aortic dissection. 2,4-8

Specific Treatment on Heart Organ Damage in Hypertensive Emergency
Commonly in hypertensive emergencies, patients with cardiac damage presented acute coronary syndrome and acute heart failure. Patients with acute coronary syndromes need to lower their target