postgraduaat_hypertensie2024.pptx

# Understanding arterial hypertension Arterial hypertension encompasses the fundamental concepts, definition, epidemiology, measurement techniques, classification, and management of high blood pressure. ## 1\. Understanding arterial hypertension ### 1.1 Introduction to arterial hypertension Arterial hypertension (AHT), a significant cardiovascular risk factor, has seen a doubling in prevalence since 1990, particularly in low and middle-income countries, with projections indicating 1.6 billion affected individuals by 2025. It is a primary risk factor for acute myocardial infarction, heart failure, and cerebrovascular accidents (CVA). The most severe complications include hypertensive emergencies, characterized by hypertension-mediated organ damage (HMOD), which are suspected to affect two to three percent of individuals with AHT. ### 1.2 Measurement of blood pressure Accurate blood pressure measurement is crucial as many clinical decisions are based on these readings. Various methods are employed: * **Consultation measurement:** Standard blood pressure readings taken during medical appointments. * **Conventional RR-measurement (RIVA-ROCCI):** Utilizes auscultatory methods with mercury or aneroid sphygmomanometers. * **Methodological principles:** * Always measure bilaterally on the first contact; the higher value is considered. * Measure both lying and standing to assess for orthostatism. * **Tip:** Pseudohypertension can occur in calcified vessels, necessitating invasive measurement with an intra-arterial catheter. * **Self-measurement by the patient at home (HBPM - home blood pressure measurement):** Allows for multiple readings in a familiar environment. * **Automated ambulatory BP monitoring (ABPM - ambulatory BP measurement):** Provides continuous monitoring over a 24-hour period. * **Invasive measurement:** Performed with an arterial catheter, typically in critical care settings. * **Palpation:** Used in urgent settings when a conventional device is unavailable. #### 1.2.1 Variability of measurement and causes of inaccuracy Inaccurate blood pressure readings can arise from several factors. The inter-arm blood pressure difference (IAD) is a common finding associated with peripheral vascular disease and increased mortality. A significant IAD, for example, greater than 10 mmHg, has been shown to be a predictor of cardiovascular events and all-cause mortality. #### 1.2.2 Current technology: automated blood pressure measurement Modern automated devices use oscillometry, eliminating the need for a stethoscope. They are available for both wrist and upper arm measurements, with a preference for upper arm devices. Validated devices can be found on specialized websites. #### 1.2.3 Automated blood pressure measurements: Applications and benefits Automated devices are applicable in both hospital and home settings. * **Home blood pressure measurement (HBPM):** * **Ambulatory blood pressure measurement (ABPM):** * **Advantages:** More readings, better reproducibility, reduction of the "white coat" effect, higher predictive value for morbidity, and improved assessment of blood pressure control. * **Disadvantages:** Potential for self-medication and patient anxiety. * **Usefulness:** Applicable for both diagnosis and follow-up. #### 1.2.4 Ambulatory blood pressure management (Portometrie - ABPM) ABPM (Portometrie) is indicated in several scenarios: * Elevated blood pressure in patients without end-organ damage and low cardiovascular risk. * Discrepancies between consultation and home blood pressure readings. * Therapy-refractory hypertension. * Suspicion of hypotensive episodes in hypertensive patients. * Suspicion of sleep apnea syndrome. * Significant variability in consultation blood pressure. * Elevated consultation blood pressure in pregnant women with suspected pre-eclampsia. ABPM aims to assess therapy control, detect over-treatment, and identify patterns like the "dipper profile" and "morning surge." ### 1.3 Definition of arterial hypertension The definition of hypertension is critical and distinguishes between different clinical scenarios: * **White coat hypertension:** Consultation blood pressure $\\ge 140/90$ mmHg, but ambulatory or home measurements are below $130-135/85$ mmHg. This is associated with a slightly increased cardiovascular risk compared to normotensives. * **Isolated office hypertension:** Similar to white coat hypertension. * **Isolated ambulatory hypertension:** Hypertension diagnosed based on ambulatory or home measurements ($\\ge 130-135/85$ mmHg) while consultation blood pressure is normal or low. These individuals are exposed to the long-term risks of sustained AHT. * **Masked hypertension:** Blood pressure is normal during consultation but elevated during ambulatory monitoring. The distinction between systolic and diastolic blood pressure is important in diagnosis and management. ### 1.4 Epidemiology of arterial hypertension The epidemiology of AHT highlights its widespread nature and increasing prevalence. #### 1.4.1 Incidence of AHT Data on the incidence of AHT underscores its growing impact globally. ### 1.5 Pathogenesis and diagnostic workup of arterial hypertension Understanding the underlying mechanisms and conducting a thorough diagnostic workup are essential for effective management. #### 1.5.1 Contributing factors and risk stratification A comprehensive evaluation includes: * **Personal history:** Previous blood pressure readings, cardiovascular risk factors, and medication history (efficacy, side effects). * **Family history:** Familial occurrence of hypertension. * **Medications:** Oral contraceptives, steroids, thyroid hormones, NSAIDs/COX2-inhibitors can influence blood pressure. * **Clinical examination:** Weight, height, BMI, thyroid palpation, examination of large blood vessels, cardiac auscultation, and abdominal palpation for polycystic kidneys or bruits. * **Cardiovascular risk factors:** * Male $\\ge 55$ years, Female $\\ge 65$ years * Nicotine abuse * Dyslipidemia (Total cholesterol $\\ge 190$, LDL $\\ge 115$, HDL $< 40$ (M) / $< 46$ (V), Triglycerides $\\ge 150$) * Family history (Male $< 55$, Female $< 65$) * Impaired fasting glucose ($102-125$ mg/dl) or impaired glucose tolerance test * Diabetes mellitus ($\\ge 126$ mg/dl) or post-loading glucose $> 198$ mg/dl * Abdominal obesity (waist circumference $\\ge 102$ cm (M) / $\\ge 88$ cm (V)) * CRP $> 1$ mg/dl #### 1.5.2 Routine and facultative investigations * **Routine tests:** * Blood tests: complete blood count, electrolytes (potassium), uric acid, creatinine, glucose, lipids. * Urine analysis: micro-albuminuria dipstick, urine sediment. * ECG. * **Facultative investigations:** * Echocardiography. * Carotid duplex ultrasound. * Quantitative proteinuria (if urine dipstick is positive). * Fundoscopy. * Glucose tolerance test (if fasting glucose $> 100$ mg/dl). * ABPM (Portometrie). #### 1.5.3 Risks of untreated hypertension Untreated hypertension poses significant risks, categorized as: * **Subclinical:** "Target organ damage" (TOD). * **Clinical:** Associated clinical conditions (ACC). **Subclinical end-organ damage includes:** * Left ventricular hypertrophy (ECG Sokolow-Lyon $> 38$ mm or echocardiography). * Carotid artery duplex: Intima-media thickness (IMT) $\\ge 0.9$ mm or plaque. * Ankle-brachial index $< 0.9$. * Elevated creatinine (Male $1.3-1.5$, Female $1.2-1.4$ mg/dl). * Creatinine clearance $< 60$ ml/min. * Micro-albuminuria ($30-300$ mg/24 hours or albumin-creatinine ratio Male $> 22$, Female $> 31$ mg/g creatinine). **Associated clinical conditions include:** * Cerebrovascular disease. * Heart disease: infarction, angina, revascularization, heart failure. * Kidney disease: creatinine $> 1.5$ mg/dl (M) / $> 1.4$ mg/dl (V), proteinuria $> 300$ mg/24 hours. * Peripheral vascular disease. * Retinopathy: hemorrhages, exudates, papilledema. #### 1.5.4 Risk stratification Based on the collected information, a classification for total cardiovascular risk can be established. This classification helps stratify patients into low, moderate, high, and very high added risk categories, indicating an approximate 10-year risk of cardiovascular disease. #### 1.5.5 Physiology of blood pressure regulation Blood pressure is regulated by several systems: * **Chemoreceptors:** Regulate electrolytes. * **Baroreceptors:** Located in the aorta and carotid sinus. * **Sympathetic nervous system:** Releases catecholamines, causing vasoconstriction and influencing heart rate and contractility. It also stimulates the Renin-Angiotensin-Aldosterone System (RAAS). * **RAAS:** Renin release is triggered by reduced renal perfusion, sympathetic stimulus, or macula densa signals (e.g., hyponatremia). ### 1.6 Classification of hypertension: primary and secondary Hypertension is broadly classified into two main categories: * **Primary (Essential) Hypertension:** Accounts for $89-95%$ of cases and has no identifiable cause. * **Secondary Hypertension:** Accounts for $2-10%$ of cases and is caused by an underlying medical condition. #### 1.6.1 Causes of secondary hypertension Numerous conditions can lead to secondary hypertension: * **Sleep apnea syndrome.** * **Renal diseases:** * Renovascular disease (e.g., renal artery stenosis). * Parenchymal kidney disease. * **Endocrine hypertension:** * Pheochromocytoma. * Primary hyperaldosteronism. * Cushing's syndrome. * Thyroid disorders. * **Coarctation of the aorta.** #### 1.6.2 Hypertension and the kidney The kidney plays a dual role in hypertension; it can be both a cause and a consequence. * **Cause:** Approximately $50%$ of secondary hypertension is renal in origin (renovascular or parenchymal). Etiologies of end-stage renal failure often include diabetic nephropathy and nephroangiosclerosis due to AHT. * **Consequence:** Chronic hypertension can lead to kidney damage. Diagnostic evaluation for kidney involvement includes creatinine and urine sediment analysis, renal ultrasound, and potentially kidney biopsy, renogram, CT, or MRI. #### 1.6.3 Hypertension in patients on kidney dialysis For patients on dialysis, hypervolemia and the absence of renal vasodepressors can contribute to hypertension. Blood pressure often decreases with the initiation of dialysis due to fluid correction. If AHT persists, medication may be necessary on non-dialysis days. In rare cases of therapy-refractory AHT, nephrectomy might be considered. ### 1.7 Management of arterial hypertension The management of AHT involves a comprehensive approach addressing lifestyle modifications and, when necessary, pharmacological interventions. #### 1.7.1 Lifestyle modifications These are crucial for all hypertensive patients: * **Weight control:** AHT patients are often heavier; weight loss can reduce blood pressure by $5-8$ mmHg. * **Salt restriction:** Adhering to guidelines of $2$ grams of sodium (equivalent to $5$ grams of sodium chloride) per day is recommended, especially for salt-sensitive individuals (black patients, diabetics, older adults, metabolic syndrome, CKD). * **Aerobic exercise:** Aim for $2 \\times 30$ minutes per week at $70-80%$ of maximal workload. * **Alcohol limitation.** * **Smoking cessation.** * **DASH (Dietary Approaches to Stop Hypertension) diet:** Emphasizes fruits and vegetables, with reduced intake of saturated fats. #### 1.7.2 Pharmacological treatment The choice of medication depends on individual patient characteristics and comorbidities. * **Importance of BP reduction:** Lowering blood pressure is paramount, and specific therapies may offer additional benefits beyond BP reduction, particularly in patients with diabetes, atrial fibrillation, or kidney failure. * **First-line agents:** Thiazide diuretics, spironolactone, calcium channel blockers, ACE inhibitors, ARBs, direct renin inhibitors, beta-blockers, and centrally acting medications are all considered. * **Combination therapy:** Multiple medications are often required to achieve target blood pressure. * **Target blood pressure goals:** * **Kidney failure:** Target $< 140/90$ mmHg for low proteinuria, and $< 130/80$ mmHg for high proteinuria. * **Geriatric population ($> 80$ years):** Start medication for Grade 2 hypertension ($\\ge 160$ mmHg), with a target of $< 140/80$ mmHg. * **Diabetes:** Target $< 140/90$ mmHg, potentially $< 130/85$ mmHg in some cases, with nefroprotective effects from ACE inhibitors or ARBs. * **Micro-albuminuria:** A trigger for early intervention. ### 1.8 Hypertensive emergencies and urgencies Hypertensive emergencies and urgencies represent acute elevations in blood pressure requiring specific management. #### 1.8.1 Definitions * **Hypertensive urgencies:** Severe blood pressure elevation (typically $> 180/110$ mmHg) without evidence of acute end-organ damage or symptoms. The term "uncontrolled hypertension" is now preferred, and rapid BP reduction is generally not required. * **Hypertensive emergencies:** Severe blood pressure elevation (usually $> 180/120$ mmHg, but can be lower with existing organ damage) associated with acute hypertension-mediated organ damage that necessitates immediate blood pressure reduction to prevent further damage or promote regression. #### 1.8.2 Hypertensive emergencies: classification and management These are heterogeneous and require rapid diagnosis and tailored treatment. * **Classification:** Based on the type of hypertension-mediated end-organ damage (heart, retina, brain, kidneys, large arteries). * **Management:** Primarily parenteral, fast-acting, and titratable medications. The speed of BP reduction and target BP depend on the clinical context. * **Malignant hypertension and hypertensive encephalopathy:** * Reduce mean arterial pressure (MAP) by $20-25%$ over several hours. * First-line agents: Labetalol or Nicardipine. * Alternatives: Nitroprusside or Urapidil. * Oral treatment with ACE inhibitors may be used cautiously at low doses, especially if RAAS is highly activated. * **Acute ischemic stroke:** * Therapeutic duality: balancing the need to reduce perifocal edema against the risk of reduced perfusion. * Indications for BP reduction: Severe $\\ge 220/120$ mmHg, or MAP reduction of $15%$ over 1 hour. * Target BP in normotensives: $160-170/95-100$ mmHg. * Target BP in hypertensives: $180-185/105-110$ mmHg. * IV Labetalol or Nicardipine. * For thrombolysis, BP must be $< 185/110$ mmHg initially and $< 180/105$ mmHg for $24$ hours. * **Intracerebral hemorrhage (ICH):** * Aggressive BP reduction to $< 140$ mmHg in the first hour is beneficial if the patient is clinically stable. * For BP $> 220$ mmHg, rapid reduction to $< 220$ mmHg followed by gradual reduction over hours. * Medication choice: Labetalol, Nicardipine, Urapidil. Nitroglycerine and sodium nitroprusside are contraindicated due to ICP increase. * **Acute aortic syndrome:** * Immediate reduction of systolic BP to $100-120$ mmHg and pulse to $< 60$ bpm within $20$ minutes. * Beta-blockers (Esmolol or Labetalol) are first-line for BP and pulse control, often with nitroprusside, nitrates, or nicardipine. * **Acute coronary syndrome:** * Reduce afterload without increasing heart rate. * Nitroglycerine with a beta-blocker, or Labetalol. * Calcium channel blockers (Diltiazem, Verapamil) if beta-blockers are contraindicated. * **Acute hypertensive pulmonary edema:** * Reduce preload and afterload. * Nitroglycerine or sodium nitroprusside. * Consider non-invasive ventilation with CPAP and diuretics for volume overload. * **Hypertension during pregnancy (preeclampsia):** * Start medication for BP $\\ge 150/95$ mmHg (or $\\ge 140/90$ mmHg in gestational hypertension). * Goal BP $< 140/90$ mmHg. * For BP $> 160/110$ mmHg, IV Labetalol or Methyldopa is indicated. * Magnesium sulfate is used for seizure prophylaxis in preeclampsia. * IV Labetalol is preferred over Hydralazine due to adverse perinatal effects. * Diuretics, nitroprusside, and RAAS blockers are contraindicated. #### 1.8.3 Prognosis and follow-up The prognosis for hypertensive emergencies has significantly improved with adequate treatment. Key prognostic indicators include troponin levels, kidney function, the degree of BP control, and proteinuria in follow-up. Intense follow-up is essential. #### 1.8.4 Challenges in management * Identification of subclinical organ damage (e.g., routine troponin measurements, brain MRIs). * Establishment of uniform nomenclature and classification systems. * Development of standardized treatment strategies (medication choice, BP targets, speed of reduction, oral vs. IV administration). #### 1.8.5 Specific medications used in hypertensive emergencies * **Sodium nitroprusside:** Direct vasodilator acting on both arterial and venous beds. Side effects include cyanide toxicity. * **Nitroglycerine:** Direct vasodilator, primarily venous. Can cause cerebral vasodilation and increased ICP. * **Nicardipine:** Dihydropyridine calcium channel blocker, arterial vasodilator. Minimal chronotropic or inotropic effects. * **Labetalol:** Alpha and non-selective beta-blocker. No significant chronotropic effect due to beta-blockade. Contraindicated in COPD, heart failure, and AV block. * **Urapidil:** Alpha-1 adrenoceptor antagonist and 5-HT1A agonist. Reduces reflex tachycardia. * **Esmolol:** Short-acting beta-blocker, primarily used peri-anesthetically. * **Enalapril:** ACE inhibitor. Less effective in Black individuals. Caution in volume depletion and renal artery stenosis. * * * # Hypertensive emergencies and urgencies This section explores critical hypertensive conditions, differentiating between emergencies and urgencies based on organ damage and outlining their management. ### 2.1 Definitions Hypertensive emergencies and urgencies are defined by the presence or absence of target organ damage, respectively. ### 2.2 Hypertensive urgency Hypertensive urgency, now often referred to as "uncontrolled hypertension," is characterized by a severe elevation in blood pressure, typically exceeding 180/110 mmHg, but without evidence of acute, ongoing target organ damage. Patients are usually asymptomatic. The current consensus suggests abandoning the term "hypertensive urgency" and considering it as a state of uncontrolled hypertension requiring controlled blood pressure reduction without the risk of inducing hypotension. #### 2.2.1 Management of uncontrolled hypertension * **Goal:** Gradual reduction of blood pressure without causing hypotension. * **Treatment:** Oral antihypertensive medications are generally sufficient. * **Captopril:** Sublingual administration (25 mg) can be used for rapid onset (5-15 minutes), with effects lasting 4-6 hours. Caution is advised in renovascular hypertension and in cases of high renin levels or volume depletion due to the risk of hypotension. * **Nifedipine:** Sublingual administration (5-10 mg) has a rapid onset (1-5 minutes, peak effect within 20 minutes). However, it carries a risk of reflex tachycardia and abrupt, severe blood pressure drops and is not FDA approved for this indication. Nicardipine 30 mg orally may be an alternative. * **Labetalol:** Oral administration (200 mg) has an onset of 0.5-2 hours and lasts 6-8 hours, with doses potentially repeatable up to 1200 mg. Contraindications apply. * **Clonidine:** A central alpha-agonist, but associated with sedation and rebound hypertension. * **Monitoring:** Blood pressure should be rechecked within 2 hours of initiating additional medication to achieve safe blood pressure levels. * **Caution:** Avoid telephone instructions without clinical assessment, as this may overlook serious underlying issues like urinary retention, arthritis, or delirium. ### 2.3 Hypertensive emergencies Hypertensive emergencies are defined as a state of severely elevated blood pressure (usually > 180/120 mmHg, but sometimes lower depending on the clinical context) associated with acute, life-threatening hypertension-mediated organ damage. These conditions necessitate immediate blood pressure reduction to prevent further extension of organ damage or to achieve regression of existing damage. #### 2.3.1 Affected organs The organs commonly affected include the heart, retina, brain, kidneys, and great arteries. #### 2.3.2 Classification Classification is based on the type of hypertension-mediated end-organ damage, which dictates the treatment strategy, target blood pressure, and timeframe for reduction. ##### 2.3.2.1 Renal emergencies This category includes: * Renal crisis due to collagen diseases. * Acute glomerulonephritis. * Excess circulating catecholamines (e.g., pheochromocytoma). * Drug interactions with MAO inhibitors. * Sympathomimetic drugs, cocaine. * Rebound hypertension after stopping antihypertensives. * Perioperative hypertension. ##### 2.3.2.2 Malignant hypertension Malignant hypertension is characterized by: * Severe blood pressure elevation, usually exceeding 200/120 mmHg. * Progressive retinopathy with hemorrhages, cotton wool spots, and papilledema. * Potentially associated with acute kidney failure. * May involve thrombotic microangiopathy with Coombs-negative hemolysis (elevated LDH, low haptoglobin, schistocytes) and thrombocytopenia. This is termed acute hypertensive microangiopathy. * Poor prognosis if left untreated, with prognosis strongly influenced by kidney function. * Requires aggressive parenteral therapy, with preferred agents being Labetalol or Nicardipine, or alternatives like Nitroprusside or Urapidil. * **Retinopathy in Malignant Hypertension:** * Flame-shaped hemorrhages. * Cotton wool spots (Grade 3). * Papilledema (Grade 4). * Fundoscopic examination is crucial for diagnosis. * **Thrombotic Microangiopathy (TMA) in Malignant Hypertension:** * Endothelial damage due to high shear forces. * Activation of coagulation, leading to platelet-rich microthrombi that obstruct the microcirculation. * Platelet consumption and intravascular hemolysis. * Often shows regression within 24-48 hours with blood pressure control. ##### 2.3.2.3 Hypertensive encephalopathy This condition involves a severe rise in blood pressure leading to neurological symptoms such as seizures, cortical blindness, lethargy, and coma. * **Pathophysiology:** Disruption of cerebral autoregulation, leading to cerebral hyperemia and edema, particularly in the posterior regions. Microscopic hemorrhages and infarction can occur. Posterior Reversible Encephalopathy Syndrome (PRES) is a typical finding on MRI, characterized by white matter lesions, distinguished from other causes of PRES by the presence of elevated blood pressure. * **Presentation:** Nausea, vomiting, papilledema, convulsions, and coma. Retinopathy may be absent in about one-third of patients. * **Management:** Mean Arterial Pressure (MAP) reduction of 20-25% over several hours. Labetalol and Nicardipine are preferred due to their effect on cerebral blood flow without increasing intracranial pressure. Urapidil is another option. Oral ACE inhibitors may be used cautiously at low doses, especially in cases of highly activated RAAS, with NaCl infusion to manage hypotension. ##### 2.3.2.4 Acute heart failure and cardiogenic pulmonary edema This is a frequent presentation of hypertensive emergencies. * **Pathophysiology:** Acute blood pressure rise increases left ventricular filling pressures, leading to pulmonary edema. This can occur in both heart failure with reduced ejection fraction (HFrEF) and preserved ejection fraction (HFpEF). * **Management:** The management is detailed in the heart failure lectures. Prognostic indicators include troponin levels and the degree of hypertension. ##### 2.3.2.5 Acute coronary syndrome (ACS) This includes STEMI, non-STEMI, and unstable angina. * **Pathophysiology:** Sudden blood pressure elevation can cause endothelial damage and intravascular thrombosis, potentially leading to Type 1 myocardial infarction, especially in individuals with pre-existing coronary insufficiency. Structural changes in hypertensive hearts (left ventricular hypertrophy, microvascular alterations) can lead to ventricular-vascular uncoupling and Type 2 infarction. * **Management:** Reduction of afterload without increasing heart rate is crucial to reduce diastolic filling time and myocardial oxygen consumption. Nitroglycerine combined with a beta-blocker is often used, or Labetalol or Urapidil. If beta-blockers are contraindicated, diltiazem or verapamil may be considered. ##### 2.3.2.6 Acute myocardial injury This differs from ACS by the absence of demonstrable ischemia (symptoms, ECG changes, troponin elevation, Q waves, regional wall motion abnormalities, or coronary thrombus). Only elevated troponin levels are present, with an identical pathophysiology to ACS. ##### 2.3.2.7 Acute aortic syndrome This encompasses acute aortic dissection, intramural hematoma, penetrating atherosclerotic ulcer, and aortic rupture. * **Presentation:** Low prevalence among hypertensive emergencies. * **Management:** Requires immediate reduction of systolic blood pressure to 100-120 mmHg and pulse rate to less than 60 beats per minute within 20 minutes to decrease shear stress. Beta-blockers like Esmolol or Labetalol are the first choice, often combined with nitroprusside, nitrates, or nicardipine for optimal blood pressure control. Hypotension needs careful management, considering causes like blood loss, hemopericardium, valvular dysfunction, or left ventricular failure. ##### 2.3.2.8 Intracerebral hemorrhage (ICH) ICH is often associated with hypertension. * **Pathophysiology:** Elevated mean arterial pressure (MAP) can worsen bleeding and outcomes, although adequate perfusion is also necessary. * **Management:** The optimal approach is debated. The INTERACT2 trial suggested aggressive blood pressure lowering to a systolic blood pressure (SBP) of less than 140 mmHg in the first hour for patients with SBP between 150-220 mmHg, provided they remain clinically stable. This approach was found to be safe and improve functional outcomes. For patients with SBP greater than 220 mmHg, a rapid reduction to less than 220 mmHg is recommended, followed by a gradual decrease over several hours to 140-160 mmHg if clinically stable. * **Medications:** Labetalol, nicardipine, and urapidil are commonly used. Nitroglycerine and sodium nitroprusside are contraindicated due to potential increases in intracranial pressure (ICP). ##### 2.3.2.9 Subarachnoid hemorrhage (SAH) * **Management:** Blood pressure control is crucial to reduce the risk of rebleeding while avoiding infarction and vasospasm. For most patients without suspected elevated ICP or altered consciousness, SBP should be maintained below 160 mmHg and MAP below 110 mmHg. If consciousness is altered, a more conservative approach with ICP monitoring and ventriculostomy may be considered, with blood pressure therapy guided by cerebral perfusion pressure (CPP) of 70 mmHg. Labetalol, nicardipine, and enalapril are used, with vasodilators being contraindicated. ##### 2.3.2.10 Hypertensive emergencies in pregnancy (preeclampsia/eclampsia) * **Definition:** Preeclampsia is characterized by elevated blood pressure, edema, and proteinuria, potentially progressing to seizures (eclampsia). * **Management:** Medication is initiated with repeated BP readings > 150/95 mmHg. In cases of gestational hypertension, medication starts above 140/90 mmHg. Methyldopa, labetalol, and calcium channel blockers (CCBs) are used, aiming for a target BP < 140/90 mmHg. SBP > 160/110 mmHg constitutes an emergency, requiring IV labetalol or methyldopa. * **Preeclampsia Management:** Immediate BP reduction to < 160/105 mmHg, with a target of 140-150/90-100 mmHg. IV labetalol is a common choice (maximum 800 mg/24 hours), requiring fetal monitoring. Timely initiation of oral methyldopa and long-acting nifedipine is important. IV nicardipine is an alternative. Oral long-acting nifedipine has also shown to be safe. * **Contraindications:** Diuretics (reduce placental flow), RAAS blockers (teratogenic), and nitroprusside. ##### 2.3.2.11 Amphetamine and cocaine intoxication * **Management:** Initial management with benzodiazepines. Phentolamine (alpha-blocker), nicardipine, nitroprusside, or clonidine can be used. Beta-blockers are relatively contraindicated and may not prevent coronary vasospasm. In cases of ACS, aspirin, nitrates, and possibly coronary angiography are indicated. ##### 2.3.2.12 Pheochromocytoma * **Pathophysiology:** Adrenergic hyperstimulation. * **Management:** Labetalol is contraindicated. Phentolamine (alpha-blocker), nicardipine, and nitroprusside are used. ### 2.4 Pathophysiology of Hypertensive Emergencies The exact pathophysiology is not fully understood but involves several key determinants: * **Sudden increase in blood pressure:** Often occurs in individuals with pre-existing hypertension. * **Triggers:** Poor compliance or cessation of antihypertensives, stress, high salt intake, recreational drugs, NSAIDs, and inadequate control of major risk factors. * **Key Determinants:** * Activation of the Renin-Angiotensin-Aldosterone System (RAAS). * Endothelial dysfunction. * Disrupted vascular autoregulation. ### 2.5 Clinical Presentation of Hypertensive Emergencies * **No specific blood pressure threshold:** The rate of blood pressure increase is more critical than a fixed threshold. * **Rapid diagnostics:** Essential. * **Anamnesis:** * **Symptoms:** Headache, visual disturbances, chest pain, dyspnea, vertigo, neurological symptoms. * **Causes:** Non-compliance, dietary indiscretions, medications (steroids, NSAIDs, cyclosporine, sympathomimetics, cocaine). * **Secondary forms:** Renal diseases, renal artery stenosis. * **Clinical Examination:** Focus on cardiovascular and neurological assessment. Repeated blood pressure measurements in both arms and potentially on the lower limb (for aortic dissection) are crucial. Laboratory tests and ECG should be performed urgently. ### 2.6 Management Principles * **Determined by organ damage:** The choice of treatment is dictated by the specific type of organ damage and the clinical context. * **Parenteral treatment:** Generally preferred for rapid onset, titrability, and avoidance of undesirable side effects. * **Essential medications:** Nicardipine and Labetalol are considered essential drugs for intensive care units. * **Speed and target BP:** The required speed of blood pressure reduction and target pressures vary depending on the clinical presentation. * **Hypertensive acute pulmonary edema and aortic dissection:** Require rapid blood pressure reduction. * **Intracranial bleeding:** The evidence for rapid reduction is less clear. * **Individualized approach:** Management strategies can differ between institutions based on local experience and preferences. ### 2.7 Specific Medications Used in Hypertensive Emergencies * **Sodium Nitroprusside:** * **Mechanism:** Direct vasodilator, reducing both afterload (systemic vascular resistance) and preload (left ventricular end-diastolic pressure). * **Adverse Effects:** Fatigue, nausea, disorientation, psychosis. Risk of cyanide toxicity with high doses, especially with renal and hepatic impairment. Can increase ICP. * **Nitroglycerine:** * **Mechanism:** Direct vasodilator, reducing afterload and preload. Dilates epicardial coronaries. * **Adverse Effects:** Headache, hypotension. Tolerance can develop with prolonged use. Does not cause neonatal respiratory depression or hypotension during cesarean sections. Can cause cerebral vasodilation and increase ICP. * **Calcium Channel Blockers (e.g., Nicardipine):** * **Mechanism (Dihydropyridine):** Arterial vasodilator, dilates epicardial coronaries. Minimal effect on heart rate or contractility. * **Adverse Effects:** Nausea, vomiting, headache, flushing, hypotension. * **Other CCBs:** Nimodipine (cerebral vasodilator, used in aneurysmal SAH), Isradipine, Verapamil, Diltiazem. * **Labetalol:** * **Mechanism:** Selective antagonist of postsynaptic alpha-adrenoreceptors and non-selective beta-adrenoreceptor antagonist, leading to vasodilation without significant reflex tachycardia. * **Adverse Effects:** Nausea, vomiting, vertigo, flushing, paresthesias, postural hypotension. * **Contraindications:** COPD, congestive heart failure, second or third-degree AV block, bradycardia. * **Urapidil:** * **Mechanism:** Selective postsynaptic alpha-1 adrenoceptor antagonist and presynaptic 5-HT1A agonist. * **Adverse Effects:** Headache, vertigo, hypotension. Does not affect ICP. * **Enalapril:** * **Mechanism:** Angiotensin II antagonist, particularly effective in high-renin hypertensive crises. * **Adverse Effects:** Hypotension in volume-depleted patients or those on diuretics. May worsen renal function in cases of renal artery stenosis. * **Esmolol:** * **Mechanism:** Short-acting beta-blocker. * **Use:** Peri-anesthesia. ### 2.8 Prognosis and Follow-up * **Improved Prognosis:** Adequate treatment has significantly improved the prognosis of hypertensive emergencies. * **Prognostic Indicators:** Troponin levels, renal function, degree of blood pressure control, and proteinuria during follow-up are important prognostic factors. * **Intensive Follow-up:** Required for patients who have experienced a hypertensive emergency. ### 2.9 Challenges * **Identification of subclinical organ damage:** The role of routine troponin testing or brain MRI in identifying subclinical damage is an area of ongoing discussion. * **Uniform nomenclature and classification:** Standardizing terminology is important for clear communication and research. * **Uniform treatment strategies:** Developing consensus on optimal medication, speed of reduction, target blood pressure, and route of administration (IV vs. oral) is crucial. ### 2.10 Perioperative Hypertension While not always an emergency, parenteral therapy is frequently used. Careful blood pressure management is vital to avoid complications at vascular suture sites (thrombosis vs. bleeding). Restarting oral medications or using IV nicardipine or labetalol are common approaches. Preoperative assessment for factors like pain, anxiety, hypovolemia, hypoxia, and withdrawal syndromes is important. ### 2.11 Other Specific Populations * **Acute Ischemic Stroke:** A dual therapeutic approach is considered: managing perifocal cerebral edema and impaired autoregulation. Restrictive therapy may be indicated, particularly if SBP > 220 mmHg. * **Acute Stroke with Thrombolysis:** Blood pressure must be < 185/110 mmHg before thrombolysis, with a target of MAP - 15% over 1 hour. BP should be maintained below 180/105 mmHg for the following 24 hours to reduce the risk of hemorrhagic transformation. * **Intracerebral Bleeding (ICB):** Aggressive blood pressure lowering is generally favored, especially in the first hour. * **Acute Aortic Dissection:** Immediate reduction of SBP to 100-120 mmHg and pulse rate to < 60 bpm within 20 minutes. * **Severe Pregnancy-Related Hypertension:** Requires prompt management to protect mother and neonate. * **Pheochromocytoma:** Requires specific management due to adrenergic hyperstimulation, with alpha-blockers being essential. * * * ## Common mistakes to avoid * Review all topics thoroughly before exams * Pay attention to formulas and key definitions * Practice with examples provided in each section * Don't memorize without understanding the underlying concepts

| Term | Definition | |---|---| | Arterial Hypertension (AHT) | A condition characterized by persistently elevated blood pressure in the arteries, recognized as a primary cardiovascular risk factor contributing to conditions like acute myocardial infarction, heart failure, and cerebrovascular accidents. | | Cardiovascular Risk Factor | An attribute or characteristic that is associated with an increased risk of developing cardiovascular disease. These include factors like hypertension, dyslipidemia, smoking, diabetes, and obesity. | | Myocardial Infarction | Also known as a heart attack, this occurs when blood flow to a part of the heart muscle is severely reduced or blocked, typically by a blood clot, causing damage to the heart muscle. | | Heart Failure | A chronic condition where the heart muscle cannot pump blood as well as it should, leading to symptoms such as shortness of breath, fatigue, and swelling in the legs, ankles, and feet. | | Cerebrovascular Accident (CVA) | Commonly referred to as a stroke, this is a medical emergency that occurs when the blood supply to part of the brain is interrupted or reduced, preventing brain tissue from getting oxygen and nutrients. | | Hypertensive Emergencies | A severe and rapid increase in blood pressure, usually above $180/120$ mmHg, accompanied by evidence of acute, life-threatening organ damage, requiring immediate reduction in blood pressure. | | Hypertensive Urgencies | A significant rise in blood pressure, typically over $180/110$ mmHg, without evidence of acute organ damage. These are now often referred to as uncontrolled hypertension and do not require immediate blood pressure reduction. | | Hypertension-Mediated Organ Damage (HMOD) | Damage to various organs (heart, brain, kidneys, eyes, blood vessels) caused by the sustained elevated pressure of hypertension over time. | | Home Blood Pressure Measurement (HBPM) | A method of monitoring blood pressure at home by the patient, using a validated device, to obtain multiple readings over time, which can provide a more accurate assessment than office-based measurements alone. | | Ambulatory Blood Pressure Measurement (ABPM) | Also known as portometrie, this involves continuous blood pressure monitoring over a 24-hour period using a portable device, offering insights into blood pressure variability, the white-coat effect, and nocturnal dipping patterns. | | White Coat Hypertension | A phenomenon where a patient's blood pressure is elevated when measured in a clinical setting (doctor's office) but is normal when measured at home or via ambulatory monitoring. | | Masked Hypertension | A condition where blood pressure is normal during office visits but elevated during out-of-office measurements (HBPM or ABPM), posing a risk for long-term cardiovascular complications. | | RAAS (Renin-Angiotensin-Aldosterone System) | A hormonal system that regulates blood pressure and fluid balance in the body. Its activation can lead to vasoconstriction and sodium and water retention, increasing blood pressure. | | Orthostatic Hypotension | A form of low blood pressure that occurs when a person stands up from a sitting or lying position. It can cause dizziness, lightheadedness, or fainting. | | Left Ventricular Hypertrophy (LVH) | An increase in the thickness of the muscle walls of the left ventricle of the heart, often caused by chronic hypertension. It is a sign of target organ damage. | | Carotid Duplex Ultrasound | An imaging technique used to assess blood flow and the condition of the carotid arteries, detecting plaque buildup or thickening of the arterial wall (IMT), which are signs of vascular damage. | | Ankle-Brachial Index (ABI) | A non-invasive test that compares the blood pressure in the ankles to the blood pressure in the arms to assess for peripheral artery disease. An ABI below $0.9$ indicates possible PAD. | | Micro-albuminuria | The presence of small amounts of albumin in the urine, which is an early indicator of kidney damage, particularly in individuals with hypertension or diabetes. | | Malignant Hypertension | A severe and rapidly progressing form of hypertension characterized by extremely high blood pressure (often $>200/120$ mmHg) with evidence of acute, widespread organ damage, particularly involving the retina, kidneys, and brain. | | Hypertensive Encephalopathy | A neurological condition caused by a sudden, severe rise in blood pressure, leading to brain swelling, confusion, seizures, and potentially coma. | | Posterior Reversible Encephalopathy Syndrome (PRES) | A neurological disorder characterized by reversible white matter edema, typically in the posterior regions of the brain, often associated with severe hypertension, autoimmune diseases, or certain medications. | | Acute Coronary Syndrome (ACS) | A term used for a range of conditions associated with sudden, severe flow to the heart muscle. This includes heart attack (myocardial infarction) and unstable angina. | | Acute Aortic Syndrome | A spectrum of conditions involving the aorta, including aortic dissection, intramural hematoma, and penetrating atherosclerotic ulcers, often triggered by severe hypertension. | | Autoregulation (Cerebral) | The brain's ability to maintain a constant cerebral blood flow despite changes in systemic blood pressure. This mechanism can be overwhelmed in severe hypertension. | | Vasospasm | The constriction of blood vessels, which can reduce blood flow and lead to ischemia. It is a concern in conditions like subarachnoid hemorrhage. | | Perfusion Pressure | The pressure gradient that drives blood flow through a tissue or organ. In the brain, maintaining adequate perfusion pressure is crucial for preventing ischemia. | | Framingham Risk Score | A tool used to estimate an individual's 10-year risk of developing cardiovascular disease based on factors such as age, sex, blood pressure, cholesterol levels, and smoking status. | | SCORE Chart | A risk assessment tool that estimates the 10-year risk of fatal cardiovascular disease based on age, sex, smoking status, systolic blood pressure, and cholesterol levels. | | Dipper Profile | Refers to the normal nocturnal dipping pattern of blood pressure, where blood pressure decreases by $10-20\%$ during sleep. A lack of dipping (non-dipper) is associated with increased cardiovascular risk. | | Morning Surge | A rapid increase in blood pressure that typically occurs in the early morning hours, before waking. An exaggerated morning surge is linked to an increased risk of cardiovascular events. | | Preeclampsia | A serious pregnancy complication characterized by high blood pressure, edema, and proteinuria, typically developing after the 20th week of gestation. It can progress to eclampsia, a life-threatening condition. | | Eclampsia | The most severe form of preeclampsia, characterized by seizures in addition to high blood pressure and proteinuria. | | Magnesium Sulfate | A medication used to prevent and treat seizures in women with preeclampsia and eclampsia. It also has a vasodilatory effect. | | RAAS Blockade | The inhibition of the renin-angiotensin-aldosterone system, typically achieved with ACE inhibitors or angiotensin II receptor blockers (ARBs), to lower blood pressure and reduce cardiovascular risk. | | Teratogen | A substance or agent that can cause birth defects. Certain medications, such as RAAS blockers, are teratogenic and should be avoided during pregnancy. | | Phentolamine | An alpha-adrenergic blocking agent used to treat hypertensive emergencies, particularly those related to pheochromocytoma, by causing vasodilation. | | Urapidil | An antihypertensive medication that acts as both an alpha-1 adrenergic receptor antagonist and a 5-HT1A receptor agonist, leading to vasodilation and reduced sympathetic activity without significant reflex tachycardia. | | Esmolol | A short-acting beta-blocker primarily used in peri-anesthetic settings for rapid control of heart rate and blood pressure. | | Nicardipine | A dihydropyridine calcium channel blocker that causes arterial vasodilation, used to treat hypertensive emergencies. | | Natrium Nitroprusside | A potent direct vasodilator that reduces both preload and afterload, used in severe hypertensive emergencies. It is metabolized to cyanide, requiring caution in patients with renal or hepatic impairment. | | Nitroglycerine | A vasodilator that reduces preload and afterload, and dilates epicardial coronary arteries. It is used in hypertensive emergencies, particularly those involving acute coronary syndromes and heart failure. | | Labetalol | A combined alpha and beta-adrenergic blocker used to treat hypertensive emergencies, including those during pregnancy. It lowers blood pressure without causing significant reflex tachycardia. | | Enalapril | An ACE inhibitor that blocks the production of angiotensin II, a potent vasoconstrictor. It is used to treat hypertension, particularly in patients with heart failure or kidney disease. | | Clonidine | A central alpha-agonist that reduces sympathetic outflow from the brain, leading to a decrease in blood pressure. It can cause sedation and rebound hypertension if stopped abruptly. |