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Hypertensive disorders By Dr. Haitham Nabeel Your Date Here Your Footer Here Hypertension Your Date Here Your Footer Here Objectives After completion of this lecture you will understand the : Diagnosis of h...

Hypertensive disorders By Dr. Haitham Nabeel Your Date Here Your Footer Here Hypertension Your Date Here Your Footer Here Objectives After completion of this lecture you will understand the : Diagnosis of hypertension Stages of hypertension Investigations Threshold of treatment Monitoring blood pressure control Pharmacological and non pharmacological treatment Target blood pressure Investigations for secondary causes Your Date Here Your Footer Here 3 Blood pressure BP follows a normal distribution in the general population and there is no specific cut-off above which the risk of cardiovascular risk suddenly increases. The diagnosis of hypertension is therefore made when systolic and diastolic values rise above a specific threshold that corresponds to the level of BP at which the risk of cardiovascular complications and benefits of treatment outweigh the treatment costs and potential side effects of therapy. Your Date Here Your Footer Here 4 Pathogenesis & etiology In more than 95% of cases, however, no specific underlying cause of hypertension can be found. Such patients are said to have essential hypertension. In about 5% of cases, hypertension is secondary to a specific disease, as summarised in the next slide. Your Date Here Your Footer Here 5 Causes of secondary hypertension Your Date Here Your Footer Here 6 Risk factors Nonmodifiable risk factors Positive family history Ethnicity Advanced age Modifiable risk factors Obesity Diabetes Smoking, excessive alcohol or caffeine intake Diet high in sodium, low in potassium Physical inactivity Psychological stress Your Date Here Your Footer Here 7 Clinical features Hypertension is usually asymptomatic until the diagnosis is made at a routine physical examination or when a complication arises. Reflecting this fact, a BP check is advisable every 5 years in adults over 40 years of age to pick up occult hypertension Physical Examination signs in hypertensive patients: Signs of left ventricular hypertrophy, accentuation of the aortic component of the second heart sound, and a fourth heart sound. Afib is common Your Date Here Your Footer Here 8 Diagnosis of hypertension If clinic blood pressure is between 140/90 mmHg and 180/120 mmHg → offer ambulatory blood pressure monitoring (ABPM) If ABPM is unsuitable or the person is unable to tolerate it → offer home blood pressure monitoring (HBPM) Confirm diagnosis of hypertension in people with a clinic blood pressure of 140/90 mmHg or higher and ABPM daytime average or HBPM average of 135/85 mmHg or higher. Your Date Here Your Footer Here 9 White coat hypertension (white coat effect) Definition: arterial hypertension detected only in clinical settings or during blood pressure measurement at a physician's practice Etiology: anxiety experienced by the patient Clinical features: consistently normal blood pressure measurements and normalization of elevated blood pressure outside of a clinical setting Diagnostics Take different blood pressure measurements several minutes apart (after the patient had time to relax) Take blood pressure measurements on several visits (at least 2) Your Date Here Your Footer Here 10 Stages of hypertension NICE guidelines, August 2020. Your Date Here Your Footer Here 11 ACC/AHA classification of hypertension 2017 Your Date Here Your Footer Here 12 Investigations Aims to : 1-assess cardiovascular risk 2-determine the presence of target organ damage Your Date Here Your Footer Here 13 Target organ damage Damage to organs such as the heart, brain, kidneys and eyes. Examples are left ventricular hypertrophy, chronic kidney disease, hypertensive retinopathy or increased urine albumin:creatinine ratio. Your Date Here Your Footer Here 14 Example What is the 10 year cardiovascular risk for a 50-year- old male, hypertensive (BP 15/9), smoker and non- diabetic with total cholestrol 240mg/dl ? A/5-9% Your Date Here Your Footer Here 16 Investigations For all people with hypertension offer to : HbA1C electrolytes creatinine , eGFR total cholestroln and HDL cholestrol Urinalysis for blood, protein, glucose and ACR ratio 12 lead ECG Fundoscopy Thyroid function tes Your Date Here Your Footer Here 17 Investigations Additional investigations are appropriate in patients younger than 40 years of age or those with resistant hypertension include: Chest X-ray: to detect cardiomegaly, heart failure, coarctation of the aorta Echocardiogram: to detect or quantify left ventricular hypertrophy Renal ultrasound: to detect possible renal disease Renal angiography: to detect or confirm the presence of renal artery stenosis Urinary catecholamines: to detect possible phaeochromocytoma Urinary cortisol and dexamethasone suppression test: to detect possible Cushing’s syndrome Plasma renin activity and aldosterone: to detect possible primary aldosteronism Your Date Here Your Footer Here 18 When to start antihypertensive ? 1-persistent stage 2 HT 2- stage 1 HT A-if patient over 80 if their clinic blood pressure is over 150/90 mmHg Your Date Here Your Footer Here 19 When to start antihypertensive ? B- if patient under 80 years: Start anti hypertensive if he has 1 or more of the following: target organ damage established cardiovascular disease renal disease Diabetes an estimated 10-year risk of cardiovascular disease of 10% or more. Your Date Here Your Footer Here 20 Established cardiovascular disease Past medical history of stroke or transient ischemic attack, heart attack, angina, narrowed peripheral arteries or an interventional procedure Your Date Here Your Footer Here 21 When to start antihypertensive ? C-if patient under 60: estimated 10-year risk below 10% D-if patient under 40 : consider seeking specialist evaluation of secondary causes of hypertension more detailed assessment of the long-term balance of treatment benefit and risks. Your Date Here Your Footer Here 22 What if BP>180/120? Is there any symptoms or signs indicating same-day referral ? signs of retinal haemorrhage or papilloedema life-threatening symptoms such as new onset confusion, chest pain, signs of heart failure, or acute kidney injury. suspected phaeochromocytoma (for example, labile or postural hypotension, headache, palpitations, pallor, abdominal pain or diaphoresis). Your Date Here Your Footer Here 23 What if BP>180/120? If NO , carry out investigations for target organ damage : If target organ damage is identified→ consider starting antihypertensive drug treatment immediately, without waiting for the results of ABPM or HBPM. If no target organ damage is identified →repeat clinic blood pressure measurement within 7 days Your Date Here Your Footer Here 24 Your Date Here Your Footer Here 25 Non-pharmacological management The big four : Weight loss DASH diet and decreasing sodium intake Regular exercise Reduce alcohol consumption Other changes : Smoking cessation Avoidance of NSAIDS Increase dietary potassium Your Date Here Your Footer Here 26 Pharmacological treatment There are 4 steps If blood pressure is not adequately controlled move a step higher Before considering next step treatment for hypertension discuss with the person if they are taking their medicine as prescribed The main drugs in hypertension Mx include ACE , ARB, CCB , DIURETICS. When choosing antihypertensive drug treatment for adults of black African or African–Caribbean family origin, consider an angiotensin II receptor blocker (ARB), in preference to an angiotensin-converting enzyme (ACE) inhibitor Your Date Here Your Footer Here 27 Step 1 treatment A- offer an ACE inhibitor or an ARB to adults starting step 1 antihypertensive treatment who: have type 2 diabetes and are of any age or family origin are aged under 55 but not of black African or African– Caribbean family origin. If an ACE inhibitor is not tolerated, for example because of cough, offer an ARB. Do not combine an ACE inhibitor with an ARB to treat hypertension Your Date Here Your Footer Here 28 Step 1 treatment B- offer a calcium-channel blocker (CCB) to adults starting step 1 antihypertensive : are aged 55 or over and do not have type 2 diabetes are of black African or African–Caribbean family origin and do not have type 2 diabetes (of any age). If a CCB is not tolerated, for example because of oedema, offer a thiazide-like diuretic such as indapamide in preference to a conventional thiazide diuretic such as bendroflumethiazide or hydrochlorothiazide. Your Date Here Your Footer Here 29 Dual therapy there was not enough evidence to determine confidently the benefits or harms of starting treatment with dual therapy Your Date Here Your Footer Here 30 Step 2 treatment If BP is not controlled on first step treatment , add another first line drug. Ex/patient on ACE inhibitor and not controlled ? Step 2 treatment options include : CCB , thiazide like diuretics Your Date Here Your Footer Here 31 Step 3 treatment If hypertension is not controlled in adults taking step 2 treatment, offer a combination of: an ACE inhibitor or ARB and a CCB and a thiazide-like diuretic. Your Date Here Your Footer Here 32 Step 4 treatment regard them as having resistant hypertension. Before considering further treatment for a person with resistant hypertension: Confirm elevated clinic blood pressure measurements using ambulatory or home blood pressure recordings. Assess for postural hypotension. Discuss adherence Your Date Here Your Footer Here 33 Step 4 treatment Consider further diuretic therapy with low-dose spironolactone for adults with resistant hypertension starting step 4 treatment who have a blood potassium level of 4.5 mmol/l or less caution in people with a reduced estimated glomerular filtration rate monitor blood sodium and potassium and renal function within 1 month of starting treatment and repeat as needed thereafter Your Date Here Your Footer Here 34 Step 4 treatment Consider an alpha-blocker or beta-blocker for adults with resistant hypertension starting step 4 treatment who have a blood potassium level of more than 4.5 mmol/l. If blood pressure remains uncontrolled in people with resistant hypertension taking the optimal tolerated doses of 4 drugs, seek specialist advice Your Date Here Your Footer Here 35 Antihypertensive drugs Your Date Here Your Footer Here 36 Treatment according to subgroups Patients with CHF Diuretics, aldosterone antagonists, ACEIs, and ARBs ARBs can be combined with sacubitril Beta blockers Safe to use in compensated CHF Must be used cautiously in decompensated CHF Contraindicated in cardiogenic shock Patients with diabetes mellitus ACEIs, ARBs, CCBs, thiazide diuretics, beta blockers ACEIs/ARBs are protective against diabetic nephropathy. Beta blockers can mask hypoglycemia symptoms. Your Date Here Your Footer Here 37 Treatment according to subgroups Patients with asthma ARBs, CCB, thiazide diuretics, cardioselective beta blockers (nonselective beta blockers can cause bronchoconstriction) Avoid ACEIs (can cause bradykinin-induced cough). Treatment of hypertension in pregnancy First-line treatment: methyldopa, labetalol, hydralazine, and nifedipine Second-line treatment: thiazides, clonidine Contraindicated: furosemide, ACEI, ARB, renin inhibitors (e.g., aliskiren) Your Date Here Your Footer Here 38 Refractory hypertension Refractory hypertension refers to the situation where multiple drug treatments do not give adequate control of BP. Although this may be due to genuine resistance to therapy in some cases, a more common cause of treatment failure is non-adherence to drug therapy. Resistant hypertension can also be caused by failure to recognise an underlying cause, such as renal artery stenosis or phaeochromocytoma Your Date Here Your Footer Here 39 Monitoring BP Use clinic blood pressure measurements to monitor the response Consider ABPM or HBPM, in addition to clinic blood pressure measurements, for people with hypertension identified as having a white-coat effect In people with a significant postural drop or symptoms of postural hypotension, treat to a blood pressure target based on standing blood pressure Your Date Here Your Footer Here 40 BP targets Reduce clinic blood pressure to below 140/90 mmHg and maintain that level in adults with hypertension aged under 80 Reduce clinic blood pressure to below 150/90 mmHg and maintain that level in adults with hypertension aged 80 and over. When using ABPM or HBPM to monitor the response to treatment. Reduce and maintain blood pressure at the following levels: below 135/85 mmHg for adults aged under 80 below 145/85 mmHg for adults aged 80 and over. Your Date Here Your Footer Here 41 Your Date Here Your Footer Here 42 Hypertensive crises Your Date Here Your Footer Here Definitions Hypertensive crisis (acute severe hypertension): an acute increase in systolic blood pressure ≥ 180 mm Hg and/or diastolic blood pressure ≥ 120 mm Hg. Hypertensive urgency: hypertensive crisis that is either asymptomatic or with isolated nonspecific symptoms (e.g., headache, dizziness, or epistaxis) without signs of organ damage Hypertensive emergency: hypertensive crisis with signs of end-organ damage, mainly in the cardiovascular, central nervous, and renal systems. Your Date Here Your Footer Here 44 Etiology Drug-related Nonadherence to antihypertensives Drugs that may exacerbate hypertension (e.g., MAO inhibitors, TCAs, NSAIDS, cocaine, amphetamines, ecstasy, stimulant diet pills) Consumption of foods rich in tyramine (e.g., wine, chocolate, aged cheese, cured meat) during therapeutic use of MAOIs Pheochromocytoma, hyperthyroidism Acute and rapidly progressive renal disorders Collagen vascular diseases (e.g., SLE) Eclampsia/Pre-eclampsia Head trauma, spinal cord disorders Your Date Here Your Footer Here 45 Clinical features Hypertensive urgency Asymptomatic or isolated, nonspecific symptoms (e.g., headache, dizziness, or epistaxis) Hypertensive emergency Signs and symptoms of end-organ dysfunction Cardiac Heart failure exacerbation, pulmonary edema: dyspnea, crackles on examination Myocardial infarction: chest pain, diaphoresis Aortic dissection: chest pain, asymmetric pulses Your Date Here Your Footer Here 46 Clinical features Neurologic Hypertensive encephalopathy: headache, vomiting, confusion, seizure, blurry vision, papilledema Ischemic or hemorrhagic stroke: focal neurological deficits, altered mental status Renal: Acute kidney injury (azotemia and/or oliguria, edema) and microhematuria Pathophysiology: severe hypertension → acute thrombotic microangiopathy → thrombosis of glomerular capillaries and red blood cell extravasation and fragmentation as well as luminal thrombosis of arterioles → infarction and necrosis of endothelial and mesangial cells → decreased glomerular blood flow → acute kidney damage Biopsy: petechial subcapsular hemorrhages, renal infarction, and segmental capillary loop necrosis with crescent formation Your Date Here Your Footer Here 47 Clinical features Ophthalmic Acute hypertensive retinopathy: blurry vision, decrease in visual acuity, retinal flame hemorrhages, papilledema Other Microangiopathic hemolytic anemia: fatigue, pallor Your Date Here Your Footer Here 48 Management Approach to management Confirm blood pressure manually and on bilateral upper extremities. Determine if there are signs of end-organ damage. Focused history/physical Select screening tests For hypertensive emergencies ABCDE approach Admit patients (ideally to ICU). Lower the blood pressure acutely using IV agents and aim for targets based on the affected end-organs Evaluate and treat underlying disorders. For hypertensive urgency Select, reinstitute, or modify oral antihypertensive therapy. In patients with a new diagnosis, evaluate for secondary causes of hypertension. Arrange follow-up, monitoring, and counseling. Your Date Here Your Footer Here 49 Red flags for hypertensive crisis Dyspnea Chest pain Altered mental status Focal neurologic symptoms Your Date Here Your Footer Here 50 Diagnostics Evaluate for signs of end-organ damage Laboratory studies CBC: signs of microangiopathic hemolytic anemia BMP: altered electrolytes and/or elevated creatinine and urea, which suggest kidney failure BNP: elevated in heart failure Troponin: elevated in myocardial ischemia Urinalysis: signs of glomerular injury (e.g., proteinuria, hematuria) ECG: left ventricular hypertrophy, signs of cardiac ischemia (e.g., ST depressions or elevations) Chest x-ray: cardiomegaly, pulmonary edema Your Date Here Your Footer Here 51 Diagnostics Additional evaluation to consider Urine pregnancy test Toxicology screen CT chest with IV contrast if chest pain is concerning for aortic dissection Consider TTE if clinical features suggest pulmonary edema. Consider CT head if neurological symptoms are present. Your Date Here Your Footer Here 52 Management Hypertensive urgency Outpatient treatment is recommended. Move patient to a quiet room for 30 minutes. Reinstitute or increase the dosage of existing oral antihypertensive therapy. For patients with nonspecific symptoms that do not constitute end- organ damage (e.g., isolated headache, nonspecific dizziness, and epistaxis), consider a rapid-acting oral antihypertensive agent prior to discharge (e.g. Captopril). Monitor the patient for a few hours to ensure BP is improving. For patients with a first diagnosis of hypertension, consider evaluation for secondary hypertension. Discharge and follow-up Ensure close follow-up with an outpatient provider. 53 Hypertensive urgency is usually caused by nonadherence to antihypertensive therapy. Aggressive intravenous antihypertensive therapy is not required. Clinical pearl! Your Date Here Your Footer Here 54 Management Hypertensive emergency General principles ICU admission and immediate initiation of intravenous antihypertensive therapy Continuous cardiac monitoring Consider intra-arterial blood pressure monitoring. Identify and treat any contributing comorbidities (e.g., chronic renal failure). IV fluids if signs of volume depletion Monitor BMP every 6 hours. Your Date Here Your Footer Here 55 Management Rate and target of blood pressure reduction General goal Reduce BP by max. 25% within the first hour to prevent coronary insufficiency and to ensure adequate cerebral perfusion pressure. Reduce BP to ∼ 160/100–110 mm Hg over the next 2–6 hours. Reduce BP to patients baseline over 24–48 hours. Special cases Indications for the rapid lowering of systolic BP (usually to < 140 mm Hg) in the first hour of treatment include severe pre- eclampsia or eclampsia, aortic dissection, and pheochromocytoma with hypertensive crisis Your Date Here Your Footer Here 56 Management Intravenous antihypertensives Calcium channel blockers Nicardipine Clevidipine Nitric-oxide dependent vasodilators Sodium nitroprusside Nitroglycerin Direct arterial vasodilators: hydralazine Antiadrenergic drugs Selective beta-1 antagonist: esmolol Nonselective beta blocker with alpha-1 antagonism: labetalol Nonselective alpha antagonist: phentolamine D1 agonist: fenoldopam ACE inhibitor: enalaprilat Your Date Here Your Footer Here 57 Management Choice of intravenous antihypertensive drugs Consider the following factors when choosing an antihypertensive: Desired rate of decrease in blood pressure End-organ system affected Underlying disorder Presence or absence of comorbidities (e.g., heart failure, COPD) Pharmacokinetics and adverse effects of the agent Availability in our great country Your Date Here Your Footer Here 58 Mean arterial pressure should not be lowered by more than 25% within the first hour, except in special cases. Reducing the blood pressure too rapidly can lead to hypoperfusion and ischemia in certain organs (e.g., brain, kidney, heart). Clinical pearl! Your Date Here Your Footer Here 59 Aortic dissection Your Date Here Your Footer Here Epidemiology Incidence Peak incidence: 60–80 years of age In patients with Marfan syndrome: peak incidence 30–50 years of age) Sex: ♂ > ♀ Localization Ascending aorta: ∼ 65% of cases Descending aorta, distal to the left subclavian artery: 20% of cases Aortic arch: 10% of cases Abdominal aorta: 5% of cases Your Date Here Your Footer Here 61 Etiology Acquired Hypertension (most common risk factor) Approx. 70% of patients with aortic dissection have elevated blood pressure, which can lead to propagation of the dissection and increases the risk of rupture. Exception: In patients < 40 years of age, less than 40% of cases are due to hypertension. Trauma (e.g., deceleration injury in a motor vehicle accident, or iatrogenic injury during valve replacements or graft surgery) Vasculitis with aortic involvement (e.g., syphilis, Takayasu arteritis) Use of amphetamines and cocaine Third-trimester pregnancy (or early postpartum period) Atherosclerosis Congenital Connective tissue disease (Marfan syndrome, Ehlers-Danlos syndrome) Bicuspid aortic valve Coarctation of the aorta Your Date Here Your Footer Here 62 Stanford classification Stanford type A aortic dissection: any dissection involving the ascending aorta (defined as proximal to the brachiocephalic artery), regardless of origin Can extend proximally to the aortic arch and distally to the descending aorta Generally requires surgery Complications include aortic regurgitation and cardiac tamponade. Stanford type B aortic dissection: any dissection not involving the ascending aorta Descending aorta; originating distal to the left subclavian artery Most cases can be managed with medical therapy (e.g., beta blockers, vasodilators). Your Date Here Your Footer Here 63 Classifications of aortic dissection Stanford classification – Type A: dissection involves the ascending aorta or aortic arch – Type B: dissection involves only the descending aorta (distal to the origin of the left subclavian artery) DeBakey classification – Type I: dissection involves the ascending and descending aorta – Type II: dissection involves only the ascending aorta (up to the brachiocephalic artery) – Type III: dissection involves only the descending aorta (distal to the origin of the left subclavian artery) Your Date Here Your Footer Here 64 Pathophysiology Transverse tear in the aortic intima (“entry”) → blood enters the media of the aorta and forms a false lumen in the intima-media space → hematoma forms and propagates longitudinally downwards. Rising pressure within the aortic wall → rupture Occlusion of every single branching vessel (e.g., coronary arteries, arteries supplying the brain, renal arteries, arteries supplying the lower limbs) → ischemia in the affected areas. A second intimal tear may result in a “reentry” into the primary aortic lumen. Your Date Here Your Footer Here 65 Aortic dissection A tear in the tunica intima (entry tear on illustration) allows blood to enter into the tunica media. The column of blood then extends longitudinally, most commonly in the outer half of the tunica media. This creates a false lumen, which may rupture back into the true lumen of the aorta (re-entry tear on illustration) or rupture through the tunica adventitia. Your Date Here Your Footer Here 66 Clinical features Sudden and severe tearing/ripping pain Location Anterior chest (ascending) or back (descending) Interscapular or retrosternal pain Neck and jaw Abdomen or periumbilical, colicky pain Character: migrates as the dissected wall propagates caudally Hypertension or hypotension Asymmetrical blood pressure and pulse readings between limbs Syncope, diaphoresis, confusion or agitation A heart murmur (an aortic regurgitation in a proximal dissection) Your Date Here Your Footer Here 67 Diagnostics Approach Assess the risk of acute aortic dissection using the aortic dissection detection risk score (ADD-RS). Check ECG in all patients to exclude other causes of severe chest pain. Consider which imaging modality is indicated CXR: low to moderate-risk patients Definitive imaging (e.g., CTA, MRA): high-risk patients, unexplained hypotension, abnormal CXR, no alternative diagnosis Your Date Here Your Footer Here 68 Aortic dissection detection risk score (ADD-RS) Your Date Here Your Footer Here 69 ECG Should be ordered for all patients. Findings are variable and include: Normal findings Signs of left ventricular hypertrophy Nonspecific changes, such as ST depression and T-wave changes ST elevation due to coronary artery occlusion. BUT…ST elevation is more commonly associated with acute coronary syndrome (ACS) than aortic dissection. Therefore, unless there are high- risk conditions or features suggestive of aortic dissection, patients with ST elevation should be treated for ACS and immediate coronary artery reperfusion therapy arranged. Your Date Here Your Footer Here 70 initial imaging in low to moderate risk patients Chest x-ray (AP view) Characteristic findings: May be normal Widened mediastinum (> 8 cm) at the level of the aortic knuckle Alteration of the mediastinal contour seen on serial imaging Mediastinal mass Calcium sign: displacement of the intimal calcification of > 6 mm Your Date Here Your Footer Here 71 Widened mediastinum X-ray chest (PA view) of a patient with a Stanford type A dissection Widening of the mediastinum is accompanied by a prominent aortic knob on the left side and convexity in the region of the ascending aorta on the right side. Cardiac silhouette enlargement is also visible, which could indicate aortic regurgitation or pericardial effusion. Your Date Here Your Footer Here 72 Normal chest x-ray findings do not rule out aortic dissection. If clinical suspicion for acute aortic dissection persists, perform a second imaging study. Clinical pearl! Your Date Here Your Footer Here 73 Definitive imaging Definitive imaging is used to determine the type of lumen, location, and extent of the dissecting membrane. The identification of a false lumen is highly suggestive of aortic dissection. Indications All high-risk patients: ADD-RS score of 2 or 3 Moderate and low-risk patients (ADD-RS score of 0 or 1) with: Unexplained hypotension No other diagnosis to explain the symptoms Any concerning features present on chest x-ray Your Date Here Your Footer Here 74 Modalities CT angiography of the chest, abdomen, and pelvis Indications: stable patients, surgical planning Advantages: very high sensitivity and specificity (considered to be the gold standard). Magnetic resonance angiography (MRA) of the chest, abdomen, and pelvis Indications: stable patients, contraindications to CTA Transesophageal echocardiography (TEE) Indications: Unstable patients Intraoperative visualization Renal insufficiency or contrast allergy. Your Date Here Your Footer Here 75 Stanford type A aortic dissection CT thorax (with contrast; axial view) A mucosal flap (green line) can be seen dividing the lumen of the ascending (A) and descending (D) aorta. This radiological appearance confirms a Stanford type A aortic dissection. T: pulmonary trunk Your Date Here Your Footer Here 76 Management Approach Urgent cardiothoracic surgical consult for all patients with suspected or confirmed dissection, regardless of location. Stanford A dissection: immediate surgery. Stanford B dissection: treat conservatively (watchful waiting and ongoing medical therapy) unless complications occur. Blood pressure control is essential in all patients to prevent progression of the dissection Supportive care Admission to surgical ICU with close monitoring and surveillance imaging Your Date Here Your Footer Here 77 Medical therapy Control hypertension and heart rate: target SBP 100–120 mm Hg and HR ≤ 60 beats per minute Start with IV beta blocker: to avoid reflex tachycardia Esmolol Labetalol Followed by vasodilator (e.g., IV sodium nitroprusside) Contraindications to beta blocker: start calcium channel blocker Verapamil Diltiazem Patients with dissection of the descending aorta who remain stable on IV treatment can be transitioned to oral medications and discharged with outpatient imaging surveillance. Your Date Here Your Footer Here 78 Start beta-blocker therapy before vasodilators to avoid a reflex tachycardia! Clinical pearl! Your Date Here Your Footer Here 79 Medical therapy Hypotensive patients Hemodynamic support: target MAP of 70 mm Hg or euvolemia. IV fluids Vasopressor support: if the patient remains hypotensive. Norepinephrine Phenylephrine Inotropes: should be avoided as they can increase sheer stress on the aortic wall through increased force of ventricular contraction. Identify and treat any comorbidities that may be contributing Cardiac tamponade Severe aortic insufficiency Expedite operative management. Your Date Here Your Footer Here 80 Surgical therapy Indications All patients with Stanford A dissection Patients with Stanford B dissection who develop complications: End-organ damage (ischemia) Hypotension Persistent severe chest pain or hypertension Propagation of dissection Expanding aneurysm Expanding hematoma Rupture Your Date Here Your Footer Here 81 Ascending aortic dissection is a surgical emergency! Clinical pearl! Your Date Here Your Footer Here 82 Supportive care Patients may require sedation Analgesia (e.g., morphine) Identify and treat any complications (e.g., mesenteric ischemia, acute kidney injury) Your Date Here Your Footer Here 83 Avoid thrombolytic therapy in patients with suspected aortic dissection! Clinical pearl! Your Date Here Your Footer Here 84 Complications Aortic rupture and acute blood loss: acute back and flank pain (tearing pain), symptoms of shock → indication for emergency surgery Complications of Stanford type A dissections Myocardial infarction (coronary artery occlusion) Aortic regurgitation (extension of the dissection into the aortic valve): new diastolic heart murmur and (exertional) dyspnea Cardiac tamponade combined with cardiogenic shock Pericarditis (slow extension of the dissection into the pericardium) Stroke (extension of the dissection into the carotids) Your Date Here Your Footer Here 85 Complications Complications of both Stanford type A dissection and Stanford type B dissections Bleeding into the thorax, mediastinum, and abdomen Arterial occlusion followed by ischemia of the: Celiac trunk, superior/inferior mesenteric artery → acute abdomen, ischemic colitis. Renal arteries → acute renal failure (oliguria, anuria) Spinal arteries → weakness of lower extremities or acute paraplegia Complete occlusion of the distal aorta → Leriche syndrome (aortoiliac occlusive disease) Your Date Here Your Footer Here 86 THANK YOU! Do you have any questions?

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