Dr. Ali Ragab | Critical Care Study Notes Pass Critical Care ICU questions and answers (ASU) Cardio Dr. Ali Ragab WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Hypertension in ICU * Hypertensive crisis; definition, pathophysiology, and management (2007 - 2009) + Na Nitroprusside in Malignant hypertension; doses, monitor, (diagnose and treat) (2010) Ce Hypertensive crisis © SBP > 180 mmHg or DBP > 120 mmHg. * This includes hypertensive emergency and hypertensive urgency. Hypertensive urgency * Hypertensive crisis without target organ damage. Hypertensive emergency * Hypertensive crisis with target organ damage - central nervous em (c.g. encephalopathy or hemorrhage) - myocardial (e.g. ischemia or pulmonary edema) ~ hematologic (e.g. hemolysis) - renal (c.g, acute renal failure) - pregnancy (eclampsia or preeclampsia). Accelerated malignant hypertension * Hypertensive emergency + fundoscopic findings (papilledema + acute retinal hemorrhages and exudates). rnc * Mild to moderate } in BP > arterial and arteriolar vasoconstriction (autoregulation) > maintains tissue perfusion at relatively constant level and prevents the increase in pressure from being transmitted to the smaller or more distal vessels. * Severe } in BP > failure of autoregulation > } pressure in arterioles and capillaries > damage of the vascular wall > disruption of vascular endothelium > plasma constituents (e.g, fibrinoid material) enter vascular wall > narrowing or obliterating the vascular lumen. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Ey * Within the brain - failure of autoregulation > breakthrough vasodilation > cerebral edema and hypertensive encephalopathy. [Et Primary or essential hypertension (95% of cases) * Unknown cause. Secondary hypertension (5% of cases) Renal disease * Intrinsic renal disease (GN - PAN - systemic sclerosis - chronic pyelonephritis ~ polycystic kidneys). * Renovascular disease (renal artery stenosis - atheromatous - fibromuscular dysplasia). Endocrine disease * Cushing’s syndrome - Conn’s syndromes - pheochromocytoma - acromegaly ~ hyperparathyroidism ~ hyperthyroid. Others * Coarctation - pregnancy - liquorice. * Drugs (steroids - MAOI - oral contraceptive pill - cocaine). * History of hypertension. * History of CNS - cardiac - aortic - renal disease. * History of obstetrics/ gynecology diseases. * Antihypertensive meds (dose changes ~ compliance). * Cocaine/amphetamine use. © @NS (mental status changes - headache - weakness ~ vision changes). * Cardiac (chest pain - SOB - dyspnea on exertion - orthopnea). * Renal (hematuria ~ decreased UOP). WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Geist * Vitals (BP in both arms and legs - heart rate - O2 saturation). * Fundoscopie (hemorrhages ~ exudates - papilledema). © @VS (5; ~ S; - murmurs - f JVP - peripheral edema - pulse deficits). © Pulmonary (crackles/rales). © Neurological (mental status changes - focal neurological deficits). * CBC - electrolytes ~ BUN/ Creatinine - glucose. * Urinalysis (RBCs - casts). © Cardiac enzymes. * ECG (ST and T Wave Changes - Q Waves - LVH). * CXR (Wide mediastinum ~ pulmonary edema). General goals First minutes to hour * Reduce 25% of the initial MAP. * Avoid aggressive BP reduction (may lead to ischemia of the kidneys / brain / myocardium because of arterial autoregulation). Next several hours © | BP to (160/100 mmHg). * After 24 hours of maintaining BP in 160/100 range > further BP therapy can be initiated to achieve the final goal BP. Patients with cardiovascular disease * Patients with (acute LV failure - myocardial ischemia - aortic dissection) > aggressive treatment to achieve BP < 120/80 mmHg. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Patients with ischemic strokes * Managed with BP target higher than usual. Transition from parenteral to oral * Once BP is controlled > start oral therapy and slowly decrease parenteral therapy. Volume status * Patients with hypertensive emergencies + volume depletion > volume repletion to maintain organ perfusion while controlling BP. OT Secondary causes sion in patients without prior history * Pain - anxiety ~ new onset of angina - hypercarbia. * Excessive arousal after sedation - withdrawal - volume overload. Management * Usually self-limited situation. * Low doses of short-acting agents should be used to avoid drops in BP. Clinical features: * Headache - nausea ~ vomiting ~ delirium ~ encephalopathy. Head CT * In patients with mental status changes + focal neurologic deficit. Management Goal * Lminute to 1 hour > | MAP no more than 20-25% * Over next 5 hours > target BP 160/110 mmHg. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Antihypertensive agents * Sodium nitroprusside traditionally used. * Other options (labetalol - fenoldopam - nicardipine). If neurologic status worsens > | infusion and consider other etiologies. Groin Etiology * Myocardial ischemia/infarction - LVF with acute pulmonary edema. History * Chest pain - SOB/dyspnea on exertion - orthopnea - PND. * Cardiac risk factors (DM - HTN - f Chol - t age - smoking, etc.). * Dietary indiscretion * History of CAD/CHE or drugs (ASA - nitrates). Physical Exam © THR-1RR- | SaQ2- 7 JVP - $3/S: - crackles/rales - LL edema. * 1 Cardiac enzymes - } BNP. * ECG (dynamic ST/T wave changes ~ Q waves). * CXR (cardiomegaly - bilateral infiltrates with pulmonary edema). Management * GIN > titrated to symptom relief. * Bblocker > add for all except acute LV failure. * Loop diuretics > add if pulmonary edema present. * ACEI > should be initiated unless contraindicated. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Etiology * ARF - acute GN ~ scleroderma renal crisis - renal artery stenosis. History * Hematuria - | UOP. © Recent upper respiratory tract infection. * History of chronic renal insufficiency. * Medications (ACEi ~ NSAIDs ~ cyclosporin - steroids - diuretics). Physical Exam Skin findings of scleroderma ~ abdominal Bruits ~ gross hematuria. Diagnostic Studies * 1 SCreat. ~ urinalysis (RBCs /protein/casts). Management Goals © Within minutes to hour > | MAP by 10-20%. * Over next 5 hours > | BP by another 10%. Anti-hypertensives * Nicardipine. * Fenoldopam. © Sodium nitroprusside (risk of cyanide toxicity). * ACEI (in scleroderma renal crisis) Hemodialysis © Tfnecessary. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Etiology * Pheochromocytoma. * Tyramine ingestion with MAO inhibitor. * Cocaine or amphetamines. * Rebound hypertension. History * Headache ~ sweating - palpitations. * History of depression/MAOi use with dietary indiscretion. * Medications (clonidine - f blockers). Physical Exam * 1 HR - hyperhidrosis - restlessness - agitation. * Café-au-lait spots - port wine stains - neurofibromas. Diagnostic Studies * Urine/serum toxicology. * Serum catecholamines/urine metanephrines. Management Pheo/MAOI/cocaine * Alpha blocker (phentolamine) + B blocker (after starting B-blocker). * BZDs (in cocaine intoxication). Rebound HTN * Etiology > clonidine or f blocker withdrawal. * Management > re-instituting single dose of withdrawn drug. If above strategies yield little response * Alternative therapies (e.g. sodium nitroprusside - labetalol). WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Symptoms * Headache - nausea - vomiting - vision changes. Fundoscopic * Hemorrhages - exudates - papilledema. Management Goal * In minutes to hour > | MAP by 20-25% * Over next 5 hours > | BP to 160/110 if tolerated. Antihypertensive agent * Sodium nitroprusside. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Angiotensin converting enzyme inhibitors * Non-selective competitive irreversible inhibition to angiotensin I binding site > | conversion of angiotensin I to angiotensin II (potent vasoconstrictor) > venous and arteriolar vasodilatation. RNa « First-dose hypotension (in salt/water depletion or hypersensitivity). «Renal failure (in renovascular disease - ARF - hyperreninemic HTN). © Dry cough (due to increa * Severe angioneurotic edema (causing upper airway obstruction). ET CES * Bilateral renal artery stenosis. sed production of kinins). * History of hereditary or idiopathic angioneurotic edema. * Pregnancy. CSS * Stop ACEi in ICU patients until vital organ (specifically renal) function is stabilized and the patient no longer requires inotropic support. * HTN > 25 mg PO q8~12h (max 450 mg/day). * Acute HTN > 5-25 mg SL (onset 20-30 min - duration 4 hours). * Heart fallure > 6.25 mg q8h (max 450 mg/day). ee © HTN > (25-5 mg/day PO) (1.25 mg q6h IV). © Heart failure > (2.5 mg/day PO) (1.25-5 mg q6h IV). WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Angiotensin receptor blockers (ARBs) * Blocks binding of angiotensin II to type 1 angiotensin II receptors. * Losartan 25-100 mg/day. * Valsartan 80-160 mg/day (max 320 mg/day). ARBs may be used as alternative to ACEI (they shouldn't be combined). * Cough. * Angioneurotic edema. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Alpha-adrenergic antagonists Mechanism of action * Non-selective competitive antagonist at alpha receptors > arteriolar and venous vasodilatation > | systemic blood pressure. Dosage © Bolus > 1-10 mg - infusion > 5-30 mg/h (IV). © Onset = 2 minutes ~ duration = 10-15 minutes. Mechanism of action * Non-selective non-competitive at alpha receptor antagonist. Dosage * HTN pheochromocytoma > 10 mg PO ql2h (up to 40 mg q8h). © Onset = several hours - duration = 3-4 days. In prolonged use * Prolonged use > 7 B-adrenergic effects > | HR > combination therapy with 6-blockade is recommended Mechanism of action * Relatively arterio-selective competitive alpha 1 receptor antagonist. Dosage © HTN > 1 mg PO fh (increase dose to 20 mg/day) Indications © Used for essential or renovascular (hyperreninemia) hypertension, * Frequently used in combination with B-blockers WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Mechanism of action . Competitive antagonist at (a1) - (fi) - (B2) adrenergic receptors. Arterial and venous vasodilation > | systemic blood pressure. Negative inotropy > | COP > | systemic blood pressure. Reflex tachycardia is attenuated by beta blockade. Dosage HTN > 200-400 mg PO q12h. Hypertensive emergency > 20 mg IV then 40-80 mg IV ql0min. Continuous IV infusion > 1-2 mg/min. Onset = 5-10 minutes - duration = 2-6 hours Adverse effects . Bronchospasm and hyperkalemia > related to B-blockade Mechanism of action . Non-selective B-blocker with a: antagonist activity. Dosage . Heart failure > 3.125 mg PO ql2h (7 every 2 weeks to 25 mg PO q12h). HTN > 6.25 mg PO qi2h (1 every 2 weeks to 25 mg PO q12h). WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Beta-adrenergic antagonists « Negative inotropic and chronotropic > |COP > | BP. Propranolol * HTN > 40 mg PO qi2h (max 640 mg/day). * SVTPO dose > 10-30 mg q6-8h. * SVTIV dose > 1-3 mg at 1 mg/min; repeat q2-5min (total 5 mg). * Portal HTN > 10 mg PO q8h; titrate up to 60 mg q6h. Carvedilol * See before. [Selective BE Atenolol * 25-100 mg/day PO. Bisoprolol * HTN > 25-5 mg PO qDay (max 20 mg qDay). * Heart failure > 1.25 mg PO qDay (max 10 mg qDay). Esmolol * LD =0.25-0.5 mg/kg over 1 min; then 50-100 meg/kg/min for 4 min. * Bradycardia - hypotension - bronchoconstriction - hyperkalemia. * Aggravation of peripheral vascular ischemia. * Masking sympathetic response to hypoglycemia. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes EE Calcium channel blockers (CCBs) © Dihydropyridines (e.g. nifedipine - nimodipine - amlodipine). * Non-dihydropyridine (c.g. verapamil - diltiazem) * Magnesium (physiological calcium antagonist). Mechanism of action * Predominant arteriolar vasodilator + minimal venous vasodilator, * No direct depressant effect on heart rate conduction. * Peripheral vasodilatation > | systemic blood pressure > sympathetic stimulation > } COP and t HR > counter the negative (inotropic - chronotropic ~ dromotropic) effects of nifedipine. Dosage © 5-10 mg oral/sublingual. * Onset = 2-5 minutes ~ duration = 20-30 minutes, Adverse effects + Profound hypotension > in patients with (ventricular dysfunction - aortic stenosis - concomitant beta blockade) - (for this reason the use of sublingual nifedipine for treating hypertensive emergencies is no longer recommended). retic resistant peripheral edema > due to redistribution of extracellular fluid rather than sodium and water retention. Mechanism of action * Highly lipid-soluble > CNS > selective cerebral arterial vasodilation. * Used to |cerebral arterial vasospasm following aneurysmal SAH. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Dosage * Dose = 60 mg/4hrs orally (in ancurysmal SAH). * Can be given at 30 mg/2hrs to reduce variation in blood pressure. * IV nimodipine is not recommended due to its profound effect on BP. vasodilation > systemic hypotension > | CBF. * Cerebral vasodilatation > 1 ICP (with | intracranial elastance). Mechanism of action * Similar pharmacodynamic profile to nifedipine. * Amlodipine exerts specific anti-inflammatory effects in (HTN - diabetic nephropathy) and in modulating HDL in patients with hypercholesterolemia. Dosage © 5-10 mg oral/day © Onset = 24-96 hours ~ duration = 24 hours. * Primary effect > AV node > used as antiarrhythmic for SVT > concomitant therapy with B-blockers or digoxin is not recommended. * Not active as nifedipine in its effects on smooth muscle > limited role as vasodilator > less pronounced |systemic blood pressure. * Verapamil has a negatively inotropic effect Dosage * HTN > 80 mg qShr initially; maintenance 80-320 mg q12hr (PO) © SVT > 2.5.5 mg IV over 2 minutes; repeat 5-10 mg after 15-30 min © Chronic AF > 240 - 480 mg PO q6-8hr WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Therapeutic effects * Cardiovascular profile > similar to verapamil * Vasodilatory effect > intermediate between nifedipine & verapamil * Diltiazem exerts minimal cardio-depressant effects and is less likely to potentiate beta blockers. Dosage © HTN > 120-240 mg q24hr © AF & Atrial flutter > 20 mg IV over 2 min; repeat 25 mg after 15 min * Continuous infusion in AF and atrial flutter > 10 mg/hr RePatrine Therapeutic actions © Direct arteriolar and venous vasodilator > | BP. * Established role in the treatment of pre-eclampsia and eclampsia. * Perioperative management of pheochromocytoma. * Treatment of autonomic dysfunction in tetanus. Dosage * 40-60 mg/kg loading (or 6 gm) * 2-4g/hinfusion. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Centrally acting agents [Clonidine Mechanism of action * Centrally acting a:-agonist > ++ inhibitory neurons in vasomotor centre > | sympathetic outflow from CNS > vasodilation associated with negative inotropy and reduction in heart rate. * Clonidine has centrally acting analgesic properties > suitable drug in patients with postoperative hypertension. Peripherally © ++ Pre-junctional az-receptors > | norepinephrine release. © ++ Post-junctional ai-receptors > vasoconstriction. Rebound hypertension * Rebound hypertension following initial reduction of BP (due to variable duration of the central and peripheral effects). Dosage © HTN > 0.1 mg PO ql2h (max 2.4 mg). * Gancer pain > cpidural infusion at 30 meg/h. Ce Mechanism of action * Methyldopa metabolized to methyl-norepinephrine > stimulate a2 receptors > | sympathetic outflow. Indications * Accelerated essential ~ renovascular - pregnancy induced HTN. * Limited role in hypertensive emergencies. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Dosage «HTN > 250 mg PO q8-12h (max 3 gm/day). * HTN crisis > 20-40 mg/kg/day divided IV q6h. Adverse effects * Depression (minimized if the daily dose is <1 gm). * May lead to positive direct Coombs test in 20% of patients. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Direct vasodilators Mechanism of action * Dilates arterioles and venules > | afterload and | preload. When infused intravenously * Nanitroprusside + (oxy-Hb) > (met-Hb) + cyanide + nitric oxide. * Nitric oxide is responsible for vasodilatory effect of Na nitroprusside Dosage * 0,25-10 meg/kg/min (start low and go slow). * Onset = immediate - duration = 1-2 minutes. Precautions * Prolonged exposure to light > release of hydrogen cyanide. * The solution is light sensitive > protection from exposure to light by wrapping administration sets in aluminum foil. Adverse effects Cardiovascular system (intracoronary steal phenomenon) * Arteriolar vasodilation (coronary) > blood flow away from ischemic areas > exacerbate myocardial ischemia (intracoronary steal). Central nervous system © Cerebral vasodilator > 1 CBF and blood volume > f ICP. * Rapid | MAP > exceed autoregulation capacity > | CBF. Pulmonary * Pulmonary vasodilator effect > attenuate hypoxic pulmonary vasoconstriction > 7 intrapulmonary shunting and | PaQ2. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Cyanide toxicity * Free cyanide + methemoglobin > cyanmethemoglobin. * Cyanide is metabolized in the liver and kidneys to form thiocyanate. * Consider toxicity in patients who become resistant to sodium nitroprusside despite maximum infusion rates and who develop unexplained lactic acidosis. Treatment of suspected cyanide toxicity jal management * Stop infusion and start 100% oxygen Sodium thiosulphate (150 mg/kg) * Converts cyanide to thiocyanate (which is excreted renally). Hydroxycobalamin (5 gm over 15 minutes) * Binds cyanide to produce cyanocobalamin. Mechanism of action * GIN > generates nitric oxide > dilates venous system > | preload, * GIN > cerebral vasodilation > use with caution in patients with known or suspected f ICP (headache due to this mechanism . « GTN > dilates coronary vessels > } coronary blood flow to ischemic areas > | angina pectoris. This is in contrast to Na nitroprusside (which cause coronary steal phenomenon). Dosage * 5-200 meg/min (max 400 meg/min) - (IV - SL - PO - transdermal * Onset = 2-5 min - duration = 5-10 min. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Adverse effects * Tachyphylaxis is common with glyceryl trinitrate (doses should not be increased if patients no longer respond to standard doses). Hydralazine Mechanism of action * Hydralazine > potent arterio-sclective direct-acting vasodilator (++ of cGMP and inhibition of smooth muscle). Dosage * IV bolus (10-20 mg) then 20-50 mg q6-8h. * Onset = 10-20 min - duration = 1-4 hours. Adverse effect * Direct and reflex sympathetic activity > } COP and } HR. * Prolonged use > renin release > sodium and water retention. * Immunological side-effects (with chronic use) > lupus syndrome ~ vasculitis ~ hemolytic anemia - rapidly progressive GN. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes EE Diuretics Mechanism of action * | (Na-K -CL-H,0) reabsorption in ascending limb of loop of Henle. * Direct venodilator effect. Dosage * Frusemide > PO (20-240 mg/day) - IV (40-200 mg/day). Side effects * | BP-|Na-| Mg -alkalosis - hypovolemia - hypoter * Hyperuricemia (precipitate gout). * Hyperglycemia (may interfere with DM control). * Nephritis and ototoxicity. [Thiazide diuretics Mechanism of action * | (Na-K -CL - water) reabsorption in the distal tubules. Dosage * Dihydrochlorothtazide: (25-100 mg/day PO). * Chlorthalldone (25-100 mg/day PO). Side effects * No ototoxicity. * Thrombocytopenia - hypersensitivity reactions - hypercalcemia. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Prine eed Mechanism of action * | Na/water reabsorption and K/H secretion in distal tubules. Types Aldosterone antagonist * Spironolactone (25-400 mg/day PO). Non-aldosterone antagonists * Triamterene (100-200 mg/day PO). * Amiloride (10-20 mg/day PO). Side effects * Hyperkalemia. * Acidosis. * Gynecomastia (with prolonged use of spironolactone). WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes EE Acute heart failure [Definitions CCS Heart failure * Clinical syndrome resulting from any cardiac disorder that impairs the ability of the ventricle to fill with or eject blood. Systolic Dysfunction (EF is < 40%) * Impaired myocardial contractility > | LVEF and SV > | COP. Diastolic dysfunction (heart failure with preserved EF) (EF >40%) * Impaired diastolic filling with normal systolic function > } LV filling pressures > venous congestion (pulmonary and systemic). High-output heart failure * for normal COP in the face of metabolic needs (failure occurs when COP fails to meet these needs). Ventricular dilatation * 1 Preload > } ventricular dilatation > 1 contractility according to starling law > 7 COP (within limits). Ventricular hypertrophy * 7 Afterload > } muscle mass > } contractility > } COP. * Hypertrophy (not associated with } in blood supply) > ischemia of the hypertrophic muscle fibers > fibrosis and > | contractility. Tachycardia * | SV 7 HR to maintain COP (COP = SV X HR). * Marked tachycardia > | COP due to decreased filling time. © Marry's low (HR is inversely proportionate to blood pressure). * Bainbridge reflex (7 RA pressure > 7 HR). WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Redistribution of blood flow * | COP > ++ sympathetic > diversion of blood flow from less vital organs (e.g. skin) to more vital organs (e.g. brain and heart) Hypervolemia * | COP > | GFR > f renin > t Ang II > f aldosterone > salt and water retention > f blood volume > 1 preload + f cardiac contraction. © 7 ADH > water retention. * [fit exceeds certain limits > | cardiac contractility > edema. LA Ce Ce CEO eer tay . NYHA class I (no dyspnea during ordinary activity). NYHA class Ill (dyspnea during ordinary activity). NYHA class III (dyspnea during less than ordinary activity). NYHA class IV (dyspnea at rest). Left sided heart failure Right sided heart failure Decreased preload + Mitral stenos * Left atrial myxoma, Increased preload + Mitral regurge. + Aortic regurge. * PDA and VSD. * Hyperdynamic circulation Increased afterload * Aortic stenosis. * Systemic hypertension. * Coarcitation of aorta, Decreased contractility + Myocarditis. * Cardiomyopathy. * Ischemia heart disease. Arrhythmias Decreased preload * Tricuspid stenosis. + Right atrial myxoma. Increased preload © Tricuspid regurge. * Pulmonary regurge * VSD and ASD. * Hyperdynamic circulation ad stenosis. hypertension. * Pulmonary embolism Decreased contractility + Myocarditis. * Cardiomyopathy. * Ischemia heart disease. Arrhythmias WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Meneses cae) * HTN - Endocarditis * Failure to take meds (very common). ~ Anemia - Rheumatic disease - Thyrotoxicos © Arrhythmia (common). * Infection/Ischemia/ Infarction (common) * Lung problems (PE - pneumonia - COPD). * Endocrine (pheochromocytoma - hyperaldosteronism). * Dietary indiscretions (common). Benin ae res Left failure Right fi re tow [+ | BP-| capillary refill - cold. |* LSHF symptoms cardiac |. Fatigue and syncope. + Tricuspid regurgitation output |. Pulsus alternans. © 93 (right-sided) (Forward) |, Mitral regurgitation. +. Venous [+ Dyspnea. * Elevated JVP. congestion |. Orthopnea - PND. © Hepatomegaly. (Backward) |, Cough with frothy sputum. | Pulsatile liver. * Crackles. Peripheral edema, Meee According to NICE (if ECG and BNP are normal > heart failure is unlikely). ECG * Evidence of ischemia (ST-T wave abnormalities). * Previous myocardial infarction (Q waves). * Conduction delays and arrhythmias (SVT and ventricular) Chest x-ray * Cardiomegaly (cardiothoracic ratio > 50%). Kerley B lines * Kerley B lines. Short horizontal lines © Prominent interstitial markings. near periphery of the lung near costophrenic * Pleural effusion. angles. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Ey Echocardiogram (transthoracle) * LVEF - cardiac enlargement - wall motion abnormalities - valvular disease ~ pericardial effusion. BNP BNP Is secreted by ventricles due to LV stretch and wall tension * Serum BNP >400 > consistent with HF (specificity is reduced in patients with renal dysfunction). * Serum BNP <100 > good negative predictive value to exclude HF Cardiac troponins. * Cardiac troponins are measured in blood after myocyte necrosis. * Released after 4 hrs. - peaking at 12-24 hrs * Cardiac troponins may be released in conditions other than acute remains 7 for 10 days. coronary ischemia such as sepsis and after chemotherapy. Routine laboratory tests * CBC - electrolytes - BUN ~ creatinine - fasting glucose - LFTs - fasting lipid profile - urinalysis - thyroid function tests. Investigations for the cause * Serum tests for rheumatologic diseases (ANA - ANCA, etc.). « Amyloidosis (serum and urine protein electrophoresis). * Pheochromocytoma (catecholamines). Coronary angiography * Performed in patients with angina or evidence of ischemia by ECG or stress testing. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Management of acute heart failure CSTmnrrnncnrn en) * Maintain arterial saturations of 94-98% (88-92% if COPD). Creo een) * CPAP or BiPAP may be used to avoid intubation. * Intubation and mechanical ventilation should be considered in deteriorating patient and those with DCL. * Parenteral opiates > | sympathetic tone > | ventricular afterload. * Diamorphine 1.25-5mmg IV slowly. * Furosemide 40-80mg IV slowly. * Larger doses required in renal failure. Pererieen Nitroglycerin * Start infusion at 5 mcg/min (max 200 mcg/min). * GTN spray 2 puffs SL or 2 x 0.3 mg tablets SL. Optimize filling pressure Underfilled patient * Target MAP 70 mmHg and CVP 8-10mmHg. * Give plasma expander 100 mL qi5min IV. Well/overfilled hypotensive patient * Inotropic support. * Target MAP 70 mmHg. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes [EW Drugs and dosing . Dopamine doses * Dopamine. (meg/kg/min) * Dobutamine 25-15 meg/kg/min. + Renal dose =1-3, * Milrinone bolus (50 meg/kg); infusion + Inotropic dose = 2-8. (0.375-0.75 mcg/kg/min). ccc iadly Ege Low COP + low MAP + high SVR * Inodilator is required (e.g, dobutamine or milrinone) * Levosimendan would also be suitable choice in this setting, * If COP rises but MAP falls > norepinephrine to maintain MAP. High COP + low MAP + low SVR + E.g. sepsis > norepinephrine after adequate volume resuscitation. Low COP + MAP at or above target + high SVR * Dilating agent (e.g. glyceryl trinitrate) or inodilator. High PAP + high RAP * Pulmonary vasodilator is indicated. Reduced catecholamine receptor responsiveness Reduced catecholamine receptor responsiveness occurs in © Chronic heart failure (downregulation of B-receptors). * Long-term B-agonist infusions. Alternative strategies * Phosphodiesterase inhibitors (milrinone). * Levosimendan (intracellular calcium sensitizer). WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Mechanism of action © Milrinone competitive inhibition of phosphodiesterase I enzyme (responsible for breakdown of cAMP) > } intracellular cAMP > improving myocardial contractility (independent of B-receptor). * Levosimendan intracellular Ca sensitizer; it binds to and sensitizes cTnC to Ca without raising intracellular calcium > improving myocardial contractility (independent of B-receptor). Mechanical support for the heart Intra—aortic balloon pump (IABP) * IABP > | afterload + } coronary perfusion + | cardiac work. Indication of IABP insertion * Cardiogenic shock complicating acute MI. * Weaning from cardiopulmonary bypass. © High-risk PCI. * Bridging therapy to cardiac transplantation. Absolute contraindications to IABP * Moderate-to-severe aortic regurgitation. * Aortic dissection. Complications include * Limb ischemia - bleeding - infection. Extracorporeal membrane oxygenation (ECMO) * VA ECMO provides circulatory and respiratory support. VA ECMO has been used in * Peri-operatively in cardiac surgery. * Inrefractory cardiogenic shock. © During cardiopulmonary arrest. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes [EH Ventricul: assist devices (VADs) * Left ventricular assist devices (LVADs) or biventricular assist devices (BIVAD) should be considered in severe and intractable heart failure with reversible cause or if heart transplantation is feasible. Complications of VADS include * Device failure - bleeding - infection - thromboembolism. Early revascularization therapy * Effective therapy myocardial salvage during ACS. * Late percutaneous intervention (up to 72 hrs. post-MI) has been shown to be of benefit in cases with cardiogenic shock. * Further dose of furosemide 40-80mg. * Consider CPAP. * 1 Nitrate infusion (without dropping SBP <100mmHg). * Consider alternative diagnoses (e.g. hypertensive heart failure - aortic dis: tion - pulmonas Weights reduction embolism - pneumonia). * Daily weights > aim reduction of 0.5 kg/day. Diuretics * Change to oral furosemide or bumetanide. * [fon large doses of loop diuretic > consider thiazide (e.g. metolazone 2.5-5mg daily PO). ACE-inhibitor « ACEi if LVEF <40%. « If ACEi is contraindicated > consider hydralazine and nitrate. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Beta-blockers * Consider B-blocker and spironolactone (if LVEF <35%). * Optimize management of AF (if present). © Consider anticoagulation. Management of chronic heart failure CC ed * Treat the cause (e.g. arrhythmias - valve disease) * Treat exacerbating factors (anemia - thyroid diseas ~ infection - } BP). * Avoid exacerbating factors > e.g, NSAIDS (fluid retention) and verapamil (~ve inotrope). Diuretics improve symptoms but without mortality benefit. Drugs and doses * Furosemide 40 mg - bumetanide 1-2 mg - torsemide 10-20 mg. Side effects © Hypokalemia and renal impairment. Consider adding K* sparing diuretic if * K'<3.2 mmol/L. © Concurrent digoxin therapy. * Pre-existing K* losing conditions. Potassium sparing diuretics « Eplerenone 25-50 mg daily. * Spironolactone 125-25 mg daily. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes If refractory edema Consider adding thiazide * Metolazone 5-20 mg/day. © Hydrochlorothiazide 25-50 mg daily. TIT nen hr eas) Ge considerations * Consider in all those with left ventricular systolic dysfunction * Improves symptoms and prolongs life. Drugs and doses (ACE-i) © Captopril 6.25-12.5 mg q6-8h (target 50 mg tid). * Enalapril 2.5 mg bid (target 10 mg bid). * Lisinopril 2.5-5 mg daily (target 10-20 mg bid). © Ramipril 1.25-2.5 mg bid (target 5 mg bid). Drugs and doses (ARB) * Valsartan 40 mg bid (target 160 mg bid). © Losartan 25 mg daily (target up to 100 mg daily). Eee erst * B-blockers reduce mortality in heart failure. Action * B-Blockers > blocking the toxic effects of chronic adrenergic stimulation on the heart. Drugs and doses * Bisoprolol 1.25 mg/day (up to 10 mg/day). * Carvedilol 3.125 mg q12h ( up to 25-50 mg q12h). * Metoprolol 12.5-25 mg/day. Start low and go slow (wait 2 weeks between each dose increment). WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes EE PT nee Splronolactone > | mortality when added to conventional therapy. Indications * Insymptomatic patients despite optimal therapy. * In post-MI patients with LVSD. Drugs and doses * Eplerenone 25-50 mg/day. * Spironolactone 12.5-25 mg/day. Indications * Helps symptoms even in thos with sinus rhythm. * Considered for patients with LVSD who have signs or symptoms of heart failure while receiving standard therapy (e.g. ACEi and p- blockers) or in patients with AF Dosing of digoxin * Digoxin 0.125-0.25 mg/day. * Maintain serum K* at 4-5 mmol/L (| K* « digoxin toxicity). * Serum therapeutic levels = 0.8-2 ng/mL. Drug interaction * Antibiotics (c.g. erythromycin - tetracycline) > f digoxin levels. * Quinidine - verapamil - flecainide - amiodarone > 7 digoxin levels. Digoxin toxicity Digoxin toxicity may be caused or exacerbated by * Drug interactions * Hypokalemia - Hypoxemia - Hypothyroidism - Hypovolemia. * Renal insufficiency. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Vasodilators * Combination of hydralazine and isosorbide dinitrate should be used if intolerant of ACEi and ARBS as it reduces mortality. * It also reduces mortality when added to standard therapy (including ACEi) in black patients with heart failure * Stop smoking. * Stop drinking alcohol. * Eat less salt * Fluid restriction (1.5L/day PO). WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Ey Levosimendan Levosimendan uses in ICU (2011) Lie tC * Intracellular calcium sensitizer > binds to and sensitizes troponin C to calcium without raising intracellular calcium > improving myocardial contractility (independent of B-receptor) * Stimulates ATP-sensitive K* channels > vasodilatation, in addition to myocardial anti-stunning/ischemic effects. * Athigh dose > PDE-inhibition. * LD 6-12 mcg/kg over 10-min followed IVI at 0.1-0.2 mcg/kg/ min. * Decompensated heart failure (acute and chronic). * Post-resuscitation myocardial dysfunction. * Perioperative optimization of cardiac patients with cardiomyopathy. * Sepsis not responding to positive inotropes. * Hypotension - headache - nausea - vomiting (more common). © Hypokalemia and arrhythmias (less common) * Absorption ~ IV or PO. * Distribution - highly protein bound. * Metabolism - hepatic with t % of 70 hours. * Elimination - renal. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Acute coronary syndrome © Chest pain of 7 hours in 48 years old hypertensive patient, how to manage (2010). « Non-ST elevation myocardial infarction (2007). * Postoperative chest pain In 65 year-old man + ECG revealed ST segment elevation in V1-4, How to manage? (2012), Unstable angina (cardiac blomarker Is not elevated) Ischemic chest pain characterized by one of the following 1. Recent origin or more (frequent - severe - prolonged) than usual. 2. More difficult to control with drugs. 3. Occurring with rest or with minimal exertion. NSTEMI * Troponin positive ischemic chest pain without ST segment elevation. STEMI * Troponin positive ischemic chest pain with ST segment elevation. * Rupture of atheromatous plaque > exposure of collagen > platelet aggregation (via glycoprotein IIb/Ila receptors) > initiates clotting cascade > thrombus formation. In STEMI * Complete occlusion with no collateral blood supply > complete myocardium infarction > ST segment elevation. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes In NSTEMI * Incomplete occlusion or collateral blood supply > thrombus formation > myocyte ischemia but not infarction > no ST segment elevation. Non-modifiable * Age - male gender - family history of IHD. Modifiable * Smoking - HTN - DM - hyperlipidemia - obesity - sedentary lifestyle ~ cocaine use. Symptoms * Acute central chest pain (>20 min) often associated with (nausea - sweatiness ~ dyspnea - palpitations). Silent MI * ACS without chest pain (in elderly and diabetic patients). * Silent MIs may present with (syncope ~ pulmonary edema - epigastric pain and vomiting ~ postoperative hypotension or oliguria ~ acute confusional state ~ stroke - diabetic hyperglycemic states). Signs * Distress ~ anxiety ~ pallor ~ sweatiness - } or | pulse - f or [BP. * Signs of heart failure (J JVP - 3 heart sound - basal crepitations). * Pan systolic murmur (papillary muscle dysfunction/rupture ~ VSD). * Pericardial friction rub (pericarditis). WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Differential diagnosis of chest discomfort Conditions with immediate life-threatening potential 1, ACS. 2. Acute aortic dissection. 3. Pulmonary embolism. 4, Esophageal rupture. 5. Tension pneumothorax. Other common conditions 1. Acute myocarditis. 2. Transient apical ballooning syndrome. 3. Acute pericarditis. 4. Costochondritis and related musculoskeletal conditions. 5. Gastroesophageal reflux disease. 6. Esophageal spasm. 7. Pleurisy. 8. Referred pain from abdominal organs e.g. spleen and gall bladder. 12-lead ECG ECG should be done within 10 minutes of patient's arrival to ER 1. If initial ECG is not diagnostic > perform ECG every 15-30 min to evaluate for evolving ST-segment clevations or depressions. 2, If there are ST-segment depressions in anterior precordial leads (V:- V3) > perform posterior leads (V7-Vs) to detect posterior MI ECG changes in UA/NSTEMI * ST depression - inverted T wave - non specific changes - or normal. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes ECG changes in STEMI Normal Hyperacute Acute Indeterminate 1. Hyperacute (0-20 minutes) - Tall vealed T waves + progressive upward coving STE. 2. Acute (minutes to hours) - persisting STE - gradual loss of R wave - progressive inversion of T waves. 3. Early (hours to days) - loss of R wave - development of pathological Q waves - return of ST segments to baseline - persistence of T wave inversion. 4. Indeterminate (days to weeks) - pathological Q waves - persisting T wave inversion. 5. Old (weeks to months) - persisting deep Q waves ~ normalized ST segments and T waves. ECG patterns of myocardial Injury STE ‘Artery I - Ml ~ aVF (Reciprocal | RCA — posterior descending changes in aVL). branch. Vs-a (Reciprocal changes in Il [LAD - diagonal branch. - Il - aVF). Septal [Vi TAD — septal branch. Lateral |Vs-<—1-aVL. Left circumflex ~ circumflex or diagonal branch. RV___| Vi - VaR- Vik (Right ECG). [RCA — proximal branches. Posterior | Posterior ECG (V7. Left circumflex — posterior ST depression in Vi-2 with | circumflex or RCA right — prominent R waves suggests | posterior descending. posterior STEMI. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Other causes of STE and T wave changes (should not receive thrombolytic therapy) * Pericarditis (global ST elevation with PR depression). « Early repolarization (notched J-point mainly in antero-lateral leads). * Old LV aneurysm. * Metabolic disturbance (hyperkalemia - hypercalcemia). * Apical ballooning syndrome (Takotsubo). * Normal variant (non-ischemic STE mainly V2-3). Cardiac biomarkers Troponin * Troponin T and I (most sensitive and specific markers). * Check troponin (two blood samples 3 hours apart). © Other cardiac enzymes (CKMB - CK) are sensitive but le Timeline for serum markers in evaluation of ACS Marker Rises Peaks Normalizes Troponin 2-6h | 12-24h 7-104 Myoglobin 12h 46h 24h CK-MB 3-4h 12-24h 12d Non-dlagnostic ECG and normal initial cardiac blomarkers Possible UA/NSTEMI who have non-diagnostic ECG and normal initial cardiac biomarkers > observe for 6-12 hrs. ve studies > treat for ACS. 2. If no further pain and -ve studies > consider stress test. 1, If recurrent ischemic pain or po Echo * Regional wall abnormalities. Chest x-ray * Look for (cardiomegaly ~ pulmonary edema - wide mediastinum). WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Coronary CT * Consider in non-diagnostic ECG and negative cardiac biomarkers. « It has high negative predictive value > determine patients who are safe for discharge from ER. TIMI Risk Score for UA/NSTEMI Item Score Age 2 65 years 1pt Markers (clevated cardiac biomarkers). Ipt ECG (ST-segment deviation > 0.5 mm). Tpt Risk factors (23 for CAD). Ipt Ischemia (= 2 anginal events previous 24h). | I pt GAD (stenosis 250%). 1pt Aspirin use in the preceding 240. Ipt If TIMI risk score 23 > consider early LMWH and angiography. Management of ACS — without ST elevation * Analgesia (c.g. morphine 5-10 mg IV + metoclopramide 10 mg IV). «Nitrates (GIN spray or sublingual tablets as required). CREM Aspirin * Aspirin 300 mg PO followed by 75 mg/day. * Mechanism = irreversible inactivation of COX enzyme ...... WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Second antiplatelet agent Clopidogrel (300 mg PO then 75mg/day PO) * For those with confirmed ACS. * Mechanism = inhibit platelet activation and aggregation through irreversible binding to P2Y12 class of ADP receptors on platelets. Ticagrelor (180 mg then 90mg/12h PO) © Preferred alternative in higher risk group. * Mechanism = inhibit platelet activation and aggregation through reversible binding to P2Y12 class of ADP receptors on platelets. Prasugrel (60 mg then 10 mg/day PO) * Alternative to clopidogrel for those undergoing PCI. « Mechanism = inhibit platelet activation and aggregation through irreversible binding to P2Y12 class of ADP receptors on platelets. Intravenous GP IIb/Ila inhibitors * Mechanism = prevent fibrin binding to platelets > inhibit platelet aggregation * Agents > abciximab - tirofiban - eptifibatide. It is recommended that clopidogrel and ticagrelor be stopped 5 days prior to elective CABG and prasugrel 7 days prior to elective CABG. * Fondaparinux (factor Xa inhibitor) 2.5 mg/day until discharge. © LMWH (c.g, enoxaparin 1 mg/kg/12h until discharge). © UFH (aim aPTT 50-70s) until discharge. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes ed © Drugs (e.g. bisoprolol 2.5 mg/day). Contra-indication * Cardiogenic shock ~ heart failure ~ asthma/COPD ~ heart block. If contraindicated > consider rate limiting CCB * Verapamil 80-120mg/8h PO. * Diltiazem 60-120mg/8h PO. * Donot use (8-blockers + verapamil) > can precipitate asystole. Neer * IV nitrate if pain continues. * Eg. GTN 50 mg in 50mL 0.9% saline at 2-10 mL/h. * Titrate to pain and maintain SBP >100 mmHg. * Omit if recent sildenafil use. * Should be given to all patients unless there are Cl. * Monitor renal function. * Start early > e.g. atorvastatin 80 mg/day. Angiography Urgent (<120 min after presentation) if * Ongoing angina and evolving ST changes. * Signs of cardiogenic shock. © Life-threatening arrhythmias. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Early (<24h) * IfGRACE score >140 and high-risk patient. Within 72h * Iflower-risk patient. GRACE = Global Registry of Acute Coronary Events. Risk is scored based on age, heart rate, BP, renal function, Killip class of heart failure, and other events, e.g. raised troponin. Very complicated to calculate so recommendation by European Society of Cardiology is to use an online calculator Management of ACS — with ST elevation * Aspirin (300 mg PO - if not already given). ‘Second antiplatelet agent * Clopidogrel (300 mg PO). © Consider ticagrelor or prasugr if no history of stroke/TIA and <75 years) as alternatives clopidogrel to as they are superior in outcome. Intravenous GP IIb/IIIa inhibitors « Abciximab - tirofiban - eptifibatide. * (c.g. morphine 5-10 mg IV + metoclopramide 10 mg IV). * Routine use now not recommended in the acute setting unless patient is hypertensive or in acute LVF. © Useful as anti - anginal in chronic/stable patients. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes RIE cn * In those presenting <12h after symptom onset (see below). Primary PCI * Bivalirudin monotherapy. © UFH titrated to aPTT + GP IIb/IIIa inhibitor. Fibrinolytic therapy © UFH administered IV 60 U/kg bolus then 12 U/kg/h. © Enoxaparin 30 mg bolus IV + 1 mg/kg SC every 12 h. © Fondaparinux 2.5 mg IV initial dose then SC every 24 h. Warfarin Indicated for 1. LV thrombus. 2. Mechanical heart valve. 3. Atrial fibrillation. Caution * Triple therapy (ASA + clopidogrel + warfarin) > 7 bleeding risk. * E.g, bisoprolol 2.5 mg/day PO. * Targeted to heart rate of 50 to 60 bpm. * CI (cardiogenic shock - heart failure - asthma/COPD - heart block). tien * Treat hypotension and oliguria with fluids (avoid nitrates and diuretics). WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Reperfusion therapy ECG criteria * ST elevation > 1 mm in 2 2 adjacent limb leads. * ST elevation > 2 mm in 2 2 adjacent chest leads. * LBBB (unless known to have LBBB previously). * Posterior changes: deep ST depression and tall R waves in leads V1.3. Primary PCI * Recommended for all patients presenting within 12 hours of symptom onset with STEMI + can be transferred to primary PCI centre within 120 min of first medical contact. «If this is not possible > thrombolysis + transfer to primary PCI centre after the infusion for either rescue PCI (if residual ST elevation) or angiography (if successful). Thrombolysis + If primary PCI not available within 120 minutes > administer fibrinolytics within 30 minutes of arrival if symptom onset < 12 hours and no contraindications. Fibrinolytic therapy Alteplase Tenecteplase | Reteplase | Streptokinase Fibrin He Ht + = selective Hi 5 min 17 min 14 min 20 min Dose | 15mg bolus then | 053mg/kg | Two10- |” 15million units 0.75 mg/kg over 30 | single-dose. | unit bolus | over 30-60 min, min; then 0.5 mg/kg doses 30 over 60 min min apart Possible No No No Yes allergy WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes EN Contraindications to fibrinolytic therapy Absolute contraindications Relative contraindications Intracranial bleed (at any time). ‘© Current anticoagulant use. * Ischemic siroke (within 6 months). ‘© Major surgery (2 weeks). * Closed head trauma (within 3 mont! «Prolonged CPR (>10 min) + Suspected aortic dissection. + Pregnancy. + Uncontrolled hypertension (>180/100 mmHg). | « Retinopathy. * Known structural vascular lesion. + Peptic ulcer disease Intracranial tumor. Grit Elective PCI rt * Indicated 3 - 24 hrs after successful fibrinolysis to reduce recurrence. Emergent (rescue) PCI Indicated following fibrinolysis for patients with * Cardiogenic shock - heart failure - anterior infarction. * Failed fibrinolysis (<50% ST segment resolution - ongoing chest pain - rising cardiac biomarkers). Patients with STEMI who don’t receive reperfusion (e.g. presenting after 12 hours) > treat with fondaparinux or enoxaparin/ UFH if not available. Medical management without stent * Aspirin 75-162 mg indefinitely plus clopidogrel 75 mg/day or ticagrelor 90 mg twice daily for at least 1 month uninterrupted and ideally for 1 year Bare metal stent * Aspirin 162-325 mg for 1 month then 75-162 mg indefinitely plus clopidogrel 75 mg/day or prasugrel 10 mg/day or ticagrelor 90 mg twice daily for at least 1 month and ideally for 1 year. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Drug-eluting stent * Aspirin 162-325 mg for 1 month then 75-162 mg indefinitely plus clopidogrel 75 mg/day or prasugrel 10 mg/day or ticagrelor 90 mg, twice daily for at least 1 year uninterrupted. Sree Five classes of drugs currently receive strong recommendation from AHA for long-term medical therapy 1. Aspirin 2, Clopidogrel. 3, Beta-blockers, 4. ACE inhibitors. 5. Statins (target LDL <70 mg/dL - HDL >40 mg/dL). WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.com aDr. Ali Ragab | Critical Care Study Notes [EIN Complications of myocardial infarction Recurrent ischemia or infarction [Prevention Anti-thrombotic therapy Aspirin ‘* Of benefit across wide spectrum of patients with IHD. Clopidogrel - prasugrel - ticagrelor * Added to ASA in patients with ACS (particularly if undergoing PCI). © Used in conjunction with PCI. * Do not provide benefit when used with thrombolysis. Anticoagulation Intravenous UFH * Maintain infarct-related artery patency in patients undergoing thrombolysis or PCI. Alternatives to UFH * LMWH (c.g. enoxaparin) * Direct thrombin inhibitors (e.g. bivalirudin - fondaparinux). B-Blockade * Oral B-blockade > should be provided to all patients. * IV B-blockade > tachyarrhythmias or uncontrolled severe HTN. * Contraindications > | HR - cardiogenic shock ~ severe HF - | BP. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes [EH (ete Rapid escalation of medical therapy * Nitrates - ASA - Clopidogrel - Heparin or LMWH - B blockers. * Assess and treat secondary causes (CHF - arrhythmia - anemia etc.). Recurrent pain + ST elevation © Urgent catheterization or thrombolysis. Recurrent pain + no ST elevation * Stable > clective catheterization. * Unstable > urgent catheterization (IABP if needed). * CABG (if needed). Right ventricular infarction * RV infarction occurs in 30% of patients with inferior MI. (rnc « Proximal occlusion of RCA > RV infarction > | contractile performance of RV > | LV preload and systemic hypotension. * Diastolic abnormalities > systemic venous hypertension. * AVN or SAN block (in inferior MI with RV involvement) > conduction system disease. * Neck > jugular venous distension. * Chest > clear lungs. * Abdomen > congested liver. * Peripheral > systemic hypotension. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes [EE LFSC CT Eto * STE in V.R ¢ precordial ST segment depressions. Differential diagnosis DD for RV infarction includes 1, Hypotension resulting from LV infarction. 2. Pericardial tamponade. 3, Constrictive pericarditis. 4, Pulmonary embolism. Reperfusion therapy * Initial treatment of RV infarction > early reperfusion therapy. Volume expansion * Volume expansion (mainstay of therapy) > t CVP > fill LV adequately (CVP up to 15-20 mmHg). * If volume expansion does not restore SBP > 90 mmHg > consider dobutamine or dopamine to t RV output. Avoid venous vasodilator * Inisolated RSHF venous vasodilators (c.g. nitrates) should be avoided. Bradycardia * Sinus bradycardia or AV block + HD instability > consider temporary ventricular pacing WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes [EZ Left ventricular dysfunction (pump failure) * Hypotension - shock - pulmonary edema. [Treatment Airway management and oxygenation * Ensure adequate oxygenation + ETT. Hemodynamic management Blood pressure control * Maintain SBP 2 90 mm Hg (MAP > 65 mmHg). * Cardiogenic shock > inotropes or mechanical circulatory support. Pulmonary congestion * Diuretics nitrates > | pulmonary congestion. * Avoid excessive preload reduction (target PCWP 15-20 mmHg). Early reperfusion * Emergent angiography and revascularization should be considered. Mechanical complications DAC Ce Ce 1. Rupture of inter-ventricular septum. 2. Rupture of ventricular free wall. 3. Rupture of papillary muscle. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Ey Presentation * | BP - cardiogenic shock ~ new systolic murmur. Transthoracic echocardiography (ITE) * Diagnostic test of choice, [Treatment Free wall rupture * Pericardiocentesis + surgical repair. MR or VSR * Supportive measures (e.g. IABP) + surgical repair. Thromboemboli CTE Cy ¢ LV mural thrombus > arterial and venous emboli. * RV or deep venous thrombi > PE. Anticoagulation * First-line therapy (continued for 3 to 6 months). Fibrinolytic therapy * Consider in patients with cardioembolic stroke but should be undertaken with great caution. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes [J Pericarditis Errrn * Usually begins 1-4 days after ML * It is common with STEMI than with NSTEMI. * Asymptomatic pericardial effusion. + Early symptomatic > pericarditis + effusion. © Pericardial rub > dry pericarditis. * Dressler syndrome > late pericarditis which occurs 2-10 weeks post- MI duc to autoimmune phenomenon. [Treatment Aspirin * ASA> | pain and | inflammation. * Dose > up to 650 mg q4h may be required. Acetaminophen or colchicine * Acetaminophen or colchicine can also be considered. Other NSAIDs © Other NSAIDs > infarct thinning + coronary artery vasoconstriction. Corticosteroids © Should be avoided (induce scar thinning and rupture). Minimizing anticoagulation * Minimizing anticoagulation to avoid hemorrhagic pericarditis. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes [EZ Arrhythmias complicating MI Ventricular fibrillation * Aim > Urgent reversion to perfusing rhythm. * Management > CPR - Defibrillation - amiodarone or lidocaine. Ventricular tachycardia * Aim> * Management > Cardioversion - amiodarone - lidocaine. storation of normal sinus rhythm (NSR). Accelerated idioventricular rhythm (AIVR) * Aim > observation unless hemodynamically unstable. * Management > increase sinus rate (atropine ~ atrial pacing). EDEN eC LL Sinus tachycardia © Aim > reduction of heart rate. * Management > Identify and treat underlying cause. Atrial fibrillation or atrial flutter * Aim > Reduction of ventricular rate + restoration of NSR. * Management > cardioversion (if unstable) - BB - CCBs - digoxin - amiodarone. Paroxysmal SVT * Alm > reduction of ventricular rate + restoration of NSR. * Management > vagal maneuvers ~ adenosine - same as AF. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes [ER Sinus bradycardia * Aim > increase HR only if hemodynamically compromised. * Management > atropine - temporary pacing. Junctional escape * Alm > increase HR only if hemodynamic compromise. * Management > atropine - temporary pacing. High—degree AV block * Alm > increase HR. * Management > atropine - aminophylline ~ temporary pacing. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes [EJ Aortic stenosis * Senile calcification - congenital (bicuspid valve) - RHD. rnc * Aortic stenosis > LV outflow obstruction > 7 afterload > concentric LVH and diastolic dysfunction > heart failure. Symptoms The classic triad includes * Angina - exertional syncope ~ heart failure. Other presentations * Dyspnea - di s faints. * Systemic emboli if infective endocarditis. * Sudden death Signs * Pulse > slow rising with narrow pulse pressure (parvus et tardus). * Apex > heaving and non-displaced apex beat (LV heave). © Murmurs > ejection systolic murmur (aortic area). * Heart sounds > decreased (or absent) aortic component of S2 EcG * LVH with strain pattern - P mitrale - LAD - poor R wave progression - LBBB or complete AV block (calcified ring) Chest X-ray * LVH - calcified aortic valve - post stenotic dilatation of ascending aorta. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Doppler echo Estimate the gradient across valves; severe stenosis if: * Peak gradient 2 40 mmHg (poor LV not able to generate gradient). © Valve area <1 cm?, * Aortic jet velocity > 4 m/s (or is increasing by >0.3 m/s per year). Cardiac catheter * Assess > valve gradient - LV function - CAD. Aortic valve replacement * Prompt valve replacement is usually recommended. * Bicuspid aortic valve and ascending aortic dilation > concomitant ascending aortic replacement may be necessary. Percutaneous valvuloplasty/replacement * Consider if the patient is not medically fit for surgery. Aortic regurgitation Acute « Infective endocarditis - ascending aortic dissection ~ chest trauma. Chronic * Congenital. * Connective tissue disorders (Marfan’s syndrome ~ Ehlers Danlos). * Rheumatic fever. * Rheumatoid arthritis - SLE - Takayasu arteritis. * Seronegative arthritides (ankylosing spondylitis - Reiter’s syndrome). * Hypertension. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Gy * Osteogenesis imperfecta. * Syphilitic aortitis. (Crees * Acute severe AR > abruptly reduces ventricular compliance > high filling pressures and heart failure. * Chronic AR > 7 preload (} EDV) + 7 afterload (t SBP) > LV cavity dilation + eccentric ventricular hypertrophy > | systolic function and heart failure. CIeinierrnecen Symptoms « Exertional dyspnea - orthopnea - PND - palpitations - syncope. Signs * Pulse > collapsing (water hammer) ~ wide pulse pressure. * Apex > displaced hyperdynamic apex beat. * Murmur > high-pitched early diastolic murmur. © Corrigan’s sign (carotid pulsation). © De Musset’s sign (head nodding with each heart beat). © Quincke’s sign (capillary pulsations in nail beds). * Duroziez’s sign (in the groin). * Traube’s sign (pistol shot sound over femoral arteries). * Austin Flint murmur (denotes severe AR). Ce ECG * LVH. Chest X-ray * Cardiomegaly - dilated ascending aorta - pulmonary edema WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Echo * Assess size and shape of the aortic root. * Identify the cause of AR. * Assess (ventricular chamber dimensions - volumes ~ EF). Doppler and color-flow Imaging Severe AR i «Effective regurgitant orifice area > 0.30 cm?. «© Regurgitant volume 2 60 mL/beat. Cardiac catheterization * Assess (severity - aortic root - LV function - CAD - other valves). Medical treatment The main goal of medical therapy is to reduce systolic hypertension * ACEI - IV or oral vasodilators. * IABP and -blockade are contraindicated. * Echo every 6-12 months to monitor. ‘Surgical treatment Indications for surgery * Severe AR with enlarged ascending aorta. * Increasing symptoms - enlarging LV - deteriorating LV function. * Infective endocarditis refractory to medical therapy. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes [J Mitral regurgitation (MR) Acute mitral regurgitation; causes, clinical picture and management (2009) Functional (LV dilatation). Annular calcification (elderly). Rheumatic fever. Infective endocarditis. Mitral valve prolapse. Ruptured chordae tendinea. Papillary muscle dysfunction/rupture (e.g. post-MI). Connective tissue disorders (Ehlers Danlos - Marfan’s). Cardiomyopathy. Congenital (may be associated with other defects e.g. ASD). (Cries MR | COP > LVand LA pressure > LV and LA dilatation > CHF and pulmonary HTN. Symptoms Chronic severe MR . Exertional dyspnea - symptoms of | COP (c.g. weakness ~ fatigue). Acute severe MR Pulmonary edema ~ | BP - cardiogenic shock. Signs Murmur > pansystolic at the apex radiating to axilla. Heart sounds > Soft S; - split S: - loud P2 (pulmonary hypertension). Diastolic rumble may be audible in severe MR (functional MS). WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes J ECG * AF -P mitrale if in sinus rhythm (1 LA size) - LVH. Chest X-ray * Enlarged LA and LV - mitral valve calcification - pulmonary edema, Echocardiogram * Assess LV function and MR severity and etiology. Sev MR if * Effective regurgitant orifice 2 0.40 cm?, © Regurgitant volume 2 60 mL/beat. Cardiac catheterization * Confirm diagnosis - exclude other valve disease - assess CAD. Ce Medical treatment Atrial fibrillation * Rate control + anticoagulation. Stabilization of acute severe MR © | Afterload (e.g, nitroprusside) + inotropes (e.g, dobutamine) # IABP. Management of pulmonary edema « Diuretics - nitrates - mechanical ventilation. Anticoagulation « AF - history of embolism - prosthetic valve - additional MS. Surgical treatment * Indication > deteriorating symptoms. * Aim > repair or replace the valve before LV is irreversibly impaired. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Mitral stenosis Normal mitral valve orifice area is 4-6 cm? * Rheumatic fever. * Congenital. * Mucopolysaccharidoses. «Endocardial fibroelastosis. © Malignant carcinoid. * Prosthetic valve. Symptoms usually begin when the orifice becomes < 2 em? Symptoms Pulmonary hypertension * Dyspnea - hemoptysis. Pressure from large left atrium on local structures «© Hoarseness (recurrent laryngeal nerve). * Dysphagia (esophagus). * Bronchial obstruction. Others * Fatigue - palpitations - chest pain - systemic emboli - infective endocarditis. Signs * Malar flush on cheeks (due to | COP). * Low pulse volume. * AF (due to enlarged LA). * Tapping non-displaced apex beat (palpable S;) + RV heave. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes [J On auscultation * Loud. * Opening snap. * Rumbling mid-diastolic murmur. * Graham Stell murmur may occur. Severity * More severe stenosis > longer diastolic murmur and closer opening snap is to So. ECG * AE; P-mitrale; RVH; progressive RAD Chest X-ray * LA enlargement (double shadow in right cardiac silhouette). * Pulmonary edema. * Mitral valve calcification. Echocardiogram * Severe stenosis if the valve orifice < 1 cm?/m? body surface area. Cardiac catheterization Indications for cardiac catheterization * Previous valvotomy. * Signs of other valve disease. * Angina. * Severe pulmonary hypertension. * Calcified mitral valve. Atrial fibrillation * Rate control (BB - CCBs) + Anticoagulation (warfarin). WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Pulmonary venous congestion * Diuretics > | preload and pulmonary venous congestion. If this fails to control symptoms > * Balloon valvuloplasty (if pliable non-calcified valve). © Open mitral valvotomy or valve replacement. uspid regurgitation * Functional (RV dilatation). * Rheumatic fever. * Infective endocarditis (IV drug abuser). * Carcinoid syndrome. * Congenital (e.g. ASD). * Drugs (c.g. ergot-derived dopamine agonists). ‘Symptoms * Fatigue - hepatic pain on exertion (hepatic congestion) - ascites - edema - symptoms of the causative condition Signs * Giant v waves and prominent y descent in JVP - RV heave. * Pansystolic murmur (at lower sternal edge in inspiration). * Pulsatile hepatomegaly - jaundice - ascites. * Diuretics for systemic congestion © Drugs to treat underlying cause. * Valve repair or replacement. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes JJ Tricuspid stenosis * Rheumatic fever. * Congenital. * Infective endocarditis. Symptoms * Fatigue ~ ascites - edema. Signs * Giant a wave and slow y descent in JVP. * Opening snap. * Early diastolic murmur (at left sternal edge in inspiration). * Echocardiogram. « Diuretics. * Surgical repair. Pulmonary stenosis Congenital * Congenital (e.g. Turner syndrome - Fallot’s tetralogy - rubella). * Acquired (rheumatic fever - carcinoid syndrome). WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes J CTE RS OTE Symptoms . Dyspnea - fatigue - edema - ascites. Signs . Dysmorphic facies (congenital causes). Prominent a wave in JVP - RV heave. Ejection click - ejection systolic murmur (radiates to left shoulder). Widely split S:. RAD - P pulmonale - RVH - RBBB. Chest X-ray . Prominent pulmonary arteries (post-stenotic dilatation). Other Investigations Echo/TOE. Cardiac catheterization is diagnostic. Pulmonary valvuloplasty or valvotomy. Pulmonary regurgitation Any cause of pulmonary hypertension. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes * Decrescendo murmur in early diastole at the left sternal edge (the Graham Steell murmur if associated with mitral stenosis and pulmonary hypertension). Prosthetic valve complications Clinical presentation * Systemic embolism > stroke. * Mechanical obstruction > heart failure. Suspect in patients with * New dyspnea - muffled valve closure sounds - new murmurs. Investigations Echo * Assess severity of prosthetic obstruction. Transesophageal echo * Define thrombus size and degree of limitation in movement. Treatment Re-operation * Preferred for left-sided valve thrombosis with symptomatic heart failure and large clot burden. Thrombolysis * Consider for poor surgical candidates. * Primary therapy for those with right- or left- sided valve thrombosis with small clot burden and mild symptoms. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes * Fibrinolytic therapy with streptokinase or rtPA followed by IV heparin and aspirin until INR is therapeutic. Le Te ES Clinical presentation * Infection - embolism - heart failure. Investigations * Blood cultures and TEE are key to diagnosis. Treatment * Antibiotics. + Re-operation to remove infected tissue and foreign material. Bio prosthesis * Frequent and progressive due to degeneration. © Reoperation after stabilization. Mechanical vz * Sudden due to defective material (rare). © Urgent re-operation, Presentation * Heart failure or anemia due to hemolysis. © Murmur may not be audible. Investigations * Echocardiography is key to diagnosis. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes ZI Treatment * Re-operation (urgency determined by severity of heart failure and infectious cause). WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Acute pericarditis Ce * Inflammation of the pericardium. Idiopathic or secondary to * Bacteria (TB - Lyme disease - Q fever - pneumonia - rheumatic fever - Staphs - Streps - mycoplasma - legionella). Viruses (coxsackie - EBV - CMV - adenovirus - varicella - HIV). Fungi and parasitic (in immunocompromised). Autoimmune (SLE - RA - vasculitis - IBD - sarcoid - Dressler’s). Drugs (procainamide - hydralazine - INH - chemotherapy). Metabolic (uremia - hypothyroidism). Others (trauma - surgery - malignancy - radiotherapy - MI - CHF). . . . . . . © Chest pain 7 by inspiration or lying flat and | by sitting forward. © Pericardial friction rub may be heard. «Fever may occur. Perrecenns ECG * Concave (saddle-shaped) ST segment clevation + PR depression Blood tests * CBC - ESR - KFTs - electrolytes ~ cardiac enzymes. + Tests relating to possible etiologies. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes [ZJ Chest X - ray * Cardiomegaly may indicate pericardial effusion. Echo * If suspected pericardial effusion. NSAIDs * NSAIDs with gastric protection for 1-2 weeks. * Ibuprofen (400-800 mg q8h) or indomethacin (25-50 mg q6h). Aspirin * Aspirin with gastric protection for 1-2 weeks. * May be utilized if there is no response to the NSAIDs. * Aspirin (up to 900 mg q6h). For post-MI pericarditis > sterolds and NSAIDs should be avoided * | Coronary blood flow. © 1 Myocardial infarction size. * 1 Blood pressure. * Incidence of myocardial rupture. Colchicine © + Colchicine 500 meg q24~12h for 3 months (| risk of recurrence). Etiology «Treat the cause. Steroids * If not improving or autoimmune > consider steroids or other immunosuppressive therapies. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Pericardial effusion * Accumulation of fluid in the pericardial sac (normally 10-50 mL). Pericarditis (causes of pericarditis). Myocardial rupture (hemopericardium—wound ~ post MI). Aortic dissection. Pericardium filling with pus. Malignancy. ee eee CER OT * Dyspnea - chest pain - muffled heart sounds. Signs of local structures compression * Hiccoughs (phrenic N). * Nausea (diaphragm). * Bronchial breathing at It base (Ewart’s sign: compressed It lower lobe). Chest X - ray * Enlarged globular heart (if effusion > 300mL). EcG * Low-voltage QRS complexes. * Alternating QRS morphologies (electrical alternans), Echocardiography * Echo-free zone surrounding the heart. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes EZ Etiology © Treat the cai Pericardiocentesis * Diagnostic (suspected bacterial pericarditis). * Therapeutic (cardiac tamponade). * Pericardial fluid for (culture - ZN stain/TB culture - cytology). Constrictive pe rditi: [Definition * The heart is encased in rigid pericardium. [causes * Unknown - elsewhere TB - after pericarditis (causes of pericarditis) CEL Features of right heart fallure * TJVP (prominent x and y descents) - HSM - ascites - edema. Other features * Kussmaul’s sign (JVP rising paradoxically with inspiration). Examination * Soft diffuse apex beat. * Quiet heart sounds - S; - diastolic pericardial knock. [eEorrorns Chest X-ray ¢ Small heart + pericardial calcification. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes cT/MRI * Helps distinguish from restrictive cardiomyopathy. Dopp! chocardiography * Dilated IVC with | respiratory variation and increased expiratory diastolic flow reversals in the hepatic veins. Medical treatment * Diuretics for volume overload. * If inflammatory component is present > anti-inflammatory drugs. Surgical treatment * Surgical removal of as much of the pericardium as possible. Cardiac tamponade Cerner rss * Pericardial effusion > 1 intrapericardial pressure > | ventricular filling > | COP and cardiac arrest. * THR - | BP - pulsus paradoxus - } JVP - muffled S; and S:. Beck's triad 1. Falling BP. 2. Rising JVP. 3, Muffled heart sounds * Low-voltage QRS # electrical alternans. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Echo is diagnostic * Echo-free zone (>2 cm or > 1cm if acute) around the heart + diastolic collapse of right atrium and right ventricle. [Management Urgent drainage * Seek expert help, * Send fluid for (culture - ZN stain/TB culture ~ cytology). Emergency echocardiographic-guided pericardiocentesis is recommended. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Aortic dissection [Definition * Blood splits the aortic media at high pressure. Pathophysiolog: Dissection extends and occludes branches of aorta leading to © Hemiplegia (carotid artery). © Unequal arm pulses and BP or acute limb ischemia. + Paraplegia (anterior spinal artery). © Anuria (renal arteries). * Aortic valve incompetence ~ inferior MI - cardiac arrest (if dissection moves proximally). Stanford classification system * Type A> dissection involves ascending aorta (70%). * Type B > dissection distal to the origin of left subclavian artery (30%). Lee SR CR * Degeneration of aortic wall (old age - chronic hypertension). * Connective tissue disorders (Marfan or Ehlers-Danlos syndrome). * Inflammatory disorders (Giant cell arteritis ~ Takayasu arteritis). * Iatrogenic injury (Catheterization - IABP - aortic and cardiac surgery). * Congenital (bicuspid aortic - coarctation - Turner or Noonan syndrome). © Other (pregnancy - cocaine use). * Sudden tearing chest pain (+ radiation to back) * Hypertension WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Less common signs * Murmur of aortic insufficiency. * Hypotension and shock. * Pericardial tamponade. * Myocardial ischemia. * Congestive heart failure. * Malperfusion syndromes (limb ischemia - neurologic impairment or paraplegia ~ mesenteric ischemia - renal insufficiency) ores Echocardiography cnr * Diagno: * Suggestive Contrast enhanced CT intimal flap in proximal aorta. ortic root dilatation ~ aortic insufficiency. * Diagnostic = intimal flap with in aorta - dual lumens. © Suggestive = aortic root dilatation - pericardial effusion. Magnetic resonance imaging * Diagnostic = intimal flap with in aorta - dual lumens. * Suggestive = aortic root dilatation - pericardial effusion. ‘Aortography * Diagnostic = intimal flap with in aorta - dual lumens. * Suggestive ortic root dilatation - pericardial effusion. Chest radiography «Limited diagnostic utility. * expanded mediastinum (rare). Electrocardiogram * Nonspecific. * Ischemic changes (if type A dissection involves coronary arteries). WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Blood test * Not reliable for rapid detection of AD. * 1 D-dimer may be helpful in intermediate-risk patients Management Type A dissection * Type A dissection is surgical emergency. Type B dissection «Type B dissection is managed medically. * Surgery reserved for patients with limb or visceral ischemia or contained rupture. CE Pain relief > | sympathetic tone * Morphine sulfate (1-2 mg IV q 3-5 min). Control blood pressure and heart rate Heart rate reduction Metoprolol (2.5-5 mg IV q2min x 3 doses; then 5-10 mg IV q4h). Esmolol (500 mcg/kg IV bolus; then 50 meg/kg/min). Propranolol (1 mg IV q3-5 min (max 10 mg); then 2-6 mg IV q4-6h). Target heart rate > 60-70 bpm. ee ee Heart rate/blood pressure reduction * Labetalol (20 mg IV; then 2 mg/min and titrate to 10 mg/min). © Target heart rate > 60-70 bpm. * Target SBP > 100-110 mmHg. Blood pressure reduction * Na nitroprusside > (0.25 mcg/min IVI; titrate to 10 mcg/kg/min). * Target SBP > 100-110 mmllg, WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes [Ey Blood pressure reduction in setting of renal artery Involvement * Enalaprilat (0.625-1.25 mg IV q6h). * Target SBP > 100-110 mmllg, * Control hypertension > BB or CCB therapy. Irene Type A * 50% with medical management. © 20% with surgical repair. Type B * 10% with medical therapy. Penetrating aortic ulcer Pathophysiology Hypertension + severe atherosclerotic lesion (in elderly) > ulcer > * Penetrates intimal layer > dissection (rare). * Ulceration through adventitia > pscudoaneurysm or aortic rupture. tal al presentation * Acute onset chest pain + radiating to the back and hypertension. * Contrast CTA - TEE - MRA. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Medical management Medical therapy is the initial choice in absence of (false aneurysm - frank rupture - recurrent pain). * Control BP > | shear stress and pulse pressure against the ulcer. * Risk factor modification (lipid-lowering ttt and smoking cessation). * In hemodynamic instability - aortic rupture ~ pseudoaneurysm. + Endovascular stent grafting can be used safely in selected patients. Ruptured aortic aneurysm CS * Acute hemodynamic instability and (back - chest - abdominal pain). Ruptured AAA The classic triad of (<1/3 of patients) 1, Abdominal pain. 2. Hypotension. 3. Pulsatile abdominal mass. Ruptured TAA * Acute hemothorax or hemorrhagic pericardial effusion/ tamponade. DIE tae Cos * Stable patient > CT or abdominal ultrasound. * Unstable patient + suspected rupture > immediate surgical exploration. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes (ete Emergent surgery + Symptomatic or aneurysms with suspected rupture. * Endovascular repair. Elective surgery Elective repair is recommended when * Diameter of thoracic aorta reaches 6 cm (5 cm in Marfan syndrome). * Diameter of abdominal aorta reaches 5 to 5.5 cm. © Expanding at >1 cm/year. * 60% will die before presentation to medical attention. * Operative mortality is approximately 50%. * Mortality is 100% without surgical intervention. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes EE Narrow complex tachycardia Ce * ECG > HR >100 bpm + QRS duration <120ms (<3 small squares). Narrow QRS complexes occur when ventricles are depolarized via the normal conduction pathways. Denner Sinus tachycardia * Normal P wave followed by normal QRS * Not arrhythmia > Do not attempt to cardiovert > if necessary (i.e. no response to fever/hypovolemia) > rate control with BB. Atrial tachyarrhythmias Atrial fibrillation (AF) * Absent P wave + irregular QRS complexes. Atrial flutter * Atrial rate 260-340 bpm (sawtooth baseline). * Ventricular rate often 150 bpm (2:1 block). © Due to re-entrant circuit usually in right atrium. * 23 P wave morphologies + irregular QRS complexes. Junetional tachycardia * AV node is part of the pathway. * P wave either buried in QRS complex or occurring after QRS complex. * AVNR tachycardia includes accessory pathway (e.g. WPW). WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Management - VT versus SVT with aberrancy * If in doubt > treat as VI (the commonest cause) - giving AVN blocking agents to treat SVT with aberrancy when the patient is in VT can cause dangerous hemodynamic instability. * If WPWis suspected > avoid drugs that slow AV conduction. Hemodynamically unstable patient DC cardioversion * Up to 3 synchronized DC shocks. * 70-120} for the first (120-150] for AF) then 120-360] subsequently Management of precipitating factors * Correct (K ~ Mg - Ca). Amiodarone * 300mg IV over 220min; then 900 mg/24h IVI via central line. * Consider repeat shock Hemodynamically stable + regular rhythm Vagal manoeuvres * Vagal manoeuvres (carotid sinus massage - Valsalva manoeuvre) transiently increase AV block. Adenosine * Adenosine > transient AV block (short half-life 10-15s. © Give 6 mg IV bolus into large vein (if unsuccessful after 2 min give 12 mg then one further 12 mg bolus). * Side effects = chest tightness - dyspnea - headache - flushing. sthma - 24/34 degree AV block * Potentiated by dipyridamole - antagonized by theophylline. * Contraindications WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes [Ey Hemodynamically stable + Irregular rhythm (treat as AF) Rate control * B-blocker (c.g. metoprolol 1-10 mg IV). * Rate-limiting CCBs (c.g. verapamil 5-10 mg IV). * Digoxin — alternative in heart failure ~ (LD 500 meg PO then 500 mcg PO after 8h and further 250 mcg PO after 8h). * Amiodarone (may also control rhythm—see below). Anticoagulation * Consider anticoagulation with warfarin or NOAC to | risk of stroke. Rhythm control - chemical cardioversion * Amiodarone 300mg IV over 20-60 min then 900mg over 24h. * Flecainide 300mg PO (if no structural heart damage). Rhythm control - DC cardioversion * Ifonset < 48h or if effectively anticoagulated for >3wk. * Synchronized DC cardioversion under sedation. EXEEEney Ld Sinus tachycardia * Identify and treat underlying cause. Supraventricular tachycardia 1. Adenosine - Atenolol - Amiodarone. 2. If unsuccessful > DC cardioversion. Multifocal atrial tachycardia * Most commonly occurs in COPD. © Correct hypoxia and hypercapnia, * Consider verapamil if rate remains >110bpm. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Wolf-Parkinson-White (WPW) syndrome * Congenital accessory pathway between atria and ventricles. * Short PR interval * Wide QRS complex due to slurred upstroke or delta wave. © WPW type A (+ve 5 wave in V1). © WPW type B (-ve 5 wave in Vi). * Degeneration to VE and sudden death. z e a 2 = ¢ Z e Ey * Flecainide - propafenone - sotalol - amiodarone. Ablation * Electrophysiology and ablation of the accessory pathway. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Atrial fibrillation (AF) * Recent onset AF in old male (2007 - 2012 - 2013) * Management of rapid atrial fibrillation (2010) © AF = irregular atrial rhythm at 300-600 bpm (AV node responds intermittently > irregular ventricular rhythm). Common causes © Heart failure ~ HTN - IHD - mitral valve disease. * Pulmonary embolism - pneumonia. © Hyperthyroidism - | K- | Mg. * Caffeine. * Alcohol. * Post-operative. Lone AF * Means no cause found. ‘Symptoms * Asymptomatic - chest pain - palpitations - dyspnea - faintness. Signs «© Pulse (irregularly irregular + apical pulse rate > radial rate) © 4* heart sound (variable intensity). © LVF (signs of LVF). Examine the whole patient: AF is often associated with non-cardiac disease. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes ECG + P wave (absent P waves). © QRS complexes (irregular and narrow). Blood tests * Urea ~ creatinine - electrolytes ~ cardiac enzymes - thyroid functions. Echocardiography * Look for (LA enlargement - | LV function - structural abnormalities). Unstable patient (| BP - myocardial ischemia - syncope — heart failure) * ABCDE. * Synchronized DC cardioversion (start at 120-150J) + amiodarone. * Do not delay treatment in order to start anticoagulation, Stable patient + AF started <48h ago * Rate or rhythm control may be tried * Start heparin in case cardioversion is delayed. Stable patient + AF started >48h ago or unclear time of onset * Rate control (¢.g, with bisoprolol or diltiazem). « Ifrhythm control is chosen > anticoagulate for >3wks first. Further management © Correct electrolyte imbalances (K - Mg ~ Ca). * Treat associated illnesses (e.g. MI - pneumonia). * Consider anticoagulation (see anticoagulation below). WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes CEM ey Rate control « BB or rate. imiting CCBs are 1* choice (if this fails > add digoxin then consider amiodarone). * Do not give BB with verapamil. * Aim > HR < 90 bpmat rest and (200 - age in years) bpm on exertion. Anticoagulation * See anticoagulation below. Rhythm control Rhythm control may be appropriate if * Symptomatic or CCF * Younger patients. 1 presentation with lone AF. * AF from corrected cause Elective DC cardioversion © Do echo first > check for intracardiac thrombi. © If there is risk of cardioversion failure (past failure ~ past recurrence) > amiodarone for 4 weeks before and 12 months after cardioversion. Elective pharmacological cardioversion * Flecainide > 1* choice (contraindicated if structural heart diseass * Amiodarone > alternative to flecainide. In refractory cases * AVN ablation with pacing. * Pulmonary vein ablation. * Maze procedure. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes [EZ Anticoagulation and AF [Acute AF AF started <48h © Use heparin until full risk assessment for emboli is made. AF started >48h * Therapeutic anticoagulation (23 wks before elective cardioversion). * Trans-esophageal guided cardioversion (if urgent cardioversion). Use no anticoagulation if * Stable sinus rhythm has been restored + * No risk factors for emboli + AF recurrence unlikely. * Paroxysmal > terminates in <7 days (may recur). * Persistent > lasts >7 days. * Permanent > continuous AF despite treatment. The need for anticoagulation should be assessed using CHA2DS:-VASc score to assess embolic stroke risk > consider anticoagulation if score ($ > 0) or (7 > 1) and balancing this against the risks of anticoagulation to the patient assessed with HAS-BLED score. CHA2DS2-VASc * CHE (1) ~ HTN (1) - Age 65-74 (1) Age >74 (2) - DM (1) - previous Stroke/TIA/thromboembolism (2) - Vascular disease (1) - Sex Category (1 if female). HAS-BLED — 1 point for each * HTN - Abnormal renal or liver functions - Stroke history ~ Bleeding - Labile INR - Elderly > 65yrs ~ Drugs (antiplatelet agents or NSAIDs). WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Atrial flutter © Atrial flutter = SVT characterized by succession of rapid atrial depolarization waves. * P waves = sawtooth appearance. * Flutter waves may be visible after carotid sinus massage or adenosine. As the underlying atrial rate is often around 300/ min the ventricular or heart rate is dependent on the degree of AV block (c.g, if there is 2:1 block the ventricular rate will be 150/ min). Similar to AF regarding rate and rhythm control and the need for anticoagulation WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Bradycardia * Bradycardia = HR < 60 bpm. * Asymptomatic. Fatigue ~ nausea - dizziness ~ syncope - chest pain - breathlessness. * Sudden cardiac death can occur. Cardiac causes * Degenerative changes (fibrosis of conduction pathways). Post MI~especially inferior MI (RCA supplies SAN and AVN). * Sick sinus syndrome. «Iatrogenic (ablation - surgery). * Aortic valve disease (e.g, infective endocarditis). * Myocarditis - cardiomyopathy - amyloid - sarcoid - SLE. Non-cardiac origin * Vasovagal (very common). * Endocrine (hypothyroidism - adrenal insufficiency). * Metabolic (hyperkalemia - hypoxia). © Hypothermia. © TICP (Cushing's triad = | HR + 7 BP + irregular breathing). Drug-induced * B-blockers - verapamil - diltiazem - amiodarone - digoxin. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes EE Treatment of the cause * Perform ECG ~ check electrolyt * Correct metabolic defects. * Give antidotes to medicines likely to have caused bradycardia (e.g, glucagon if BB overdose). do digoxin levels Patients with adverse signs or risk of asystole Atropine Adverse signs * Give atropine 500 meg IV. Shock. Syncope. Heart failure. Myocardial ischemia, * If no satisfactory response > repeat atropine | 500 mcg IV every 3-5 mins (max 3 mg) ; Interim measures Risk of asystole © Transcut s pacing. ranscutaneous pacing anaes « Isoprenaline 5 mcg/min IVI. a Te * Adrenaline 2-10 meg/min IVI. + Ventricular pause >3s, * Alternatives: aminophylline or dopamine. | *_ Complete heart block 4 with broad QRS. © Glucagon (if bradycardia due to BB or CCB). Patients without adverse signs or risk of asystole * Observation. Atrioventricular block [Definition * Delay or failure of impulse conduction from atria to ventricles. * 1 degree > atrial impulses are delayed. * 2° degree > atrial impulses are blocked intermittently. * 3" degree > atrial impulses are blocked completely. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Torre * PR interval > 200 ms - each P wave is followed by QRS Etiology * Increased vagal tone. © Drugs (e.g. digoxin). + IHD (particularly inferior MD). * Rheumatic fever. Management © Itusually causes no symptoms and requires no treatment. * Ifassociated with digoxin > stop drug or | the dose. EEA Mobitz type | (Wenckebach) * Delay in AV conduction increases with each atrial impulse until an atrial impulse fails to conduct © ECG = progressive lengthening of PR interval over culminating in non- conducted P wave. Clinical features © Itmay occur with inferior ML * Type 1 is common in fit healthy people (high vagal tone). Management * Treatment is rarely necessary. Mobitz type II * Intermittent failure of conduction of atrial impulses to the ventricles without preceding increases in PR interval. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes EcG * PR interval remains constant prior to the blocked P wave. Clinical features © Itis likely to be associated with structural heart disease * AV block may be intermittent or persistent. * The adverse prognosis relates to the frequency of progression to complete AV block. Management * Slower symptomatic ventricular rates may require pacing. LULZ * No atrial impulses are conducted to the ventricles (atrial and ventricular contractions are dissociated). * SAN continues to depolarize the atria - ventricular activation depends on standby escape pacemaker located below the block Escape pacemaker may be * Close to the His bundle narrow QRS + (40-60 bpm) © Distal in ventricular tissue wide QRS + (20-40 bpm). * No ectopic escape pacemaker > ventricular asystole > Stokes- Adams attack or death if the episode is prolonged. EcG * Normal regular P-waves completely dissociated from QRS complexes. Etiology * Idiopathic fibrosis of the conduction system (most common). * MI- valvular heart discase - cardiac surgery. * Congenital form of complete heart block. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Management Cardiac pacing is usually required > } HR and COP. Right bundle branch block . Conduction block in right branch of bundle of His > slow activation of the free wall of the RV > broad QRS. Rapid depolarization of the septum and free wall of LV is normal. QRS duration >120 ms. M shaped QRS in Vi-2. Positive QRS in lead Vi. Broad S waves in leads I and Vs.s(>40 msec) Secondary T wave inversion in leads V1.2. Normal variant. Massive pulmonary embolism. Right ventricular hypertrophy. Ischemic heart disease. Congenital heart disease. Left bundle branch block Delayed activation of the interventricular septum and the free wall of the left ventricle. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes * QRS duration >120 ms. * Broad notched R waves in leads I, aVL and usually Vs.s. * Deep broad $ waves in leads V1.2. * Secondary ST and T changes are usually present. * CAD - cardiomyopathy ~ LVH. * LBBB makes diagnosis of MI difficult and the development of new LBBB fulfils ECG criteria of acute infarction. Hemiblocks CMEC TEES CTE eEY The left branch of the bundle of His divides into * Left anterosuperior division. * Posteroinferior division. Left anterosuperior > supply anterior superior lateral wall of left ventricle. Posteroinferior > supply posterior inferior diaphragmatic surface of the left ventricle. Left anterior hemiblock There is left-axis deviation * Small q and prominent R in leads I and aVL. * Small r and prominent S in leads II, ITI and aVF. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes (rrr Th is usually right-axis deviation * Small rand prominent S in leads J and aVL. * Small q and prominent R in leads II, III, and aVF. Temporary Cardiac Pacing * Temporary pacing in ICU (2006) * Reestablish circulatory integrity and normal hemodynamics in acutely compromised bradyarrhythmia or tachyarrhythmia by maintaining appropriate HR until it resolves or until long-term therapy initiated. renee « Transcutaneous. « Transvenous. Indications of Pacing in Acute MI * Sinus bradycardia (<50 bpm) + SBP < 80 mmHg (unresponsive to ttt). * Mobitz type II 2 degree AV block. * 3" degree heart block. * Alternative RBBB and LBBB. * RBBB or LBBB with 1 degree AV block. * Newly acquired (LBBB - RBBB and LPFB - RBBB and LAFB). Indications for Pacing in the Absence of MI Bradyarrhythmia * Prolonged sinus pauses (3s). * Symptomatic sinus bradycardia. * Symptomatic second- or third- degree AV block. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes * Complete heart block secondary to structural heart disease. * Asystole. * Alternating bundle branch block. Tachyarrhythmias © SVT or VT unresponsive to medical therapy. * Symptomatic sustained pause~dependent VT. * Symptomatic TDP associated with structural heart disease, metabolic abnormalities or drug effects. Prophylaxis in conditions which may promote bradycardia ‘* General anesthesia with concomitant conduction block. * Cardiac surge - VSD closure - Ostium primum repair). * Percutaneous coronary intervention with associated bradycardia. * Right heart catheterization or endocardial biopsy in patient with LBBB. (TV surge * Cardioversion with sick sinus syndrome. * New AV block or BBB with endocarditis before cardiac surgery * Lyme carditis with associated conduction block. « Electrophysiology studies. * Pharmacologic treatment with drugs that worsens bradycardia. CTE CES . Thasystotic arrest victims: no survival benefit from temporary pacing. * Risks outweigh benefits: in patient with MI who received thrombolytic agent and being aggressively treated with _antiplatelet/ anticoagulation agents. * Asymptomatic patient with stable escape rhythm (may become pacing dependent) * Bradyarrhythmia secondary to profound hypothermia. © Relative contraindication if it is not possible to achieve right ventricle (RV) capture: that is, prosthetic tricuspid valve or RV infarct WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes CEs * Pneumothorax = Sepsis * Cardiac perforation * Pacing failure: from loss of capture, loss of electrical continuity in pacing circuit, or electrode displacement. Permanent pacemakers (PPMS) TAT + Complete AV block (Stokes-Adams attacks, asymptomatic, congenital) * Mobitz type II AV block * Persistent AV block after anterior MI. * Symptomatic bradycardias (e.g. sick sinus syndrome) © Heart failure (cardiac resynchronization therapy). © Drugs stant tachyarrhythmias. Single chamber (SC) * Lead in only one chamber, usually the right ventricle (RV). * Used primarily in patients with chronic atrial fibrillation (AF). Dual chamber (DC) * Leads in both the right atrium (RA) and RV. * Able to mimic normal cardiac physiology with sequential atrial to ventricular (A-V) pacing and have less AF than RV-only devices. Biventricular (BIV) devices * Leads in the RV and LV, as well as typically the RA. * Simultaneously or sequentially pace the RV and LV. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Broad complex tachycardia Ce * ECG = HR >100 + QRS complexes >120ms (>3 small squares). * Sustained VT = VT lasting > 30 seconds. If no clear QRS complexes > it is VF or asystole or problems with ECG machine or stickers. * Palpitations ~ SOB ~ chest pain ~ syncope. * Significant CAD - cardiomyopathy ~ myocarditis - valvular disease Denner * VF-VT-TDP (polymorphic VT). © Antidromic AVRT (e.g. WPW). «SVT with BBB or metabolic causes of broad QRS. * Ventricular ectopics (if >3 together at rate >100 > this is VT). Differentiating VT from SVT with aberrancy ECG findings in favor of VT QRS >160 ms. +ve or -ve QRS in all chest leads (all +ve R or alll -ve QS). Marked left axis deviation or QRS positive in aVR. AV dissociation or 2:1 or 3:1 Mobitz II heart block. General considerations * Connect patient to cardiac monitor and have defibrillator to hand. * Correct (hypoxia - electrolyte abnormalities). * Obtain 12-lead ECG (request CXR) and obtain IV access. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes If hemodynamically unstable VT Synchronized DC shock * Up to 3 synchronized DC shocks > 20-150} for the first then 150-360] subsequently (biphasic). Correct electrolytes * Correct hypokalemia > up to 60 mmoL KCL at 30 mmoL/h via CVC. * Correct hypomagnesemia > 2 gm MgSOs over 30 min via CVC. Amiodarone * Amiodarone 300 mg IV over 2 20min; consider repeat shock; then 900 mg/24h IVI via central line amiodarone (peripherally only in emergency). For refractory cases * Consider procainamide or sotalol. If hemodynamically stable VT Correct electrolytes * Correct hypokalemia > up to 60 mmoL KCL at 30 mmoL/h via CVC. * Correct hypomagnesemia > 2 gm MgSO over 30 min via CVC. Amiodarone * Amiodarone 300 mg IV over 20-60 min (avoid if long QT) via CVC. Refractory cases * Consider synchronized DC shock. Maintenance anti-arrhythmic therapy may be required © If VT occurs after MI > IV amiodarone infusion for 12-24h. © If 24h after MI > oral anti-arrhythmic > sotalol (if good LV function) or amiodarone (if poor LV function). WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Prevention of recurrent VT * Surgical isolation of the arrhythmogenic area or ICD may help. Management of VF * non-synchronized DC shock (there is no R wave). LEE Ce Cc * Manage as SVT with e.g. adenosine. Ventricular extra systoles (ectopics) * These are the commonest post-MI arrhythmia - but they are also seen in healthy people (often >10/h). * Patients with frequent ectopics post-MI have worse prognosis (there is no evidence that antidysrhythmic drugs improve outcome). CE es Definition * Form of VT with constantly varying axis (often in the setting of long QI syndromes). Causes © Congenital. * Drugs (e.g. some antidysrhythmic ~ tricyclics - antimalarials - antipsychotics). Management Congenital long-QT syndromes * Treated with high doses of B-blockers. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Acquired long-QT syndromes * Stop all predisposing drugs. * Correct hypokalemia and give MgSO; (2 gm IV over 10 min). * Over-drive pacing (pace at faster rate then slow reduce) or isoprenaline IVI to } HR. Ventricular fibrillation ECG shows irregular waves of varying morphology and amplitude. an AA Where 0 * IHD (most common) - cardiomyopathy. © Anti-arrhythmic drugs. * Severe hypoxia. * Non-synchronized DC cardioversion. DC shock * Immediate non-synchronized DC shock at 200 J - if ineffective > repeated at 200-360 and 360 J (or biphasic equivalent). Basic and advanced life support * If DC shock sequence fails > basic and advanced life support. Anti-arrhythmic drugs * Amiodarone (the drug of choice). © Other anti-arrhythmic drugs (lidocaine - Mg - procainamide). WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Sick-sinus syndrome [Definition * Sinus node dysfunction > slowing to the point of sinus bradycardia or sinus pauses or generating tachyarrhythmias such as atrial fibrillation and atrial tachycardia. * Sinus node fibrosis (typically in elderly patients). * Palpitation - dizziness - syncope. Permanent pacemakers * For patients with symptomatic bradycardia or sinus pauses. Antiarrhythmic drugs * Bradycardia-tachycardia syndrome may require both pacing (for the bradycardia) and antiarrhythmic drugs (for the tachycardia). Atropine and low-dose Isoproterenol * May be useful prior to pacing in hemodynamically unstable patient. Anticoagulation * Consider anticoagulation if episodes of AF occur. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Long-QT syndrome [Definition * Channelopathies > 1 repolarization phases > predisposing the patient to ventricular arrhythmias (classically TDP). Bazett’s formula QT. = QT/VRR The QT interval should be measured in either lead II or Vs. PR interval t os. \ \ T Pe u ores LJ Pe Giintovar * Prolonged QT. (> 440 ms in men or > 460 ms in women). © QT. >500 > f risk of TDP. © Short QT. (< 350 ms). Causes of long-QT syndrome © | K-|Mg-| Ca- | temperature. * Myocardial ischemia - post cardiac arrest. © TIC. © Congenital long QT syndrome. © Drugs (amiodarone - sotalol - TCA - macrolides ~ antihistaminic). WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Causes of short QTc (<350 ms) © Hypercalcemia. * Congenital short QT syndrome. * Digoxin effect. * Unexplained syncope or aborted sudden death. * Syncope or sudden death may be precipitated by (emotions - physical activity - auditory stimuli) causing acute adrenergic arousal. Polymorphous VT with shock * 18 line management DC shock with magnesium (drug of choice). * Identify and eliminate precipitating factors of acquired LQTS » > pharmacological intervention (isoprenaline or adrenaline) or electrical pacing. © Unresponsive rhythms or recurren: Patients presented with (or history of) syncope or aborted sudden death 15 line management > BB (aim: exercise HR <130 beats/min). * Symptomatic bradycardia despite BB > permanent pacemaker. * Recurrence with previous ttt > stellate sympathetic ganglionectomy. * If failed triple therapy > implantable defibrillator is required. Asymptomatic patients with incidental LQTS * Have very low risk of syncope or sudden death «Prophylactic measures are generally not required and close follow-up is sufficient. Class IA, IC and Ill drugs * Class IA, IC and III drugs may increase QT interval and should be avoided in polymorphous VT and torsade de pointes. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Infective endocarditis (IE) [Definition * Infection of heart valves or related structures by blood-borne spread of the infective organism. Perrine © High-pressure jet > mechanical damage to endothelium > allowing microbes to attach to the endothelium > infection and disruption of the endothelium > exposure of extracellular constituents > triggering coagulation cascade and adhesion of platelets > vegetation. * Staphylococcal infection > abscess formation in the lungs when the infection is right-sided or in and around the aortic root when the aortic valve is affected Bacteria * Strep. viridans (most common) - Strep. Bovis - Staph. aureus. * Enterococci ~ Coxiella burnetii. * HACEK Gram -ve bacteria (Hacmophilus - Actinobacillus - Cardiobacterium - Eikenella - Kingella) © Diphtheroids ~ Chlamydia. Fungi * Candida - Aspergillus ~ Histoplasma, Other * SLE (Libman-Sacks endocarditis) - malignancy. * Congenital heart disease (VSD or PDA). * Degenerative valve disease (MVP - senile aortic valve disease). * Intracardiac devices - prosthetic valves. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes «IV drug abusers. © Immunosuppressed patients. Ce Signs of Infection * Fever ~ weight loss ~ night sweats - rigors. Murmurs * Changing or new murmur. Signs of cardiac decompensation * Hemodynamic changes (c.g. | DBP in AR). * Heart failure due to (overwhelming valve destruction - coronary embolism - heart block). Embolism * Vegetations from infected area can embolize to (brain - spleen - kidneys - lungs - peripheral vascular - coronary ~ ocular vessels). Evidence of immune complex formation Cutaneous manifestations © Splinter hemorrhage (under nail beds) Retinal hemorrhages + Roth’s spots (central pale area). «Janeway lesions (purpuric lesions on the palms or sol © Osler’s nodes (infarcts in the pulp of the digits). In other parts of the body * Vasculitis - arthritis - glomerulonephritis (microscopic hematuria). WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Modified Duke crit for diagnosis of infective endocarditis Major criteria Posi re blood culture «Typical organism in 2 separate cultures. * Persistently +ve blood cultures (e.g. 3 >12h apart) * Single positive blood culture for Coxiella burneti Endocardium involved * Positive echocardiogram (vegetation ~ abscess ~ pseudoaneurysm - dehiscence of prosthetic valve). * Abnormal activity around prosthetic valve on PET/CT. © Paravalvular lesions on cardiac CT. Minor criteria 1. Predisposition (cardiac lesion - IV drug abuse) 2. Fever >38°C. 3. Vascular phenomena (emboli - Janeway’s lesions etc.) 4. Immunological phenomena (glomerulonephritis - Osler’s nodes etc.) 5. Positive blood culture that does not meet major criteria. How to diagnose © 2 major or 1 major and 3 minor or 5 minor Hematology * 7 ESR (often >100 mm in the first hour). * 1 CRP (often >100 mg/L). * Normocytic anemia and neutrophilia. Blood cultures * Blood cultures should be taken before antibiotics (if possible). * If the patient is known to have had antibiotics > culture medium can be modified to neutralize the effects of antimicrobials. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes * Allsamples should be cultured for anaerobic and aerobic organisms. * Cultures can be negative despite active infection due to previous antibiotic treatment. Other cultures * All material excised at surgery should be cultured. Serology * Less common causes of IE can be demonstrated by serology (e.g. Bartonella ~ Legionella - Chlamydia ~ Coxiella burnetii). Urinalysis * Microscopic hematuria in glomerulonephritis. Polymerase chain reaction (PCR) * Demonstration of DNA from microbes can aid detection of fastidious organisms (i.e. organisms that require specific nutrients for culture). Chest X-ray * Show evidence of enlarged heart or pulmonary edema * Tricuspid IE > may show lung abscesses with or without fluid levels. Eca * Conduction disorders (t PR interval or higher levels of heart block). * Hemodynamic changes due to valve damage (LVH - RVH). Echocardiogram * TTE may show vegetations (only if >2 mm). * TOE (more sensitive). WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Antibiotic therapy for infective endocarditis Blind therapy — native valve or prosthetic valve implanted > 1 year ago © Ampicillin or flucloxacillin + gentamicin. * Vancomycin + gentamicin (if penicillin allergic). * Meropenem + vancomycin (if thought to be Gram -ve). Blind therapy — prosthetic valve * Vancomycin + gentamicin + rifampicin. Staph — native valve * Flucloxacillin for > 4 weeks. * Ifallergic or MRSA > vancomycin Staph — prosthetic valves * Flucloxacillin + gentamicin + rifampicin for 6 weeks. © If penicillin-allergic or MRSA > vanco + gentamicin + rifampicin. Strept — fully sensitive to penicillin * Benzylpenicillin 1.2 gm/4h IV for 4~6wks. Strept—less sensitive * Benzylpenicillin + gentamicin. * If penicillin allergic or penicillin resistant > vancomycin + gentamicin. Enterococci * Amoxicillin + gentamicin. * If penicillin allergic > vancomycin + gentamicin — for 4 weeks (6 weeks if prosthetic valve). HACEK organisms * Ceftriaxone for 4 weeks with native valve or 6 weeks with prosthetic. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Fungal * Candida—amphotericin, © Aspergillus—voriconazole. Indications of surgical treatment © Heart failure ~ valvular obstruction - repeated emboli ~ fungal IE - persistent bacteremia - myocardial abscess - unstable infected prosthetic valve. * Antibiotic prophylax IE undergoing invasive procedures. « If they are given antibiotics for other reasons during procedure, the antibiotic should cover the common IE organisms. is no longer recommended for those at risk of WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Cardiomyopathies * Intrinsic myocardial disease not secondary to (congenital - hypertensive - coronary - valvular or pericardial disease). Classifled by anatomic and physiologic abnormalities 1. Dilated cardiomyopathies (DCMs). 2. Hypertrophic cardiomyopathies (HCMs). 3. Restrictive cardiomyopathies (RCMs). Features: Dilated | Hypertrophic Restrictive LVEF <45% 65-90% 50-70% - <40% (late) LV cavity size t Normal or | Normal or f (late) Stroke volume | Markedly | | Normal orf Normal or | Volume to mass ratio T 1 Markedly | Diastolic compliance | Normal to | | Markedly | Markedly | Dilated cardiomyopathies * Cardiac enlargement (LVED dimension >55 mm) + | contractile function (LVEF < 45%) are disease hallmarks. Cae Ei) Cert * Toxins (cocaine - heroin). © Drugs (chemotherapies — antiretroviral - chloroquine - TCA). * Metabolle (uremia - deficiency e.g, thiamine, selenium, carnitine) * Endocrine (hyper/hypothyroidism - DM - pheochromocytoma). * Infectious - viral (coxsackie B - HIV); parasitic (toxoplasmosis); spirochetal (Lyme disease). * Collagen disease (SLE - PAN - dermatomyositis - progressive systemic sclerosis). WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes * Neuromuscular disease (Duchenne muscular dystrophy ~ myotonic dystrophy - Friedreich's ataxia). * Miscellaneous (tachycardia - radiation - peripartum). * Idiopathic (presumed viral or idiopathic). Perrine * | Systolic contractile function > ventricular dilatation with functional mitral tricuspid regurge > 1 filling pressures > chronic dyspnea. Symptoms * Fatigue - dyspnea - pulmonary edema - RVF - emboli - AF - VT. Physical findings * TJVP -liver enlargement ~ hepatojugular reflux - peripheral edema. * S;and S gallops (may wax and wane in intensity). © Mitral or tricuspid regurgitation murmurs. Ce Echocardiography (the most useful) * Assess (systolic and diastolic function - chamber size ~ ventricular wall thickness ~ valvular pathology). Blood work * CBC -KFTs - LFTs - electrolytes ~ troponin - TSH - TIBC. EcG * Variable ST and T wave abnormalities - poor R wave progression - conduction defects (e.g. BBB) ~ arrhythmias (non-sustained VT). Chest X-ray * Global cardiomegaly - signs of CHE - pleural effusion. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Endomyocardial blopsy * Not routine (used to rule out treatable cause). Coronary angiography * Inselected patients to exclude IHD. Cornerstones pharmacological therapy * Loop diuretic (furosemide - bumetanide - torsemide). * ACEI or ARB. * B-blocker. * Digoxin and aldosterone antagonists (reserved for patients with chronic advanced symptoms e.g. NYHA class III or IV). Avold acute volume expansion * Acute volume expansion > 7 valvular regurge > | forward stroke volume and | cardiac index. Hemodynamic goals for DCM © PCWP (15-18 mm Hg). © C1 22L/min/m). For hemodynamically unstable patients * B-agonist (dobutamine) or phosphodiesterase III Inhibitor (milrinone) > for acute management of low COP state. * Oral vasodilators should be replaced with short-acting IV agents (e.g. nitroprusside or nitroglycerin). Elective surgery * Should be postponed for patients with newly diagnosed DCM to initiate pharmacologic therapy and allow time (6-12 weeks) for spontaneous recovery of systolic function. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Arrhythmias © Rapid AF > rate control (e.g. BB - digoxin ~ IV amiodarone). * Symptomatic VI > IV amiodarone and Xylocaine. * Asymptomatic non-sustained VT > generally do not require pharmacologic suppression. Hypertrop! «LV outflow tract obstruction from asymmetric septal hypertrophy. * HCM is the leading cause of sudden cardiac death in the young. Ca Symptoms Dyspnea on exertion * Due to | diastolic filling and { filling pressures Angina e chest pain * Due to T LV mass and concomitant atherosclerotic CAD. Syncope and near syncope * Due to outflow tract obstruction - ventricular arrhythmias - inadequate diastolic filling. Sudden death * VF is amenable to implantable defibrillators. Signs * Signs of congestive cardiac failure. * Jerky pulse ~ a wave in JVP - double apex beat ~ systolic thrill at lower left sternal edge ~ harsh ejection systolic murmur. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes (rrr * Autosomal dominant trait; mutations in genes that encode key sarcomere contractile and regulatory proteins. * Pathologic hallmark = unexplained myocardial hypertrophy (intra~ ventricular septum typically > ventricular free wall). * HCM may be obstructive or non-obstructive according to the presence or absence of dynamic subaortic outflow tract pressure gradients. EcG * LVH - progressive T wave inversion. © Deep Q waves (lead I- aVL - Vs.). * AF - ventricular ectopies - VT. Echocardiogram (the most useful) * Asymmetrical septal hypertrophy. «Small LV cavity with hypercontractile posterior wall. * Midsystolic closure of aortic valve. Magnetic resonance Imaging © Helpful when echocardiography is inconclusive for diagnosis. Cardiac catheterization * Assess (severity of gradient - CAD - mitral regurge) - but may provoke VT. [Treatment Pharmacologic therapy BB or verapamil * For symptoms (the aim is reducing ventricular contractility). + Amiodarone © For arrhythmias (AF ~ VT). WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes + Anticoagulate «For paroxysmal AF or systemic emboli. + Diuretics * Should be used judiciously for acute volume overload. Catecholamines ? * Catecholamines (particularly B-agonists like dobutamine) should be avoided whenever possible (they will } dynamic outflow obstruction). Surgical management * Septal myectomy or alcohol septal ablation. * Reserved for patients with dyspnea and marked outflow tract obstruction despite optimized pharmacologic therapy. Restrictive cardiomyopathies Ce stolic function in non- * Impaired ventricular filling with preserved dilated non-hypertrophied ventricle secondary to factors that decrease myocardial compliance (fibrosis or infiltration). Common etiologies * Amyloidosis ~ Hemochromatosis ~ Sarcoidosis. * Loffler’s eosinophilic endocarditis. * Endomyocardial fibros © Idiopathic. GEOre ess * Rigid non-compliant ventricular myocardium > 1 filling pressures. * Clinical and hemodynamic features mimic constrictive pericardial disease. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes EE CTE RS OTE * Features of RVF predominate (} JVP with prominent x and y descents - hepatomegaly - edema - ascites). * Kussmaul’s sign ~ $3 ~ Si - MR - TR. Echocardiography * Concentric LVH and normal ventricular size. * Bi-atrial enlargement. * Doppler evidence of restrictive physiology (short isovolumetric relaxation time). Increased myocardial echogenicity (speckling) suggests infiltrative process (e.g, amyloidosis) confirmed by: * Rectal biopsy (70% sensitivity). * Abdominal fat pad biopsy (80% sensitivity). * Endomyocardial biopsy (>99% sensitivity). Cardiac MR or high-resolution CT imaging * To exclude pericardial constriction if diagnosis remains uncertain. Treat underlying disease * Control HR ~ anticoagulate if AFib. * Low doses of diuretics to decrease congestive symptoms Heart transplant * For CHF refractory to medical therapy. Cardiac amyloidosis * May respond to prednisone and melphalan immunosuppression. ACE inhibitors and B-blockers * Generally ineffective and should be avoided during hospitalization. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes EE Syncope Sudden and transient loss of consciousness with loss of postural tone. Prrieeess . Transient hypoxia and/or hypoperfusion of cerebral cortices and reticular activating system (SBP < 70 mmHg or interruption of CBF for 8-10 seconds usually results in syncope). Ce ue Arrhythmia Bradyarrhythmia (e.g. SAN or AVN disease). Tachyarrhythmia (e.g. SVT or ventricular arrhythmias). Low cardiac output . Valve stenosis ~ pump failure. Pulmonary embolism - pulmonary hypertension. Atrial myxoma. Aortic dissection. Cardiac tamponade. Autonomic insufficiency DM - Parkinson disease. Reflex mediated . Orthostatic hypote: Neuro-cardiogenic (e.g, vasovagal). Carotid sinus hypersensitivity. Situational (cough ~ defecation - micturition). Volume depletion ~ drugs. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes SEN Deere Neurologic event * Cerebrovascular accident - TIA - seizure. * Hyperventilation with hypocapnia © Migraine. * Narcolepsy. * Subclavian steal. Psychiatric * Anxiety or panic disorder. * Major depression. * Somatization. © Substan bus Metabolic * Hypoadrenalism - Hypoglycemia ~ Hypothyroidism. History * Tongue biting - aching muscles - disorientation > neurologic cause. * Rapid onset + short duration of DCL + loss of postural tone + complete rapid recovery > cardiac cause. * Medication history > substance abuse. Physical examination © Murmurs - bruits ~ signs of heart failure > cardiovascular etiology. * Diplopia - headache - focal signs > neurologic etiology Orthostatic blood pressure measurements should be taken. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes EN Electrocardiogram * Bradycardia - heart block - pauses >3 seconds with sinus arrest. * Pre-excited QRS complexes ~ paroxysmal SVT. * Long or short QT intervals - Brugada syndrome. * Pacemaker malfunction. Laboratory tests * Blood chemistries ~ hematologic studies - cardiac biomarkers. Cardiac evaluation Echocardiography * For patients with known or suspected cardiac disease. Exercise tolerance test * For patients with syncope during or shortly following exercise. Telemetry/24-hour Holter monitoring * Diagnostic in (20%) of patients with repeat syncopal event. Electrophysiology study * Detect ventricular and supra-ventricular arrhythmias. * Patients with normal hearts and normal ECGs rarely require electrophysiology testing. Implantable loop recorder * Useful for patients with infrequent but recurrent episodes of syncope with suspicion of arrhythmogenic caus Evaluation of autonomic control/reflex-mediated syncope Tilt table test * Used to support diagnosis of neuro-cardiogenic (vasodepressor or vasovagal) syncope WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Carotid sinus massage * Firm massage of carotid artery for 5-10 seconds > baroreflex- mediated bradycardia + hypotension. Avoid in patients with recent TIA/stroke and in those with carotid bruits (reasonable to proceed if Doppler studies exclude significant carotid stenosis). Neurologic evaluation (head CT) * Reserved for patients with neurologic abnormality or head trauma [Admission Hospital admission Severe structural or CAD © Heart failure - low ejection fraction - previous MI. ECG features «* Non-sustained VT. * Sinus bradycardia (<50 bpm). * Bifascicular block. * Sino-atrial block. * Pre-excited QRS complex. * Increased QT interval. Clinical features * Syncope during exertion or supine position. * Palpitations or chest pain at the time of syncope. * Family history of sudden cardiac death. * Moderate to severe orthostatic hypotension. Important comorbidities * Severe anemia - electrolyte disturbance - frequent syncope. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes EE ICU admission . Sustained VT or symptomatic non-sustained VT. Second- or third~ degree heart block. Symptomatic bradycardia or pauses >3 seconds. Severe CHE. Evidence of acute ischemia. Ongoing hemodynamic instability. Severe aortic stenosis. Indications for implantation of pacemakers Symptomatic sinus pauses or sinus bradycardia. Bradycardia and second- or third~ degree AV block. Recurrent syncope caused by carotid sinus stimulation (minimal carotid sinus pressure induces ventricular asystole > 3 seconds duration in the absence of any medication that depresses SAN or AVN conduction) Indications for implantation of ICD . Hemodynamically significant sustained VT or VE. Long QT syndrome or polymorphic VT with recurrent syncope on BB. Brugada syndrome. Neurally mediated syndromes Patient education Avoid potential triggers. Sit or lie down + perform isometric contractions at the onset of prodromal symptoms. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.comDr. Ali Ragab | Critical Care Study Notes Orthostatic intolerance * Hydration (2 to 3 L/day). * Salt repletion (approximately 10 gm NaCl/day). Midodrine and fludrocortisone * Benefit patients with autonomic failure. Pacemaker implantation * Consider in recurrent medically refractory vasovagal syncope associated with marked bradycardi * Consider in severe bradycardic response to carotid sinus massage after other potential causes of syncope are excluded. WhatsA pp @ 01155887066 ~ Facebook @ ali_ragab_ali@yahoo.com