CARDIO-VASCULAR CLASS-Venous Thromboembolism Including Pulmonary Embolism.... 2- Systemic Hypertension 3- Pulmonary Hypertension. 4-Acute Heart Failure.pptx

Venous Thromboembolism Including Pulmonary Embolism....
2- Systemic Hypertension
3- Pulmonary Hypertension.
4-Acute Heart Failure. epidemiology,introduction,treatment, management

1. CARDIO-VASCULAR 4-Acute Heart Failure 1-Venous Thromboembolism Including Pulmonary Embolism.... 2- Systemic Hypertension 3- Pulmonary Hypertension.

2. Venous Thromboembolism Including Pulmonary Embolism QUE- A 42-year-old male presents to the ER with fever and shortness of breath since 2 days. He is tachypneic, hypoxic and hypotensive. a) Enumerate differential diagnosis of non-infectious causes of fever. b) Echocardiography in pulmonary embolism. c) Approach to a patient with suspected PE and with hemodynamic instability. QUE- Revised Geneva Score for diagnosis of pulmonary embolism. b) Newer anticoagulants in treatment of VTE.

3. Introduction & Epidemiology Definition : PE = clotted blood in pulmonary arterial circulation. Source : Usually from DVT (legs, arms, pelvis, jugular vein, IVC). VTE = PE + DVT Incidence ↑ with age → peak: 1/100 per year at age 80 . PE = 2nd leading cause of sudden unexpected non-traumatic outpatient death (autopsy data). Pathophysiology Clot formation = coagulation > fibrinolysis. Thrombophilias → ↑ clot risk. Classification : Provoked VTE = surgery, trauma, immobility, cancer, infection, chronic disease, estrogen , pregnancy/postpartum, age >50. Unprovoked VTE = no clear trigger (majority in ED). Recurrence Unprovoked VTE → 15% recurrence in 1 yr. Provoked VTE → 5% recurrence; but higher mortality (due to cancer/ comorbids ).

4. Markers of RV failure / high risk : ↑ RV/LV ratio (CT/echo). ↑ troponin / BNP. Acute pulmonary HTN signs on ECG. Mechanisms of Death in PE Abrupt near-total occlusion → PEA/asystole (His-Purkinje ischemia). Progressive RV failure & shock (hours–days). Clot Formation & Progression Sites: popliteal, femoral, pelvic, axillary, jugular, great veins . ⅓ of DVT pts have PE (even if asymptomatic). 75–80% hospitalized PE pts have DVT , vs. 40% ambulatory PE pts . Symptoms when ≥20% pulmonary vasculature occluded (in healthy pts). Right Heart Dysfunction Large clot burden → ↑ pulmonary arterial pressure → RV dilation & damage → troponin & BNP release.

5. Factor Key Points Age ↑ risk after 50 y, rises until 80 yr Obesity Risk at BMI >35 kg/m², increases with BMI Pregnancy / Postpartum Any trimester & postpartum period Prior VTE Highest recurrence with unprovoked VTE, men, persistent ↑ d-dimer Solid cancers Adenocarcinoma, metastatic disease; remote inactive cancer not significant Hematologic cancers Acute leukemia, myeloma; ↑ with l-asparaginase, thalidomide derivatives Thrombophilias Non-O blood type, lupus anticoagulant, shortened aPTT, factor V Leiden, protein C/S & antithrombin deficiency Recent surgery / Trauma ↑ risk with intubation/epidural; persists ≥4 wks , varies by surgery Immobility Acute limb immobility of ≥2 joints = highest risk Bed rest Becomes significant after ~72 h Indwelling catheters Cause ~50% of arm DVTs Long-distance travel Risk significant after >6 h continuous travel Smoking Population risk, potentiates obesity/other factors CHF Risk related to severity of systolic dysfunction Stroke Greatest risk in first month post-event Estrogen Highest risk in first few months; all estrogen contraceptives (oral, transdermal, vaginal) Inflammatory conditions IBD, lupus, nephrotic syndrome; risk ↑ with disease severity

6. Clinical Features of Pulmonary Embolism

7. Proposed algorithm for evaluation of suspected pulmonary embolism

8. Factors Known to Alter the d-Dimer Level From Expected Values Potential False-Positive Levels Potential False-Negative Levels Age >70 y Symptoms lasting >5 d Pregnancy Presence of small clots Active malignancy or metastasis Isolated small pulmonary infarction Surgical procedure in previous week Isolated calf vein thrombosis Liver disease Lipemia Rheumatoid arthritis Infections Trauma

9. Clinical Feature Points Clinical signs and symptoms of DVT 3.0 Alternative diagnosis less likely than PE 3.0 Heart rate >100 beats/min 1.5 Immobilization ≥3 days or surgery in the previous 4 weeks 1.5 Previous DVT/PE 1.5 Hemoptysis 1.0 Malignancy 1.0 4 = PE likely ≤4 = PE unlikely GESTALT = clinical sense that integrates: Risk factors (immobility, prior PE/DVT, cancer, OCPs, etc.) Symptoms (sudden dyspnea , pleuritic chest pain, syncope, hemoptysis ) Signs (tachycardia, hypoxia, leg swelling) Modified Wells’ Score for Pulmonary Embolism Scoring:

10. Q wave III: 1 Inverted T wave III: 1 S1-Q3-T3 pattern: +2 Maximum score = 21 ECG Scoring Method for Severity of Pulmonary Embolism Tachycardia (>100/min): 2 RBBB: Incomplete 2, Complete 3 T-wave inversion (V1–V4): 4  • V1: <1 mm =0, 1–2 mm =1, >2 mm =2  • V2: <1 mm =1, 1–2 mm =2, >2 mm =3  • V3: <1 mm =1, 1–2 mm =2, >2 mm =3 S wave I:

11. Antithrombotic Therapy for Deep Vein Thrombosis (DVT) and Pulmonary Embolism (PE) Therapy Dosage Comments Unfractionated Heparin 80 units/kg IV bolus, then 18 units/kg/h infusion Preferred if outpatient therapy not appropriate or in severe renal failure LMWH Outpatient treatment preferred — Dalteparin 100 IU/kg SC q12h OR 200 IU/kg SC daily — Enoxaparin 1 mg/kg SC q12h OR 1.5 mg/kg SC daily — Tinzaparin 175 IU/kg SC daily — Factor Xa inhibitor — — Fondaparinux <50 kg → 5 mg SC daily; 50–100 kg → 7.5 mg SC daily; >100 kg → 10 mg SC daily Avoid in renal failure

12. Target-specific anticoagulants — — Rivaroxaban (Xarelto®) 15 mg BID × 21 days, then 20 mg daily with food No heparin requirement; good for outpatient Apixaban (Eliquis®) 10 mg BID × 7 days, then 5 mg BID No heparin requirement; good for outpatient Dabigatran (Pradaxa®) 150 mg BID Requires 5–10 days heparin run-in; renal excretion Thrombolytic therapy tPA/Alteplase: 10 mg IV bolus, then 90 mg over 2 h For PE with hemodynamic compromise; follow with UFH or LMWH

13. Systemic Hypertension QUE- Define hypertension and hypertensive emergency. b) Treatment (including therapy goals) of hypertensive emergency I acute ischemic stroke for thrombolysis. c) Treatment (including therapy goals) of hypertensive emergency in aortic dissection Hypertensive Crisis Defined as acute elevation of BP with: Systolic >180 mmHg and/or Diastolic >120 mmHg Hypertensive Emergency Hypertensive Urgency

14. Hypertensive Emergencies Diagnostic Category Signs and Symptoms Evidence of Acute End-Organ Damage Acute aortic dissection Chest pain, back pain Unequal blood pressures (>20 mm Hg difference) in upper extremities Abnormal CT angiogram of chest and abdomen/pelvis or transesophageal echocardiogram of the aorta Acute pulmonary edema Shortness of breath Interstitial edema on chest radiograph Acute myocardial infarction Chest pain, nausea, vomiting, diaphoresis Changes on ECG or elevated levels of cardiac biomarkers Acute coronary syndrome Chest pain, nausea, vomiting, diaphoresis Clinical diagnosis, changes on ECG, or elevated levels of cardiac biomarkers Acute renal failure May have systolic or diastolic abdominal bruit Elevated serum creatinine level, proteinuria Severe preeclampsia, eclampsia Seizures, shortness of breath, headache, or vision abnormalities (blurred vision, flashing lights, scotomata) Proteinuria (no longer required for diagnosis), low platelet count, renal insufficiency, elevated liver enzyme levels, pulmonary edema

15. Hypertensive retinopathy Blurred vision Retinal hemorrhages , cotton-wool spots, hard exudates, sausage-shaped veins Hypertensive encephalopathy Altered mental status, nausea, vomiting, headache Papilledema, arteriolar hemorrhage / exudates on fundoscopy, cerebral edema (posterior white matter) on MRI Subarachnoid hemorrhage Headache, focal neurologic deficits Abnormal CT brain; red blood cells on lumbar puncture Intracranial hemorrhage Headache, new neurologic deficits Abnormal CT brain Acute ischemic stroke New neurologic deficits Abnormal MRI or CT brain Acute perioperative hypertension Bleeding unresponsive to direct pressure Clinical diagnosis; manifestations of other hypertensive emergencies

16. Treatment of Hypertensive Emergencies by Diagnosis

17. DX Therapy Goals Agents Risks Comments Aortic dissection Reduce shear forces by ↓ BP and PR Lower SBP to 100–120 mm Hg ↓ PR ≤60 beats/min Esmolol* IV bolus, then continuous infusion OR Labetalol* IV bolus or continuous infusion Nicardipine IV continuous infusion (after β-blocker) Nitroprusside infusion (after β-blocker) β-blockers: Respiratory distress in asthma/COPD; test dose of esmolol recommended, switch to diltiazem if intolerant Nitroprusside: cyanide/thiocyanate toxicity in renal dysfunction or therapy >24–48 h Measure BP in both arms, treat higher BP Always use β-blocker before vasodilators (avoid reflex tachycardia) Acute HTN pulmonary edema Reduce BP by 20%–30% Promote diuresis via vasodilation Symptomatic relief Nitroglycerin* SL, topical, or IV infusion Clevidipine infusion Nitroprusside infusion Enalaprilat IV Nicardipine infusion Nesiritide IV ACE inhibitors: may worsen renal function Nitroprusside: cyanide/thiocyanate toxicity with renal dysfunction or therapy >24–48 h IV nitrates: low dose dilates capacitance vessels, high dose dilates arterioles Nesiritide : mixed outcomes; ASCEND-HF trial showed no significant benefit

18. Acute MI Reduce ischemia Avoid >25% reduction in MAP Nitroglycerin * SL, aerosol, or IV infusion Esmolol* infusion Labetalol or metoprolol IV bolus Nitrates contraindicated if PDE inhibitors used (sildenafil <24 h, tadalafil <48 h) β-blockers contraindicated in CHF, low-output states Monitor for hypotension (consider RV infarct, volume depletion) SBP >180 mm Hg or DBP >110 mm Hg is relative contraindication to thrombolytics Acute sympathetic crisis (cocaine, amphetamines, MAOI toxicity) Reduce sympathetic drive Symptom relief Aim SBP <140 mm Hg in 1st hour Benzodiazepine* IV bolus Nitroglycerin SL, topical, or IV infusion Phentolamine* IV or IM Nicardipine or clevidipine infusion Benzodiazepines: risk of respiratory depression Labetalol: controversial in cocaine-induced HTN Benzodiazepines are 1st line in cocaine-induced HTN Phentolamine is 1st line for pheochromocytoma CCBs (nicardipine, clevidipine ) are 3rd line after benzodiazepines + nitrates Acute renal failure Reduce BP gradually (≤20% acutely) Fenoldopam infusion Nicardipine infusion Clevidipine infusion Nitroprusside: avoid (cyanide/thiocyanate toxicity) ACE inhibitors: avoid acutely —

19. Eclampsia, preeclampsia Aim SBP <140 mm Hg in 1st hour Hydralazine* IV bolus Labetalol* IV bolus Nifedipine* oral Hydralazine: reflex tachycardia, hypotension Labetalol: fetal bradycardia, caution in asthma/COPD/HF Nifedipine: maternal tachycardia, overshoot hypotension All are 1st line agents Nifedipine ideal if no IV access Contraindicated: ACE inhibitors, ARBs, renin inhibitors, nitroprusside Hypertensive Encephalo pathy Decrease MAP by 20%–25% in 1st hour Avoid rapid ↓ to prevent hypoperfusion Labetalol IV bolus/infusion Nicardipine infusion Clevidipine infusion Avoid β-blockers in drug-induced crisis Avoid nitroglycerin (worsens cerebral autoregulation) Cerebral autoregulation impaired—lower BP cautiously Subar Achnoid hemorrhage SBP <160 mm Hg to prevent rebleed (BP goals not well defined) Nicardipine infusion Labetalol IV bolus (10–20 mg) or infusion Esmolol bolus + infusion Clevidipine infusion Avoid hypotension (maintain cerebral perfusion) Nimodipine ↓ mortality (not for BP lowering, but may ↓ BP) Clazosentan may be alternative to nimodipine with similar hypotensive effects

20. Diagnosis Therapy Goals Agents Risks Comments Intracerebral Hemorrhage (ICH) - If SBP >220 mmHg → aggressive IV infusion- If SBP 150–220 mmHg → IV boluses to lower SBP to 140 mmHg - Labetalol IV bolus or continuous infusion- Nicardipine IV infusion- Esmolol IV bolus + infusion - Excessive BP lowering <150 mmHg not associated with morbidity - Early hemorrhage growth in first 6h- Aggressive control (SBP 130–139 mmHg) reduces hematoma growth, morbidity, mortality Acute Ischemic Stroke (rtPA candidate, BP ≤185/110 mmHg) - Treat if BP >185/110 after 3 readings- Goal: ≤185/110 mmHg before reperfusion - Labetalol 10–20 mg IV over 1–2 min; may repeat once- Nicardipine 5 mg/h IV, titrate ↑ by 2.5 mg/h every 5–15 min (max 15 mg/h)- Clevidipine 1–2 mg/h IV, double dose q2–5 min (max 21 mg/h)- Nitroprusside if uncontrolled or DBP >140 mmHg - Excessive lowering may worsen ischemia - During & after reperfusion: If SBP >180–230 or DBP >105–120 → Labetalol infusion 2–8 mg/min OR Nicardipine 5–15 mg/h OR Clevidipine up to 21 mg/h Acute Ischemic Stroke (not reperfusion candidate) - Treat if ≥220/120 mmHg (on 3 readings 15 min apart)- Reduce BP by ~15% in first 24h - Same agents & doses as rtPA candidate - Excessive reduction may worsen perfusion - Early treatment if ACS, aortic dissection, preeclampsia/eclampsia- Do not reduce SBP >15% in first 24h- Withdrawal syndrome possible if on β-blockers or clonidine

21. Condition Blood p. Goal First-Line Therapy Second-Line Therapy Heart Failure <130/80 mm Hg Diuretic with ACE inhibitor β-Blocker Post–Myocardial Infarction <130/80 mm Hg β-Blocker, ACE inhibitor or ARB Aldosterone antagonist High Coronary Artery Disease Risk <130/80 mm Hg β-Blocker, Calcium channel blocker (if angina pectoris) ACE inhibitor, Calcium channel blocker, or Diuretic Recurrent Stroke Prevention <140/90 mm Hg Thiazide diuretic with ACE inhibitor or ARB — Diabetes <130/80 mm Hg - Nonblack: Thiazide diuretic, ACE inhibitor, ARB, or CCB - Black: Thiazide diuretic or CCB Above alone or in combination Chronic Kidney Disease <130/80 mm Hg ACE inhibitor or ARB Above alone or in combination with other drug class Indications for Specific Antihypertensive Therapy

22. Pulmonary Hypertension

23. Normal pulmonary circulation : High-flow, low-resistance. Normal PA systolic: 15–30 mmHg Normal PA diastolic: 4–12 mmHg Definition : mPAP >25 mmHg at rest OR >30 mmHg with exertion. Definitive diagnosis : Right heart catheterization (echo = screening). Group 1: Pulmonary Arterial Hypertension • Idiopathic • Genetic/heritable abnormalities • Drug or toxin induced • Associated with known risk factors for pulmonary arterial hypertension ( HIV , portal hypertension, pulmonary veno -occlusive disease, collagen vascular disorders) Group 2: Pulmonary Venous Hypertension (left heart disease) • Left ventricular systolic or diastolic dysfunction • Mitral or aortic valve disease World Health Organization Classification of Pulmonary Hypertension

24. Group 3: Chronic Hypoxemic Lung Disease • Obstructive lung disorders (chronic obstructive pulmonary disease) • Interstitial lung disease • Idiopathic pulmonary fibrosis • Collagen vascular disorders • Sleep-disordered breathing (obstructive sleep apnea ) • Chronic exposure to high altitude Group 4: Chronic Thromboembolic Pulmonary Hypertension Group 5: Miscellaneous • Lymphatic obstruction • Hematologic disorders: myeloproliferative disorders • Systemic disorders: sarcoidosis, neurofibromatosis • Metabolic disorders: glycogen storage disease, thyroid disorders.

25. Clinical Features Most common symptom : Dyspnea (>50%). Others: Fatigue, chest pain, syncope, exertional presyncope. Advanced: Early satiety, anorexia, orthopnea , PND, edema . Exam : Often normal early. Later → TR murmur, JVD, hepatomegaly, ascites, loud P2, edema Diagnostic Testing ECG- Most common: Right axis deviation . Others: RVH (R/S >1 in V1, qR in V1, S1Q3T3, RBBB, RA enlargement). Arrhythmias: AF, flutter, AVNRT. Labs   Non-specific. ↑ Troponin, ↑ BNP → worse prognosis. ↑ LFTs, lactate, coagulopathy → poor prognosis. Imaging CXR : RA/RV/hilar PA enlargement; may show edema , ILD, hyperinflation. Echocardiography : Best initial test. Findings: RVH, ↓ RV fx , TR, septal bowing, RV:LV >1. CT Pulmonary Angio : To rule out PE + assess RV.

26. Treatment Principles (ED Management) Goals : Oxygenation, volume balance, support RV function, maintain perfusion, ↓ afterload. 1. Oxygen & Ventilation Target SpO₂ >90%. Avoid intubation if possible (PPV worsens RV failure). If required: Lung-protective strategy (TV 6–8 mL/kg, lowest PEEP, plateau <30, avoid hypercapnia). 2. Volume Avoid overload (↑ RV dilation, ↓ LV filling). If hypovolemic → cautious bolus (100–250 mL crystalloid). Diuresis later if fluid overloaded. 3. RV Function Dobutamine : 2 → titrate to 10 mcg/kg/min (risk tachy , hypotension). Milrinone : 0.125–0.75 mcg/kg/min (risk hypotension, requires monitoring).

27. 4. Maintain Right Coronary Perfusion Vasopressors for hypotension: First-line : Norepinephrine (0.05 mcg/kg/min, avoid high dose). Avoid: Dopamine (tachyarrhythmias), phenylephrine (less effective). 5. RV Afterload Reduction Outpatient drugs: Prostanoids , endothelin receptor antagonists, PDE-5 inhibitors. ED use : Restart home prostanoid infusion immediately if interrupted. Inhaled vasodilators ( epoprostenol , nitric oxide) for acute decompensation. Avoid initiating IV vasodilators in ED . Class Drug Key Features Notes / Adverse Effects Prostanoids (Potent vasodilators, antiplatelet & antiproliferative properties) Epoprostenol IV infusion; half-life 2–5 min; can be given as aerosol for acute PH with RV failure Requires continuous infusion Treprostinil IV or SC; half-life 4–5 h Not for acute RV failure Iloprost Inhaled/aerosol; outpatient alternative if unable to tolerate parenteral prostanoids Not for acute RV failure Tadalafil Oral, longer acting Not for acute RV failure Commonly Prescribed Outpatient Pulmonary Vasodilators Endothelin Receptor Antagonists Bosentan Oral Elevated transaminases, ↓ hemoglobin Ambrisentan Oral Same class effects; not for acute RV failure Phosphodiesterase-5 Inhibitors Sildenafil Oral Headache, flushing, dyspepsia; contraindicated with nitrates (risk of hypotension)

28. Acute Heart Failure Pathophysiology of heart failure. b) Biomarkers in diagnosis of heart failure. c) Management of sympathetic crashing acute pulmonary edema . Que- Mention the classification of heart failure alongwith the common presentation symptoms and physical findings. Introduction and Epidemiology Acute heart failure (AHF) includes a spectrum from gradual symptoms (e.g., leg swelling, dyspnea ) to abrupt pulmonary edema . Includes both: Acute decompensation of chronic heart failure New-onset heart failure “Congestive heart failure” is outdated and refers to fluid overload signs.

29. Pathophysiology HF is a clinical syndrome with symptoms: dyspnea , edema , fatigue. Caused by structural or functional cardiac dysfunction impairing pump function. Leads to: Reduced exercise tolerance Fluid retention Pulmonary/splanchnic congestion Compensatory adaptations (renal, vascular, muscular) maintain short-term function but worsen long-term outcomes. Neurohormonal Activation Triggered by ↓ cardiac output: Activation of RAAS and sympathetic systems Increased norepinephrine, vasopressin, endothelin, TNF-α Results in: Sodium & water retention ↑ Systemic vascular resistance .↑ Myocardial workload and O₂ demand Natriuretic Peptides Counter-regulatory hormones: Atrial NP (atria), B-type NP (ventricles), C-type NP (endothelium) Promote: Vasodilation/Natriuresis/ Inhibition of RAAS and sympathetic systems B-type NP is produced as: NT- proBNP (inactive, t½ ~2 hrs) BNP (inactive, t½ ~20 min) Ischemic Triggers and Pulmonary Edema Acute MI → pump failure → HF or cardiogenic shock. Acute pulmonary edema : Results from rapidly declining CO and ↑ systemic vascular resistance May be sudden, severe, and fatal Even mild BP elevation can be worsen.

30. Classification Characteristics Hypertensive AHF - Signs/symptoms of AHF with preserved LV function- Systolic BP >140 mm Hg- Chest radiograph: pulmonary edema- Symptom onset <48 hours Pulmonary Edema - Respiratory distress- Rales on chest auscultation- Reduced oxygen saturation from baseline- Pulmonary edema confirmed by chest X-ray Cardiogenic Shock - Evidence of tissue hypoperfusion- Systolic BP typically <90 mm Hg- Refer to Chapter 50 for details Acute-on-Chronic HF - Mild to moderate symptoms of AHF- Systolic BP 90–140 mm Hg- Does not meet criteria for hypertensive HF, pulmonary edema , or cardiogenic shock- Typically increased peripheral edema - Symptom onset over several days High-Output Failure - High cardiac output- Typically with tachycardia, warm extremities- Pulmonary congestion present Right Heart Failure - Low-output state- Jugular venous distention- Hepatomegaly- May have hypotension C lassification of Acute Heart Failure

31. SYSTOLIC AND DIASTOLIC HEART FAILURE Definition and Classification Systolic Heart Failure ( HFrEF ) : Ejection fraction (EF) <50%; impaired ventricular contraction → increased intracardiac volume and afterload sensitivity → pulmonary congestion and edema under stress. Diastolic Heart Failure ( HFpEF ) : Preserved EF; impaired ventricular relaxation and decreased compliance → elevated atrial pressure → preload sensitivity. More common with aging, chronic hypertension (causing LV hypertrophy), and coronary artery disease DIAGNOSIS History and Physical Examination No single finding is highly sensitive or specific. Initial clinical judgment: sensitivity 61%, specificity 86%. Most useful history: prior HF (sensitivity 56%, specificity 80%). Risk factors: HTN, diabetes, valvular disease, old age, male sex, obesity. Clinical gestalt in ED comparable to BNP value for diagnosis. Symptoms: Highest sensitivity: dyspnea on exertion (84%). Most specific: PND, orthopnea , edema (76–84%). Physical finding with highest positive likelihood: S3 (LR+ = 4.0).

32. CHEST RADIOGRAPHY Findings: pulmonary venous congestion, cardiomegaly, interstitial edema . Absence of findings doesn’t rule out HF (20% may have normal CXR in HF). Late-stage HF may have few radiographic signs despite elevated PCWP. ECG AND BIOMARKERS ECG: Identifies triggers (e.g., ischemia, MI, arrhythmias). BNP/NT- proBNP : Correlate with filling pressures and ventricular stretch. BNP <100 or NT- proBNP <300 pg /mL largely excludes HF. Gray zone: BNP 100–500 pg / mL. POCUS (Point-of-Care Ultrasound) Helps assess LV function, volume status, and pulmonary congestion. Three key questions: Bedside US use to identify acute heart failure (AHF) in dyspneic ED patients- Pulmonary congestion (B-lines) Volume overload (IVC size >2 cm or <50% collapsibility) - LV ejection fraction (normal, moderate, severe) B-lines: ≥3 per view = pathologic (interstitial/alveolar edema ). Must distinguish B-lines from pulmonary fibrosis/pneumonia. Rapid IVC and LV assessment aids acute HF diagnosis. Not a replacement for formal echocardiography. NT- proBNP age cutoffs: <50 yrs : 450 pg /mL /.- 50–75 yrs : 900 pg / mL . - 75 yrs : 1800 pg /mL Elevation also occurs in PE, pneumonia, sepsis, renal failure.

33. TREATMENT General Approach Driven by acuity, hemodynamics , and volume status. Maintain O₂ saturation ≥95%; use oxygen liberally when unknown. In critically ill: secure airway (ET intubation if needed). Noninvasive positive-pressure ventilation (NIPPV): reduces intubation, improves symptoms and acidosis. High-velocity nasal insufflation: alternative to NIPPV. Hypertensive Acute Heart Failure Pulmonary edema may occur even at SBP 150 mmHg. Aim: Afterload reduction using vasodilators. Nitroglycerin Routes: Sublingual, IV, transdermal (slow onset). SL: 0.4 mg every 5 min until IV started. IV: 0.5–0.7 mcg/kg/min; titrate up to 200 mcg/min. Adverse effects: hypotension, headache, rarely methemoglobinemia. Hypotension → consider RV infarct or hypovolemia → give IV fluids.

34. Nitroprusside Potent arterial vasodilator for refractory cases. Dose: 0.3 mcg/kg/min IV, titrate every 5–10 min (max 10 mcg/kg/min). Monitor for hypotension, thiocyanate toxicity. Loop Diuretics in Hypertensive HF Used after vasodilators. Alone may worsen renal function and increase mortality. Contraindications to Vasodilators Avoid in hypoperfusion, hypotension, RV infarct, aortic stenosis, HOCM, volume depletion. Consider phenylephrine for HOCM with shock. Monitor renal function, electrolytes, urine output. Repeat/double dose if poor response. Avoid NSAIDs (worsen HF). Diuretics may cause hypokalemia , ototoxicity, QT prolongation. Normotensive Acute Heart Failure Signs: SOB, JVD, rales, S3 with normal vitals. Primary treatment: Diuresis. Loop Diuretics IV preferred due to bowel edema in HF. Options: Furosemide Bumetanide (1 mg = 40 mg furosemide) Torsemide (20 mg = 40 mg furosemide) Onset: 10–15 minutes IV. DOSE trial: Start at 1–2.5× daily PO dose IV every 12h. Naive patients: furosemide 40 mg IV.

35. Other Medications Morphine : Not preferred; may worsen outcomes. If needed, small IV doses (2–4 mg). ACEi /ARBs : Consider after stabilization; oral ACEi reduce mortality in HFrEF . β-Blockers : Not initiated acutely, unless for rate control. Calcium Channel Blockers : Avoid; negative inotropic effect. NSAIDs : Contraindicated in acute HF. Vasodilator Dose Titration/End Point Complications Sublingual NTG 0.4 mg every 1–5 min Blood pressure Hypotension IV Nitroglycerin 0.5–0.7 mcg/kg/min (starting dose) Symptoms Headache, hypotension Nitroprusside Start: 0.3 mcg/kg/min; Max: 10 mcg/kg/min Blood pressure, symptoms Hypotension, cyanide/thiocyanate toxicity, coronary steal Vasodilators for Acute Heart Failure

36. Step Comments Administer oxygen to maintain SpO₂ ≥95%; give sublingual nitroglycerin Repeat 1–2 sprays/tablets every 5 minutes as needed If severe dyspnea, consider NIV or endotracheal intubation Use NIV early to avoid intubation if tolerated If BP >150/100 mm Hg, add IV nitroglycerin or nitroprusside If BP drops <100 mm Hg, stop nitrates and monitor for hypotension or shock If BP <150/100 mm Hg after sublingual NTG and improved symptoms Consider switching to transdermal nitroglycerin Start IV loop diuretic (furosemide or bumetanide) Initiate after vasodilator in the setting of volume overload Assess for high severity/risk Red flags: altered mental status, persistent hypoxia despite NIV, hypotension, ↑ troponin, ischemic ECG changes, tachycardia/ pnea , ↓ urine output Admit to ICU if high severity or risk of decompensation Any ongoing cardiorespiratory compromise or acute ischemia warrants ICU If good response, no high-risk features, and adequate social support Consider ED observation or discharge Admit remaining patients Use clinical judgment as scoring systems may miss some at-risk patients Management of Hypertensive Acute Heart Failure – Stepwise Approach THANK YOU