Cardio High Yield Notes PDF

Hypertension What is it? Hypertensive urgency→ Severely elevated blood pressure without symptoms or end organ damage Hypertensive emergency → occurs with elevated BP and evidence of end organ damage Causes Chronic HTN (med noncompliance) Rebound HTN (med withdrawal) Sympat...

Hypertension What is it? Hypertensive urgency→ Severely elevated blood pressure without symptoms or end organ damage Hypertensive emergency → occurs with elevated BP and evidence of end organ damage Causes Chronic HTN (med noncompliance) Rebound HTN (med withdrawal) Sympathetic drugs (cocaine, amphetamine) Pre-eclampsia Ischemic stroke CVA Head trauma Thyroid storm Hyperaldosteronism Risk factors Presenting signs and symptoms Hypertensive emergency → ○ Mental status changes, intracranial hemorrhage, retinopathy, aortic dissection, cardiac ischemia, CHF, acute renal failure Physical exam/ presentation Hypertensive encephalopathy → headache confusion, N/V, seizures CHF → acute pulmonary edema, LV dysfunction, AMI Acute kidney injury/ acute renal failure → acute hypertensive necrosis, microscopic hematuria, elevated Cr Vascular compromise → aortic dissection, aortic aneurysm/rupture Diagnosis Hypertensive urgency (screening for end-organ damage) ○ Serum creatine, urinalysis, chest xray, ECG Treatment Hypertensive urgency ○ Control BP within 24-48 hours ○ Discharge reliable pts with follow up ○ Urgent follow up is required for potential medication titration ○ HCTZ → 1st line Hypertensive emergency → requires rapid but controlled BP reaction with IU meds ○ Aim to reduce mean BP by 25% within 1st hour ○ Gradual lowering of BP to avoid complications Target SBP of 160-180 mmHg After that you can make further reductions gradually with oral meds  ○ Meds → Nitroprusside → potent vasodilator (lowers BP in seconds, cessation leads to rapid return) Requires ICU and intra arterial monitoring Can cause cyanide toxicity Labetalol → combo of alpha and beta blocker Affective in most hypertension emergencies. Preferred aortic dissection, useful in pregnancy, and patients with ICH/CVA Hydralazine → vasodilator used in pregnancy with hypertension emergency Increases uterine blood flow at arteriole level Contraindications: ACS, aortic dissection Fenoldopam → dopamine agonist (decrease PVR) Good alternative to nitroprusside to avoid cyanide toxicity Good for renal toxicity, AKI, or ARF Enalaprilat → IV ACE inhibitor Effective in CHF/ stroke Nust be renally dosed if you have renal issues Nicardipine → IV CCB/dihydropyridines Good for subarachnoid hemorrhage and CVA patients Esmolol → IV Beta blocker Aortic dissection Contraindicated in CHF Short acting/titrable Especially useful in intubation induced hypertension, STEMI/NSTEMI, VF/VT ○ DOES NOT CAUSE TACHYCARDIA QUICK NOTE: Acute phase ischemic stroke (CVA) ○ Do NOT lower blood pressure unless its >185/110 in candidates for reperfusion treatment (tPa) This is because their BP goal is 220/120 in noncandidates for reperfusion treatment tx (tPa) Aortic dissection ○ Must be rapidly lowered within 20 minutes to SBP of 100-120 ICH/SAH ○ Consult neurosurgery  Neurologic (TBI, CVA, ICH) ○ 1st line → Nicardipine Cardiac (acute CHF) ○ 1st line → nitroglycerin, nitroprusside, enalapril Myocardial Infarction ○ 1st line → metoprolol/esmolol NTG/nitroprusside best when there’s a PE Aortic Dissection ○ 1st line → Esmolol/labetalol +/- nitroprusside Renal (AKI/ARI/ARF) ○ 1st line → Fenoldopam Pregnancy (preeclampsia/eclampsia) ○ 1st line → hydralazine/labetalol Sympathetic overdrive (cocaine OD, pheochromocytoma) ○ 1st line → phentolamine +/- benzo Distributive shock What is it? A type of circulatory shock characterized by severe peripheral vasodilation, leading to inadequate tissue perfusion despite normal or increase CO Key mechanisms ○ Peripheral vasodilatation: reduced systemic vascular vascular resistance → pooling of blood and decreased circulating volume ○ Maldistribution of blood flow: preferential blood flow to non-vital organs ○ Capillary leakage: increase permeability leading to 3rd space fluid losses ○ Compensatory response: increase CO (tachycardia) may initially compensate but become insufficient Causes Septic shock → systemic infection triggering an excessive in inflammatory response Anaphylactic shock → severe allergic reaction (IgE mediated) Neurogenic shock → Spinal cord injury/CNS damage affecting autonomic control Endocrine shock → acute adrenal insufficiency (addisonian crisis) Presenting S/S Septic shock → fever, hypotension, warm extremities early progressing to cold extremities Anaphylactic shock → urticaria, angioedema, bronchospasm, hypotension Neurogenic shock → hypotension with bradycardia Endocrine shock → hypotension, hyponatremia, hypokalemia Treatment 1. Resuscitation:  a. Fluid therapy: Crystalloids (saline) initial 30mL/kg bolus b. Vasopressors: norepi= 1st line (for hypotension unresponsive to fluids) 2. Targeted therapy: a. Septic shock: early antibiotics, source control, corticosteroids (if adrenal insufficiency) b. Anaphylactic shock: epinephrine, antihistamines, corticosteroids c. Neurogenic shock: IV fluids, vasopressors, atropine Management: Septic shock → ○ Within 1 hour of recognition: early recognition and antibiotics ○ Lactate measurement, fluid resus, vasopressors to maintain MAP >65 ○ Consider corticosteroids, BG control and early goal directed therapy Anaphylactic shock → ○ 1st line of treatment: epi IM ○ Adjunctive therapy: antihistamines (H1 and H2 blockers), corticosteroids, beta agonists (bronchospasms) Neurogenic shock → ○ Initial → maintain spine immobilization Fluids and vasopressors to restore vascular tone atropine= bradycardia ○ Long term care Monitor for complications like DVT, pressure ulcers Cardiogenic shock What is it? A form of shock where the heart’s inability to pump effectively results in reduced CO → inadequate tissue perfusion ○ Heart can’t meet metabolic demands of tissue Causes MI → MCC (STEMI) Acute HF Arrhythmias Mechanical causes Cardiomyopathy RVF Presenting features Cardiac output → decreased Systemic vascular resistance → increased Pulmonary capillary wedge pressure → increased  Blood pressure → hypotension Central venous pressure → increased Treatment Initial stabilization ○ Oxygen therapy: O2 sat> 90% ○ Vasoactive drugs: norepi/dopamine to support BP ○ Inotropes: dobutamine to increase contractility Revascularization (if due to MI) ○ Percutaneous coronary intervention (PCI): first line treatment for STEMI with shock ○ CABG: for patients with extensive coronary DZ Hypovolemic shock What is it? A form of shock due to reduced intravascular volume, leading to decreased preload, SV and CO ○ Inadequate perfusion due to significant blood/fluid loss Causes 1. Hemorrhagic hypovolemic shock (blood loss) a. Trauma (external/internal bleeding) b. GI hemorrhage c. Ruptured aneurysm d. Postpartum hemorrhage 2. Non Hemorrhagic hypovolemic shock (fluid loss0 a. GI losses: Severe vomiting, diarrhea b. Renal losses: diuretic overuse, diabetes c. Skin losses: burns, excessive sweating d. 3rd space losses: Pancreatitis, bowel obstruction Presenting signs and symptoms Class I (mild) → blood loss < 15% (750mL); minimal symptoms Class II (mod) → blood loss 15-30% (750-1500mL); tachycardia, mild hypotension Class III (severe) → blood loss 30-40% (1500-2000mL); significant hypotension, confusion, oliguria Class IV (life threatening) → blood loss >40% (>2000mL), severe hypotension, anuria, lethargy, coma Treatment Start with crystalloid fluids Give in 1mL increments No set drip rate= bolus ○ 18g IV → 1L in 10-15 mins  ○ 20g IV → 1L in 20 mins ○ 22g IV → 1L in 30 mins After 2-3 liters, if theres no response with hypotension consider vasopressors and diagnosis of shock SO IF NO RESPONSE TO 2-3 BOLUS IS MADE → DX OF SHOCK Crystalloids: ○ Normal saline or lactated ringer’s → first line Colloids: ○ Used in same setting but crystalloids preferred Blood products ○ Indicated: if Hb is