Low Mg, Ca or K can all cause QT prolongation
|Preload Reduction *Patients with diastolic|
dysfunction (right MI) are often
preload dependent, so use
|Loop diuretics Vasodilators Nitrogen – primarily venodilation Nitroprusside and BNP Analogs (nesiritide) are arterial and venous. Morphine ACEI, ARB, Aldosterone antagonists|
|Afterload Reduction||Vasodilators ACEI, ARB, Aldosterone antagonist|
|Positive Inotrope||Beta 1 agonist (dobutamine) Misc (high dose dopamine) Type 3 Phosephodiastereas inhibitor(milrinone)|
|Pulse||Beta blockers Non–DHP Calcium Channel Blockers Antiarrhythmics|
|Oxygenation and Ventilation||Non-invasive ventilation with BiPap or CPAP|
Calcium Channel Blockers worsen systolic function in systolic failure – ionotropic effects
- LVEF of 50-75 is normal
- HFpEF = heart failure with normal ejection fracture
- HFrEF = heart failure with reduced ejection fracture
Acute Decompensated Heart Failure:
- If patient is on a beta blocker, don’t use dobutamine, use milrinone.
- Nitro and diuretics cause vasodilation to improve edema.
- Continue recommended therapies while treating:
- Beta-blockers- do not initiate a new beta blocker until stabilized, but do not discontinue)
- Digoxin – in HF level is 0.5-2.0 – in arrhythmia, it’s 1.5-2.5 – digoxin has a narrow therapeutic index so know.
- Avoid drugs with negative ionotropy: class 1 sodium channel blocking antiarrhythmics (mexiletine, tocainide, procainamide, quinidine, disopyramide, flecainide, propafenone)
- In heart failure: only amiodarone and dofetilide
- Wolfe Parkinson White: procainamide or ibutilide
- Hypothyroid: non-DHP, avoid beta blockers
- Pregnancy: digoxin, non-DHP, no warfarin or heparin
- Do not use fenoldopam in patients with stroke, dopamine agonist can cause cerebral vasodilation and reduced blood flow to the brain
- 1a agents cause Torsades, usually avoid in structural heart disease
- 1b agents have little atrial affinity
- Sotolol: 50/50 sodium and potassium blockade, Torsades, especially in renal disease
- amio: TSH, pulmonary, liver, eyes, get baseline chest x-ray
|1c||flecainide||X||convert (rare)||PSVT and
can be used in HF
|adenosine||PSVT in pregnancy||
This site has a great rundown on the mechanism and actions and how these agents shift the action potential. You probably don’t need to know all that for the BCPS. Just know how to pick an agent for a specific patient population.
|STEMI, PPCI||UHF, bivalirudin|
|STEMI, fibrinolytic||UHF, enoxaparin, fondaparinux||bivalirudin not studies with lytics|
|NSTE-ACS, early invasive||enoxaparin, bivalirudin, fondaparinux, UFH||if you’re going to cath lab, all|
if placing a stent, no fondaparinux
|NSTE-ACS, ischemia-guided||enoxaparin, fondaparinux, UFH|
- Stop heparin after the intervention.
- Everyone with ACS gets dual anti-platelets for 12 months, regardless of stent or not.
- Usually aspirin + clopidogrel, ticagrelor or prasugrel
- Prasugrel has the highest bleeding risk
- Clopidogrel has the most drug interactions
- Ticagrelor is BID
- Prasugrel has a longer surgery hold time
- Ticagrelor is a reversible inhibitor
- Can only use prasugrel if going for PCI.
- Some people also get a glycoprotein IIaIIIb (abciximab, eptifibatide, tirofiban)
- Usually aspirin + clopidogrel, ticagrelor or prasugrel
- In elective caths, a bare-metal stent gets 1 month, a drug-eluting stent gets 6 months.
- You can have multiple antiplatelets, but only one anti-coagulant
Heparin: 60 units/kg then 12/units kg
Angiomax: 0.75 mg/kg then 1.75 mg/kg
Troponin is the primary biomarker used. If a person has negative cardiac enzymes, treatment is not as emergent. They indicate myocardial necrosis. NSTEMI, STEMI or new LBB will usually see elevated enzymes. Obtain enzymes at presentation and 3-6 hours after.
|myoglobin (1st to show up, 1st to leave)||1-2 h||4-6 h||24 h|
|CK-M8||3-4 h||12-24 h||2 days|
|Troponin||3-6 h||12-24 h||7 days|
Remember MONABS meets chest pain at the door for all Acute Coronary Syndrome.
- M: Morphine -it may be harmful in ACS. It causes vasodilation, reduces blood volume, preload, blood pressure and can cause reflex tachycardia. It can also make blood thinners work less effectively. It’s still often used for acute pain and anxiety.
- O: Oxygen if oxygen sat is < 94%, start at 4 L per nasal cannula to keep above 95%
- N: Nitro to cause vasodilation, decreases preload and afterload. Recommended for ischemia, heart failure, hypertension or anterior MI. Do not use if hypotensive, bradycardic or tachycardic. No diagnostic value.
- A: Aspirin, everyone gets aspirin, decreases all-cause 30-day mortality, add clopidogrel, ticarelor or prasugrel (prasugrel only if straight to PCI) +/- eptifiditide in high risk.
- B: Beta blockers
- S: Statins
Management After ACS is as easy as ABCDE:
- Aspirin, anti-anginals, ACEI/ARB, aldosterone antagonists
- Beta blockers, blood pressure
- Cholesterol, cigarettes
- Diet, diabetes, dual antiplatelet therapy
- Excercise, education
Acute Coronary Syndrome can be Divided into STEMI and NSTEMI
NSTE (non ST-segment elevation):
There are two main treatment algorithms for non-stemi
|Ischemia Guided ASA P2Y12 Inhibitors Clopidogrel or ticagrelor only Anticoagulants UFH enoxaparin fondaparinux||Early Invasive ASA P2Y12 Inhibitors Clopidogrel or ticagrelor Can use prasugrel if going to PCI Anticoagulants UFH enoxaparin fondaparinux (not if STEMI) bivalirudin Can consider GPI (eptifibatide, tirofiban, abciximab (no kidney adjustment needed)|
- A STEMI usually means immediate angiography unless angiography is not available.
- TIMI risk score: predicts mortality. When TIMI score is higher than 3, aggressive treatment like LMWH, GPIIa/IIIb inhibitors and invasive strategies are warranted.
- Medium and high-risk patients: aspirin and another platelet inhibitor + ADP inhibitor if going to cath lab (eptifibatide or tirofiban, abciximab can be used if immediately going to cath). Give as close to PCI as possible. If on dialysis can only use abciximab.
- High risk: troponin + high TIMI score: give UFH as pre-treatment.
- If not planning on cath, aspirin + another platelet inhibitor
- Dual antiplatelets for 12 months after stenting. Hold effient for 7 days prior to non-emergent surgery, hold clopidogrel and ticagrelor for 5.
- If CABG, stop LMWH 12-24 hours prior to surgery, stop gpIIa/IIIb inhibitors 4 hours prior. Arixtra 24 hours prior.
- Anticoagulants are given to all ACS patients in addition to platelet therapy. See chart above.
Indicated in STEMI when PCI cannot be performed within 120 minutes AND symptoms started within the last 12 hours. Patients should receive anticoagulation for a minimum of 48 hours but up to 8 days or when revascularization is performed with enoxaparin, UHF or fondaparinux. Cath is preferred and has mortality benefits.
Just remember *****Any blood anywhere, usually only used in stroke****
- Relative contraindications (use with caution):
- BP > 180/110 – Remember this, but you can treat BP and use lytic.
- Ischemic stroke > 3 months before
- Major surgery < 3 weeks before
- Tramautic or prolonged (> 10 minute) CPR
- Internal bleeding within 2-4 weeks.
- Active peptic ulcer
- Non-compressible vascular puncture
- Known intracranial pathology (like dementia)
- Oral anticoagulants
- Absolute contraindications (DO NOT USE):
- Any prior hemorrhagic stroke
- Ischemic stroke within the last 3 months (except past 4.5 hours)
- Intracranial neoplasm or arteriovenous malformation
- Active internal bleeding
- Aortic dissection
- Considerable facial trauma or closed-head trauma in past 3 months
- Intracranial intraspinal surgery within 2 months
- Severe uncontrolled HTN that is not responsive to treatment
- For streptokinase, treatment within the past 6 months.
- Doses are different in ACS than in stroke.
- Alteplase: 15 mg then 0.75 mg/kg over 40 minutes
- Reteplase: 10 units, repeat in 30 minutes
- Tenectplase: <60 kg – 30 mg IV, 60-69 kg – 35 mg IV, 70-79 kg – 40 mg IV, 80-89 kg – 45 mg IV, greater than 90 kg – 50 mg IV.
- Must follow up lytic with anticoagulants: UHF, fondaparinux or enoxaparin.
Stages of CHF:
|Stages of CHF||NYHA Functional Class|
|A||High risk of heart failure but
no structural disease or
|B||Structural heart disease but
without signs or symptoms of
|I||Asymptomatic HF. No limitations
in physical activity caused by HF
|C||Structural heart disease with
prior or current symptoms of
|II||Slight limitation of physical
activity. Asymptomatic at rest
but symptoms with normal level
|III||Marked limitation in physical
activity because of HF symptoms.
Asymptomatic at rest.
|IV||Symptoms even at rest. Unable to
carry out any physical activity.
|D||Refractory HF requiring
All patients with EF less than 40% get assessed by the five fingers of ABCDE.
- ACEI: Everyone gets ACEI or ARB. Proven to decrease mortality and symptoms. Use caution if SBP < 80, SCr > 3 or K > 5.0. Contraindicated in angioedema. Can use ARB in angioedema, but they may also cause so educate patient and use caution. Theoretically, aliskiren should not confer a risk of bradykinin-induced angioedema, because unlike ACE inhibitors, it has no known effect on bradykinin metabolism, however, caution is still recommended.
- Beta Blocker: Beta blockers decrease mortality and symptoms. The only ones used for heart failure are bisoprolol, carvedilol and metoprolol SUCCINATE only. Combine with ACEI. If hypotension is a problem, reduce ACEI before beta blocker.
- C stages of heart failure (II-IV) may get aldosterone antagonist added to ACEI and Beta blocker, especially with past cardiac hospitalization or increase in BNP or post-acute MI. Do not give if CrCl < 30.
- Digoxin can be added for symptoms. It not good at reducing exercise related dyspnea.
- Edema and fluid retention can be corrected with diuretics. There is no mortality benefit, but quality of life may improve.
- Hydralazine/isosorbide dinitrate – add to all African Americans with III or IV stage HF>
- Sacubitril/valsartan – in stages II or III, replacing ACEI with Entresto can decrease mortality.
- Ivabradine – can reduce hospitalization in stages II and III, must be on optimal Beta blocker and have HR > 70 at rest.
- Also: be sure to control HTN, counsel on smoking cessation, EtOh abuse, correct thyroid disease and dyslipidemia.
- Calcium channel blockers with negative inotropic effects (diltiazem and verapamil) may be harmful.
Meds that Exacerbate CHF:
- Thiazolidinediones: rosiglitazone, pioglitazone
- TNF- alpha antagonist: infliximab, etanercept
- NDHP Calcium Channel Blockers: verapamil, diltiazem
- Newly Started Beta Blockers: titrate slowly
- NSAIDs/COX-2 Inhibitors: prostaglandin increases renin release, also causes fluid retention
- Glucocortocoids: sodium and water retention
- Sodium-containing medications: Zosyn, Timentin, Colace, antacids
- Itraconazole: cardiovascular toxicity
- Doxorubicin: cardiovscular toxcity
- Cilostazol: arrhythmias and death
CHF or LVEF <40%
|Stroke, TIA, thromboembolism||2|
|Age 65-74 years||1|
If score is:
- 0 – Don’t need ASA or oral anticoagulant (OAC)
- 1 – ASA
- 2+ – OAC
CHA₂DS₂-VASc Score for Atrial Fibrillation Stroke Risk (another way to remember)
- Congestive heart failure : + 1
- Hypertension: + 1
- Age >= 75: +2
- Diabetes: +1
- Stroke or thromboembolism: +2
- Vascular disease: +1
- Age 65-74: + 1
- Sex Category Female: +1
Is score is 1 – ASA only, if 2 use another agent as follows:
- DabigaTran (Pradaxa): 150 mg BID except in CrCl 30-50 or with dronedarone or ketoconazole, liver disease. Idarucizumab is a reversal agent. T – direct Thrombin inhibitor.
- RivaroXAban (Xarelto) – higher risk of bleeding, 20 mg daily, reduce in renal disease, Xa inhibitor
- ApiXAban (Eliquis) – 5 mg daily, reduce in renal disease. Xa inhibitor
- Warfarin – more effective than clopidogrel and ASA, but less effective than above and more monitoring.
Drugs for Afib (see antiarrhythmics for more info)
- Both the Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) and Rate Control vs. Electrical Cardioversion for Persistent Atrial Fibrillation (RACE) studies found no differences in survival between rate control and rhythm control in terms of mortality or morbidity.
- Rate control:
- esmolol, metoprolol, diltiazem, verapamil
- With accessory pathway: amiodarone only
- With heart failure: digoxin only
- Goal is resting rate of <90
- Pharmacological Conversion/Rhythm Control
- dofetilide, flecainide, ibutilide, propafenone, amiodarone can be used as pharmacological conversion in afib.
- flecainide, propafenone, and sotalol are recommended as first-line therapies in patients with lone AF
- hypertensive patients with left ventricular hypertrophy are at an increased risk of torsades de pointes, propafenone and flecainide are suitable choices in the absence of ischemia.
- in patients with cardiovascular disease without heart failure, sotalol is the first-line recommendation
- in patients with cardiovascular disease with heart failure, amiodarone is the preferred choice, with dofetilide as a reasonable second-line alternative.
Anticoagulation in afib
- For cardioversion:
- If stable afib: be therapeutic on warfarin for 3 weeks (which means at goal INR for 3 weeks) before and 4 weeks after cardioversion
- If unstable or they’ve been in afib less than 48 hours, convert and then continue for 4 weeks, INR 2-3 or initiate dabigatran, rivaroxaban or apixaban
- TEE Guided conversion > 48 h = LMWH or UFH at the time of TEE, perform and if no thrombus seen, 4 weeks afterward.
|Hypertensive Urgency SBP >=180 or DBP >=110 No target organ damage Can lower over several hours or days. May not even admit. Can use oral agents like captopril, clonidine, nifedipine or labetalol.||Hypertensive Emergency SBP >=180 or DBP >=110 Target organ damage (vision, neuro, kidneys, heart, etc) Avoid sudden or drastic decrease in BP Always admit. Decrease MAP 20-25% within the first hour. Use IV agents like sodium nitroprusside, nitroglycerin, hydralazine, enalaprilat, fenoldopam, nicardipine, clevidipine, esmolol or labetalol.|
- In aortic dissection, you must decrease blood pressure rapidly to 100-120, pulse 60-70.
- Use labetalol or esmolol alone or in combination with nicardipine, clevidipine or nitroprusside.
- Avoid hydralazine in aortic dissection.
- If giving a beta-blocker, give before the vasodilator because vasodilators can cause rebound tachycardia.
Blood pressure goals:
- Pre: < 140 and <90 (lifestyle modifications)
- Stage 1 HTN 140-159 or 90-99 (lifestyle and medications)
- Stage 2 HTN > 160 or >100 (lifestyle and 2 meds)
|JNC 8||When to start treatment||Goal|
|>=60 years old||>=150/90||<150/90|
|<60 years old||>=140/90||<140/90|
|>=18 years old + DM or CKD||>=140/90||<140/90|
*If urine albumin excretion >= 30 mg, some guidelines suggest 130/80*
|Patient Group||Initial Therapy|
|non-black +/- diabetes||thiazide, CCB or ACEI/ARB|
|black +/- diabetes||CCB or thiazide|
|>= 18 + CKD + HTN||ACEI or ARB|
|Stroke or TIA||ACEI or ARB|
|Coronary disease||Beta-blocker, ACEI or ARB|
|HFrEF||ACEI or ARB, Beta blocker, AA or diuretic|
|HFpEF||ACEI or ARB, beta blocker or diuretic|
Common Adverse Effects:
- Beta-blockers: caution in asthma or COPD. Greater risk of developing diabetes also can mask signs of hypoglycemia. A decrease in HR can cause reflex tachycardia.
- Thiazides: May worsen gout, not for patients with <30 CrCl, greater risk of developing diabetes. Decreases sodium and potassium, increases calcium.
- ACE or ARB: Do not use in pregnancy. Monitor K. Do not use in bilateral renal stenosis. Angioedema. Lisinopril can cause pancreatitis.
- icatibant: protein used for angioedema attack. Usually, use epi. Antihistamine or corticosteroids can also be used.
- Direct renin antagonist: Do not use in pregnancy, d0 not use in combo with ACEI in diabetes, avoid use with cyclosporin or itraconazole.
- Non-DHP CCBs (diltiazem or verapamil): no direct increase in HR, can have reflex tachycardia, decrease vasodilation, do not use in Wolfe-Parkinson White, can cause heart block.
- DHP CCBs: Decrease HR, decrease AV node conduction, decrease ionotropy, decrease vasodilation.
- Loop Diuretics: no effect on HR, decrease potassium
- Metolazone before a loop diuretic: quinazoline diuretics work by inhibiting sodium transport across the epithelium of the renal tubules (mostly in the distal tubules), resulting in a decrease in sodium reabsorption and an increase in sodium, chloride, and water excretion. Loop diuretics bind reversibly to a chloride channel receptor site in the ascending limb of the loop of Henle, inhibiting the reabsorption of filtered sodium and chloride. If you give metolazone 30 minutes before a loop diuretic, it ensures the distal Na-Cl channel is already blocked when the increased sodium reaches the distal convoluted tubule, making the loop work better.
- Clonidine: decreases heart rate, causes reflex tachycardia, alcohol withdrawal, decrease sex drive, sedation, dry mouth, orthostasis
- Methyldopa: anemia, Coombs
- Doxazosin: also used for BPH, orthostasis, especially with diuretics, non-DHPs or Beta-blockers
- Hydralazine: reflex tachycardia, vasodilation, causes lupus.
- Minodoxil: vasodilation
- Fendolopam: vasodilation (dopamine agonist), use only in HTN crisis.
- Nitropress: Decrease pre-load, majorly decrease afterload (vasodilation), cyanide
- Nitroglycerin: decrease preload, afterload (vasodilation) [more pre-load decrease, less afterload decrease than nitropress]
|B1 Selective Blockers||Non-Selective Blockers (B1 and B2)||Mixed Blockers (Beta and alpha)|
|Hydrophilic||acebutolol, atenolol, bisoprolol (both), esmolol||nadolol, pindolol, sotalol|
|Lipophilic||bisoprolol (both), metoprolol, nebivolol||propranolol||carvedilol, labetalol|
- Avoid mixed and non-selective agents in asthma. Alpha blockade causes vasodilation, decreases peripheral resistance, and causes no reflex tachycardia. (acronym: Can Let No Purple People Start)
- Lipophilic agents reduce remodeling and protect against sudden death.
- Patients sometimes feel worse when starting carvedilol. Start low and titrate up.
- Estrogen increases blood pressure
- Labetalol is preferred anti-hypertensive in pregnancy, followed by nifedipine and methyldopa.