Risk of developing hypertension: adults age 45 and up have a 40 year risk of developing hypertension:- African American – 92% - Hispanic – 92%- White – 86%- Chinese – 82%
- Prevalence 47% in U.S. adults, higher in African-Americans; M = F- Of those with HTN, ~40% unaware of dx; of those dx w/ HTN, only ½ achieve target BP
- Essential (95%): onset 25-55 y; ⊕ FHx. Unclear mechanism but ? additive microvasc renal injury over time w/ contribution of hyperactive sympathetics (NEM 2002:346.913). ↑ Age → ↓ art compliance → HTN. Genetics + environment involved (Nature 2011;478:103)- Secondary: Consider if Pt <20 or >50 y or if sudden onset, severe, refractory HTN
- Optimal: <120/80- Elevated: 120–129/<80- Stage 1: 130–139/80-89- Stage 2: >140/>90Average ≥2 measurements >1-2 minutes apart. If disparity in a category between systolic and diastolic, higher value determines stage. Elevated office BP should be confirmed with out-of-office (ABPM or home cuff) co confirm; can treat stage 2 immediately. White coat (Stage 1 in office but <at home) at heightened risk of developing HTN. Masked (<Stage 1 in office but ≥ at home), if persistent, treat as HTN.
First, check for white coat hypertension – seen 20–30% of the time; i.e. if bp is 130–150/80–90 use an ambulatory BP monitorThere are 3 options for monitoring BP as an outpatient:1 - Monitoring by patient. Not accurate, prone to "emotional HTN"2 - 6-hour test-device. Checks bp q 15 minutes. Not good for high stress patients3 - 24-hour test. Excellent for nocturnal bp and if large differences in results from office/home. NOTE: normally, bp decreases by about 10% at night. Called the "nocturnal dip."With 24-hour BP monitor, here are the key numbers to know. - Average 24 hr bp > 130/80- Nocturnal bp > 120/70- Daytime average bp >135/85If any of these three are present, this confirms your dx of HTN and you can initiate a treatment plan.
1 - Optimal bp – no Rx2 - Elevated – initiate lifestyle changes (see below)3 - Stage 1 – initiate mono therapy4 - Stage 2 - initiate therapy with 2 drugs
General Population: thiazides or CCB or ACE/ARBNOTE: The co-use of ACE/ARB's did not demonstrate any mortality/morbidity benefits; in fact, combination therapy was associated with an increase in hypotensive related syncope and Renal Dysfunction. African American: thiazides of CCB'sNOTE: With AA's with ACE see an increased incidence of cough and less BP lowering.Pregnancy: CCB or BBRecent MI or dx of CHF: BB>ACE>CCBSTABLE CADE: ACE, ARB, BB or CCBSpecial Groups1 - DMX – There is some evidence (though not universally accepted) that more intensive BP lowering to <120/80 may lead to decreased microvascular complications and decreased mortality — though this is not uniformly accepted.2 - Sleep Apnea – If CPAP properly applied, you can see approx. a 10mm decrease in systolic bp. NO NEED TO DX AND TREAT SLEEP APNEA! This is not just a pulmonary dx. Remember: not sleeping is like "walking up hill all day long" ... a patient can do it, but it takes it's toll, andone of the manifestations if hypertension.3 - Salt Sensitive Patients – These patients see a more striking decrease in bp with a low salt diet. Characteristics of these patients:- >45 years old- AA- Women- Metabolic SyndromeBe careful with this group. Remember these sources of salt: Processed Foods > Eating Out > Table Salt
- Decreased risk of CVS by 35-40%- Decreased risk of CHF by up to 50%- Decreased risk of MI by up to 25%
1 - Weight Loss: See approx. decrease in BP by 1mm/per kg of weight lost2 - DASH eating program: If pt will adhere to it -11mm3 - Low Salt Diet: See 2-8mm decrease if <2000 mg/day4 - Physical Activity: 4-10mm if 4+ sessions*/week*Session defined as movement of the body for ~40mins to the point of sweating and having a little difficulty conversing. Anything less is really not exercise.5 - Change to Moderate Etoh Us: No more than 1 drink per dat, 2-4mm decrease in bp.6 - Avoid NSAIDS: See approx. 5mm decrease
1 - Taking all comers: about 25% of patients get away with lifestyle changes or one drug2 -If BP > 20/10 from goal, likely will need 2 drugs3 - Beware of pseudo-resistant HTN, usually the result of improper BP measurement or the white coat effect. But 30% of the time it's a compliance issue. The chief compliance issues are xs salt intake, xs etoh, and inadequate use of diuretics.
Usually accounts for about 10% of cases. The patients are characterized by:- Drug Resistant- HTN in patient <30 years old- New onset of diastolic HTN in patient <65 - Unprovoked xs hypokalemiaCommon Causes of Sec HTN:Sleep Apnea: Accounts for 25-50% of these patient. Order a sleep study if their Epworth sleep score is >10 (an Epworth score of at least 10 usually indicates a positive study.Primary Hyper-aldosteronism: Accounts for 10-20%. Patients usually have normal serum k+ (only about 30% have low serum k+)- See high serum Aldosterone -> 15mg/dl- Aldos/Renin ratio >20- Usually due to bilateral adrenal hyperplasia- Responds to Aldactone, so before ordering screening test, hold Aldactone for 4 weeks (Don't need to hold ACE or ARB)Renal Artery Stenosis: Can account for up to 5-25% of cases. Dx with US, CTA or MRAThyroid DiseasePhaeochromocytomaXS Etoh
STEP ONE: Optimize the Diuretics - Make sure patient is on a diuretic- Thiazides > Thiazide-like > Loops- Thuazides – The best initial choice. This group has FOUR main players: HCTZ, Chlorthalidone (Note: Chlorthalidone is 2x as potent at HCTZ and is really the preferred thiazide diuretic), Metazalone, IndepamideIf the GFR<30, you will need a loop beacause you won't see a great response to thiazides, and the loops with the best bioavailability are either Bumex or Edecrine (NOTE: Oral Edecrine is really expensive, but it's the only loop that ok wit patients with sulpha sensitivity/allergy). STEP TWO: Optimize ACE/ARBThe combination of either an ACE or ARB with a CCB has greater effect than the individual drug alone. REMEMBER: Do not use ACE/ARB together. STEP THREE: Add Aldactone of EplerenoneUsually thought of as CHF drugs, but when added as third or fourth drug, can see up to 20/10 decrease in BP
- NSAIDS: Cox 2 inhibitors- Oral Contraceptives (estrogen predominant. Note: if you D/C, see BP return to normal up to 50% of time)- Sympathomimetics: diet pills, decongestants, cocaine- Stimulants: amphetamines- Etoh- Anti-depressants-CyclosporinNote on NSAIDS: - Work by inhibiting the COX 1 and 2 enzymes- Work by inhibiting prostaglandin synthesis at the kidneys- Can cause GI bleeding- Increase the risk of CHF exacerbations- Increase the risk of MI
- Goals: (1) identify CV risk factors; (2) consider 2° causes; (3) assess for target-organ damage- History: CAD, HF, TIA/CVA, PAD, DM, renal insufficiency, sleep apnea, preeclampsia; ⊕ FHx for HTN; diet, Na intake, smoking, alcohol, prescription and OTC meds, OCP- Physical exam: √ BP in both arms; funduscopic exam, BM, cardiac (LVH, murmurs), vascular (bruits, radial-femoral delay), abdominal (masses or bruits), neuro exam- Testing K, BUN, Cr, Ca, gl, Hat, U/A, lipids, TSH, urinary albumini creatinine (if ↑ Cr. DM peripheral edema), ? renin, ECG (for LVH), CXR, TTE (eval for valve abnl, LVH)- Ambulatory BP monitoring (ABPM): consider for episodic, masked, resistant, or white coat HTN; stronger predictor of mortality than clinic BP (NE/M 20183781509): 24 h target < 130/80
- Neurologic: TIA/CVA, ruptured aneurysms, vascular dementia- Retinopathy: stage | = arteriolar narrowing; Il = copper-wiring, AV nicking; III = hemorrhages and exudates; IV = papilledema- Cardiac: CAD, LVH, HF, AF- Vascular: aortic dissection, aortic aneurysm (HTN = key risk factor for aneurysms)- Renal: proteinuria, renal failure
Every ↓ 5 mmHg → ~10% ↓ ischemic heart disease, stroke, and HF (Lancet 2021.397.1625)Lifestyle modifications (each may ↓ SBP ~5 mmHg)- weight loss: goal BMI 18.5-24.9; aerobic exercise: 90-150 min exercise/wk - diet: rich in fruits & vegetables, low in saturated & total fat (DASH, NEM 20013413). - limit Na: ideally ≤1.5 g/d or ↓ 1 g/d; ↑ K intake / use salt substitute (NEM 2021.385.1067) - limit alcohol: ≤2 drinks/d in men: 51 drink/d in women & lighter-wt Pts avoid NSAIDS- ACC/AHA: initiate BP med if BP ≥ 130/80 & either clínical ASCVD, HF, CKD, T2DM, ≥65yrs old or 10-y ASCVD risk ≥ 10%; otherwise if BP ≥140/90- In high CV risk w/o DM, SBP target <120 (via unattended automated cuff) ↓ MACE & mortality vs. <140 mmHg, but w/ ↑ HoTN,AKI, syncope, electrolyte abnl (NEM 2021.384:1921 & 385:1268)Pharmacological Options:- Pre-HTN: ARB prevents onset of HTN, no ↓ in clinical events (NEM 2006:354:1685)- HTN: choice of therapy controversial, concomitant disease and stage may help guide Rx; ? improved control with nighttime administration (EHj 2020,41:4564)- Uncomplicated: CCB, ARB/ACEl, or thiazide (chlorthalidone preferred) are 1st line; βB not. For black Pts, reasonable to start with CCB or thiazide.+ CAD (Grc 2015:131.e435): ACEl or ARB; ACE+CCB superior to ACEl+thiazide (NEM 2008.359.2417 or βB+diuretic (Loncet 2005:366:895); may require BB and/or nitrates for anginal relief, if h/o MI, βB ± ACEI/ARB ± aldo antag (see "ACS")+ HF: ARNI/ACEI/ARB, βB, diuretics, aldosterone antagonist + prior stroke: ACEl ± thiazide (Lancet 2001;358:1033)+ diabetes mellitus: ACEl or ARB; can also consider thiazide or CCB + chronic kidney disease: ACEl or ARB (NEJM 2001,345:851 & 861)+ chronic kidney disease: ACEI or ARB- Tailoring therapy: if stage 1, start w/ monoRx; if stage 2, consider starting w/ combo (eg, ACEI + CCB; NEM 2006:359.2417); start at ½ max dose; after ~1 mo, uptitrate or add drug- Pregnancy: methyldopa, labetalol, & nifed pref. Hydral OK; avoid diuretics; ∅ ACEI/ARB. Targeting DBP 85 vs. 105 safe and ↓ severe HTN (NE/M 2015:372407).Resistant HTN (BP >goal on ≥3 drugs incl diuretic; HTN 2018,72e53)- Exclude: 2° causes (see table) and pseudoresistance: inaccurate measure (cuff size), diet noncomp (↑ Na), poor Rx compliance/dosing, white coat HTN (√ ABPM)- Ensure effective diuresis (chlorthalidone or indapamide >HCTZ; loop thiazide if eGFR <30)- Can add aldosterone antagonist (Lancet 2015:386.2059), B-blocker (particularly vasodilators such as carvedilol, labetalol, or nebivolol), o-blocker, or direct vasodilator- Consider renal denervation therapy (Lancet 2018:391:2346: 2021;397:2476)
Hypertensive emergency: ↑ BP (usually SBP > 180 or DBP > 120) → target-organ damage - Neurologic damage: encephalopathy, hemorrhagic or ischemic stroke, papilledema - Cardiac damage: ACS, HF/pulmonary edema, aortic dissection- Renal damage: proteinuria, hematuria, acute renal failure; scleroderma renal crisis - Microangiopathic hemolytic anemia; preeclampsia-eclampsiaHypertensive urgency: SBP >180 or DBP >120 (? 110) w/o target-organ damagePrecipitants- Progression of essential HTN ± medical noncompliance (espec clonidine) or ∆ in diet- Progression of renovascular disease; acute glomerulonephritis; scleroderma; preeclampsia- Endocrine: pheochromocytoma, Cushing's- Sympathomimetics: cocaine, amphetamines, MAO inhibitors + foods rich in tyramineTreatment - tailor to clinical condition (Circ 2018,138.e426)- AoD, eclampsia/severe preeclampsia, pheo: target SBP <140 (<120 for AoD) in 1 hour- Emerg w/o above: ↓ BP by ~25% in 1 h; to 160/100-110 over next 2-6 h, then nl over 1-2 d- Acute ischemic stroke (w/in 72 hr from sx onset): <185/110 before lysis initiated, o/w target <220/120 (same SBP goal for ICH)- Watch UOP, Cr, mental status: may indicate a lower BP is not tolerated
HTN urgency: goal to return to normal BP over hrs to days. Reinstitute/intensify anti-HTN Rx. Additional PO options: labetalol 200-800 mg q8h, captopril 12.5-100 mg q8h, hydralazine 10-75 mg q6h, clonidine 0.2 mg load → 0.1 mg q1h.
1 - Paroxysmal: A fib that terminates with or without Rx in <7 days2 - Persistent: >7 days in duration3 - Long Standing: >12 months4 - Permanent: When the clinical decision has been made to no longer pursue restoration of NSR5 - Valvular: Secondary to mitral valve dz (has implications for anti-coagulation)NOTE: The need for anti-coagulation is not affected by either rate/rhythm strategy only by the CHADSVASC-2 score, and to some degree by the HAS-BLED score.CHADSVASC-2 SCORE- CHF: 1 point- HTN: 1 point- >75: 2 points- 65-74: 1 point- DMX: 1 point- Hx of CVA or thromboembolism: 2 points- Vasc dz: 1 point- Female sex: 1 pointResults:- 0-1: Low Risk- 1: Intermediate Risk- >2: High RiskHAS-BLED SCORE- HTN (systolic BP >160): 1 point- Abnl LFTS: 1 point- Abnormal renal function: 1 point- Hx Cva: 1 point- Hx of bleeding issues (ill defined): 1 point- Labile INR: 1 Point- >65: 1 point- Drugs which enhance bleeding ( ie ETOH): 1 pointIf score 3 or higher, this is considered an increased risk for bleeding. NOTE:HAS-BLED only has modest predictability as compared with CHADS2VASC, but it provides some guidance.
- There is no mortality difference- There is no difference in risk for CV- See decreased hospitalizations with a rate control strategy.Putting it together, which should you choose? Consider a Rhythm control strategy in the following groups of patients:1 - Patients with symptomatic A Fib.2 - Younger patients3 - First episode of A Fib4 - Tachycardia induced cardiomyopathy.5 - Patient preference
3 broad groups for acute rate control:1 - Patients whom are H/D Stable-PO drugs as an outpatient2 - Rapid Ventricular Response and H/D unstable-Cardioversion3 - Rapid Ventricular Response, but H/D stable. Here there are 2 subgroups:1) If no pre-excitation-use IV BB or IV Calcium channel blocker (you can use IV Amio, but Amio less likely to convert to NSR-but it will slow the HR down via its AV nodal blocking ability).2) If there is pre-excitation used IV procainamide.
1 - CCB or BB2 - PO Amio3 - A-V node ablation4 - Digoxin: Not really a first line agent, as it does not control HR in Exercise (it works via the parasympathetic nervous system, and during exercise you see a sympathetic surge).Some Key Issues When Deciding on Chronic Rate Control Drugs:1 - With HEFREF patient's, try not to use CCB-n the EF is already low and these could further depress it.2 - With pre-excitation patients-don't use BB, Dig or CCB-these will increase conduction down the accessory pathway and can lead to V Fib3 - Don't consider AV node ablation, unless there has been a reasonable trial of pharm control (unless really strong patient preference).Rx Options for Pharmacological Conversion to NSE — when you are trying for Rhythm Control1 - IV Flecanide or Propafenone - administered in hospital- Give BB or CCB 30 mins prior to first dose- May cause transient hypotension or Bradycardia/conversion to 1:1 flutter- Contraindicated in patients with structural Heart disease2 - IV Ibutalide – also in hospital- Can cause Torsades, but usually within first couple of hours- Contraindicated if prolonged QT interval; low Mg or K+- Usually give 1 gram IVR or MG prior- Monitor for at lease 4 hours on tele.3 - PO Amio or PO Dofetalide (Tikosyn)- Both can cause torsades- Start Dofetalide in hospital
Here are some basic characteristics of the most commonly used NOACS:Dabig:Target – thrombin1/2 Life – 12-17.Elim. – RDose – 150 bidRivoxTarget – Xa. 1/2 Life – 7-11.Elim. – R/HDose – 20 qamApix. Target – Xa. 1/2 Life – 7-11.Elim. – R/H/EDose – 5 bid*EdoxTarget – Xa.1/2 Life – 10-14Elim. – R/H/EDose – 60 qam***But if <60kg >80 years old or cr>1.5, change to2.5 bid**If <60kg or takeing Verap, Quinidine, or Multaq, decrease dose to 30 qamBleeding risk: Dabig > Rivox > Apix> edoxNon renal elimination: Best is Elliquis, so safest in Renal dz patients. Note: R=Renal H=hepatic E=entericPOSITIVES OF NOACS- Predictable pharm profile- No monitoring, ie no INRs- Possibly decreased ICH rates- Minimal food/drug interaction, but see increased levels. I.e. increased bleeding if patient on Amio, Verapamil, Quinidine, Anti-fungals, macrolide ABX, or HIV protease inhibitors.NEGATIVES OF NOACS- Need to adjust dose per renal status and wt- Cost (much more expensive than coumadin).
1 - It's pretty safe in patients with renal dz-its metabolized via the liver via the cytochrome p450 system,but there have been recent studies which indicate that patients with severe renal impairment may require a lower dose of coumadin to achieve a therapeutic INR-so be cautious.2 - If you have to reverse coumadin ie there is a high INR -here are a few tips:- IV vit k works faster than oral-no matter what some people say!- Sub q has variable absorption especially in the elderly with decreased muscle mass.- IV works in about 1-2 hours-full effect in about 24 hrs; PO in about 6.3 - Patients treated with vitamin k can become resistant to warfarin for up to one week4 - Coumadin and ETOH: acute Etoh consumption (binge drinking) will decrease the metabolism of Coumadin and therefore lead to more intense anticoagulation with an increased INR.5 - Chronic Etoh abuse leads to an increase in the hepatic metabolism of Coumadin, less intense anticoagulation.
If moderate bleeding, it's difficult but here are a few key points:- If patient is on Dabig, they need H/D- If severe bleeding and on any of the other NOACS, transfuse prothrombin complex concentrate-it contains factors 2,9 and 10.
1 - Valvular A-fib: I.e. any patient with mitral valve dz and a fib-they get Coumadin, not NOACS (NOACS are usually for non valvular a fib)2 - HCM patients (really not that rare-1/500 incidence in USA): -they get Coumadin or NOAC.3 - Non valvular A fib: With these patients it depends on the CHADS2VASC score. Here is how it breaks down: they can recieve either a NOAC or Coumadin (patient preference). - Score 0: no anti-coagulation (almost never see a zero score in our patient population)- Score 1: It's controversial. Either none, ASA or NOAC-current clinical Trials will tell us which is superior.- Score 2 or >2: Coumadin or NOAC
- 1-2% of pop. has AF (10% of those age ≥80); M > F; lifetime risk ~25%; mean age 75 y- Acute (up to 50% w/o identifiable cause)Cardiac: HF, new CMP, myo/pericarditis, ischemia/MI, HTN crisis, valve dis., cardiac surg Pulmonary: acute pulmonary disease or hypoxemia (eg, COPD fare, PNA), PE, OSA Metabolic: high catecholamine states (stress, infection, postop, pheo), thyrotoxicosisDrugs: alcohol, cocaine, amphetamines, smoking, ibrutinib Neurogenic: subarachnoid hemorrhage, ischemic stroke- Chronic: ↑ age, HTN, ischemia, valve dis. (MV, TV, AoV), CMP, hyperthyroidism, obesity- Aggressive mgmt of HTN, OSA & EtOH (NE/M 2020;382:20) to ↓ risk
- H&P, ECG, CXR, TTE (LA size, thrombus, valves, LV fxn, pericardium), K, Mg, Cr, TFTs- In acute AF <48°, ~70% spont. convert to SR w/in 48 hrs (NEIM 2019;380:1499)
- Consider if: 1st AF, sx, tachycardia-mediated CMP, or difficult to rate controlIf AF >48 h 2-5% risk stroke w/ cardioversion (pharmacologic or electric) ∴ either TEE to r/o thrombus or ensure therapeutic anticoagulation ≥3 wk priorIf needs to cardiovert urgently, often anticoagulate acutely (eg, IV UFH)- For AF <36 hrs, no ∆ in % in SR at 4 wks w/ early cardioversion vs. wait & see (βb + a/c), with spont cardioversion in 69% and cardioversion required in 28% (NE 2019:380:1499)- Likelihood of success ∝ AF duration & atrial size; control precipitants (eg, vol status, thyroid)- Before electrical cardiovert, consider pre-Rx w/ AAD (eg, ibutilide), esp. if 1st cardiovert failed- For pharmacologic cardioversion, class Ill and IC drugs have best proven efficacy- If SR returns (spont. or w/ Rx), atria may be mech. stunned; also, high risk of recurrent AF over next 3 mo. ∴ Anticoag postcardioversion ≥4 wk (? unless AF <48 h and low risk).
- Consider if sx w/ rate control (eg, HF), difficult to control rate, or tachycardia-mediated CMP- If minimally sx or asx, previously no clear benefit vs. rate control - For recent AF (~1 mo), rhythm-control w/ AAD (fecainide, amio) & cardioversion (if persist AF) superior to usual care for achieving SR and ↓ adverse CV events
- Controlling triggers in pulm veins effective when little atrial fibrosis; as AF persists, substrate more complex- Pulm vein isolation (radiofreq or cryo; NE/M 2016;374:2235): ~70% success; superior to AAD (AMA 2014;311:692:NEM 2021;384305 & 316) & ↑ QoL (JAMA 2019:321:1059)- If NYHA II-IV + EF <35%, ablation ↓ D/HF hosp vs. rate/rhythm meds (NEM 2018378417)- AV node ablation + PPM if other Rx inadequate (NEIM 2001:344:1043 & 2002;346:2062)
- All valvular AF because stroke risk very high- Nonvalvular AF (NVAF): stroke risk ~4.5%ly but varies; a/c → 68% ↓ stroke but ↑ bleeding- CHA2DS2-VASc to guide Rx: CHF (1 point); HTN (1); Age ≥75 y (2); DM (1), Stroke/TIA (2); Vascular disease (eg, MI, PAD, Ao plaque) (1): Age 65-74 (1); ♀ Sex category (1 )Annual risk of stroke (Lancet 2012;379:648): at low end, ~1% per point: 0 → ~0%, 1 → 1.3%, 2 → 2.2%, 3 → 3.2%, 4 → 4.0%; at higher scores, risk ↑↑ (5 → 6.7%, ≥6 → ≥10%)- Score ≥2 in ♂ or ≥3 in ♀ → anticoagulate; scores 1 in ♂ or 2 in ♀ → consider anticoag or ASA or no Rx; score 0 → reasonable to not Rx- Rx options: DOAC (NVAF only) prefered over warfarin (INR 2-3); if Pt refuses anticoag. ASA + clopi or, even less effective, ASA alone (NEM 2009360.2066)- AF + CAD/ PCl: consider DOAC + clopi (not ticag or prasugrel) + ASA (d/c ~1-4 wks) (Cr 2021;143583); consider DOAC only after 12 mos (ACC 2021:77629)- If concern for procedural bleed, interrupt OAC (1-2 d DOAC, 45 dVKA). If CHA2DS2-VASc ≥ 7 (or ≥5 w/h/o CVA/TIA), consider bridge w/ UFH/LMWH, otherwise do not (ACC 201769735).
- If contraindic. to long-term OAC, consider perc. left atrial appendage (LAA) occlusion (ACC 2022:79:1). Nb, ideally warfarin + ASA x 45 d → DAPT out to 6 mo → ÁSA.- Consider surgical LAA occlusion if undergoing cardiac surgery (NE/M 2021;384.2051)
- Macroreentrant atrial loop. Typical involves cavotricuspid isthmus (if counterclockwise, flutter waves ⊖ in inf leads, if clockwise, ⊕). Atypical: other pathways related to prior scar:- Risk of stroke similar to that of AF, ∴ anticoagulate same as would for AF- Ablation of typical (cavotricuspid isthmus) AFL has 95% success rate
{Insert hemolytic anemia & properties and antidotes}
This refers to giving short acting blood thinners (usually LMWH sq) in the perioperative period when Coumadin therapy is interrupted and its anti-coagulation effects are sub therapeutic.In general patients with mechanical heart valves, A fib or DVT/PE are considered for bridging therapy.
Many Cardiologists have different approaches, but here is ours:First, check the CHADS2VASC Score.- If it's <4 and there has been no prior CVA/TIA, no need for bridging heparin- If >7, or recent TIA/CVA, you need bridging- If 5-6, or hx of remote TIA/CVA, then you need to asses the bleeding riskHere are some factors associated with a high risk of bleeding:- major bleed in the past 3/12 - hx of ICH- hx of plt abnormality- ASA use- hx of prior bleeding with bridgingLimit bridging to where the thrombotic risk > bleeding risk. This applies to bridging on both ends (i.e. pre and post op)
In general, as soon as hemostasis is achieved. - Coumadin: Same day of surgery- LMWH: 24-48 hours post op (ask the surgeon)- NOACS: 24-48 hours post op (ask the surgeon)
- Afib (irregular rhythm, no clear P waves)- Bradycardia (< 50 bpm), Tachycardia (> 110 bpm)- PVCs, pauses, or new arrhythmias- New symptoms (Palpitations, lightheadedness/dizziness)
- Ensure patient wearing device- Ensure device is charged and leads are attached
- ECG-gated, noncontrast CT- Used to estimate presence & amount of calcified coronary plaque- CAC, measured via Agatston score, provides useful surrogate of overall amount of plaque (but not % stenosis)- Advantages: simple, reproducible, low cost, predicts risk better than many traditional risk factors- Limitations: does not change w/ Rx, may slightly increase w/ statins, no large RCTs available evaluating hard outcomes, not useful in young Pts (avoid if <40 yrs, except for selected cases)
- Improved risk assessment among as Pts, if information will enhance preventive care- In intermediate-risk or selected borderline-risk adults (ie, 10-yr ASCVD risk of 5-20%), if decision about statin use remains uncertain, reasonable to use CAC score to withhold postpone, or initiate statin therapy- May be useful in selected low-risk sx Pts: CAC=0 → low risk; CAC >0 → further testing may be useful; also may be added w/ SPECT or PET MPI
- Higher plaque burden → higher risk of future ASCVD events- CAC=O can "derisk" (ie, reclassify to lower risk). When 10-yr risk of ASCVD <20% this can be used among individuals who prefer to avoid/defer statin Rx.- If severe or extreme CAC, stress testing (ETT or PET) may be considered; invasive coronary angiography never appropriate next step
- Clinical syndrome caused by functional and/or structural deficiencies in the heart leading to reduced ejection of blood and/or impaired ventricular filling- Symptoms of heart failure (HF) often due either to elevated intracardiac filling pressures and/or to inadequate forward flow to meet metabolic demands of peripheral tissues- Formal classification based on LVEF (J Cardiac Fail 2021;27:387; Circ 2022;145:895)HFrEF (reduced): ≤ 40%HFmrRF (mildly reduced): 41-49%, typically w/ spont. or provokable ↑ filling pressures HFpEF (preserved): ≥50%, typically w/ spont. or provokable ↑ filling pressures HFimpEF (improved): baseline ≤40%, follow-up >40% w/ 10% ↑ from baseline- Informal classifications based on clinical assessments:Systolic (inability to expel sufficient blood) vs. diastolic (failure to relax and fill normally) dysfunction; in most cases both are presentLeft-sided (pulmonary edema) vs. right-sided (↑ JVP, hepatomegaly, peripheral edema)Low output ( CO [eg, secondary to Ml or DCM]; more common) vs. high output (↑ stroke volume ↑CO [eg, thyrotoxicosis or AVF fistula]; less common)
- HF is a clinical syndrome diagnosed based on the presence of typical clinical symptoms and physical exam signs- Diagnosis may be enhanced by supportive laboratory data (commonly natriuretic peptides) and cardiac imaging (often echocardiography or cardiac MRI)
- Symptoms of elevated filling pressure: dyspnea, orthopnea (or recumbent cough), paroxysmal nocturnal dyspnea, rapid weight gain, peripheral edema, increasing abdominal girth, bloating- Symptoms of poor perfusion: fatigue, exercise intolerance, anorexia/early satiety, oliguria, altered mental status (in severe cases)- Risk factors or etiologic clues:Structural heart disease: known congenital, valvular, or myocardial diseaseAtherosclerosis risk factors (smoking, DM, HTN, hyperlipidemia) or known coronary heart diseaseRisk factors for diastolic dysfunction (HTN, DM, obesity)Family history (perform 3-generation) for HF, CAD, or sudden cardiac death Substance use disorder: alcohol, cocaine, methamphetamineAntecedent viral syndrome or unusual physical/emotional stress Drug or environmental exposures: cardiotoxic chemotherapy (eg, anthracyclines), immunomodulatory therapy (eg, immune checkpoint inhibitors)Sx of underlying systemic illness or connective tissue disease such as amyloidosis, sarcoidosis, SLE, rheumatoid arthritis, scleroderma, hypothyroidism
- Congestion ("dry" vs. "wet"; wet defined as PCP >15 mmHg and/or RA >8 mmHg)↑ JVP, ⊕ hepatojugular reflux, S3 gallop (in Pts w/ HF → ~40% ↑ risk of HF hosp. or pump failure death; NEJM 2001;345:574)Rales, dullness at lung base w/ egophony (pleural effusion)- Perfusion ("warm" vs. "cold"; cold defined as cardiac index <2.2 L/min/m2):Narrow pulse pressure (<25% of SBP) → CI <2.2 (91% Sens, 83% Spec)Other signs of low perfusion:- tachycardia, cool & pale extremities (forearms & legs), ↓ UOP- soft S1 (↓ dP/dt), pulsus alternans (pathognomonic of severe LV systolic dysfunction), altered mental status, muscle atrophy, cachexia (unintentional ≥5% wt loss in 6 mos)Other signs to look for:- laterally displaced apical impulse (LV enlargement)- murmur (could be primary valvular disease vs. functional MR/TR)- parasternal lift (RV dysfunction)- periodic breathing/Cheyne-Stokes respiration
- CXR: pulmonary edema, pleural effusions, cardiomegaly, cephalization, Kerley B-lines (frequently nondiagnostic in acute on chronic HF due to lymphatic adaptation)- Natriuretic peptides (BNP or NT-proBNP) help HF dx and are important for prognosis Levels higher in women, ↑ age, renal dysfunction, AF; lower in obesity; ↑ BNP (but not NT-proBNP) in Pts on newly initiated ARNI due to neprilysin inhibitionBNP diagnostic accuracy in ED Pts p/w SOB (NEJM 2002;347:161)≥50 pg/ml: NPV >95%, PPV ~70%, Sens >95%, Spec ~62% ≥150 pg/ml: NPV ~85%, PPV ~83%, Sens ~85%, Spec ~83%NT-proBNP diagnostic accuracy in ED Pts p/w SOB (JC 2005.95:948)≥450 pg/ml: NPV ~99%, PPV ~68%, Sens ~98%, Spec ~76% ≥1000 pg/ml: NPV ~91%, PV ~78%, Sens ~87%, Spec ~86%- Cardiac troponin (hsTnT and hsTl) is commonly elevated in Pts w/ worsening HF; even small elevations may be prognostically important but may not indicate myocardial ischemia/infarction (Circ 2018;137:286; Circ HF 2018;11:e005312)- Evidence of ↓ end-organ perfusion: ↑ Cr, ↓ Na, abnormal LFTs, ↑ lactic acid- Other testing may be appropriate for etiologic assessment in the right context (eg, iron studies, TSH, serum & urine electrophoresis w/ immunofixation, catecholamine levels)- Echocardiography 1 EF & ↑ chamber size (LV, RV, or both) → systolic dysfunctionhypertrophy, abnormal MV inflow & tissue Doppler LVH → ? diastolic dysfunction abnormal valves (suggestive of primary valvular disease) or pericardium ventricular wall thinning (Ml or DCM) or thickening (HCM or infiltrative)↑ estimated RVSP, which may be due to ↑ L-sided pressures and/or pulm. arterial HTN dilated IVC with diminished respirophasic variation (↑ RA pressure)- Right heart catheterization↑ PCWP(almost always seen unless already aggressively diuresed)↑ PASP expected in proportion to ↑ PCWP (ie, postcapillary pulmonary hypertension); if TPG (mean PAP - mean PCWP) >12, consider precapillary pulmonary hypertension (ie, pulmonary arterial hypertension)↓ CO and ↑ SVR (in low-output failure)↑ RA:PCWP ratio (>1:2) or diminished pulmonary artery pulsatility index (PAPi = [PA systolic - PA diastolic] / RA) <2.0 raises concern for RV dysfunction- Algorithmic approach to left-sided heart failure: hemodynamic and structural parameters can help distinguish etiology of left-sided heart failure including LV end-diastolic pressure (LVEDP), presence of LVH, end-systolic volume (ESV), and stroke volume (SV)
- A: At high risk for HF, but w/o structural heart disease or symptoms of HF- B: Structural heart disease, but w/o signs or symptoms of HF- C: Structural heart disease w/ prior or current symptoms of HF- D: Refractory heart failure requiring specialized intervention
- Class I: no sx w/ ordinary activity- Class Il: sx w/ ordinary activity- Class III: sx w/ minimal activity- Class IV: sx at rest
ECG (in all cases)- Q waves or poor R wave progression: ischemic heart disease, DCM - LVH: hypertensive heart disease or HCM - low limb lead voltage: NICM or infiltrative - heart block: infiltrative- atrial arrhythmias: tachycardia-induced cardiomyopathy - ventricular arrhythmias: ischemic CMP, arrhythmogenic CMP, sarcoidTTE (in all cases)- LV & RV size & function (EF)- valvular disease (and whether either 1° or 2° ["functional"] due to atrial/ventricular dilation) any findings indicative of infiltrative disease (eg, severe diastolic filling abnormalities) any findings indicative of pericardial disease (qv; pericardial effusion, septal bounce)Coronary angiography (invasive or noninvasive): should be considered in all adult Pts w/CAD risk factors or anginal sxCardiac MRI (in select cases) w/ multiparameter eval of cardiac structure & fxn including:- LVEF, RVEF, and volumes- Regional wall motion abnormalitiesPresence, pattern, & extent of late gadolinium enhancement (LGE) such as:- Subendocardial or transmural infarct: CAD- Mid-wall LGE: idiopathic DCM, HCM, myocarditis, sarcoidosis, Chagas Epicardial LGE: sarcoidosis, myocarditis, Anderson-Fabry, Chagas- Global endocardial LGE: amyloidosis, systemic sclerosis, s/p heart transplant Myocardial inflammation or infiltration: myocarditis, sarcoidosis, amyloidosis- Restrictive cardiomyopathy vs. constrictive pericardial diseaseSe/Sp of 100%/96% vs. coronary angiography for dx etiology of HF (Circ 2011;124:1351)Additional imaging (occasionally)- Tc-99m-PYP scanning (TTR amyloidosis)- 18-FDG-PET (sarcoidosis)Genetic testing if concern for familial HCM/DCMEndomyocardial biopsy: principally when myocarditis or infiltrative disease suspected based on clinical presentation or imaging; complications rare (RV perforation/tamponade, arrhythmia, PA rupture)
