Aortic insufficiency; Non-pharmaceutical and pharmaceutical treatment of HTN Flashcards
General approach to HTN treatment and management
- Lifestyle changes for management of ALL HTN patients
- Identify indications for pharmacological treatment
- Select first line treatments based on individual patient characteristics and comorbidities
- Titrate treatment to reach target BP [Target BP for 65 and younger < 130/80 mmHg; Target BP for 65 and older < 140/90 mmHg]. Always ensure individual approach over general approach
- Regular follow-ups to ensure adherance to regime, changes/resistance in BP control or development of unwanted side effects
Non-pharmacological treatments of HTN [which type of patients, methods]
Eligible patients:
- ALL patients with HTN, especially those with Elevated or Stage 1 HTN [ < 150mmHg and < 90mmHg] with < 10% 10 year ASCVD risk
- Trialed for 3-6 months before considering drug based management
- Changes in lifestyle in addition to pharmacological therapy shows the most potent effects
Management plans: Weight loss most effective measure
DIET
- DASH diet [rich in fruits, vegetables, whole grains; avoids trans and saturated fats]: Potential to reduce upto 11 mmHg SBP
- Decrease dietary Sodium [< 1500mg daily intake]: Potential to reduce upto 5-6 mmHg SBP
- Increase dietary Potassium [by increasing fruit and vegetable intake]
- Decrease alcohol intake
EXERCISE
- Aerobic [90-150 min/week]: Potential to reduce upto 5-8 mmHg SBP
- Dynamic resistance/weight training
- Isometric resistance
Smoking cessation alone significantly reduces CVD risk in the future
Psychosocial factors or other social determinants of health must be addressed along with lifestyle changes to ensure adherence and effectiveness
Increased Potassium intake NOT RECOMMENDED for CKD patients
Indications for Antihypertensive Treatment
Controversial and vary according to age
ALL adults with SBP > 140mmHg OR DBP > 90 mmHg
Adults with SBP >130 mmHg or DBP > 80mmHg AND one of the following:
- Clinical ASCVD [IHD, PAD, previous stroke] or CHF
- 10-year ASCVD risk > 10% [for ages 65 and older including DM]
Based on 2017 ACC/AHA guidelines
How to consider initial medication for HTN
Patients Initial BP:
- SBP 130-139mmHg or DBP 80-89mmHg: Consider monotherapy with first-line drugs
- SBP > 140mmHg or DBP > 90mmHg AND average blood pressure > 20/10mmHg above target: Consider combination therapy of first-line drugs [prescribe single, combination pills when possible to ensure greater patient adherence]
Additional Factors:
- Consider major comorbidities and include Second-line and changes in drug choice based on response
- Adverse effects not tolerable to patients, change drug choice
- Always revisit treatment plan and individualize approach to treatment
First-line anti-hypertensive drug of choice
ACE inhibitors: [-pril class drugs] Nephroprotective
- Lisinopril
- Enalapril
- Captopril
Angiotensin Receptor Blockers [ARBS]: [-artan class drugs] Nephroprotective
- Losartan
- Valsartan
Thiazide DIuretics: [isolated Systolic HTN; Black american patients initial choice]
- Chlorthalidone
- Hydrochlorothiazide
Dihydropyridine CCB: [can be combined with all other first line choices; indications same as thiazide diuretics]
- Amlodipine
- Nifedipine
Non-dihydropyridine CCB: [less commonly used]
- Diltiazem
- Verapamil
First line drugs for Primary HTN are Thiazide Diuretics, ACEIs, ARBs and dihydropyridine CCBs
Commonly used combination therapy drugs for HTN
ACEIs/ARBs + dihydropyridine CCBs/Thiazide diuretics
DO NOT prescribe ACEIs and ARBs together or in combination with Direct Renin Inhibitors, as this increases risk of Hyperkalemia and Renal dysfuntion
Common comorbidities with HTN
- History of stroke/TIA
- Stable Ischemic Heart Disease
- CKD
- Diabetes
- CHF
- Asthma
- Osteoporosis
- Gout
- Migraine
In Osteoporosis: Thiazide diuretics [helps prevent calcium loss]
In Gout: Thiazide diuretics avoided [increases uric acid levels]; ARBs, ACEIs and CCBs used
In Migraine: Beta blockers/CCBs used
Treatment options for HTN + History of stroke/TIA
- Monotherapy: ACEIs/ARBs/Thiazide diuretic
- Comb therapy: Thiazide + ACEIs/ARBs
- Goal: BP < 130/80 mmHg in most patients
Treatment options for HTN + Stable IHD
- Initial: ACEIs/ARBs + Beta blockers
- Add on for angina patients: dihydropyridine CCBs
- Add on for non-angina patients: dihydropyridine CCBs/Thiazides/Aldosterone antagonists
- Goal: BP < 130/80 mmHg
Treatment options for HTN + CKD
- Initial patients with microalbuminemia + diabetes/over proteinuria: ACEIs/ARBs
- Initial patients with microalbuminemia without diabetes: ACEIs/ARBs
- Combination: ACEIs/ARBs + CCBs +/- Thiazide diuretic
- Goal: SBP < 120mmHg [if tolerated]
CKD recommendation based on 2021 KDIGO CKD guidelines
Treatment options for HTN + Diabetes
- Initial patients with microalbuminemia or overt proteinuria: ACEIs/ARBs [protective against diabetic nephropathy]
- Inital patients without microalbuminemia: any first line agent
- Goal: BP < 130/80 mmHg
Treatment options for HTN + CHF
HFrEF:
- Beta blockers [carvediol/metoprolol succinate/bisprolol] use catiously in decompensated CHF, contraindication in cardiogenic shock
- Diuretics [including aldosterone antagonists[
- ACEIs/ARBs
- Angiotensin receptor-neprilysin inhibitor
- Goal: BP < 130/80 mmHg
HFpEF:
- Diuretics for current volume overload
- ACEIs/ARBs + Beta blockers for no current volume overload
- Avoid nitrates
- Goal: SBP < 130 mmHg
DO NOT use dihydropyridine CCBs in HFrRF for myocardial depressing eff
Common Second-line antihypertensive drug choices
Beta Blockers [first line only in IHD, HF, AFib, Thoracic aorta disease, Thyrotoxicosis, Migraine, Essential tremor comorbid patients]
Combined alpha and beta:
- Carvediol
- Labetalol
Noncardioselective:
- Nadolol
- Propranolol
Cardioselective:
- Atenolol
- Bisoprolol
- Metoprolol succinate
Loop Diuretics: [preferred diuretic in patients with symptomatic HF and CKD, if GFR < 30mL/min]
- Furosemide
- Torsemide
Potassium-sparing Diuretics
Aldosterone Antagonists: [in HTN due to primary hyperaldosteronism]
- Spironolactone
- Eplerenone
- Finerenone [nonsteroidal]
Epithelial Sodium Channel Blockers [not very effective; consider add on for hypokalemia receiving thiazide diuretics]
- Amiloride
- Triamterene
Direct Renin Inhibitors: [rarely used]
- Aliskiren
Alpha-1 Blockers: [Pheochromocytoma induced HTN; adjunct in BPH patients]
- Prazosin
- Doxazosin
Alpha-2 Agonists: [rarely used]
- Clonidine
- Methyldopa
Direct Arterolar Vasodilators:
- Hydralazine [drug of choice in pregnant patients]
- Minoxidil [given with loop diuretics]
What is Aortic Insufficiency?
Aortic Insufficiency aka Aortic Regurgitation is a condition where the Aortic valves do not close completely at the end of systole, allowing blood to flow back into the Left Ventricle [aka regurgitation] causing changes in the heart ex. LV hypertrophy [to match SV from high end-diastolic volume in LV], Congestion in left side of heart and pulmonary circulation, LHF, etc
AR is basically precursor to Heart Failure
Etiologies of Aortic Insufficiency
Divided into Acute and Chronic causes
Acute:
- Infective Endocarditis [most common valvular cause]
- Aortic Dissection [most common non-valvular cause]
- Chest Trauma
- Iatrogenic [post TAVR or percutaneous ballon dilation of aorta]
Chronic:
Primary Valvular causes
- Congeital Bicuspid Aortic Valve
- Calcified Aortic valves [~ 76% of AS patients also have AR]
- Rheumatic Heart disease [more common in lower-income countries]
Aortic dilatation causes
- Connective Tissue disorders [Marfan syndrome, Ehlers-Danlos syndrome]
- Chronic HTN
- Aortic aneurysm
- Aortitis of any etiology [especially tertiary syphilis]
Aortic Dilatation causing AR does not always or necessarily involve the Aortic Valves themselves in the pathophysiology, however they do lead to AR at some point in some patients
General, Acute and Chronic mechanisms
Basic Pathophysiology of Aortic Regurgitation
General:
- Regurgitation decreases Diastolic Pressure, subsequent beat pushes more blood than normal SV causing increased Systolic Pressure
- Widened pulse pressure [Higher Sys and Lower Dys] manifests as Corrigan’s sign [carotid artery] and Water hammer pulse [peripheral limb arteries]
Acute AR:
- Acute presentation of AR, heart cannot compensate for excess blood end of diastole in LV, backflow and congestion of blood all the way into pulmonary circulation = Pulmonary edema and Dyspnea
- Decreased cardiac output in severe cases = Cardiogenic shock and MI
Chronic AR:
- Longer duration allowing heart to compensate increased EDLV volume, heart increases CO by increasing SV [compensated HF]
- Overtime chronically increased EDLV forces remodelling of LV [eccentric hypertrophy] and decreased contractility = Systolic dysfunction of LV [decompensated HF]
Corrigan’s sign and Water hammer pulse is where on palpation we feel rapid upstroke of pulse and prompt collapse of vessel
Signs and Symptoms, Auscultation
Acute AR Clinical features
Signs and Symptoms:
- Dysnpea
- Pulmonary Edema
- Underlying causative agent symptoms [Chest pain in aortic dissection, Fever in Infective endocarditis]
Auscultation:
- Soft S1 [early closing of Mitral valve due to increased EDLVP]
- Soft and short early diastolic murmur
Signs and Symptoms, Auscultation
Chronic AR Clinical features
Signs and Symptoms:
- Can be asymptomatic for decades
- Palpitations
- Corrigan’s sign
- Water Hammer pulse
- Quincke sign [visible capillary pulse when presuure is applied to the tip of a fingernail]
- De Musset sign [rhythmic nodding or bobbing of head in synchrony with heartbeats]
- Traube sign [pistol shot like sound heart over femoral artery on auscultation]
- Exertional Dyspnea
- Angina [coronary artery shift to systolic filling, reduced reserve blood; reduced diastolic perfusion pressure with bradycardia esp at night]
- Syncope
- Orthopnea
- Early fatigability
- Point of maximal impulse moves more inferolaterally than normal [increased heart size]
Auscultation:
- S3 [volume overload sign]
- High pitched, blowing decrescendo early diastolic murmur [S2 becomes indistinguishable sometimes; heard best on left sternal borders for valve based and right sternal borders for aorta based AR; worsens with squatting or handgrip due to increased afterload]
- Austin Flint murmur
- Severe cases murmur resembles AS [Crescendo-decrescendo midsystolic murmur]
Austin Flint Murmur - Rumbling, low pitched middiastolic or presystolic murmur heard best at apex. Regurgitant blood stikes anterior leaflet of mitral valve which leads to premature closing of the mitral leaflets
Tools we can use to diagnose AR
- Echocardiography [TTE, TEE]
- CMR
- CTA
- Catheterization [Diagnostic hemodynamic cardiac catheterization with aortography, Coronary angiography]
- CXR
- Lab studies [Blood cultures, BNP/NT-proBNP]
- ECG
ECG - signs of LVH, ST depressions, T wave inversion in I, avL, V5 and V6
CXR - Ddx of dyspnea and LVH sillhouette
General approach towards diagnosing AR
- In acute presentation of symptoms, ECG, CXR and TTE are done to form a quick prelim dx and find Ddx for angina, dysnpea
- CTA or TEE is done if Aortic dissection is suspected as this is an emergency
- In chronic presentation of symptoms, TTE and ECG [sometimes] should be enough to form a diagnosis
- If TTE is inconclusive, TEE/CMR/Catheterization/Exercise Stress test can help find a causative agent
Echocardiography findings for AR
Indications and Supportive Findings
Indications:
- To assess structure and function of valve, LV and to find severity of AR through heart values [LVEF, end-diastolic LV size and pressure, volume of regurgitated blood, velocity of regurgitaiton jet and its width to aortic outlet area]
- TTE is the modality of choice [non-invasive, quick]
- TEE when TTE is inconclusive or suspected presence of Aortic dissection, acute presentation of symptoms, preoperative risk assessment
Supportive Findings:
General findings:
- Abnormal Aortic valve leaflets [Calcifications, Bicuspid nature, vegetations]
- Regurgitation jet on Doppler flow tracking
- Fluttering of anterior Mitral valve leaflet
- Dilated aorta [this usually indicates either an Aortic root cause of AR or a result of Chronic AR. In acute AR this may be a sign of Aortic dissection]
Specific AR findings:
- Reduced CO
- Elevated EDLVP
- Early Mitral valve closing
- Rapid pressure equilibriation between Aorta and LV
- Increased LV size and volume [sign of chronic AR. CMR can also be used as sometimes TTR cannot accurately assess LV remodelling]
Acute and Chronic
Approach and Management for AR
Approach:
- Acute AR presentation requires immediate surgery
- Hemodynamics are stabilized in acute presentations to prepare or assess for surgery
- Prophylactic treatments for Infective Endocarditis and Aortic dissection is done
- Chronic AR surgery is mainstay [based on AR presentation]
- Comorbidities are managed alongside
Surgical Management:
- Acute severe AR, Stage D AR and Stage C AR with reduced LVEF, > 50mm LVESD are all considered for Aortic Valve Replacement surgery
- David Procedure or Aortic Root reconstruction is an alternative choice which is valve sparing repair of aortic sinuses and ascending aorta
- Antithrombotic therapy depends on choice of valve replacement [mechanical or bioprosthetic]
Medical Management:
Acute AR:
- Hemodynamic stabilization prior to surgery [Inoconstrictors or Inodilators for cardiogenic shock management, Afterload reduction with vasodilators in acute HF like Nitroprusside]
- Beta blockers in Aortic Dissection
Chronic AR:
- HTN management [Beta blockers usually contraindicated as this increases Diastole leading to more regurgitation of blood]
- HF management
- Prophylactic antibiotics for prostatic valves or history of Infective Endocarditis, Rheumatic heart disease
Serial Echocardiography monitoring is done as follow-ups and frequency depends on classified Stage of AR
