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Goals of Diagnosing HTN
Detect & stage HTN severity; detect TOD; assessing overall CV risk; detect secondary causes of HTN
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HTN stats
1 in 3 in US = HTN; 66 mil in US 20 yo & older; 95% are essential HTN; 2005 in US, direct & indirect cost of HTN = $59.7 Billion
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HTN pt awareness stats
63% aware of the dx; only 45% receiving tx; 34% under ctrl using a threshold criterion of 140/90
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Factors of essential HTN:
Genetic defect, inc dietary Na intake, intrinsic renal differences, stress, obesity, drug or substance abuse
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Primary HTN: other factors:
Variable plasma renin activity; variable symp n.s. response & catecholamines; insulin resistance & DM; inadequate dietary K+ & Ca+ ; resistant vessels
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Renal artery stenosis in HTN: MOA
Excessive renin release in response to decrease in renal blood flow & perfusion pressure
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Renal vascular HTN: 2 pathologic processes (resulting in stenosis)
85% atherosclerosis of proximal renal arteries (pts usu also have CAD); 15% fibromuscular dysplasia (esp in F 15–50 yrs; genetic predisposition)
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Fibromuscular dysplasia (FMD) is characterized by:
fibrous thickening of the intima, media, or adventitia of the renal artery
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Congenital abnormality which results in narrowing of the aorta, usually in the ascending region, which increase PVR due to the stenosis
Coarctation of the Aorta
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Coarctation of the Aorta: incidence
Rare (1:10,000) & usually accompanies other abnormalities such as bicuspid aortic valve or Turner Syndrome
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Hyperaldosteronism: most common etiologies:
unilateral aldosterone-producing adenoma or bilateral adrenal hyperplasia
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If Pheochromocytoma undiagnosed:
Outpouring of catecholamines during unrelated surgical/ radiologic procedure can lead to severe, abrupt hypertensive crisis & mortality rate over 80%
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Obstructive sleep apnea & HTN
HTN = response to chronic, intermittent hypoxia during nocturnal apneic episodes
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Cushing Syndrome: tx for HTN
HTN is reversible if cause is eliminated (ie, pituitary adenoma, corticosteroid Rx)
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HTN & chronic kidney dz: epidemiology
HTN is second most common cause of chronic kidney disease (> 25% of cases)
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Most easily recognized treatable risk factor for stroke, MI, CHF, peripheral vascular dz, aortic dissection, atrial fibrillation & end-stage kidney disease
HTN
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HTN in younger pts (< 50 yrs): Hemodynamic fault =
vasoconstriction at the level of the resistance arterioles
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Isolated systolic HTN: associated risks
BP of 160/60 (pulse pressure of 100 mmHg) carries 2x the risk of fatal coronary heart dz as 140/110 (pulse pressure of 30 mmHg) (PP = SBP – DBP)
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Diastolic BP age pattern
Peaks in the early 50’s, then declines for men and women (Systolic BP continues to rise for both throughout life)
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Resistant Hypertension
Defined as persistence of BP > 140/90 despite tx with full doses of 3 or more different classes of meds in rational combination (& including a diuretic); important to know pt is compliant
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4 Categories of Resistant HTN
Pseudoresistance; Inadequate medical regimen; Nonadherence or ingestion of pressor substances; secondary HTN
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Pseudoresistance:
Usually caused by white coat effect superimposed on chronic HTN that is well controlled with meds outside the office
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Resistant HTN: Inadequate medical regimen
Absence of appropriate diuretic; Renal fn impairment which affects drug clearance; monotherapy or inadequate dosing of meds
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Resistant HTN: Nonadherence or ingestion of pressor substances
a. Medication nonadherence; b. Lifestyle modification noncompliance; obesity, high salt diet, excessive alcohol intake; c. Habitual use of tobacco, cocaine, meth, phenylephrine or NSAIDS (cause renal Na+ retention)
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Resistant HTN: Secondary HTN:
If you’ve exhausted the first 3 categories, time to look for secondary cause of HTN
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Most commonly overlooked secondary causes of Resistant HTN:
Chronic kidney dz & primary aldosteronism
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Hypertensive Urgency
Severe elevation of BP; No evidence of progressive TOD; benefit from BP lowering in a few hrs; absence of raised intracranial pressure
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Hypertensive Emergency
Acute, severe elevation in BP; evidence of rapidly progressive TOD (eg, MI, pulmonary edema or renal failure); requires immediate, gradual reduction of BP (NOT to the normal range); always look for secondary causes
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Hypertensive Emergency: tx
Controlled, gradual lowering of BP; 10% decrease in first hour, then 15% over next 3–12 hrs to BP of no less than 160/110; rapid correction of BP to norm levels puts pt at high risk for worsening cerebral, renal or cardiac ischemia
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Malignant Hypertension:
Type of Hypertensive Emergency; usually accompanied by other end organ damage
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Malignant Hypertension is most common in:
Young adults, prior renal dz, AA males, PG, or collagen vascular dz
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Dz w/ Compelling Indications for tight HTN ctrl
CHF; High Coronary Dz Risk; Chronic Kidney Dz; DM; Post-MI; Recurrent Stroke Prevention
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Beta blocker : MOA
Blockade of parts of the symp NS (reduce PVR); Lowers HR; Initially lowers cardiac output; Reduces circulating renin
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Fn of Angiotensin II
Normally stims release of Na+-retaining hormone aldosterone (adrenal corticol cells); normally amplifies vasoconstriction (systemic and renal)
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ACEI AEs
Cough; Angioedema; Hyperkalemia; Rash; CI in PG; use cautiously in renal artery stenosis (RAS)
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ARBs: MOA
Act to block Angiotensin II from binding points; same effect as ACEI, without some of the AEs
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ARBs AEs
Hyperkalemia; Angioedema (rare, 10% cross-over); CI in PG; Cautious use in RAS
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Diuretics: MOA
Act to block Na+ (and K+) from being absorbed, thus increasing urine Na+. Water follows Na+ out of the body. Blood volume is less (lowering BP)
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Diuretics: AEs
Hypokalemia; Volume depletion; Gout; increased insulin resistance; hyponatremia; increased chol levels
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CCBs: MOA
Blocks vascular smooth mx contractility (resulting in vasodilatation & afterload reduction). Also result in coronary vasodilatation & are used in coronary artery spasm
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CCBs: Dihydropyridines (DHPs) vs nonDHPs
DHPs more vascular selective; nonDHPs are more cardio-selective with more inhibitory effects on the SA/AV node
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Essential HTN =
established primary HTN
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Hallmark of essential HTN =
elevated peripheral vascular resistance
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Variations in BP determined by:
variations in ECF volume, heart contractility, & vascular tone
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Def of HTN = repeated readings of:
SBP over 140 &/or DBP over 90
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Evidence supports tx of high risk pts at lower threshold of:
of 130/80 mmHg.
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HTN: High risk groups include:
DM, chronic kidney dz, CV or Cerebrovascular dz, or LVH on EKG
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Factors of essential HTN affect:
ECF volume, heart contractility, or vascular tone
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HTN contributes to what % of M/F AA deaths?
30% M & 20% F
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Most common secondary cause of HTN
Chronic renal dz (proteinuria, high creat)
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?% of pts w/ chronic renal dz have HTN
85%
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Chronic renal dz & HTN: MOA
expanded plasma volume & peripheral vasoconstriction
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Renal artery stenosis prevalence in HTN pts
less than 2%
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HTN pts w/ renal artery stenosis: proportions
75% unilateral stenosis; 25% bilateral
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Problem w/ renovascular HTN
Renal artery stenosis causes 30% of medically refractory HTN
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Catecholamine-producing large tumors of adrenals
Pheochromocytoma
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HTN & CPAP use for OSA
CPAP improves risk of developing HTN & CV dz
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HTN prevalence in DM pts
75% of diabetics have HTN
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Aldosterone-like effect precipitates persistent HTN in:
Cushing Syndrome
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Leading cause of death worldwide
arterial HTN
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Using std size cuff on obese pt:
Gives falsely elevated result
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Ambulatory BP monitor can detect:
Lack of nocturnal dip (assoc w/higher CVD risk)
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BP & substances
Avoid tobacco/caffeine 30 min prior; document if pt took meds
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Ambulatory BP monitor & TOD
Better TOD predictor than office measurements
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Those that develop HTN before 50 yrs:
SBP > 140 mmHg & DBP > 90 mmHg
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What symptom must be present for a dx of Malignant Hypertension?
Papilledema
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Most patients who develop HTN after 50 yrs have:
Isolated Systolic HTN
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Defn Isolated Systolic HTN
systolic BP over 140 mmHg with diastolic BP <90 mmHg
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Isolated Systolic HTN: hemodynamic fault =
decreased distensibility of the large conduit arteries
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Majority of uncontrolled HTN occurs among:
older pts with isolated systolic HTN.
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JNC: SBP opinion
In pts over 50, SBP over 140 is a more important CVD risk than DBP
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DHP CCBs: AEs
Ankle edema; Flushing; HA; Increased HR
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Diltiazem/Verapamil: AEs
Bradycardia; Constipation
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Most common cause of Hypertensive Emergency
Acute CHF with pulm edema (37%)
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JNC7: tx of uncomplicated HTN for most pts
thiazide diuretic
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HTN lifestyle mods
Wt; ETOH; aerobic activity; Na+ to 2.4 mg/day; K+; DASH diet
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Most single HTN meds lower BP:
at most 20/10 mm Hg (so most pts on more than 1 drug)
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Compelling Indications: CHF
Diuretic; Beta-blocker; ACEI; ARB; AA
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Compelling Indications: High Coronary Dz Risk
Beta; ACEI; CCB; Diuretic
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Compelling Indications: Post-MI
Beta; ACEI; AA
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Compelling Indications: DM
Beta; ACEI; Diuretic; ARB
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Compelling Indications: Chronic Kidney Dz
ACEI; ARB
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Compelling Indications: Recurrent Stroke Prevention
ACEI; Diuretic
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HTN eval labs
UA; serum Cr, glu, K+, Na+ ; Lipids (TC, trigs, HDL, LDL); 12-Lead EKG (LVH)
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HTN TOD
Neuro; Ophthalmologic; CV; Renal; Vascular
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First Line Tx for HTN
*Thiazide* ; beta; ACEI; ARB; other diuretics; CCB
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ACEIs
Block formation of angiotensin II; blocking Angiotensin II results in vasodilatation and Na+ loss
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Excessive Na+-K+ exchange which results in hypokalemia; associated with HTN
Hyperaldosteronism
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Complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill with or eject blood (systolic or diastolic)
CHF
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Clinical syndrome caused by a variety of underlying conditions that lead to inadequate cardiac output
CHF
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Clinical syndrome of CHF =
Body’s maladaptive response to a low-flow state which produces symptoms of dyspnea and volume overload
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3 major adaptive mechanisms to compensate for CHF
Frank-Starling mechanism (rapid); Neurohumoral system activation (rapid); Myocardial remodeling (slow)
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Frank-Starling mechanism
Increased ventricular filling during diastole results in increased volume of ejected blood during systolic contraction (CO = HR x SV; norm is about 5L/min)
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Neurohumoral release
Norepinephrine stimulates cardiac contraction & activation of renin-angiotensin-aldosterone system; fn = to maintain arterial pressure & perfusion of vital organs
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Cardiac Remodeling (decline in function)
Compensatory response following injury to cardiac tissue; LV dilates, damaged area forms scar (over time progresses to noncompliance of ventricle, inhibiting relaxation & filling)
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ACEI effect on heart remodeling
Decrease (reverse) remodeling, improving cardiac performance
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Diastolic Left Heart Failure:
Relaxation or Filling: heart does not relax normally, filling pressures are high but EF is normal (over 55%)
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Systolic Dysfunction
Defect is in the expulsion of blood from the left ventricle, leading to inadequate cardiac output
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Causes of Systolic Left Heart Failure
Ischemic heart dz (most common) due to MI hit or chronic ischemia; Longstanding HTN; Valvular Heart Dz; Idiopathic; Myocarditis (L & R); Toxins (ETOH, Cocaine, Thyroid, Pb); Sepsis
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Relationship: CHF & age
HF incidence due to Diastolic dysfunction increases with age (due to increasing noncompliance of LV from long-standing HTN)
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Systolic component of CHF caused by:
chronic loss of contracting myocardium due to prior MI & acute loss of myocardial contractility induced by transient ischemia
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Diastolic component of CHF is due to:
ventricles reduced compliance due to chronic scarring & acute loss of distensibility during ischemia
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Rare instances of high output HF is assoc with:
Elevated cardiac index but low SVR; chronic activation of symp N.S. & RAA systems; chronic volume overload and remodeling; heart cannot meet the metabolic demands; ultimately result in same neurohormonal imbalances as low output HF
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Sudden triggers for Acute HF
Massive MI; Tachyarrhythmia with a very rapid rate; rupture of valve secondary to infective endocarditis
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Causes of Right HF
Left HF; Congenital Heart Lesion (ASD); Right Valve Dz (Tricuspid, Pulmonic); Pulmonary Dz
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Pulmonary Dz =
COPD, Interstitial Lung Dz; Pulmonary emboli; Pulmonary HTN (idiopathic, connective tissue dz)
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Why do initial CHF S/S occur w/ exertion?
Exertion: Decrease ventricular filling time; Increase HR; Inability to increase CO (end result = supply & demand mismatch); ischemia may worsen situation
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CHF S/S
SOB/dyspnea on exertion; edema (LE, abdomen (ascites), sacral/low back if bedbound); PND; orthopnea; fatigue, weakness, anorexia, nausea, wt change; tachycardia/palpitations
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CHF Phys Exam findings
Skin (pallor, cyanosis, cool/moist); Tachypnea/ accessory mx use?; JVP elevation; HJR, hepatomegaly
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Cardiac Exam: Right HF:
Right sided S3 or S4; TR murmur, loud P2 (delayed closing of pulmonic valve
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CHF: Systemic Findings
Hepatomegaly; Pulsatile liver, tender RUQ; Ascites, Abd Swelling; edema (Low Back or sacrum if in bed); diminished or bounding pulses; Pulse, Pressure, 02 sat, weight
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CHF: Cardiac Cath consists of:
Left ventriculogram; Arch shot; Coronary angiography to assess for blockages
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Left ventriculogram:
Evaluate LV fn w/ calculated EF, assess wall motion, look for evidence of Mitral Regurgitation
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Arch shot:
Assess for Aortic Insufficiency, defects in aorta (dissection/aneurysm)
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CHR: Echo: Assess:
Assess for EF (LV function); for LVH; RV & Pulmonary pressures; Cardiac valves/murmurs; diastolic fn/ relaxation; WMAs; Pericardium (for effusion or mass)
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Management Algorithm
S/S; H&P; EKG /Labs (assess etiology); Echo (MRI): preserved EF (diastolic) or poor EF (Systolic); cardiac cath (r/o ischemia, assess valve gradients, filling pressures, consider bx; start acute or chronic tx; reduce concomitant risk factors
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Pharm mgmt of CHF
ACEI; ARBs; Beta Blockers; Nitrates + hydralazine; AAs; diuretics; digoxin; statins
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CHF: Pharm mgmt w/ proven mortality benefit
ACEI; ARBs; Beta Blockers; Nitrates + hydralazine; AAs
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CHF: Non-Pharm chronic tx
Multi-disciplinary team approach; Wt mgmt (Na+ / Fluid balance; ETOH/Toxin avoidance; Behavioral/ Risk modification; Palliative Care/ Hospice when appropriate
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Exercise in CHF pts
Pts limited in even daily activity by poor functional status; even if cannot fix heart make body more efficient at given work load to allow independence; allows for wt Loss, mx strength, rehab enough to be able to get transplant
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Resynchronization therapy (Biventricular pacing): indications
If low EF, Wide QRS > 130 ms and Class III or IV
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Anticoagulation for CHF
Consider Coumadin (chronically) for Low EF; Hosp pt: prophylactic anticoag; aspirin if CAD (but no evidence for non-ischemic)
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Anticoagulation for CHF: Chronic Definite Use (Unless CI)
A-fib; LV Thrombus; Previous thrombo-embolic CVA; Coagulopathy; LV Aneurysm
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Decompensated CHF:
Pt is clinically deteriorating or unstable; begin early & aggressive tx as sort out Etiology
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Acute CHF S/S
Severe SOB, Rales, Hypoxic, Cyanotic, Pale; CP; Tachy, BP may be hyper or hypo; cool or not perfused, poor pulses; distress (tachypneic, accessory mx); poor mental status
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Tests to determine cause of Decompensated CHF
EKG (ischemia), HTN, atrial or other arrhythmia; Echo to assist dx; CXR to assess pulmonary edema
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Acute Decompensated CHF: Tx
Diuretics (Natriuretics); O2 (CPAP or BiPAP); morphine? ; Nitrates (Vasodilators); Inotropes (Dobutamine, Milrinone); Hold/Do not start Beta; ACE/ ARB or other afterload reduction; Balloon pump; ID & tx underlying cause
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Acute Pulmo Edema (flash Pulmo Edema)
Overcome fluid balance btw vascular bed & lung interstitium; pts are tachypneic, tachycardic, hypertensive, hypoxemic, crackles; if hypotensive, grave sign
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Causes of Acute Pulmo Edema:
MI; Acute Valvular lesion (MR, AI); HTN/Renovascular dz; End stage valvular dz (AS, MS); Systemic illness (sepsis, anemia, thyrotoxicosis, severe resp illness); poss other causes (PE, MI)
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Acute Pulmonary Edema: Rx
IV Diuretics, nitrates, inotropes (or BNP nesiritide), pressors (BP support), ACE/ARB or hydralazine + nitrate; HOLD beta in acute phase; O2, Morphine, Anti-arrhythmics if indicated
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% of people with LV dysfn who are symptomatic
50%
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Heart Contraction & Relaxation wrt energy
Both are energy requiring
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Classifications of Left Heart Failure:
Systolic & diastolic
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Systolic Left Heart Failure
Contraction: heart does not squeeze well, low EF (<55%)
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CHF with preserved systolic function
Clinical S/S similar to systolic dysfunction
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CHF risk factors
Age; HTN; Tobacco; DM; Obesity; ETOH/Substance abuse
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Most common cause of Systolic Left Heart Failure
Ischemic heart dz
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Can Systolic & Diastolic CHF coexist?
yes
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Most common form of HF is caused by:
chronic ischemic heart dz
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Prior histories most often assoc w/ systolic CHF
CAD; valvular heart dz
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Prior histories most often assoc w/ diastolic CHF
HTN
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Diagnostic features of systolic CHF
Echo reduced EF; CXR Cardiomegaly; CXR Pulm edema
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Diagnostic features of diastolic CHF
Echo LVH; EKG LVH; CXR Pulm edema
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Echo features present in systolic HF & absent in diastolic HF
Reduced EF; LV dilation
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CHF & output
Most right/ left heart failure is low output
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Most common cause of Right HF
Left HF
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CHF pts w/low EF (<35%) are at risk of devt of:
v-tach or v-fib
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JVP elevation:
Assess R int jugular vein; Reflects right atrial pressure elevations
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HJR =
Hepatojugular reflux
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CHF PE: First assess:
Acute distress or chronically ill?
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Lung Exam: Left HF
Crackles/Rales; poss wheezing; dullness at bases; sputum (frothy/pink)
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Lung Exam: Right HF
Possibly clear; dullness at bases (consider pleural effusion)
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Cardiac Exam: Left HF:
S3 or S4 or Summation gallop; MR murmur
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CHF: dx tests help to:
classify dz; assess etiology
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What % of CHF patients have LVH?
20%
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CHF: EKG
Global low voltage possible in end stage CHF; Evidence of Ischemia or prior infarction (Q waves)
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CHF: Cardiac Biomarkers
(CK/MB, Troponin levels): indicated if suspect ischemic etiology
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Cardiac Cath: Indicated in:
MI, USA
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CHF: on CXR (PA/Lateral), what is important?
Size & Shape of cardiac silhouette
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CHF: CXR findings
Kerley B lines; Pleural effusions
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Kerley B lines =
sharp, linear densities of interlobular interstitial edema
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Pleural effusions in CHF: caused by:
increase in interstitial edema
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Pleural effusions most often assoc with:
LV dysfunction
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CHF = most common cause of what pulmonary outcome?
Pleural effusion
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Describe pleural effusions:
Typically transudative, small to moderate in size, & free flowing (LLD view may be helpful)
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CHR: Echo provides:
structural, anatomic & physiologic info about the heart
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BNP: CHF
BNP secreted from ventricles under stress in CHF
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BNP Levels
Levels vary dependent on alterations in intracardiac filling pressure
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BNP = proposed marker for :
severity of CHF & potentially useful for Rx management
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BNP may be falsely elevated in:
renal failure
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CHF Device Tx
AICD; IABP; Ultrafiltration/hemofiltration to remove fluid; LVAD
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AICD criteria
EF < 35% for most CHF etiologies
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AICD Purpose:
Prevention of sudden death; also for some HCM
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IABP =
Intra-aortic balloon pump, temporary measure for acute CHF in hospital
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AICD =
Automatic Implantable Cardioverter Defibrillators
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CHF: Nonpharm tx
Behavioral; Devices (AICDs, Pacing, LVADS or pumps); Transplant
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LVAD =
Left Ventricular Assist Device
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LVAD is considered a ____ tx
bridge therapy prior to heart transplantation
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Placement of LVAD
May be internal or external
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Frequency of heart transplants for CHF
2500/yr for CHF
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CHF Device Tx
AICD; IABP; Ultrafiltration/hemofiltration to remove fluid; LVAD
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AICD for CHF = what type prevention?
Primary or Secondary Prevention
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AICD indicated if:
Previous V-Tach, SCD
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Effect of antiarrhythmics for VT/VF
(Amiodarone, Dofetilide) do not improve survival
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Limitation in OHT (transplant) for CHF =
donor organs
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OHT for CHF: Late Survival post one year:
Determined by devt CAD or vasculopathy
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OHT for CHF: median survival =
10 years
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OHT for CHF: one-year mortality predicted by:
need for post-op dialysis or ventilation
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OHT for CHF: Hx of sepsis, CAD, DM, CVA predict:
decreased 5 year survival
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Decompensated CHF: types
Acute or Acute on Chronic
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Acute CHF: hypotension is:
Ominous (if bradycardia this may be cause, as is inappropriate)
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Decompensated CHF: Phys Exam
New murmur of MR or AI, worsened AS , rales
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Decompensated CHF: tx
Tx early & aggressively; eliminate or control inciting factors
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Acute (flash) Pulmo Edema:
S/S of rapid clinical deterioration
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