-
Chronic renal dz & HTN: MOA
expanded plasma volume & peripheral vasoconstriction
-
Renal artery stenosis prevalence in HTN pts
less than 2%
-
HTN pts w/ renal artery stenosis: proportions
75% unilateral stenosis; 25% bilateral
-
Problem w/ renovascular HTN
Renal artery stenosis causes 30% of medically refractory HTN
-
Catecholamine-producing large tumors of adrenals
Pheochromocytoma
-
HTN & CPAP use for OSA
CPAP improves risk of developing HTN & CV dz
-
HTN prevalence in DM pts
75% of diabetics have HTN
-
Aldosterone-like effect precipitates persistent HTN in:
Cushing Syndrome
-
Leading cause of death worldwide
arterial HTN
-
Using std size cuff on obese pt:
Gives falsely elevated result
-
Ambulatory BP monitor can detect:
Lack of nocturnal dip (assoc w/higher CVD risk)
-
BP & substances
Avoid tobacco/caffeine 30 min prior; document if pt took meds
-
Ambulatory BP monitor & TOD
Better TOD predictor than office measurements
-
Those that develop HTN before 50 yrs:
SBP > 140 mmHg & DBP > 90 mmHg
-
What symptom must be present for a dx of Malignant Hypertension?
Papilledema
-
Most patients who develop HTN after 50 yrs have:
Isolated Systolic HTN
-
Defn Isolated Systolic HTN
systolic BP over 140 mmHg with diastolic BP <90 mmHg
-
Isolated Systolic HTN: hemodynamic fault =
decreased distensibility of the large conduit arteries
-
Majority of uncontrolled HTN occurs among:
older pts with isolated systolic HTN.
-
JNC: SBP opinion
In pts over 50, SBP over 140 is a more important CVD risk than DBP
-
DHP CCBs: AEs
Ankle edema; Flushing; HA; Increased HR
-
Diltiazem/Verapamil: AEs
Bradycardia; Constipation
-
Most common cause of Hypertensive Emergency
Acute CHF with pulm edema (37%)
-
JNC7: tx of uncomplicated HTN for most pts
thiazide diuretic
-
HTN lifestyle mods
Wt; ETOH; aerobic activity; Na+ to 2.4 mg/day; K+; DASH diet
-
Most single HTN meds lower BP:
at most 20/10 mm Hg (so most pts on more than 1 drug)
-
Compelling Indications: CHF
Diuretic; Beta-blocker; ACEI; ARB; AA
-
Compelling Indications: High Coronary Dz Risk
Beta; ACEI; CCB; Diuretic
-
Compelling Indications: Post-MI
Beta; ACEI; AA
-
Compelling Indications: DM
Beta; ACEI; Diuretic; ARB
-
Compelling Indications: Chronic Kidney Dz
ACEI; ARB
-
Compelling Indications: Recurrent Stroke Prevention
ACEI; Diuretic
-
HTN eval labs
UA; serum Cr, glu, K+, Na+ ; Lipids (TC, trigs, HDL, LDL); 12-Lead EKG (LVH)
-
HTN TOD
Neuro; Ophthalmologic; CV; Renal; Vascular
-
First Line Tx for HTN
*Thiazide* ; beta; ACEI; ARB; other diuretics; CCB
-
ACEIs
Block formation of angiotensin II; blocking Angiotensin II results in vasodilatation and Na+ loss
-
Excessive Na+-K+ exchange which results in hypokalemia; associated with HTN
Hyperaldosteronism
-
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
-
Clinical syndrome caused by a variety of underlying conditions that lead to inadequate cardiac output
CHF
-
Clinical syndrome of CHF =
Body’s maladaptive response to a low-flow state which produces symptoms of dyspnea and volume overload
-
3 major adaptive mechanisms to compensate for CHF
Frank-Starling mechanism (rapid); Neurohumoral system activation (rapid); Myocardial remodeling (slow)
-
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)
-
Neurohumoral release
Norepinephrine stimulates cardiac contraction & activation of renin-angiotensin-aldosterone system; fn = to maintain arterial pressure & perfusion of vital organs
-
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)
-
ACEI effect on heart remodeling
Decrease (reverse) remodeling, improving cardiac performance
-
Diastolic Left Heart Failure:
Relaxation or Filling: heart does not relax normally, filling pressures are high but EF is normal (over 55%)
-
Systolic Dysfunction
Defect is in the expulsion of blood from the left ventricle, leading to inadequate cardiac output
-
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
-
Relationship: CHF & age
HF incidence due to Diastolic dysfunction increases with age (due to increasing noncompliance of LV from long-standing HTN)
-
Systolic component of CHF caused by:
chronic loss of contracting myocardium due to prior MI & acute loss of myocardial contractility induced by transient ischemia
-
Diastolic component of CHF is due to:
ventricles reduced compliance due to chronic scarring & acute loss of distensibility during ischemia
-
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
-
Sudden triggers for Acute HF
Massive MI; Tachyarrhythmia with a very rapid rate; rupture of valve secondary to infective endocarditis
-
Causes of Right HF
Left HF; Congenital Heart Lesion (ASD); Right Valve Dz (Tricuspid, Pulmonic); Pulmonary Dz
-
Pulmonary Dz =
COPD, Interstitial Lung Dz; Pulmonary emboli; Pulmonary HTN (idiopathic, connective tissue dz)
-
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
-
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
-
CHF Phys Exam findings
Skin (pallor, cyanosis, cool/moist); Tachypnea/ accessory mx use?; JVP elevation; HJR, hepatomegaly
-
Cardiac Exam: Right HF:
Right sided S3 or S4; TR murmur, loud P2 (delayed closing of pulmonic valve
-
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
-
CHF: Cardiac Cath consists of:
Left ventriculogram; Arch shot; Coronary angiography to assess for blockages
-
Left ventriculogram:
Evaluate LV fn w/ calculated EF, assess wall motion, look for evidence of Mitral Regurgitation
-
Arch shot:
Assess for Aortic Insufficiency, defects in aorta (dissection/aneurysm)
-
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)
-
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
-
Pharm mgmt of CHF
ACEI; ARBs; Beta Blockers; Nitrates + hydralazine; AAs; diuretics; digoxin; statins
-
CHF: Pharm mgmt w/ proven mortality benefit
ACEI; ARBs; Beta Blockers; Nitrates + hydralazine; AAs
-
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
-
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
-
Resynchronization therapy (Biventricular pacing): indications
If low EF, Wide QRS > 130 ms and Class III or IV
-
Anticoagulation for CHF
Consider Coumadin (chronically) for Low EF; Hosp pt: prophylactic anticoag; aspirin if CAD (but no evidence for non-ischemic)
-
Anticoagulation for CHF: Chronic Definite Use (Unless CI)
A-fib; LV Thrombus; Previous thrombo-embolic CVA; Coagulopathy; LV Aneurysm
-
Decompensated CHF:
Pt is clinically deteriorating or unstable; begin early & aggressive tx as sort out Etiology
-
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
-
Tests to determine cause of Decompensated CHF
EKG (ischemia), HTN, atrial or other arrhythmia; Echo to assist dx; CXR to assess pulmonary edema
-
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
-
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
-
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)
-
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
-
% of people with LV dysfn who are symptomatic
50%
-
Heart Contraction & Relaxation wrt energy
Both are energy requiring
-
Classifications of Left Heart Failure:
Systolic & diastolic
-
Systolic Left Heart Failure
Contraction: heart does not squeeze well, low EF (<55%)
-
CHF with preserved systolic function
Clinical S/S similar to systolic dysfunction
-
CHF risk factors
Age; HTN; Tobacco; DM; Obesity; ETOH/Substance abuse
-
Most common cause of Systolic Left Heart Failure
Ischemic heart dz
-
Can Systolic & Diastolic CHF coexist?
yes
-
Most common form of HF is caused by:
chronic ischemic heart dz
-
Prior histories most often assoc w/ systolic CHF
CAD; valvular heart dz
-
Prior histories most often assoc w/ diastolic CHF
HTN
-
Diagnostic features of systolic CHF
Echo reduced EF; CXR Cardiomegaly; CXR Pulm edema
-
Diagnostic features of diastolic CHF
Echo LVH; EKG LVH; CXR Pulm edema
-
Echo features present in systolic HF & absent in diastolic HF
Reduced EF; LV dilation
-
CHF & output
Most right/ left heart failure is low output
-
Most common cause of Right HF
Left HF
-
CHF pts w/low EF (<35%) are at risk of devt of:
v-tach or v-fib
-
JVP elevation:
Assess R int jugular vein; Reflects right atrial pressure elevations
-
HJR =
Hepatojugular reflux
-
CHF PE: First assess:
Acute distress or chronically ill?
-
Lung Exam: Left HF
Crackles/Rales; poss wheezing; dullness at bases; sputum (frothy/pink)
-
Lung Exam: Right HF
Possibly clear; dullness at bases (consider pleural effusion)
-
Cardiac Exam: Left HF:
S3 or S4 or Summation gallop; MR murmur
-
CHF: dx tests help to:
classify dz; assess etiology
-
What % of CHF patients have LVH?
20%
-
CHF: EKG
Global low voltage possible in end stage CHF; Evidence of Ischemia or prior infarction (Q waves)
-
CHF: Cardiac Biomarkers
(CK/MB, Troponin levels): indicated if suspect ischemic etiology
-
Cardiac Cath: Indicated in:
MI, USA
-
CHF: on CXR (PA/Lateral), what is important?
Size & Shape of cardiac silhouette
-
CHF: CXR findings
Kerley B lines; Pleural effusions
-
Kerley B lines =
sharp, linear densities of interlobular interstitial edema
-
Pleural effusions in CHF: caused by:
increase in interstitial edema
-
Pleural effusions most often assoc with:
LV dysfunction
-
CHF = most common cause of what pulmonary outcome?
Pleural effusion
-
Describe pleural effusions:
Typically transudative, small to moderate in size, & free flowing (LLD view may be helpful)
-
CHR: Echo provides:
structural, anatomic & physiologic info about the heart
-
BNP: CHF
BNP secreted from ventricles under stress in CHF
-
BNP Levels
Levels vary dependent on alterations in intracardiac filling pressure
-
BNP = proposed marker for :
severity of CHF & potentially useful for Rx management
-
BNP may be falsely elevated in:
renal failure
-
CHF Device Tx
AICD; IABP; Ultrafiltration/hemofiltration to remove fluid; LVAD
-
AICD criteria
EF < 35% for most CHF etiologies
-
AICD Purpose:
Prevention of sudden death; also for some HCM
-
IABP =
Intra-aortic balloon pump, temporary measure for acute CHF in hospital
-
AICD =
Automatic Implantable Cardioverter Defibrillators
-
CHF: Nonpharm tx
Behavioral; Devices (AICDs, Pacing, LVADS or pumps); Transplant
-
LVAD =
Left Ventricular Assist Device
-
LVAD is considered a ____ tx
bridge therapy prior to heart transplantation
-
Placement of LVAD
May be internal or external
-
Frequency of heart transplants for CHF
2500/yr for CHF
-
CHF Device Tx
AICD; IABP; Ultrafiltration/hemofiltration to remove fluid; LVAD
-
AICD for CHF = what type prevention?
Primary or Secondary Prevention
-
AICD indicated if:
Previous V-Tach, SCD
-
Effect of antiarrhythmics for VT/VF
(Amiodarone, Dofetilide) do not improve survival
-
Limitation in OHT (transplant) for CHF =
donor organs
-
OHT for CHF: Late Survival post one year:
Determined by devt CAD or vasculopathy
-
OHT for CHF: median survival =
10 years
-
OHT for CHF: one-year mortality predicted by:
need for post-op dialysis or ventilation
-
OHT for CHF: Hx of sepsis, CAD, DM, CVA predict:
decreased 5 year survival
-
Decompensated CHF: types
Acute or Acute on Chronic
-
Acute CHF: hypotension is:
Ominous (if bradycardia this may be cause, as is inappropriate)
-
Decompensated CHF: Phys Exam
New murmur of MR or AI, worsened AS , rales
-
Decompensated CHF: tx
Tx early & aggressively; eliminate or control inciting factors
-
Acute (flash) Pulmo Edema:
S/S of rapid clinical deterioration
-
Cause of pericarditis
coxsackievirus
-
Cardiomyopathy
dilated cardiomyopathy (MC due to CAD or ischemia)
-
Congenital heart defect
ventricular septal defect
-
Cyanotic congenital heart defect
tetralogy of fallot (VSD, RVH, pulmonary stenosis, & overriding aorta)
-
Cause of chest pain in outpatient setting
musculoskeletal cause
-
Ulcer location in chronic venous insufficiency
proximal to medial malleolus
-
Ulcer location in chronic arterial insufficiency
distal toes or lateral aspect of affected extremity
-
Site for an acute embolic occlusion
femoral artery
-
Cause of renovascular hypertension
artherosclerosis
-
Chest x-ray finding with traumatic thoracic aortic injury
widened mediastinum
-
Inherited condition associated with pulmonary embolism
Factor V leiden mutation (expressed as resistance to anticoagulant protein C)
-
Cause of atrial fibrillation
HTN & Coronary arthrosclerosis
-
Valvular abnormalities in adults
Aortic stenosis
-
Valve abnormality in rheumatic heart disease
Mitral stenosis
-
Valvular heart defect in US
mitral valve prolapse
-
Cause of CHF
Artherosclerotic coronary disease & HTN
-
Cause of arterial occlusive disease
atherosclerosis
-
Aortic catastrophe
aortic dissection
-
Cause of secondary HTN
Renal disease
-
Test for arterial insufficiency
Ankle-brachial index
-
Cause of sudden cardiac death in adolescents
hypertrophic cardiomyopathy
-
Osler nodes (painful, violaceous, raised lesions of the fingers, toes or feet)
Endocarditis
-
Janeway lesions (painLESS erythematous lesions of the palms or sole)
Endocarditis
-
Roth spots (exudative lesions in the retina)
Endocarditis
-
Pain relieved by sitting forward
pericarditis
-
Young person passes out & dies playing a sport
hypertrophic cardiomyopathy
-
Delta wave
Wolff-Parkinson White
-
Machine like murmur
patent ductus arteriosus (close w/ indomethacin, open w/ prostaglandin E1)
-
Kussmaul sign (↑ in JVP during inspiration)
Constrictive pericarditis
-
Homan’s sign
calf pain on forced dorsiflexion (DVT)
-
Punched out appearance with pale or necrotic base
ulcers secondary to chronic arterial insufficiency
-
Lower extremity edema & pigmentation changes
chronic venous insufficiency
|
|