Showing posts with label Cardiology. Show all posts
Showing posts with label Cardiology. Show all posts

06 March 2012

Non–ST-segment elevation myocardial infarction - NSTEMI




Unstable Angina and Non-ST elevation Myocardial Infarction
John Blair, MD
Myocardial Infarction .ppt

Acute Coronary Syndrome - LEARNING POINTS
http://www.medicine.uci.edu/residency/powerpoint/ACS.ppt

Trends  in clinical and demographic  features of patients  with acute myocardial  infarction
Warren  K. Laskey, MD: Candidate  for MPH
Steve  Goodman, MD, MSc, PhD
Laskey_Warren.ppt

Acute  Coronary Syndrome
Steven  R. Bruhl MD, MS
ACS_PPT_FINAL_6-14-10.ppt

Twenty  Points to Remember from the UA/NSTEMI Guideline Update
http://www.fpm.emory.edu/.ppt

Nanette  K. Wenger, MD, MACP, FACC, FAHA
SET.ppt,
ACS.ppt

NSTEMI - Conservative  vs Early Invasive Approach
Nstemi.ppt

Bleeding  and Acute Coronary Syndromes
Cardiac  Catherization Conference
Syed  Raza MD
BleedingandACS.ppt

ST  Elevation Myocardial Infarction (STEMI)
William  J. Mosley II, MD
STEMI Talk.ppt

Stanford  ACS Guidelines
David  P. Lee, M.D., John  S. Schroeder, M.D., Donald  Schreiber, M.D.
Stanford_ACS_Guidelines.ppt

Acute  MI/Stroke
Sean  Kiley
ACLSpresentation.ppt

Cardiac  Medications “The Essentials”
Kenneth  Kenyon, PharmD, BCPS
Cardiac Medications.ppt

Acute  Coronary Syndromes
Robert  Smith
Acute  Coronary Syndromes.ppt
PDFs Here 

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25 February 2012

Pulmonary artery occlusion pressure



Pulmonary Hypertension
https://pediatrics.med.unc.edu/education/uncpeds/rotations/picu/files/PHTN_Resident_Lecture.ppt

Use of Thrombolytics in Pulmonary Embolism
http://intmedweb.wfubmc.edu/download/thrombolytics.ppt.

The Use of Thrombolytics in Pulmonary Embolism
by Pamela Harm, M.D.
http://intmedweb.wfubmc.edu/download/thrombolytics.ppt

Pulmonary  Blood Flow
by Thomas  Sisson, M.D.
http://open.umich.edu/sites/default/files/2319/tsisson-pulmonarybloodflow-07-1.ppt

Control of Cardiac Output
by Daniel R. Margulies, MD, FACS
Crirtical care.ppt

Invasive Hemodynamic Monitoring
Donna Cohen, BSN, RN
Hemodynamic Pre and Dynamic

Anesthetic Management of Vascular Surgery
Vascular Surgery.ppt

Controversies  in Pulmonary Hypertension and Sickle Cell  Disease
By Kristen Sanfilippo  MD
Sanfilippo_2011-10-28.ppt

Heart,  Blood, & Lymph Disease
http://occonline.occ.cccd.edu/online/dfarrell/HeartBloodLymph.PPT


Pediatric Cardiac Disorders
pp_cardiac.ppt

Pulmonary  Artery Catheter
by Marie  Sankaran Raval M.D.
Pulmonary Artery Catheter.ppt

Cardiovascular  Nursing
Cardiovascular Cardiovascular.ppt

Central Venous Pressure Monitoring
By Dr. Aidah Abu  Elsoud Alkaissi
Central Venous Pressure.ppt

Cardiac Pathophysiology
Cardiac Pathophysiology.ppt

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23 January 2012

Tricuspid Stenosis Ppts and Latest 20 published articles



Tricuspid Stenosis: Tricuspid valve stenosis is a valvular heart disease which results in the narrowing of the orifice of the tricuspid valve of the heart. It's relatively a rare condition. The stenosis causes increased resistance to blood flow through the valve.
Heart Murmurs
by David Leder
http://www.lumen.luc.edu/lumen/meded/medicine/pulmonar/pd/heart%20murmurs.ppt

Aortic  Stenosis
http://www.learntheheart.com/CRA22-AS-PPT.ppt

Tricuspid  Valve Diseases
by M.Sahebjam M.D., Echocardiologist
http://thc.tums.ac.ir/UserFiles/File/Amozesh/Tricuspid%20Valve%20Diseases.ppt

Echocardiography, Doppler  Echocardiography
http://www.cardiovascularinstitute.org/images/Doppler_Echocardiography.ppt

Valvular Heart Disease II: The Aortic Valve
by Laura Wexler, M.D
http://www.med.uc.edu/pages/courses/icp2/icp%2011%20valve%20II-02.ppt

Valvular  Heart Disease - Aortic Stenosis
http://www.cvtoolbox.com/downloads/vhd/Aortic_Stenosis.ppt

Valvular  Heart Disease
http://www.cmft.nhs.uk/undergrad/students/documents/ValvularHeartDisease-ProfCotterSept2011.ppt

Congenital Heart Disease - Thoracic Conference
by Frank Nami, M.D.
http://www.barnabashealth.org/hospitals/saint_barnabas/mservices/surgery/staff/NamiCHD.ppt

‘How I do’ CMR in valvular heart disease
by Dr.  Saul Myerson, Clinical  Lecturer in Cardiovascular  Medicine
http://www.scmr.org/assets/files/members/documents/How_I_do_valvular_heart_disease.ppt

Valvular  Emergencies
by Dr.  Kanagala
http://www.cchseast.org/Portals/33/Residency/ValvularEmergencies.ppt

Valvular Stenosis - Board  Review
by Vikram  Chhokar MD, University  of Tennessee
http://www.uthsc.edu/cardiology/ppt/AS.ppt

Valvular  Heart Disease - Mitral Stenosis
http://www.cvtoolbox.com/downloads/vhd/Mitral_Stenosis.ppt

Valvular  Heart Disease and Anesthesia
by Wayne  E. Ellis, Ph.D., CRNA
http://wayneellisent.org/Martha%27s%20Lectures/Cardiac%20Lectures/Valvular%20Heart%20Disease%20and%20Anesthesia%201.ppt

Aortic Stenosis:  Updates in Diagnosis & Management
by Amanda Ryan, D.O.
http://www.wiredcardiologist.com/PPTs/aortic.ppt

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19 December 2011

Valvular Stenosis ppt and latest 20 publications




Valvular  Heart Disease
by Kenneth  S. Korr M.D.
http://www.brown.edu/Courses/Bio_281-cardio/cardio/Valvular2005.ppt

Valvular  Heart Disease
http://www.austincc.edu/nursmods/online/online_lev4/rnsg_2432/documents/ValvulaCardimyopathyAneurysmHrtSur08Copy_000.ppt

Valvular  Heart Disease
http://legacy.owensboro.kctcs.edu/jsmith/Valvular%20Heart%20Disease.ppt

Valvular  Heart Disease
by Steven R. Bruhl MD, MS
http://www.utoledo.edu/med/depts/medicine/residency/Didactics/pdf/Valvular_Heart_Disease_IM_8-12.ppt

Valvular Disease,  Carditis & Cardiomyopathy
http://www.mac.edu/faculty/ChristineStaake/Nursing%20331/lecture%20notes/Valvular%20Disease,%20Carditis%20and%20%20Cardiomyopathy.ppt

Valvular Heart Disease
by Laura Wexler, M.D.
http://www.med.uc.edu/pages/courses/icp2/icp%2011%20valve%20II-02.ppt

The Essentials of Valvular Heart Disease
http://www.cardiologyfellows.northwestern.edu/cculectures/The%20Essentials%20of%20Valvular%20Heart%20Disease.ppt

Valvular Stenosis
by Vikram  Chhokar MD
http://www.uthsc.edu/cardiology/ppt/AS.ppt

Cardiac  Cath Measurement of Stenotic Aortic Valve  Area
by Ryan  Tsuda, MD
http://tulane.edu/som/tuhvi/upload/cathconf09-14-04.ppt

Latest 20 publications

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20 February 2010

Pathophysiology of Pericardial Disease



Pathophysiology of Pericardial Disease

Pericardium - Anatomy

Normal pericardium is a fibro-serous sac which surrounds the heart and adjoining portions of the great vessels.
The inner visceral layer, also known as the epicardium, consists of a thin layer of mesothelial cells closely adherent to the surface of the heart. The epicardium is reflected onto the surface of the outer fibrous layer with which it forms the parietal pericardium.
The parietal pericardium consists of collagenous fibrous tissue and elastic fibrils.
Between the two layers lies the pericardial space, which contains approximately 10-50ml of fluid, which is an ultrafiltrate of plasma.
Drainage of pericardial fluid is via right lymphatic duct and thoracic duct.

Pericardial Layers:

Visceral layer
Parietal layer
Fibrous pericardium

Function of the Pericardium

1. Stabilization of the heart within the thoracic cavity by virtue of its ligamentous attachments -- limiting the heart’s motion.
2. Protection of the heart from mechanical trauma and infection from adjoining structures.
3. The pericardial fluid functions as a lubricant and decreases friction of cardiac surface during systole and diastole.
4. Prevention of excessive dilation of heart especially during sudden rise in intra-cardiac volume (e.g. acute aortic or mitral regurgitation).

Etiologies of Pericarditis


I. INFECTIVE
1. VIRAL - Coxsackie A and B, Influenza, adenovirus, HIV, etc.
2. BACTERIAL - Staphylococcus, pneumococcus, tuberculosis, etc.
3. FUNGAL - Candida
4. PARASITIC - Amoeba, candida, etc.

II. AUTOIMMUNE DISORDERS
1. Systemic lupus erythematosus (SLE)
2. Drug-Induced lupus (e.g. Hydralazine, Procainamide)
3. Rheumatoid Arthritis
4. Post Cardiac Injury Syndromes i.e. postmyocardial Infarction (Dressler's) Syndrome, postcardiotomy syndrome, etc.

III. NEOPLASM
1. Primary mesothelioma
2. Secondary, metastatic
3. Direct extension from adjoining tumor

IV. RADIATION PERICARDITIS
V. RENAL FAILURE (uremia)
VI. TRAUMATIC CARDIAC INJURY
1. Penetrating - stab wound, bullet wound
2. Blunt non-penetrating - automobile steering wheel accident
VII. IDIOPATHIC

Pathogenesis

1) Vasodilation:
 transudation of fluid

2) Increased vascular permeability
 leakage of protein

3) Leukocyte exudation
neutrophils and mononuclear cells


Pathology
depends on underlying cause and severity of inflammation

serous pericarditis
serofibrinous pericarditis
suppurative (purulent) pericarditis
hemorrhagic pericarditis

Clinical Features of Acute Pericarditis

Idiopathic/viral
* Pleuritic Chest pain
* Fever
* Pericardial Friction Rub
3 component:
a) atrial or pre-systolic component
b) ventricular systolic component (loudest)
c) ventricular diastolic component

* EKG: diffuse ST elevation
PR segment depression

Diagnostic Tests
Echocardiogram: Pericardial effusin
N.B.: absence does not rule out pericarditis
N.B.: Pericarditis is a clinical diagnosis, not an Echo diagnosis!

Blood tests: PPD, RF, ANA
Viral titers
Search for malignancy
Pericardiocentesis:
low diagnostic yield
done therapeutically

Treatment
Pain relief
analgesics and anti-inflammatory
ASA/NSAID’s
Steroids for recurring pericarditis
Antibiotics/drainage for purulent pericarditis
Dialysis for uremic pericarditis
Neoplastic: XRT, chemotherapy

Pericardial Effusion
Normal 15-50 ml of fluid
ETIOLOGY
1. Inflammation from infection, immunologic process.
2. Trauma causing bleeding in pericardial space.
3. Noninfectious conditions such as:
a. increase in pulmonary hydrostatic pressure e.g. congestive heart failure.
b. increase in capillary permeability e.g. hypothyroidism
c. decrease in plasma oncotic pressure e.g. cirrhosis.
4. Decreased drainage of pericardial fluid due to obstruction of thoracic duct as a result of malignancy or damage during surgery.

Effusion may be serous, serofibrinous, suppurative, chylous, or hemorrhagic depending on the etiology.
Viral effusions are usually serous or serofibrinous
Malignant effusions are usually hemorrhagic.


Pathophysiology
Pericardium relatively stiff
Symptoms of cardiac compression dependant on:

1. Volume of fluid
2. Rate of fluid accumulation
3. Compliance characteristics of the pericardium

A. Sudden increase of small amount of fluid (e.g. trauma)
B. Slow accumulation of large amount of fluid (e.g. CHF)

Clinical features
Small effusions do not produce hemodynamic abnormalities.

Large effusions, in addition to causing hemodynamic compromise, may lead to compression of adjoining structures and produce symptoms of:

dysphagia (compression of esophagus)
hoarseness (recurrent laryngeal nerve compression)
hiccups (diaphragmatic stimulation)
dyspnea (pleural inflammation/effusion)

Physical Findings

Muffled heart sounds
Paradoxically reduced intensity of rub
Ewart's sign:
Compression of lung leading to an area of consolidation in the left infrascapular region (atalectasis, detected as dullness to percussion and bronchial breathing)

Diagnostic studies
CXR: “water bottle” shaped heart
EKG:
low voltage
“electrical alternans”
Echocardiogram
Cardiac Tamponade

Fluid under high pressure compresses the cardiac chambers:
acute: trauma, LV rupture – may not be very large
gradual: large effusion, due to any etiology of acute pericarditis

CardiacTamponade -- Pathophysiology
Accumulation of fluid under high pressure:
compresses cardiac chambers & impairs
diastolic filling of both ventricles

 SV venous pressures
 CO systemic pulmonary congestion
Hypotension/shock JVD rales
Reflex tachycardia hepatomegaly
ascites
peripheral edema

Tamponade-- Clinical Features
Symptoms:
Acute: (trauma, LV rupture)
profound hypotension
confusion/agitation
Slow/Progressive large effusion (weeks)
Fatigue (CO)
Dyspnea
JVD
Signs:
Tachycardia
Hypotension
rales/edema/ascites
muffled heart sounds
pulsus paradoxus

Pulsus Paradoxus
Intrapericardial pressure (IPP) tracks intrathoracic pressure.
Inspiration:
negative intrathoracic pressure is transmitted to the pericardial space

 IPP
 blood return to the right ventricle
 jugular venous and right atrial pressures
 right ventricular volume
 interventricular septum shifts towards the left ventricle
 left ventricular volume
 LV stroke volume
 blood pressure (<10mmHg is normal) during inspiration

Pulsus Paradoxus
Exaggeration of normal physiology
> 10 mm Hg drop in BP
with inspiration
Tamponade -- Diagnosis

EKG: low voltage, sinus tachycardia,

electrical alternans
Echocardiography
pericardial effusion
(r/o other etiologies in dif dx)
RA and RV diastolic collapse

Right Heart Catheterization
Catheterization Findings:
Elevated RA and RV diastolic pressures
Equalized diastolic pressures
Blunted “y” descent in RA tracing
y descent: early diastolic filling (atrial emptying)
 BP and Pulsus paradoxus
Pericardial pressure = RA pressure

Jugular venous pressure waves

Normal JVP contours
(1) A-wave
1) results from ATRIAL contraction
2) Timing - PRESYSTOLIC
3) Peak of the a-wave near S1
(2) V-wave

1) results from PASSIVE filling of the right atrium while the tricuspid valve is closed during ventricular systole (Remember the V-wave is a "V"ILLING WAVE)

2) Large V-waves on the left side of the heart may be seen with mitral regurgitation, atrial septal defect, ventricular septal defect. The v-wave in the jugular venous pulse reflects right atrial events. To see the v-wave on the left side of the heart Swan-Ganz monitoring is needed

3) timing - peaks just after S2

(3) X-descent

1) results from ATRIAL RELAXATION

2) timing - occurs during ventricular systole, at the same time as the carotid pulse occurs

(4) Y-descent

1) results from a FALL in right atrial pressure associated with opening of the tricuspid valve

2) timing - occurs during ventricular diastole

(5) Generalizations

1) the A-wave in a normal individual is always larger than the V-wave

2) the X-descent is MORE PROMINENT than the Y-descent
RA Pressure Tracing

a wave: atrial contraction
v wave: passive filling of atria during
ventricular systole with mv/tv closed
y descent: early atrial emptying with mv/tv
open (early passive filling of ventricle)

Tamponade:
blunted y descent (impaired rapid ventricular filling due to compression by high pericardial pressure)

Tamponade -- Treatment
Pericardiocentesis
Pericardial Window
Balloon Pericardiotomy
Pre-pericardiocentisis
Post-pericardiocentesis
Constrictive Pericarditis
Late complication of pericardial disease
Fibrous scar formation
Fusion of pericardial layers
Calcification further stiffens pericardium
Etiologies:

Pathophysiology
Rigid, scarred pericardium encircles heart:

Systolic contraction normal
Inhibits diastolic filling of both ventricles

 SV venous pressures
 CO systemic pulmonary congestion
Hypotension/shock JVD rales
Reflex tachycardia hepatomegaly
ascites
peripheral edema
Physical exam
Kussmaul’s sign
Diagnosis
CXR: calcified cardiac silhouette
EKG: non-specific
CT or MRI: pericardial thickening

Cardiac Catheterization
Prominent y descent: “dip and plateau”:
rapid atrial emptying rapid ventricular filling then abrupt cessation of blood flow due to rigid pericardium

Elevated and equalized diastolic pressures (RA=RVEDP=PAD=PCW)
Constriction vs. Restriction

Similar presentation and physiology, important to differentiate as

constriction is treatable by pericardiectomy

Majority of diseases causing restriction are not treatable
Constrictive Pericarditis
TAMPONADE
Low cardiac output state
JVD present
NO Kussmaul’s sign
Equalized diastolic pressures
RA: blunted y descent
Decreased heart sounds

CONSTRICTION

Low cardiac output state
JVD present
Kussmaul’s sign
Equalized diastolic pressures
RA: rapid y descent
Pericardial “knock”
Constriction vs. Tamponade Summary
TAMPONADE
Pulsus paradoxus:
Present
Echo/MRI:
Normal systolic function
Large effusion
RA & RV compression
Treatment:

Pericardiocentesis
CONSTRICTION
Pulsus paradoxus:
Absent
Echo/MRI:
Normal systolic function
No effusion
Pericardial thickening
Treatment:
Pericardial stripping

Pathophysiology of Pericardial Disease.ppt

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03 October 2009

The Cardiovascular Examination



Valvular Heart Disease and the Cardiac Exam
By:Charlotte Bai, M.D.
Internal Medicine Board Review
May 28, 2009

Overview
* Clinical syndromes
* Overview of cardiac murmurs and maneuvers
* Left sided valvular lesions
o Aortic stenosis and sclerosis
o Mitral stenosis
+ Rheumatic fever prophylaxis
o Acute and chronic aortic regurgitation
o Acute and chronic mitral regurgitation
* Right sided valvular lesions
o Tricuspid valve disease
* Prosthetic valves
* Endocarditis prophylaxis
* Questions

General Appearance
* Marfan Syndrome
o Tall, long extremities
o Associated with: aortic root dilitation, MV prolapse
* Acromegaly
o Large stature, coarse facial features, “spade” hands
o Associated with: Cardiac hypertrophy
* Turner Syndrome
o Web neck, hypertelorism, short stature
o Associated with: Aortic coarctation, pulmonary stenosis
* Pickwickian Syndrome
o Severe obesity, somnolence
o Associated with: Pulmonary hypertension
* Fredreich ataxia
o Lurching gait, hammertoe, pes cavus
o Associated with: hypertrophic cardiomyopathy
* Duchenne type muscular dystrophy
o Pseudohypertrophy of the calves
o Cardiomyopathy
* Ankylosing spondylitis
o Straight back syndrome, stiff (“poker”) spine
o Associated with: AI, CHB (rare)
* Lentigines (LEOPARD syndrome)
o Brown skin macules that do not increase with sunlight
o Associated with: HOCM, PS
“Spade” hands in acromegaly
* Hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu)
o Small capillary hemangiomas on the face or mouth
o Associated with: Pulmonary arteriovenous fistula
* Lupus
o Butterfly rash on face, Raynaud phenomenon- hands, Livedo reticularis
o Associated with: Verrucous endocarditis, Myocarditis, Pericarditis
* Pheochromocytoma
o Pale diaphoretic skin, neurofibromatosis- café-au-lait spots
o Associated with: Catecholamine-induced secondary dilated CM
* Sarcoidosis
o Cutaneous nodules, erythema nodosum
o Associated with: Secondary cardiomyopathy, heart block
* Tuberous Sclerosis
o Angiofibromas (face; adenoma sebaceum)
o Associated with: Rhabdomyoma
* Myxedema
o Coarse, dry skin, thinning of lateral eyebrows, hoarseness of voice
o Associated with: Pericardial effusion, LV dysfunction

Grading the Intensity of Cardiac Murmurs
* Grade 1
o Murmur heard with stethoscope, but not at first
* Grade 2
o Faint murmur heard with stethoscope on chest wall
* Grade 3
o Murmur hears with stethoscope on chest wall, louder than grade 2 but without a thrill
* Grade 4
o Murmur associated with a thrill
* Grade 5
o Murmur heard with just the rim held against the chest
* Grade 6
o Murmur heard with the stethoscope held away and in from the chest wall

Cardiac Murmurs


* Most mid systolic murmurs of grade 2/6 intensity or less are benign
o Associated with physiologic increases in blood velocity:
+ Pregnancy
+ Elderly
* In contrast, the following murmurs are usually pathologic:
o Systolic murmurs grade 3/6 or greater in intensity
o Continuous murmurs
o Any diastolic murmur

Diagnostic Testing
* ECHOCARDIOGRAM
Aortic Stenosis
Progression of Aortic Sclerosis
* Hemodynamic progression usually slow
o Average rate of increase in aortic jet velocity of 0.3 m/s per year
o Increase in mean transaortic gradient of 7 mmHg
o Decrease in AVA of 0.1 cm2 per year
* Severe AS
o Aortic jet velocity > 4 m/s
o Mean transvalvular pressure gradient > 50 mmHg
o AVA < 1.0 cm2

Pathophysiology of Aortic Stenosis
* Obstruction of LV outflow increases intracavitary systolic pressures and leads to LV pressure overload
* Initial compensatory mechanism is myocardial hypertrophy with preservation of systolic function
* Diastolic function impaired as a consequence of increased wall thickness and abnormal myocardial relaxation
* Increased wall stress and afterload causes eventual decrease in ejection fraction

Pseudostenosis
* Occurs in patients with impaired systolic function and aortic stenosis
o Unable to generate transvalvular gradient
* Careful diagnostic testing with dobutamine infusion protocols can aid in differentiating between true AS and pseudostenosis
* If the calculated AVA increases with augmentation of cardiac output, then pseudostenosis present
* If AVA does not increase with dobutamine, then obstruction fixed and true AS present

Clinical Presentation of Aortic Stenosis
* Cardinal symptoms:
o Angina
+ Occurs in >50% of patients, not sensitive due to prevalence of CAD
o Syncope
o CHF
* Sudden cardiac death rare, <1% per year
* In earlier stages, AS presentation more subtle
o Dyspnea
o Decreased exercise tolerance
* Rarely, AS diagnosed in the setting of GI bleeding
o Heyde’s syndrome
+ Bleeding caused by AVM
+ Concurrent AS occurs at prevalence rate of 15-25%
+ Associated with an acquired von Willebrand syndrome due to disruption of vW multimers through a diseased AV

Management of Aortic Stenosis
* Prognosis in asymptomatic disease excellent
* Conservative approach with monitoring for symptoms recommended
* When severe stenosis present-
o 38% of asymptomatic patients develop symptoms within 2 years
o 79% are symptomatic within 3 years
* Once symptoms occur, AVR needed
* LV dysfunction and severe AS have increased perioperative mortality with AVR
o But outcomes still favorable with surgery
* Nitroprusside may transiently improve cardiac function as a bridge to valve replacement
o Does not supplant AVR in symptomatic patients

Aortic Valve Replacement
* Prophylatic AVR in asymptomatic patients not routinely performed due to surgical risks
o Thromboembolism, bleeding associated with anticoagulation, prosthetic valve dysfunction, and endocarditis
o Occurs at a rate of 2-3% annually
o Only should be considered:
+ If other cardiac surgery (such as CABG) planned
+ Severe LVH or systolic dysfunction
+ Women contemplating pregnancy
+ Patients remote from health care
* Surgical valve replacement with operative morbidity and mortality of 10%
* Percutaneous balloon aortic valvotomy rarely used

Mitral Stenosis
* Usually associated with history of rheumatic fever
* >40% of cases of RHD result in mitral stenosis
o Women affected more than men (2:1)
* Presentation 20-40 years after the initial episode of rheumatic fever
o If infected at a young age, latent period is a few years

Clinical Presentation of Mitral Stenosis
* Significant MS leads to ↑LA pressure and pulm HTN
* Symptoms include dyspnea with ↑ cardiac demand
o Exercise
o Pregnancy
* Survival excellent with asymptomatic or minimally symptomatic patients
o >80% survival at 10 years
* Survival in symptomatic patients much worse
o 10 year survival drops to 15% or lower (if pulm HTN present)
* Findings consistent with severe MS:
o Transvalvular diastolic pressure gradient >10 mmHg
o MVA <1.0 cm2
o Severe pulmonary hypertension (>60 mmHg)

Management of Mitral Stenosis
* Atrial fibrillation
Mitral Valve Repair
* Percutaneous valvotomy
Rheumatic Fever Prophylaxis
* Primary prophylaxis
* Secondary prophylaxis
Acute Aortic Regurgitation
Acute Mitral Regurgitation
Chronic Valvular Regurgitation
Chronic Aortic Regurgitation
Chronic Mitral Regurgitation
Treatment of Chronic Mitral Regurgitation
Timing of Intervention for Left-Sided Valvular Conditions
OTHERWISE
Repeat TTE yearly, repeat clinical evaluation biannually
OTHERWISE
Repeat TTE at least yearly, repeat clinical evaluation at least biannually depending on the severity of the LV dilitiation
OTHERWISE
Clinical evaluation at least annually, depending on the severity of the mitral stenosis
OTHERWISE
Depending on the severity of AS, at least annual clinical evaluation with TTE to monitor for symptom onset
Intervention:
AVR
Chronic Severe MR
Chronic Severe AR
Mitral Stenosis
Aortic Stenosis
Tricuspid Valve Disease
* Tricuspid stenosis is rare
o Associated with rheumatic heart disease
* TR usually occurs secondary to:
o Pulmonary hypertension
o RV chamber enlargement with annular dilatation
o Endocarditis (associated with IV drug use)
o Injury following pacer lead placement
* Other secondary causes: carcinoid, radiation therapy, anorectic drug use, and trauma
* Primary causes: Marfan’s syndrome and congenital disorders such as Ebstein’s anomaly and AV canal malformation
* Echo is diagnostic in most cases
Tricuspid Regurgitation
* Severe tricuspid regurgitation is difficult to treat and carries a poor overall clinical outcome
* Symptoms are manifestations of systemic venous congestion
* Surgical intervention usually considered if other cardiac surgery planned
* Surgical options include valvular annuloplasty or replacement

Prosthetic Valves- Mechanical
* Three types:
o Ball-cage valve
o Single tilting disk valve
o Bileaflet valve
* Durable but require life long anticoagulation
* For operative procedures, warfarin typically is discontinued for 48-72 hours and restarted postop as soon as possible, except for:
o Mechanical mitral prosthesis
o Atrial fibrillation
o Prior thromboembolic events
Ball-cage valve
Single tilting disk valve
Bileaflet valve
Prosthetic Valves- Biological
* Biological Valves
o Composed of autologous or xenograft biological material mounted on stents and a sewing ring
o Warfarin therapy not required due to lower thromboembolic potential
o Valve durability less when compared to mechanical valves
o Newer stentless valves with increased longevity

Anticoagulation Guidelines for Mechanical Valves
Prosthetic Valve Complications
* Common complications include:
o Structural valve deterioration
o Valve thrombosis
o Embolism
o Bleeding
o Endocarditis
* Endocarditis prophylaxis required for patients with all types of prosthetic valves
* Suspect valve dehiscence or dysfunction in:
o Acute CHF in the immediate postop period
o New cardiac symptoms
o Embolic phenomena
o Hemolytic anemia
o New murmurs
* TEE is the diagnostic procedure of choice
* Postop TTE should be done 2-3 months after surgery

Valve Thrombosis
* Incidence with mechanical prosthesis of 2-4 % per year
* Suspect in patients with new murmur, change in cardiopulmonary symptoms, or an embolic event
* Diagnosis based on clinical presentation, TTE/TEE, and fluroscopy
* In small thrombus, treatment with heparin may be adequate
* Optimal treatment for left sided thrombosis is emergency surgery
* Consider thrombolytic therapy for right sided thrombosis or if surgery cannot be performed with left sided disease
Endocarditis Prophylaxis

The Cardiovascular Examination.ppt

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Heart Murmurs



Heart Murmurs
By: David Leder

Outline

I. Basic Pathophysiology
II. Describing murmurs
III. Systolic murmurs
IV. Diastolic murmurs
V. Continuous murmurs
VI. Summary

Basic Pathophysiology
Murmurs = Math
Describing a heart murmur

1. Timing
o murmurs are longer than heart sounds
o HS can distinguished by simultaneous palpation of the carotid arterial pulse
o systolic, diastolic, continuous
2. Shape
o crescendo (grows louder), decrescendo, crescendo-decrescendo, plateau

3. Location of maximum intensity
o is determined by the site where the murmur originates
o e.g. A, P, T, M listening areas
4. Radiation
o reflects the intensity of the murmur and the direction of blood flow

5. Intensity
o graded on a 6 point scale
+ Grade 1 = very faint
+ Grade 2 = quiet but heard immediately
+ Grade 3 = moderately loud
+ Grade 4 = loud
+ Grade 5 = heard with stethoscope partly off the chest
+ Grade 6 = no stethoscope needed

*Note: Thrills are assoc. with murmurs of grades 4 - 6

6. Pitch
o high, medium, low
7. Quality
o blowing, harsh, rumbling, and musical
8. Others:
i. Variation with respiration

+ Right sided murmurs change more than left sided

ii. Variation with position of the patient

iii. Variation with special maneuvers

+ Valsalva/Standing => Murmurs decrease in length and intensity

EXCEPT: Hypertrophic cardiomyopathy and Mitral valve prolapse

Systolic Murmurs
* Derived from increased turbulence associated with:

1. Increased flow across normal SL valve or into a dilated great vessel
2. Flow across an abnormal SL valve or narrowed ventricular outflow tract - e.g. aortic stenosis
3. Flow across an incompetent AV valve - e.g. mitral regurg.
4. Flow across the interventricular septum

Early Systolic murmurs
1. Acute severe mitral regurgitation
2. Congenital, small muscular septal defect
3. Tricuspid regurg. with normal PA pressures

Midsystolic (ejection) murmurs
* Are the most common kind of heart murmur
* Are usually crescendo-decrescendo
* They may be:
1. Innocent
2. Physiologic
3. Pathologic

Aortic stenosis
* Loudest in aortic area; radiates along the carotid arteries
* Intensity varies directly with CO
* A2 decreases as the stenosis worsens
* Other conditions which may mimic the murmur of aortic stenosis w/o obstructing flow:

1. Aortic sclerosis
2. Bicuspid aortic valve
3. Dilated aorta
4. Increased flow across the valve during systole

Hypertrophic cardiomyopathy
Pansystolic (Holosystolic) Murmurs
1. Mitral valve regurgitation
2. Tricuspid valve regurgitation
3. Ventricular septal defect
Diastolic Murmurs
* Almost always indicate heart disease
* Two basic types:

1. Early decrescendo diastolic murmurs
2. Rumbling diastolic murmurs in mid- or late diastole

Aortic Regurgitation
* Best heard in the 2nd ICS at the left sternal edge
* High pitched, decrescendo
* Blowing quality => may be mistaken for breath sounds
* Radiation:

Mitral Stenosis
* Two components:
1. Middiastolic - during rapid ventricular filling
2. Presystolic - during atrial contraction; therefore, it disappears if atrial fibrillation develops
Continuous Murmurs

1. Cervical venous hum
2. Mammary souffle
3. Patent Ductus Arteriosus
4. Pericardial friction rub
Back to the Basics
1. When does it occur - systole or diastole
2. Where is it loudest - A, P, T, M
I. Systolic Murmurs:
1. Aortic stenosis - ejection type
2. Mitral regurgitation - holosystolic
3. Mitral valve prolapse - late systole

II. Diastolic Murmurs:
1. Aortic regurgitation - early diastole
2. Mitral stenosis - mid to late diastole

Summary
A. Presystolic murmur
o Mitral/Tricuspid stenosis
B. Mitral/Tricuspid regurg.
C. Aortic ejection murmur
D. Pulmonic stenosis (spilling through S20
E. Aortic/Pulm. diastolic murmur
F. Mitral stenosis w/ Opening snap
G. Mid-diastolic inflow murmur
H. Continuous murmur of PDA

Heart Murmurs.ppt

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Valvular Heart Disease



Valvular Heart Disease

Medical Surgical I
Types
* Mitral Stenosis
* Mitral Regurgitation
* Mitral Valve Prolapse
* Aortic Stenosis
* Aortic regurgitation
* Tricuspid valve is affected infrequently
o Tricuspid stenosis – causes Rt HF
o Tricuspid regurgitation –causes venous overload

Tricuspid Valve
Rheumatic Heart Disease
* Inflammatory process that may affect the myocardium, pericardium and or endocardium
* Usually results in distortion and scarring of the valves
* Subjective symptoms
o Prior history of rheumatic fever
o General malaise
o Pain – may or may not be present
* Objective symptoms
o Temperature
o Murmurs
o Dyspnea
o polyarthritis
* Diagnosis
o H/P
o WBC and ESR
o C-reactive protein
o Cardiac enzymes
o EKG
o Chest x-ray
o Echo
o Cardiac cath
o Cardiac output
* Nursing Care
o Vital signs
o Rest and quiet environment
o Give antibiotics, digitalis, and diuretics
o Provide adequate nutrition
o Monitor I/O
o Explain treatment and home care

Mitral Stenosis
* Usually results from rheumatic carditis
* Is a thickening by fibrosis or calcification
* Can be caused by tumors, calcium and thrombus
* Valve leaflets fuse and become stiff and the cordae tendineae contract
* These narrows the opening and prevents normal blood flow from the LA to the LV
* LA pressure increases, left atrium dilates, PAP increases, and the RV hypertrophies
* Pulmonary congestion and right sided heart failure occurs
* Followed by decreased preload and CO decreases
* Mild – asymptomatic
* With progression – dyspnea, orthopneas, dry cough, hemoptysis, and pulmonary edema may appear as hypertension and congestion progresses
* Right sided heart failure symptoms occur later
* S/S
o Pulse may be normal to A-Fib
o Apical diastolic murmur is heard

Mitral Regurgitation
* Primarily caused by rheumatic heart disease, but may be caused by papillary muscle rupture form congenital, infective endocarditis or ischemic heart disease
* Abnormality prevents the valve from closing
* Blood flows back into the right atrium during systole
* During diastole the regurg output flows into the LV with the normal blood flow and increases the volume into the LV
* Progression is slowly – fatigue, chronic weakness, dyspnea, anxiety, palpitations
* May have A-fib and changes of LV failure
* May develop right sided failure as well

Mitral Valve Prolapse
* Cause is variable and may be associated with congenital defects
* More common in women
* Valvular leaflets enlarge and prolapse into the LA during systole
* Most are asymptomatic
* Some may report chest pain, palpitations or exercise intolerance
* May have dizziness, syncope and palpitations associated with dysrhythmias
* May have audible click and murmur

Aortic Stenosis
* Valve becomes stiff and fibrotic, impeding blood flow with LV contraction
* Results in LV hypertrophy, increased O2 demands, and pulmonary congestion
* Causes – rheumatic fever, congenital, arthrosclerosis
* Atherosclerosis and calcification is primary cause in the elderly
* Complications – right sided heart failure, pulmonary edema, and A-fib
* S/S – Early: dyspnea, angina, syncope

Aortic Regurgitation
* Aortic valve leaflets do not close properly during diastole
* The valve ring that attaches to the leaflets may be dilated, loose, or deformed
* The ventricle dilates to accommodate the ^ blood volume and hypertrophies
* Causes: infective endocarditis, congenital, hypertension, Marfan’s
* May remain asymptomatic for years
* Develop dyspnea, orthopnea, palpitations, ,and angina
* May have ^ systolic pressure with bounding pulse
* Have a high pitch, blowing, decrescendo diastolic murmur

Assessment for Valve Dysfunction
* Subjective symptoms
o Fatigue
o Weakness
o General malaise
o Dyspnea on exertion
o Dizziness
o Chest pain or discomfort
o Weight gain
o Prior history of rheumatic heart disease
* Objective symptoms
o Orthopnea
o Dyspnea, rales
o Pink-tinged sputum
o Murmurs
o Palpitations
o Cyanosis, capillary refill
o Edema
o Dysrhythmias
o Restlessness

Diagnosis
* History and physical findings
* EKG
* Chest x-ray
* Cardiac cath
* Echocardiogram

Medial Treatment
* Nonsurgical management focuses on drug therapy and rest
* Diuretic, beta blockers, digoxin, O2, vasodilators, prophylactic antibiotic therapy
* Manage A-fib, if develops, with conversion if possible, and use of anticoagulation

Interventions
* Assess vitals, heart sounds, adventitious breath sounds
* ^ HOB
* O2 as prescribed
* Emotional support
* Give medications
* I/O
* Weight
* Check for edema
* Explain disease process, provide for home care with O2, medications

Surgical Management of Valve Disease
* Mitral Valve
o Commissurotomy
o Mitral Valve Replacement
o Balloon Valvuloplasty
* Aortic Valve Replacement

Mechanical Valve
Porcine Valve
Tissue Valve

Valvular Heart Disease.ppt

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25 September 2009

Cardiac Assist Devices



Cardiac Assist Devices
By: Wayne E. Ellis, Ph.D., CRNA

Types
Pacemakers
AICDs
VADs

History
* First pacemaker implanted in 1958
* First ICD implanted in 1980
* Greater than 500,000 patients in the US population have pacemakers
* 115,000 implanted each year

Pacemakers Today
* Single or dual chamber
* Multiple programmable features
* Adaptive rate pacing
* Programmable lead configuration

Internal Cardiac Defibrillators (ICD)
* Transvenous leads
* Multiprogrammable
* Incorporate all capabilities of contemporary pacemakers
* Storage capacity

Temporary Pacing Indications
* Routes = Transvenous, transcutaneous, esophageal
* Unstable bradydysrhythmias
* Atrioventricular heart block
* Unstable tachydysrhythmias
* *Endpoint reached after resolution of the problem or permanent pacemaker implantation

Permanent Pacing Indications
* Chronic AVHB
* Chronic Bifascicular and Trifascicular Block
* AVHB after Acute MI
* Sinus Node Dysfunction
* Hypersensitive Carotid Sinus and Neurally Mediated Syndromes
* Miscellaneous Pacing Indications

Chronic AVHB
* Especially if symptomatic

Pacemaker most commonly indicated for:
* Type 2 2º
o Block occurs within or below the Bundle of His
* 3º Heart Block
o No communication between atria and ventricles

Chronic Bifascicular and Trifascicular Block
* Differentiation between uni, bi, and trifascicular block
* Syncope common in patients with bifascicular block
* Intermittent 3º heart block common

AVHB after Acute MI
* Incidence of high grade AVHB higher
* Indications for pacemaker related to intraventricular conduction defects rather than symptoms
* Prognosis related to extent of heart damage

Sinus Node Dysfunction
* Sinus bradycardia, sinus pause or arrest, or sinoatrial block, chronotropic incompetence
* Often associated with paroxysmal SVTs (bradycardia-tachycardia syndrome)
* May result from drug therapy
* Symptomatic?
* Often the primary indication for a pacemaker

Hypersensitive Carotid Sinus Syndrome
• Syncope or presyncope due to an exaggerated response to carotid sinus stimulation
• Defined as asystole greater than 3 sec due to sinus arrest or AVHB, an abrupt reduction of BP, or both

Neurally Mediated Syncope
* 10-40% of patients with syncope
* Triggering of a neural reflex
* Use of pacemakers is controversial since often bradycardia occurs after hypotension

Miscellaneous
* Hypertrophic Obstructive Cardiomyopathy
* Dilated cardiomyopathy
* Cardiac transplantation
* Termination and prevention of tachydysrhythmias
* Pacing in children and adolescents

Indications for ICDs
* Cardiac arrest due to VT/VF not due to a transient or reversible cause
* Spontaneous sustained VT
* Syncope with hemodynamically significant sustained VT or VF
* NSVT with CAD, previous MI, LV dysfunction and inducible VF or VT not suppressed by a class 1 antidysrhythmic

Device Selection
* Temporary pacing (invasive vs. noninvasive)
* Permanent pacemaker
* ICD

Pacemaker Characteristics
• Adaptive-rate pacemakers
•Single-pass lead Systems
• Programmable lead configuration
• Automatic Mode-Switching
• Unipolar vs. Bipolar electrode configuration

ICD selection
* Antibradycardia pacing
* Antitachycardia pacing
* Synchronized or nonsynchronized shocks for dysrhythmias
* Many of the other options incorporated into pacemakers

Approaches to Insertion
Mechanics
Unipolar Pacemaker
Bipolar Pacemaker
Indications
1. Sick sinus syndrome (Tachy-brady syndrome)
2. Symptomatic bradycardia
3. Atrial fibrillation
4. Hypersensitive carotid sinus syndrome
* Second-degree heart block/Mobitz II


Complete heart block
* Sinus arrest/block
* Tachyarrhythmias
Supraventricular, ventricular
To overdrive the arrhythmia
Atrial Fibrillation
1. Asynchronous/Fixed Rate
2. Synchronous/Demand
3. Single/Dual Chamber
4. Programmable/nonprogrammable
Synchronous/Demand
Examples of Demand Pacemakers
DDI
VVI/VVT
AAI/AAT
Disadvantage: Pacemaker may be fooled by interference and may not fire

Dual Chamber: A-V Sequential
Facilitates a normal sequence between atrial and ventricular contraction
Provides atrial kick + ventricular pacing
Atrial contraction assures more complete ventricular filling than the ventricular demand pacing unit
A-V Sequential
Disadvantage: More difficult to place
More expensive
Contraindication: Atrial fibrillation, SVT
Developed due to inadequacy of “pure atrial pacing”
Single Chamber
Atrial
Ventricular
“Pure Atrial Pacing”
Problems with Atrial Pacing
Electrode difficult to secure in atrium
Tends to float

Ventricular
Programmability
Table of Pacer Codes
Types of Pulse Generators
Examples
Other Information
Undersensing: Failure to sense ... much more in 105 slides

Cardiac Assist Devices.ppt

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Arrhythmia



ARRHYTHMIA
Edited by Yingmin Chen

* Definition of Arrhythmia:
The Origin, Rate, Rhythm, Conduct velocity and sequence of heart activation are abnormally.

Anatomy of the conducting system
Pathogenesis and Inducement of Arrhythmia
* Some physical condition
* Pathological heart disease
* Other system disease
* Electrolyte disturbance and acid-base imbalance
* Physical and chemical factors or toxicosis


Mechanism of Arrhythmia
* Abnormal heart pulse formation
* Sinus pulse
* Ectopic pulse
* Triggered activity
* Abnormal heart pulse conduction
* Reentry
* Conduct block

Classification of Arrhythmia
* Abnormal heart pulse formation
* Sinus arrhythmia
* Atrial arrhythmia
* Atrioventricular junctional arrhythmia
* Ventricular arrhythmia
* Abnormal heart pulse conduction
* Sinus-atrial block
* Intra-atrial block
* Atrio-ventricular block
* Intra-ventricular block
* Abnormal heart pulse formation and conduction

Diagnosis of Arrhythmia
* Medical history
* Physical examination
* Laboratory test

Therapy Principal
* Pathogenesis therapy
* Stop the arrhythmia immediately if the hemodynamic was unstable
* Individual therapy

Anti-arrhythmia Agents
* Anti-tachycardia agents
* Anti-bradycardia agents
Anti-tachycardia agents
* Modified Vaugham Williams classification
* I class: Natrium channel blocker
* II class: ß-receptor blocker
* III class: Potassium channel blocker
* IV class: Calcium channel blocker
* Others: Adenosine, Digital

Anti-bradycardia agents
* ß-adrenic receptor activator
* M-cholinergic receptor blocker
* Non-specific activator

Clinical usage
Anti-tachycardia agents:
* Ia class: Less use in clinic
* Guinidine
* Procainamide
* Disopyramide: Side effect: like M-cholinergic receptor blocker

Anti-tachycardia agents:
* Ib class: Perfect to ventricular tachyarrhythmia
1. Lidocaine
2. Mexiletine
Anti-tachycardia agents:
* Ic class: Can be used in ventricular and/or supra-ventricular tachycardia and extrasystole.

1. Moricizine
2. Propafenone

Anti-tachycardia agents:
* II class: ß-receptor blocker
* Propranolol: Non-selective
* Metoprolol: Selective ß1-receptor blocker, Perfect to hypertension and coronary artery disease patients associated with tachyarrhythmia.
* III class: Potassium channel blocker, extend-spectrum anti-arrhythmia agent.
* Amioarone: Perfect to coronary artery disease and heart failure patients
* Sotalol: Has ß-blocker effect
* Bretylium
* IV class: be used in supraventricular tachycardia
* Verapamil
* Diltiazem
* Others:
Adenosine: be used in supraventricular tachycardia

Anti-bradycardia agents
* Isoprenaline
* Epinephrine
* Atropine
* Aminophylline
Proarrhythmia effect of antiarrhythmia agents
* Ia, Ic class: Prolong QT interval, will cause VT or VF in coronary artery disease and heart failure patients
* III class: Like Ia, Ic class agents
* II, IV class: Bradycardia

Non-drug therapy
* Cardioversion: For tachycardia especially hemodynamic unstable patient
* Radiofrequency catheter ablation (RFCA): For those tachycardia patients (SVT, VT, AF, AFL)
* Artificial cardiac pacing: For bradycardia, heart failure and malignant ventricular arrhythmia patients.

Sinus Arrhythmia

Sinus tachycardia
* Sinus rate > 100 beats/min (100-180)
* Causes:
* Some physical condition: exercise, anxiety, exciting, alcohol, coffee
* Some disease: fever, hyperthyroidism, anemia, myocarditis
* Some drugs: Atropine, Isoprenaline
* Needn’t therapy
Sinus Bradycardia
* Sinus rate < 60 beats/min
* Normal variant in many normal and older people
* Causes: Trained athletes, during sleep, drugs (ß-blocker) , Hypothyriodism, CAD or SSS
* Symptoms:
* Most patients have no symptoms.
* Severe bradycardia may cause dizziness, fatigue, palpitation, even syncope.
* Needn’t specific therapy, If the patient has severe symptoms, planted an pacemaker may be needed.
Sinus Arrest or Sinus Standstill
* Sinus arrest or standstill is recognized by a pause in the sinus rhythm.
* Causes: myocardial ischemia, hypoxia, hyperkalemia, higher intracranial pressure, sinus node degeneration and some drugs (digitalis, ß-blocks).
* Symptoms: dizziness, amaurosis, syncope
* Therapy is same to SSS
Sinoatrial exit block (SAB)
* SAB: Sinus pulse was blocked so it couldn’t active the atrium.
* Causes: CAD, Myopathy, Myocarditis, digitalis toxicity, et al.
* Symptoms: dizziness, fatigue, syncope
* Therapy is same to SSS

Sinoatrial exit block (SAB)
* Divided into three types: Type I, II, III
* Only type II SAB can be recognized by EKG.

Sick Sinus Syndrome (SSS)
* SSS: The function of sinus node was degenerated. SSS encompasses both disordered SA node automaticity and SA conduction.
* Causes: CAD, SAN degeneration, myopathy, connective tissue disease, metabolic disease, tumor, trauma and congenital disease.
* With marked sinus bradycardia, sinus arrest, sinus exit block or junctional escape rhythms
* Bradycardia-tachycardia syndrome

Sick Sinus Syndrome (SSS)
* EKG Recognition:
* Sinus bradycardia, ≤40 bpm;
* Sinus arrest > 3s
* Type II SAB
* Nonsinus tachyarrhythmia ( SVT, AF or Af).
* SNRT > 1530ms, SNRTc > 525ms
* Instinct heart rate < 80bmp

Sick Sinus Syndrome (SSS)
* Therapy:
* Treat the etiology
* Treat with drugs: anti-bradycardia agents, the effect of drug therapy is not good.
* Artificial cardiac pacing.

Atrial arrhythmia
Premature contractions
* The term “premature contractions” are used to describe non sinus beats.
* Common arrhythmia
* The morbidity rate is 3-5%
Atrial premature contractions (APCs)
* APCs arising from somewhere in either the left or the right atrium.
* Causes: rheumatic heart disease, CAD, hypertension, hyperthyroidism, hypokalemia
* Symptoms: many patients have no symptom, some have palpitation, chest incomfortable.
* Therapy: Needn’t therapy in the patients without heart disease. Can be treated with ß-blocker, propafenone, moricizine or verapamil.

Atrial tachycardia
* Classify by automatic atrial tachycardia (AAT); intra-atrial reentrant atrial tachycardia (IART); chaotic atrial tachycardia (CAT).
* Etiology: atrial enlargement, MI; chronic obstructive pulmonary disease; drinking; metabolic disturbance; digitalis toxicity; electrolytic disturbance.........

ARRHYTHMIA.ppt

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Cardiac Arrhythmias



Cardiac Arrhythmias
By:Elise Georgi Morris, M.D.

Objectives
* Identify common arrhythmias encountered by the family physician
* Discuss arrhythmia etiologies
* Discuss initial primary care work-up and treatment
* Practice questions

Normal Sinus Rhythm
Implies normal sequence of conduction, originating in the sinus node and proceeding to the ventricles via the AV node and His-Purkinje system.
EKG Characteristics: Regular narrow-complex rhythm

Sinus Bradycardia
* HR< 60 bpm; every QRS narrow, preceded by p wave
* Can be normal in well-conditioned athletes
* HR can be<30 bpm in children, young adults during sleep, with up to 2 sec pauses

Sinus bradycardia--etiologies
* Normal aging
* 15-25% Acute MI, esp. affecting inferior wall
* Hypothyroidism, infiltrative diseases
(sarcoid, amyloid)
* Hypothermia, hypokalemia
* SLE, collagen vasc diseases
* Situational: micturation, coughing
* Drugs: beta-blockers, digitalis, calcium channel blockers, amiodarone, cimetidine, lithium

Sinus bradycardia--treatment
* No treatment if asymptomatic
* Sxs include chest pain (from coronary hypoperfusion), syncope, dizziness
* Office: Evaluate medicine regimen—stop all drugs that may cause
* Bradycardia associated with MI will often resolve as MI is resolving; will not be the sole sxs of MI
* ER: Atropine if hemodynamic compromise, syncope, chest pain
* Pacing

Sinus tachycardia
* HR > 100 bpm, regular
* Often difficult to distinguish p and t waves

Sinus tachycardia--etiologies
* Fever
* Hyperthyroidism
* Effective volume depletion
* Anxiety
* Pheochromocytoma
* Sepsis
* Anemia
* Exposure to stimulants (nicotine, caffeine) or illicit drugs
* Hypotension and shock
* Pulmonary embolism
* Acute coronary ischemia and myocardial infarction
* Heart failure
* Chronic pulmonary disease
* Hypoxia

Sinus Tachycardia--treatment
* Office: evaluate/treat potential etiology :check TSH, CBC, optimize CHF or COPD regimen, evaluate recent OTC drugs
* Verify it is sinus rhythm
* If no etiology is found and is bothersome to patients, can treat with beta-blocker

Sinus Arrhythmia
* Variations in the cycle lengths between p waves/ QRS complexes
* Will often sound irregular on exam
* Normal p waves, PR interval, normal, narrow QRS

Sinus arrhythmia
* Usually respiratory--Increase in heart rate during inspiration
* Exaggerated in children, young adults and athletes—decreases with age
* Usually asymptomatic, no treatment or referral
* Can be non-respiratory, often in normal or diseased heart, seen in digitalis toxicity
* Referral may be necessary if not clearly respiratory, history of heart disease

Sick Sinus Syndrome
* All result in bradycardia
* Sinus bradycardia (rate of ~43 bpm) with a sinus pause
* Often result of tachy-brady syndrome: where a burst of atrial tachycardia (such as afib) is then followed by a long, symptomatic sinus pause/arrest, with no breakthrough junctional rhythm.

Sick Sinus Syndrome--etiology
* Often due to sinus node fibrosis, SNode arterial atherosclerosis, inflammation (Rheumatic fever, amyloid, sarcoid)
* Occurs in congenital and acquired heart disease and after surgery
* Hypothyroidism, hypothermia
* Drugs: digitalis, lithium, cimetidine, methyldopa, reserpine, clonidine, amiodarone
* Most patients are elderly, may or may not have symptoms

Sick sinus syndrome--treatment
* Address and treat cardiac conditions
* Review med list, TSH
* Pacemaker for most is required

Paroxysmal Supraventricular Tachycardia
* Refers to supraventricular tachycardia other than afib, aflutter and MAT
* Occurs in 35 per 100,000 person-years
* Usually due to reentry—AVNRT or AVRT

PSVT
* Initial eval: Is the patient stable?
* Determine quickly if sinus rhythm
* If not sinus and unstable, cardioversion
* Unstable sinus tachycardia---IV beta-blocker, and treat cause
* Sxs of instability would include: chest pain, decreased consciousness, short of breath, shock, hypotension—unstable sxs require shock
* If stable, determine whether regular rhythm (sinus or PSVT) vs irregular (afib/flutter, MAT)? p waves (MAT vs. AF)?
* If regular, determine whether p waves are present, if can’t see---administer adenosine (6mg, can give 2 doses) or CSM or other vagal maneuvers)

* CSM or adenosine commonly terminate the arrhythmia, esp, AVRT or AVNRT
* Can also use CCB or beta blockers to terminate, if available
* Counsel to avoid triggers, caffeine, Etoh, pseudoephedrine, stress
* No p waves —junctional tachycardia, AVRT or AVNRT, Afib
* AVRT and AVNRT: can have retrograde p waves and short RP interval
* Abnormal p waves morphology: MAT

Atrial Fibrillation
* Irregular rhythm
* Absence of definite p waves
* Narrow QRS
* Can be accompanied by rapid ventricular response

Atrial Fibrillation—causes and associations
* Hypertension
* Hyperthyroidism and subclinical hyperthyroidism
* CHF (10-30%), CAD
* Uncommon presentation of ACS
* Mitral and tricuspid valve disease
* Hypertrophic cardiomyopathy
* COPD
* OSA
* ETOH
* Caffeine
* Digitalis
* Familial
* Congenital (ASD)

Atrial fibrillation--assessment
* H & P—assess heart rate, sxs of SOB, chest pain, edema (signs of failure)
* If unstable, need to cardiovert
* Echocardiogram to evaluate valvular and overall function
* Check TSH
* Assess for RVR
* Assess onset of sxs—in the last 24-48 hours? Sudden onset? Or no sxs?

Atrial fibrillation--management
* Rhythm vs Rate control—if onset is within last 24-48 hours, may be able to arrange cardioversion—use heparin around procedure
* Need TEE if valvular disease (high risk of thrombus)
* If unable to definitely conclude onset in last 24-48 hours: need 4-6 weeks of anticoagulation prior to cardioversion, and warfarin for 4-12 weeks after

Atrial Fibrillation
* Cardioversion: synchronized (w/QRS) delivery of current to heart; depolarizes tissue in a reentrant circuit; afib involves more cardiac tissue, but cardiovert
* Defibrillation: non-synchronized delivery of current

Atrial fibrillation--management
* Rate control with chronic anticoagulation is recommended for first line approach for majority of patients; overall Afib is a stable rhythm
* Beta-blockers (atenolol and metoprolol) or calcium channel blockers (verapamil or diltiazem) recommended. Digoxin not recommended for rate control
* Anticoagulation: LMWH and then warfarin; can use aspirin for anticoagulation if CI to warfarin, not as effective

Atrial fibrillation--management
* Goal INR of 2.5 (2.0-3.0)
* Rhythm control---second line approach, if unable to control rate or pt with persistent sxs
* Can also consider radiofrequency ablation at pulm veins
* P wave from another atrial focus
* Occurs earlier in cycle
* Different morphology of p wave
* Benign, common cause of perceived irregular rhythm
* Can cause sxs: “skipping” beats, palpitations
* No treatment, reassurance
* With sxs, may advise to stop smoking, decrease caffeine and ETOH
* Can use beta-blockers to reduce frequency

1st Degree AV Block
* PR interval >200ms
* If accompanied by wide QRS, refer to cardiology, high risk of progression to 2nd and 3rd deg block
* Otherwise, benign if asymptomatic

2nd Degree AV Block Mobitz type I (Wenckebach)

* Progressive PR longation, with eventual non-conduction of a p wave
* May be in 2:1 or 3:1
Wenckebach, Mobitz type I
* Usually asymptomatic, but with accompanying bradycardia can cause angina, syncope esp in elderly—will need pacing if sxs
* Also can be caused by drugs that slow conduction (BB, CCB, dig)
* 2-10% long distance runners
* Correct if reversible cause, avoid meds that block conduction

2nd degree block Type II (Mobitz 2)
* Normal PR intervals with sudden failure of a p wave to conduct
* Usually below AV node and accompanied by BBB or fascicular block
* Often causes pre/syncope; exercise worsens sxs
* Generally need pacing, possibly urgently if symptomatic

3rd Degree AV Block

* Complete AV disassociation, HR is a ventricular rate
* Will often cause dizziness, syncope, angina, heart failure
* Can degenerate to Vtach and Vfib
* Will need pacing, urgent referral
* Extremely common throughout the population, both with and without heart disease
* Usually asymptomatic, except rarely dizziness or fatigue in patients that have frequent PVCs and significant LV dysfunction
* No treatment is necessary, risk outweighs benefit
* Reassurance
* Optimize cardiac and pulmonary disease management

Non-sustained Ventricular tachycardia
* Defined as 3 or more consecutive ventricular beats
* Rate of >120 bpm, lasting less than 30 seconds
* May be discovered on Holter, or other exercise testing

Non-sustained ventricular tachycardia
* Need to exclude heart disease with Echo and stress testing
* If normal, there is no increased risk of death
* May need anti-arrhythmia treatment if sxs
* In presence of heart disease, increased risk of sudden death
* Need referral for EPS and/or prolonged Holter monitoring

Ventricular fibrillation
* Defibrillation

Practice Questions—Case studies

References

Cardiac Arrhythmias.ppt

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Bradycardia-tachycardia syndrome



Bradycardia-tachycardia syndrome
By: Presented by Ri

Sick sinus syndrome

* Multiple manifestations on EKG
* Sinus bradycardia
* Sinus arrest
* Sinoatrial block
* Bradycardia –tachycardia syndrom

Bradycardia-tachycardia syndrome

* Alternating patterns of bradycardia and tachycardia
* Often there is a long pause (asystole) between heartbeats, especially after an episode of tachycardia
* Tachycardia: PSVT, atrial fibrillation, atrial flutter

causes

* Most cases are idiopathic
* Intrinsic causes
* Extrinsic causes
* Cardiac surgery, especially to the atria, is a common cause of sick sinus syndrome in children.

Clinical manifestations

* Many people with sick sinus syndrome have no symptoms
* Symptoms are related to the decresed cardiac output that occurs with the bradyarrythmias or tachyarrythmias
* Fainting , Fatigue , Shortness of breath, or dyspnea, Chest pains , Confusion , Palpitations
* Bradycardia-tachycardia syndrome: peripheral thromboembolism and stroke

Treatment

* If the disorder is asymptomatic (without symptoms), no treatment is necessary
* Bradycardia-tachycardia syndrome
* Associated tachycardia may be treated with medications after the person is protected from symptomatic bradycardia by a pacemaker.
* Warfarin has been shown to decrease the number of strokes and embolic events

Bradycardia-tachycardia syndrome.ppt

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Arrhythmias and EKGs



Arrhythmias and EKGs

Outline
* Sinus Arrhythmia and Sick Sinus Syndrome
* Multifocal Atrial Tachycardia
* Bigeminal Rhythms
* Preexcitation and AVRT

Mechanisms of Arrhythmogenesis
Sinus Arrhythmia
EKG Characteristics: Presence of sinus P waves
Variation of the PP interval which cannot be q attributed to either SA nodal block or PACs

When the variations in PP interval occur in phase with respiration, this is considered to be a normal variant. When they are unrelated to respiration, they may be caused by the same etiologies leading to sinus bradycardia.

Sick Sinus Syndrome
* Characterized by a collection of symptoms and ECG findings due to chronic dysfunction of the sinoatrial (SA) node:
o Chronic and severe sinus bradycardia
o Sinus pauses
o Sinus arrhythmia
o Complete sinus arrest
o Progressive development of atrial arrhythmias (a-flutter, a-fib, atrial tachycardia)
* Patients are usually elderly and present with lightheadedness and/or syncope, but it can also manifest as angina, dyspnea, and palpitations.

* About 50% of people with SSS also display some degree of dysfunction of the AV node
Sinus bradycardia (rate of ~43 bpm) with a sinus pause

Etiologies of Sick Sinus Syndrome
Familial SSS (due to mutations in SCN5A)
Infiltrative diseases
Pericarditis
Lyme disease
Hypothyroidism
Rheumatic fever
Sinus node firbosis
Atherosclerosis of the SA artery
Congenital heart disease
Excessive vagal tone
Drugs
Tachycardia-Bradycardia Syndrome
* Common variant of sick sinus syndrome severe bradycardia alternates with paroxysmal tachycardias, most often atrial fibrillation.
* There is usually a prolonged pause in the cardiac rhythm following cessation of the tachyarrhythmia.
Tachycardia-Bradycardia Syndrome
Abrupt termination of atrial flutter with variable AV block, followed by sinus arrest with a junctional escape beat.

Multifocal Atrial Tachycardia
Bigeminal Rhythms
* Arrhythmias in which each normal sinus beat is followed by a premature contraction (PAC, PJC, or PVC).
* Results in a couplet rhythm which can be detected by pulse or auscultation.
* Generally benign
Atrial Bigeminy
Ventricular Bigeminy
Preexcitation
ECG Characteristics of WPW:
1. Short PR interval
2. QRS prolongation
3. Delta wave
Preexcitation is a condition characterized by an accessory pathway of conduction, which allows the heart to depolarize in an atypical sequence.
The most common form of preexcitation is called Wolfe-Parkinson-White (WPW) syndrome, in which a direct atrioventricular connection allows the ventricles to begin depolarization while the standard action potential is still traveling through the AV node.

AV Reentrant Tachycardia (AVRT)
In patients with WPW, a reentrant rhythm can be generated where the AV node serves as one arm of the reentrant circuit, and the accessory pathway as the other.

Types of AVRT
* Orthodromic AVRT (More common) – Narrow complex tachycardia in which the wave of depolarization travels down the AV node and retrograde up the accessory pathway.
* Antidromic AVRT (Less common) – Wide complex tachycardia in which the wave of depolarization travels down the accessory pathway and retrograde up the AV node.

Mechanism of orthodromic AVRT
Mechanism of antidromic AVRT
What is this arrhythmia?
Antidromic AVRT
Classification Scheme for Arrhythmias

Arrhythmias and EKGs.ppt

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27 August 2009

Angioedema



Angioedema

Overview
* Self-Limited, subcutaneous edema resulting from increased vascular permeability
* Generally resolves over 24-48 hours
* Mast Cell / Kinin related etiologies
* Involvement of the lips, pharynx and bowel common (potentially life-threatening)
* Treated with CCS and H1/H2 blockers

Etiology
* Immunologic / IgE mediated
* Hereditary and Acquired (non-mast cell)
Ace-Inhibitors
* ACE (Kininase II) degrades bradykinin
* ACE-I results in inc levels bradykinin
* Pts with genetic deficiencies in bradykinin degradation could be at higher risk
* 0.1-0.7% of patients tx with ACE-I
* Intestinal edema may develop

ACE-I
Hereditary/Acquired
* Kinin-mediated angioedema that may be unmasked with use of ACE-I
* C1-Inh deficiency (level or fx) - Inc BKinin
Summary

* Angioedema is potentially life-threatening
* Associated pruritis and hives points to anaphylaxis
* Absence of pruritis and hives think ACE-I and/or C1-Inh deficiency
* Use caution when switching from an ACE-I to an ARB

Angioedema

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Congestive Heart Failure



Congestive Heart Failure
By:Chris Hague, PhD
Technical Advisor: Seth Goldenberg, PhD

Outline

1. What is congestive heart failure?
2. Cardiac Glycosides
3. Phosphodiesterase inhibitors
4. Beta-adrenergic receptor antagonists
5. Sympathomimetics
6. ACE inhibitors/angiotensin receptor antagonists
7. Vasodilators
8. Diuretics
9. Aldosterone antagonists

Congestive Heart Failure
Patient Classification
* Class I (asymptomatic)
* Class II (mild)
* Class III (moderate)
* Class IV (severe)

Factors contributing to CHF
* Ischemic Heart Disease: most prevalent
* CAD: less blood flow to heart, increased damage
* Myocardial Infarct: damaged tissue
* Hypertension: “overworked” heart
* Diabetes
* Lung Disease
* Cardiomyopathies: heart muscle disease
o dilated - enlarged chambers (ventricle/atria)
o hypertrophic - thickened ventricle walls
* Abnormal heart valves: inefficient pumping
o causes are genetic, infection or disease
* Congenital heart defects: present at birth
* Severe Anemia
* Hyperthyroidism
* Cardiac Arrhythmia

Effect on Cardiac Output
Overall decrease in Frank-Starling curve with CHF
Examples of CHF factors
Hypertrophic Cardiomyopathy
Congenital Heart Defects
Types of Heart Failure

* include left, right or both sides
* left ventricular heart failure
* right ventricular heart failure
Onset of disease

* chronic disease: can take years to develop
* endogenous compensatory mechanisms

Compensatory Mechanisms
Symptoms of CHF
* shortness of breath
* persistent coughing/wheezing
* edema (or excess fluid buildup in body tissues)

Symptoms of CHF
* tiredness/fatigue
* lack of appetite/nausea
* confusion/impaired thinking
* increased heart rate

Problems
* Reduced force of contraction
* Decreased cardiac output
* Increased TPR
* Inadequate organ perfusion
* Development of edema
* Decreased exercise tolerance
* Ischemic heart disease
* Sudden death

Therapeutic Overview
Goals
* alleviate symptoms
* improve quality of life
* arrest cardiac remodeling
* prevent sudden death
Drug
* Chronic heart failure
o ACE inhibitors
o Beta-blockers
o ATII antagonists
o aldosterone antagonists
o digoxin
o diuretics
* Acute heart failure
o diuretics
o PDE inhibitors
o vasodilators

Therapies
Non-drug
* Reduce cardiac work
* Rest
* Weight loss
* low Na+ diet
Cardiac Glycosides
* discovered by William Withering
* published “An Account of Foxglove and some of Its Medical Uses” in 1785
* Foxglove plant
Cardiac Glycosides
* derived from plants
o Strophanus - Ouabain
o Digitalis lanata - Digoxin, Digitoxin
* increase force of myocardial contraction
* alters electrophysiological properties
* toxic side-effects
* Digoxin most common used in USA

Digitalis lanata
Mechanism of Action
* inhibitor of Na+/K+ ATPase pump
* increased [Na+]i
* increased Ca2+ influx through Na+/Ca2+ exchanger
* new Ca2+ steady-state: increased Ca2+ release during cardiac action potential
Electrophysiological Effects
* Direct effects
o spontaneous depolarization of atrial cardiomyocytes at high doses

Electrophysiological Effects
Overall Effect on Cardiac Function

Foxglove
Therapeutic Uses
* only orally effective inotropic agent approved in US
* also for CHF secondary to ischemic heart disease
* contraindicated in patients with Wolff-Parkinson-White syndrome
* does not stop disease progression or prolong life in CHF patients

Pharmacokinetics
* long half-life (24-36 h): once daily dosing
* high bioavailability from oral dosing
* large volume of distribution
* digoxin excreted in kidneys
* digitoxin metabolized in liver, active metabolites
* intestinal flora cause variations in toxicity

Side Effects
* extremely low therapeutic index (~2)
* most effects caused by inhibition of Na+/K+ ATPase in extracardiac tissues
* CNS: malaise, confusion, depression, vertigo, vision
* GI: anorexia, nausea, intestinal cramping, diarrhea
* Cardiac: bradycardia, arrhythmias
* anti-digoxin antibody in toxic emergencies

Serum Electrolytes affect Toxicity
* Ca2+
* hypercalcemia: increases toxicity
* K+
* digitalis competes for K+ binding site on Na+/K+ ATPase
* contraindicated with K+ depleting diuretics or patients with hypo/hyperkalemia
* hypokalemia: increased toxicity
* hyperkalemia: decrease toxicity

Example of cardiac side effects
* action potential recordings from purkinje fiber cells
* toxic doses produce oscillatory after depolorizations
* leads to ventricular tachycardia (C)

Vision Effects
* yellow-tinted vision or yellow corona-like spots

Phosphodiesterase Inhibitors
* primarily used for management of acute heart failure
* positive inotropic effects
* increase rate of myocardial relaxation
* decrease total peripheral resistance and afterload

Mechanism of Action
* inhibitor of type III cAMP phosphodiesterase
* increased [cAMP]
* increased PKA phosphorylation of Ca2+ channels in cardiac muscle
* increased cardiac contraction
* relaxes vascular smooth muscle

Therapeutic Use
* Amrinone (Inocor) and Milrinone (Primacor)
* administered IV
* milrinone is ~1o fold more potent
* T 1/2 = 2.5 h for amrinone and 30-60 min for milrinone
* effective in patients taking Beta-blockers
* does not stop disease progression or prolong life in CHF patients
* prescribed to patients non-responsive to other therapies

Side Effects
* sudden death secondary to ventricular arrhythmia
* hypotension
* thrombocytopenia
* long term clinical trials associated with increased adverse effects and increased mortality
* now only prescribed for acute cardiac decompensation in patients non-responsive to diuretics or digoxin

β-adrenergic receptor antagonists
* “β-blockers”
* standard therapy for treatment of CHF
* cheap!
* reduce sudden death caused by other drugs
* Propranolol: prototype
* Carvedilol: combination effects

Propranolol
Carvedilol
Mechanism of Action
* mechanism still unclear
* antagonizes β-adrenergic receptors on cardiac myocytes
* counterbalances increased SNS activity in CHF
* prevents development of arrhythmias
* reduces cardiac remodeling
* prevents renin release

Therapeutic Use
* administered orally
* usually given in conjunction with other therapy
* effective in patients with chronic systolic heart failure in Class II (mild) to Class III (moderate)
* prevents remodeling and cardiac damage

Side Effects
* cardiac decompensation
* bradycardia
* hypoglycemia
* cold extremeties
* fluid retention
* fatigue

Direct acting sympathomimetics
* cause immediate increases in cardiac inotropy
* goal: to increase cardiac output but not effect total peripheral resistance
* used in treatment of acute life-threatening CHF

Dopamine
Dobutamine
Mechanism of Action
* Norepinephrine/epinephrine: increase CO, increase TPR
* Dopamine:
* Dobutamine:

Therapeutic Use
* administered IV, very short T 1/2
* Dopamine
o used in cardiogenic, traumatic or hypovolemic shock
o used with furosemide in diuretic resistant patients (volume overload)
* Dobutamine
o used in patients with low cardiac output and increased left ventricular end-diastolic pressure
o not for use in hypotensive patients

Side Effects
* restlessness
* tremor
* headache
* cerebral hemorrhage
* cardiac arrhythmias
* used with caution in patients taking β-blockers
* can develop dobutamine tolerance

ACE inhibitors/AT1 receptor antagonists
* Goal: to reduce afterload/preload, reduce workload on heart
* generates positive cardiac inotropy
* used in treatment of chronic CHF

ACE inhibitors/AT1 receptor antagonists
* orally active
* ACE inhibitors
* Captopril
* Enalopril
* AT1 antagonists
* Losartan
* Valsartan

Mechanism of Action
* ACE inhibitors
* AT1 receptor antagonists
* selectively inhibits ATI receptor activation
* decreased preload
* decreased afterload
* decreased cardiac remodeling
* decreased SNS effects

Therapeutic Uses
* drugs of choice in heart failure
* increase survival in long term CHF
* ACE inhibitors
* AT1 receptor antagonists
Side Effects
* ACE inhibitors
+ cough
+ angioneurotic edema
+ hypotension
+ hyperkalemia
* ACE inhibitors and ATI receptor antagonists are both teratogenic

Vasodilators
* Goal: reduce TPR without causing large decrease in BP
* reduce preload
* reduce afterload
* relieves symptoms
* increase exercise tolerance

Drugs Used
* NO Donors
o Nitroglycerin
+ acute ischemia or acute heart failure
+ orally active
+ also administered I.V. for peripheral vasodilation
+ quick onset for acute relief
o Isosorbide dinitrate/hydralazine
+ chronic administration for long-term symptom relief
+ administered I.V.

Drugs Used
* Nesiritide
o recombinant brain-natriuretic peptide (BNP)
o BNP is secreted from ventricular myocytes in response to stretch
o vasodilator: increases cGMP in SMCs
+ decrease afterload/preload
o inhibits cardiac remodelling
o suppresses aldosterone secretion
o administered IV for acute decompensated CHF
o adverse effects: hypotension, renal failure (?)

Diuretics
* used in CHF to reduce extracellular fluid volume
* primarily used in patients with acute CHF with volume overload
* IV infusion causes immediate and predictable diuresis for immediate relief
* Goal: reduce preload/afterload
* overdosing can result in excessive reduction in preload, overreduction in stroke volume
* thiazide and loop diuretics (i.e. Furosemide) commonly used as adjunct therapies in CHF

Aldosterone Antagonists

* elevated AngII levels increase production of aldosterone in the adrenal cortex (~20X increase)
* aldosterone activates mineralocorticoid receptors in renal epithelial cells in kidney
* aldosterone promotes
o Na+ retention, Mg2+ and K+ loss
o increased SNS activity
o decreased PSNS activity
o myocardial/vascular fibrosis

Therapeutic Use
* Goal: inhibit aldosterone negative effects in CHF
* aldosterone receptor antagonists
o spironolactone
o eplerenone
* both antagonists reduce mortality in patients with moderate to severe CHF
* only use in patients with normal renal function and K+ levels
* use with K+ sparing diuretic

Side Effects
* hyperkalemia
* agranulocytosis
* anaphylaxis
* hepatoxicity
* renal failure
* Spironolactone: gynecomastia, sexual dysfunction
* Eplerenone: arrhythmia, myocardial infarct/ischemia

Congestive Heart Failure

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Heart Failure



Heart Failure
By:S. Soliman MD

Definition:
* A state in which the heart cannot provide sufficient cardiac output to satisfy the metabolic needs of the body
* It is commonly termed congestive heart failure (CHF) since symptoms of increase venous pressure are often prominent
Etiology
-Inappropriate work load (volume or pressure overload)
-Restricted filling
-Myocyte loss

Causes of left ventricular failure

• Volume over load: Regurgitate valve
• Pressure overload: Systemic hypertension

Outflow obstruction
• Loss of muscles: Post MI, Chronic ischemia
Connective tissue diseases Infection, Poisons
(alcohol,cobalt,Doxorubicin)
• Restricted Filling: Pericardial diseases, Restrictive
cardiomyopathy, tachyarrhythmia

Pathophysiology
* Hemodynamic changes
* Neurohormonal changes
* Cellular changes

Hemodynamic changes
Neurohormonal changes
Cellular changes
Symptoms
Physical Signs
Framingham Criteria for Dx of Heart Failure
* Major Criteria:
o PND
o JVD
o Rales
o Cardiomegaly
o Acute Pulmonary Edema
o S3 Gallop
o Positive hepatic Jugular reflex
o ↑ venous pressure > 16 cm H2O
* Minor Criteria
LL edema,
Night cough
Dyspnea on exertion
Hepatomegaly
Pleural effusion
↓ vital capacity by 1/3 of normal
Tachycardia 120 bpm
Weight loss 4.5 kg over 5 days management

Forms of Heart Failure
* Systolic & Diastolic
* High Output Failure
o Pregnancy, anemia, thyrotoxisis, A/V fistula, Beriberi, Pagets disease
* Low Output Failure
* Acute
* Chronic
* Right vs Left sided heart failure:

Right sided heart failure :
Most common cause is left sided failure
Other causes included : Pulmonary embolisms
Other causes of pulmonary htn.
RV infarction
MS
Usually presents with: LL edema, ascites
hepatic congestion
cardiac cirrhosis (on the long
Differential diagnosis
* Pericardial diseases
* Liver diseases
* Nephrotic syndrome
* Protein losing enteropathy

Laboratory Findings
* Anemia
* Hyperthyroid
* Chronic renal insuffiency, electrolytes abnormality
* Pre-renal azotemia
* Hemochromatosis

Electrocardiogram
* Old MI or recent MI
* Arrhythmia
* Some forms of Cardiomyopathy are tachycardia related
* LBBB→may help in management

Chest X-ray
* Size and shape of heart
* Evidence of pulmonary venous congestion (dilated or upper lobe veins → perivascular edema)
* Pleural effusion

Echocardiogram
* Function of both ventricles
* Wall motion abnormality that may signify CAD
* Valvular abnormality
* Intra-cardiac shunts

Cardiac Catheterization
* When CAD or valvular is suspected
* If heart transplant is indicated

TREATMENT
* Correction of reversible causes
Diet and Activity
* Salt restriction
* Fluid restriction
* Daily weight (tailor therapy)
* Gradual exertion programs

Diuretic Therapy
* The most effective symptomatic relief
* Mild symptoms
* Side Effects
* More severe heart failure → loop diuretics
o Lasix (20 – 320 mg QD), Furosemide
o Bumex (Bumetanide 1-8mg)
o Torsemide (20-200mg)

Mechanism of action: Inhibit chloride reabsortion in ascending limb of loop of Henle results in natriuresis, kaliuresis

and metabolic alkalosis

Adverse reaction:
pre-renal azotemia
Hypokalemia
Skin rash
ototoxicity

K+ Sparing Agents
* Triamterene & amiloride – acts on distal tubules to ↓ K secretion
* Spironolactone (Aldosterone inhibitor)
recent evidence suggests that it may improve survival in CHF patients due to the effect on renin-angiotensin-aldosterone

system with subsequent effect on myocardial remodeling and fibrosis

Inhibitors of renin-angiotensin- aldosterone system

o Renin-angiotensin-aldosterone system is activation early in the course of heart failure and plays an important

role in the progression of the syndrome
o Angiotensin converting enzyme inhibitors
o Angiotensin receptors blockers
o Spironolactone

Angiotensin Converting Enzyme Inhibitors
Side effects of ACE inhibitors
* Angioedema
* Hypotension
* Renal insuffiency
* Rash
* cough
Angiotensin II receptor blockers
* Has comparable effect to ACE I
* Can be used in certain conditions when ACE I are contraindicated (angioneurotic edema, cough)
Digitalis Glycosides (Digoxin, Digitoxin)
* The role of digitalis has declined somewhat because of safety concern
* Recent studies have shown that digitals does not affect mortality in CHF patients but causes significant

Mechanism of Action
* +ve inotropic effect by ↑ intracellular Ca & enhancing actin-myosin cross bride formation (binds to the Na-K ATPase →

inhibits Na pump → ↑ intracellular Na → ↑ Na-Ca exchange
* Vagotonic effect
* Arrhythmogenic effect

Digitalis Toxicity
* Narrow therapeutic to toxic ratio
* Non cardiac manifestations
Anorexia,
Nausea, vomiting,
Headache,
Xanthopsia sotoma,
Disorientation
* Cardiac manifestations

Digitalis Toxicity Treatment
* Hold the medications
* Observation
* In case of A/V block or severe bradycardia → atropine followed by temporary PM if needed
* In life threatening arrhythmia → digoxin-specific fab antibodies
* Lidocaine and phenytoin could be used – try to avoid D/C cardioversion in non life threatening arrhythmia

β Blockers
* Has been traditionally contraindicated in pts with CHF
* Now they are the main stay in treatment on CHF & may be the only medication that shows substantial improvement in LV

function
* In addition to improved LV function multiple studies show improved survival
* The only contraindication is severe decompensated CHF

Vasodilators
Positive inotropic agents
Anticoagulation (coumadine)
* Atrial fibrillation
* H/o embolic episodes
* Left ventricular apical thrombus

Antiarrhythmics
* Most common cause of SCD in these patients is ventricular tachyarrhythmia
* Patients with h/o sustained VT or SCD → ICD implant
* Patients with non sustained ventricular tachycardia

New Methods
* Implantable ventricular assist devices
* Biventricular pacing (only in patient with LBBB & CHF)
* Artificial Heart

Cardiac Transplant
* It has become more widely used since the advances in immunosuppressive treatment
* Survival rate
Prognosis
Heart Failure

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