Heart Failure
description
Transcript of Heart Failure
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Case History
Name : Fred Field Gender : MaleAge : 63 yearsDetails :- Manufacture Kitchen
Equipments- Work long hours under
pressure, esp. in Trade Fair Weeks
- Heavy breakfast @ 8 am (egg, bacon, sausage, bread)
- Medication Taken : Antacid
Symptoms:
- Angina
- Nausea
- Edema in ankles &
joints
Diagnosis:-No MI
- Cardiomegaly
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What tests could be performed to show
whether Myocardial Infarction (MI) has
occurred?
Question 1.
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Test Results [indicating MI]Tests done for MI
Laboratory TestsEnzymes :
- CK MB
- Lactate Dehydrogenase (LDH)
Proteins : Myoglobin
Cardiac Troponins (T & I subtypes)
Physical Tests - X-rays
- ECG
- Angiogram
- MRI (Magnetic Resonance Imaging)
- Radionuclide Imaging
- Elevation of
- CKMB
- Cardiac Troponins
- LDH (*not specific)
- Myoglobin Protein (*not specific)
- Abnormal Chest X-Ray showing
cardiomegaly
- Abnormal ECG waves
- Coronary Blockage (Angiograms)
- Abnormal pictures of Heart in MRI
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Chest X-Rays
1. Superior Vena Cava2. Right Atrium3. Right Ventricle4. Aortic Knuckle5. Pulmonary Artery6. Left Ventricle7. Apex
Normal Chest X-Ray(4)
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Chest X-Rays
(fig a. Front View) (fig b. Side View)
Chest X-rays Showing Enlargement of Heart(3)
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ECG: Electro Cardiogram
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ECG: Electro Cardiogram
(Figure : ECG showing Abnormal Waves)
12-lead electrocardiogram showing ST-segment elevation (orange) in I, aVL and V1-V5 with reciprocal changes (blue) in the inferior leads, indicative
of an anterior wall myocardial infarction
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Arteriogram/Angiogram(2)
• Coronary Angiography + Cardiac Catheterization• Tested for chances of MI, when there’s–
• Unstable Angina• Atypical Chest Pain• Unexplained Heart Failure
• Uses X-rays and a special dye injected into the blood flow; the blood flow is screened for blocks
• Risks – • Arrhythmias, Heart Attacks, • Allergies to the dye,• Bleeding & infection at the injection site, • Blood clots, Stroke, • Blood vessel damage, • Hemorrhage, Hematoma• Kidney damage due to the dye Fig. Angiogram
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Arteriogram/Angiogram(2)
Figure a.Arteriogram OR
Coronary Angiogram
Figure b.Cardiac Catheterization
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Magnetic Resonance Imaging (1)
• Cardiac Nuclear Magnetic Imaging, when ECG is unclear• Avoid dangers of Angiogram, repeated exposure to radiation,
&/or use of Ionic-based dye• Used to diagnose - heart muscle damage after MI - Birth defects of the heart - Heart tumors and growths• Show - Amount of dead heart cells after MI - Heart Valve Disorders
- Pericardial Effusions - Fibrosis of Heart - Congenital Heart Abnormalities
• NO RADIATION: Radio-magnetic waves • Special dye given as IV in special tests (commonly
Gadolinium)• **Metals must be removed before the test (Magnetic Waves)
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Magnetic Resonance Imaging (6)
Panels A–D: MRI study at baseline demonstrates slight apical hypokinesis in end-systolic phase (arrows in D, C = end-diastolic phase).
In A and B, short-axis delayed-enhanced MR images show multiple foci in the sub-epicardium and the midwall (arrows in A and B) and the acute ECG shows ST-elevation (arrows).
At 3-months follow-up (E–H), systolic function normalized (G and H) and delayed-enhancement demonstrates resolution of inflammatory foci (E and F, identical location as in A and B) with ECG normalization (F/u).
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Radionuclide Imaging(7)
• To evaluate :
– coronary artery disease (CAD),
– valvular or congenital cardiac disorders,
– cardiomyopathy, and other cardiac disorders
• 3D images of the Heart
• Use Single Photon Emitting Computerized Tomography (SPECT)
• Radioisotopes Injected IntraVenously
• A gamma camera is used to capture the photon particles emitted from the
radioisotopes (same as Computerized Tomography)
• Camera is revolved around the patient, in an elliptical fashion, to capture
images from different angles and create a 3D image
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Radionuclide Imaging(7)
(Fig.) Stress and rest images from single-photon emission computed tomography (SPECT) of a 52-yr-old man with recent-onset angina. Images obtained during stress show a large area of ischemia in the territory fed by the left anterior descending (LAD) artery that is absent at rest. Angiography confirmed a 95 to 99% occlusion involving the bifurcation of the LAD at the first diagonal branch.[Source: http://www.merck.com/mmpe/multimedia/Photo1sec07ch070.html?Ref=t&ItemId=Photo1sec07ch070&RefId=sec07/ch070/ch070i]
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Laboratory Testing
• NOT much sensitive or specific – critical timing• Cardiac Markers Tested –
1. Troponin (I & T) : Structural components of cardiac muscles - Released into blood stream after MI- Elevate within 3 to 12 hours, - Uptill 5-9days (I) & 2 weeks (T)
2. Creatinine Kinase : MB fraction is more specific for MI - 15-40% of CK in Cardiac Muscle- CK MB has 2 isoforms (1&2)- Ratio of CKMB isoform 2 to 1 indicates MI (>= 1.5)
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3. Myoglobin : Present in skeletal & cardiac muscles- Elevate before CKMB- Rise in Myoglobin: Size of MI, - Negative Myoglobin: No MI
4. LDH : MUST be supplemented by other tests- 5 isoenzymes (1 to 5)- Elevates within 12-24 hrs, Dissipates in 5-14 days- Peaks at 2-3 days- Isoenzyme 2 > 1 (normal); Isoenzyme 1 > 2 (MI)
Laboratory Testing
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To Diagnose MI
• No laboratory tests are specific to diagnose MI • Must combine with physical examination and
various scanning tests • Physical Symptoms of MI (all or some*) :– Restlessness, Severe Distress, Increased
Respiratory Rate, Perspiration, Low-grade Fever, BP Changes, Arrhythmia, Cold & Pale Complexion
..Fred Field had NO myocardial infarction..
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Question 2.
How are swollen ankles and cardiac
enlargement related to heart failure?
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EDEMA in CHF
Impaired Pumping Action of Ventricles
Blood backing up in the venous side of the circulatory system
High hydrostatic pressure in the venous end of capillary beds
Water loss from plasma into interstitial spaces between cells
Edema in body & extremities (Eg. Pulmonary Edema, Edema in ankles & eyelids, etc. )
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EDEMA in CHF
Fig A. Pulmonary Edema
Fig B. Edema in Extremities Fig C. Edema in Congestive Heart Failure
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Cardiomegaly in CHF
Damaged Cardiac Fibers (due to MI, Cardio Myopathy, etc.)
Inefficient Cardiac Contractibility
The Need to improve Cardiac Contractibility
Inability of Cardiac cells to differentiate into Myocardium
Enlargement or Hypertrophy of the Myocardium
Increased stiffness of Heart Walls
Decreased ability of relaxation ,after contraction
Enlargement of Heart or Cardiomegaly
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Cardiomegaly in CHF
Fig a. Cardiomegaly
Fig b. Cardiomyopathy
Fig c. Cardiac Hypertrophy
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Question 3.
How is tissue fluid normally formed, and
how is this changed in congestive heart
failure?
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Formation of Tissue Fluid
Fig A.Normal Formation of Tissue Fluid
Fig B. Fluid Retention in Congestive Heart Failure
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Formation of Tissue Fluid(9) .. In Normal Condition & Congestive Heart Failure ..
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Question 4.
What is the mechanism of action of
thiazide diuretics, and how may they
help patients with heart failure?
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Thiazide Diuretics
????
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Diuretics
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Thiazide Diuretic• Derived from Benzothiadiazine
• Inhibit Na+,Cl- reabsorption (thiazidie-sensitive
symporters)
• K+ , Serum Uric Acid
• Risks of MI, CHF, stroke
• Cheap & affordable for general public
• First choice of Hypertension treatment
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Thiazides
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Thiazides
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ThiazidesMechanism of Action of Thiazides
Thiazide
• Lowers the Blood
Pressure
• Decreases the workload
• Prevents overload of
blood in veins
• Prevents inefficient
pumping
• Prevents overwork of
heart muscles
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ThiazidesMechanism of Action of Thiazides
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• The Laboratory tests and Physical tests such as X-Rays, ECG, Angiogram, MRI and Radionuclide Imaging proved that Fred Field have no myocardial infarction.
• Impaired pumping action of ventricles, damaged cardiac fibres and decreased oncotic pressure at the venous end cause oedema and thus results in swollen ankles and cardiac enlargement.
• Whenever hydrostatic pressure is greater than oncotic pressure, fluid will leave the capillaries into the tissue and whenever the oncotic pressure is greater than the hydrostatic pressure fluid will enter the capillaries. If not the fluid will accumulate in the tissue and cause oedema.
• Thiazide diuretics inhibit Cl binding & transport, inhibit Na+ transport, lowers ˉ
blood pressure, decrease workload, decrease K+, increase serum uric acid and thus it decrease the risks of MI, CHF and Stroke.
SUMMARY
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References1. Taylor's Cardiovascular Diseases: A Handbook by Robert B. Taylor, M.D. Editor; 2005 Springer; ISBN
0-387-22351-72. Braunwald: Heart Disease: A Textbook of Cardiovascular Medicine, 6th Ed.; 2001 W.B. Saunders;
ISBN 0-8089-2258-03. The Physics of Coronary Blood Flow by M. Zamir; 2005 Springer; ISBN 0-387-26019-64. European Heart Journal - http://eurheartj.oxfordjournals.org/content/vol26/issue14/cover.dtl5. Medline Plus Medical Encyclopedia
- http://www.nlm.nih.gov/medlineplus/ency/article/003795.htm- http://www.nlm.nih.gov/medlineplus/ency/article/003327.htm
6. Medic Zone - http://www.mediczone.co.za/index.php?7. Chest X-ray - http://www.geocities.com/balachandiran_xray/home.htm8. Methodist Hospital System - http://www.methodisthealth.com/tmhs/mdhvc.do?channelId=-
92272&contentId=235402&contentType=SERVICE_CONTENT_TYPE9. National Library of Medicine - http://www.nlm.nih.gov/cgi/mesh/2009/MB_cgi?
mode=&term=SPECT10. Merck Manuals Online Medical Library - http://www.merck.com/mmpe/sec07/ch070/ch070i.html11. Animation on Capillary Pressure : Nursing Review – http://www.youtube.com/watch?
v=aq1pDMzYXOI12. Mayo Clinic - http://www.mayoclinic.com/health/medical/IM0210613. Experimental & Clinical Research Central Berlin –
http://www.fvk-berlin.de/kfo192/index.php?id=29
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