Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
380 Cards in this Set
- Front
- Back
|
P wave
|
represents both the depolarization and the simultaneous contraction of the atriam on EKG
|
|
|
SA node
|
generates pacemaking stimuli known as automaticity
|
|
|
short flat line after the P wave
|
Depolarization slows down when it reaches the AV node producing a pause so the blood has time to enter the ventricles
|
|
|
QRS complex
|
EKG
represents ventricular depolarization and the beginning of the ventricular contraction Purkinje fibers are very fast and send the depolarization through the endocardium to the myocardial cells |
|
|
ST Segment
|
horizontal baseline that follows the S wave
This represents the plateau phase of ventricular repolarization |
|
|
T wave
|
broad hump after the ST segment
final rapid ventricular repolarization The myocardial cells recover their resting negative charge here. The end of the T wave is the end of ventricular contraction or “systole” |
|
|
QT Interval
|
Ventricular contraction or “systole”
Changes with heart rates Interval measurements can be corrected for rate = QTc Simple rule: QT rate is normal when less than half the R-R interval. |
|
|
Small Box on EKG
Large Box on EKG |
1 mm = 0.04second
5 mm = 0.2seconds |
|
|
EKG Leads
|
Limb Leads
I II III AVR AVL AVF Chest Leads V1 V2 V3 V4 V5 V6 |
|
|
Chest Leads
V1 and V2 |
”Right” chest leads
Oriented over right side of heart |
|
|
Chest Leads
V3 and V4 |
Oriented over the interventricular septum
|
|
|
Chest Leads
V5 and V6 |
“Left chest leads
Oriented over the left side of heart |
|
|
"Watch your P's and Q's and the 3 R's"
|
P waves
QRS width Rhythm (regular?) Relattion: P waves to the QRS? Rate (heart) |
|
|
EKG Interpretation
5 features |
Rate
Rhythm Axis Hypertrophy Infarction |
|
|
Rate
|
Sinus Rhythm
Originates from the SA node 60-100 beats per minute Sinus Bradycardia Originates from the SA node Less than 60 beats per minute Caused by parasympathetic nerves Sinus Tachycardia Originates from the SA node More than 100 beats per minute Caused by sympathetic nerves |
|
|
Automaticity Foci
When the SA node fails... |
Atria: 60-80 beats/min
AV Junction: 40-60 beats/min Ventricles: 20-40 beats/min |
|
|
Rate- by boxes...
(EKG) |
300 150 100 75 60 50
The distance between two dark lines is 1/300 min |
|
|
Rhythm
(heart-EKG) |
Normal (regular) rhythm
Equal distance between similar waves Arrhythmia = any abnormal rhythm |
|
|
Sinus Arrhythmia
|
A normal physiological mechanism where the autonomic nervous system causes barely detectable rate changes in sinus pacing that relate to the phase of respiration
Heart rate increases during inspiration due to the inspiration-activated sympathetic stimulation of SA node. Heart rate decreases during expiration due to the expiration-activated parasympathetic stimulation of SA node. |
|
|
Axis
(heart-EKG) |
LAD = Left Axis deviation
RAD = Right Axis deviation NA = Normal Axis EAD = Extreme Axis Deviation |
|
|
What can change axis?
|
Position of heart
Tall people may have a more vertical or “hanging” heart so axis may be more to right. Obese patients may have heart angled up to left from intra-abdominal contents Hypertrophy More electrical conduction through the increase muscle Infarction Dead tissue will not conduct depolarization so there will be a relative “decrease” in vectors in that are |
|
|
Hypertrophy
|
An increase in size or muscle mass
With cardiac muscle, you get an increase in thickness of the ventricle, and some dilation can be present too. |
|
|
Atrial Hypertrophy
|
Lead V1 is over atria so is best source of information on atrial enlargement
With atrial enlargement, the P wave is diphasic If the first part of the P wave is larger, then this is right atrial enlargement If the last part of the P wave is larger, then this is left atrial enlargement |
|
|
P wave is diphasic
last part of the P wave is larger |
this is left atrial enlargement
|
|
|
Right Ventricular Hypertrophy
|
Look at the QRS in lead V1
Usually the R is very small and the S is very big If the R becomes large in V1, then more vectors are traveling in that direction, and thus you should have Right Ventricular Hypertrophy |
|
|
Left Ventricular Hypertrophy
|
Look at the QRS complexes in the chest leads
This hypertrophy produces QRS complexes that have high amplitudes in heights and depths. So add up the depth in lead V1 and the height in V5. If greater than 35 mm, then you have LVH |
|
|
AV Block
First Degree |
PR Interval is greater than .2 sec (1 large block)
P-QRS-T sequence is consistently normal, but the PR interval is prolonged the same amount every time |
|
|
AV Block
Type 1, Second Degree |
Wenckebach phenomenon (Mobitz type !)
PR interval becomes progressively longer until the AV node drops a QRS Block located in AV node Caused by parasympathetic excess |
|
|
AV Block
Second Degree Mobitz type II |
Normal P wave is not followed by QRS, but other cycles have normal PR Intervals.
Located in His Bundles or Bundle Branches Often has widened QRS Maybe be a 2:1 or 3:1 AV block, etc P waves to QRS waves May be early warning to complete heart block |
|
|
AV Block
Third Degree or complete |
None of the atrial depolarizations conduct to the ventricles
Ventricular rate independent of atrial (P wave) rate Junctional focus Narrow QRS’s Ventricular rate 40-60 b/min Ventricular Focus PVC-like QRS’s Ventricular rate 20-40 b/min |
|
|
Bundle Branch Block
|
Block of Conduction in the Right or Left Bundle Branches
One ventricle depolarizes more slowly to cause a “joined QRS’s” (widened) to appear on EKG BBB is diagnosed when QRS is > .12 sec (3 boxes) * IN LBBB, You can not diagnose MI. |
|
|
Right Bundle Branch Block
|
Right Chest leads V1 and V2
Split R and R' |
|
|
Left Bundle Branch Block
|
Left Chest Leads V5 and V6
Split R and R' |
|
|
Hemiblocks
|
Usually occur with an infarction and an associated diminished blood supply to one of the two divisions of the Left Bundle Branch
anterior posterior |
|
|
Anterior Hemiblock
|
Pure Anterior Hemiblock has QRS widened to .10-.12 sec
Q wave in Lead 1 and S wave in Lead 3 Q1S3 Left axis deviation to -45 degrees Usually seen second to occlusion of the ant. descending artery and the resulting anterior infarction |
|
|
Posterior Hemiblock
|
Rare because the posterior division is short, thick and has a dual blood supply
RCA and LAD Right Axis Deviation Normal or slightly widened QRS Deep or unusually wide S in Lead 1 and Q in Lead III = S1Q3 |
|
|
Bifascicular Block
|
RBBB + Ant. Hemiblock
RBBB + Post. Hemiblock Ant and Post hemiblock = LBBB |
|
|
Premature Atrial Contraction
|
“PAC” is a beat that originates from an atrial automaticity focus
Produces an abnormal P wave because it does not come from the SA node P wave is earlier than expected Creates normal looking QRS The rhythm resets when the SA node is depolarized. Sometimes the AV node will not be receptive to a premature depolarization and no QRS is created PACs are common and do not generally indicate structural disease. |
|
|
PAC with aberrant ventricular conduction
|
Premature Atrial Contraction: Sometimes one of the bundle branches has not completely repolarized, so the QRS appears wide
|
|
|
Premature Ventricular Contractions
|
A ventricular focus that becomes irritable and fires a spontaneous pulse
Major causes are Hypoxia (airway obstruction, PE, decreased cardiac output, MI, etc) Low Potassium ( hypokalemia) PVC is very wide, tall, and deep compared to QRS Long pause after to allow for repolarization of the ventricles 6 or more PVCs per minutes is pathological |
|
|
Ventricular Bigeminy, Trigeminy
|
Spaced PVCs (every 2nd or every third)
|
|
|
PSVT / PAT
|
Paroxysmal = sudden
Superventricular / Atrial Tachycardia = heart rate greater than 100 Paroxysmal Tachycardia = 150-250 b p m |
|
|
Flutter b.p.m?
Fibrillation? |
250-350 b p m
350-450 b p m |
|
|
Paroxysmal Superventricular Tachycardia
Pathophysiology |
Atrioventricular nodal reentry, the most common mechanism of PSVT, occurs when two pathways exist with different conduction rates.
A premature atrial complex that is blocked in the fast pathway and redirected through the slow pathway usually triggers the tachycardia. The electrical signal proceeds down the slow pathway and then reenters the fast pathway in a retrograde direction. By the time the signal has propagated down the slow pathway and back around on the fast pathway, the slow pathway is no longer refractory and is ready to conduct the signal again, completing a continuous circuit. |
|
|
Paroxysmal Superventricular Tachycardia
Treatment |
Teach Valsalva maneuver or carotid massage
Increase parasympathetic tone and decrease conduction through AV node Decrease caffeine, nicotine, alcohol, sudafed, stress If persists acutely, may require adenosine treatment If becomes very frequent, may need oral beta-blocker, Ca++ channel blocker or rarely atrial foci ablation |
|
|
Atrial Flutter
|
Symptoms
Palpitations, fatigue, lightheaded, mild SOB, possible syncope Workup includes EKG, Transesophagealechocardiogram (TEE), CXR, Holter monitor or exercise testing Treatment in general Revision to NSR, Maintain NSR, control ventricular rate, prevent emboli |
|
|
Atrial flutter:
Pathophysiology |
Atrial flutter is caused by a single electrical wave (“short circuit”) that usually circulates very rapidly around the right atrium (upper chamber) of the heart in the exact same pattern over and over.
Note sawtooth pattern of strip rate about 300bpm Flutter wave have constant amplitude, duration, and morphology Usually in a 2:1 or 4:1 block resulting in HR of 150 or 75 bpm |
|
|
Causes of Atrial flutter
|
LV Dysfunction
Rheumatic Heart Disease (common) Congenital Heart Disease Anything that causes A Fib Hyperthyroidism, obesity, sick sinus syndrome, pericarditis, pulmonay disease, PE, MVP, rarely MI, Postop Cardiac Surgery, Atrial Septal Defect |
|
|
Atrial Fibrillation
|
Affects less than 1% of <55 year olds and >8% 85 year olds
Risk factors: HTN, LVH, DM, CAD, COPD, Cardiomyopathies Risk of stroke 4.5% per year; reduced to 1.5% with warfarin |
|
|
Symptoms of
Atrial Fibrillation |
palpitations, weakness, dizziness, decreased exercise capacity, dyspnea, maybe angina, maybe heart failure, hypotension
|
|
|
Atrial Fibrillation Treatment
|
New onset A fib: Electrical or drug cardioversion if recent onset and no atrial thrombi on transesophageal echo
Electrical success rate is 80% drug (amiodarone) success rate is 86% Chronic A fib: control ventricular rate with Ca++ channel blockers, digoxin, or Beta-Blockers |
|
|
Ventricular Tachycardia
|
Pathophysiology
Poor coronary blood flow, causing poor heart oxygenation, irritates a hypoxic ventricular focus Causes ventricular rate >100 bpm Needs to be treated quickly because of poor filling and pumping of ventricles at that rate. Causes dizziness, lightheadedness, unconsciousness, and cardiac arrest. |
|
|
Torsades de Pointes
|
Very rapid ventricular rhythm
Caused by low potassium or magnesium, medications that block potassium channels, congenital abnormalities that lengthen QT segment Rate is 250-350 bpm in brief episodes |
|
|
Torsades de Pointes
Mechanism |
The underlying basis for rhythm disturbance is delay in phase III of the action potential. The delay is mediated by the hERG potassium channel. This prolonged period of repolarization and the inhomogeneity of repolarization times among myocardial fibers allow the dysrhythmia to emerge. The initiating electrophysiologic mechanism may be triggered activity or reentry.
|
|
|
Torsades de Pointes
Treatment |
Treatment includes ACLS, potassium, Magnesium Sulfate, and overdrive pacing.
|
|
|
Ventricular Flutter
|
Produced by a single ventricular automaticity focus firing at a rapid rate of 250-350 bpm
Smooth sign wave pattern with no jagged waves Usually degenerates into ventricular fibrillation |
|
|
Ventricular Fibrillation
|
No effective cardiac output
So heart has no blood supply So multiple ventricular foci fire to try to compensate If defibrillation is not instituted in 7-10 minutes, this leads to sudden cardiac death Treatment is CPR, defibrillation and anti-arrhythmic drugs Post MI: 95% survival if rapid cardioversion by defibrillator |
|
|
Wolff-Parkinson-White Syndrome
|
Conduction from atrial to ventricle via an accessory pathway that directly connects the atrial and ventricle and bypasses the AV node
Results in earlier activation of ventricles Seen as a short PR interval (<0.12 sec) QRS fusion of early ventricle activation from acc path and later activaton from AV node This is a delta wave = slurred QRS second to slow muscle fiber to muscle fiber conduction Can have tachyarrhymias Risk of sudden cardiac death; |
|
|
Wolff-Parkinson-White Syndrome
Treatment |
treatment is ablation of accessory pathway
|
|
|
Sick Sinus Syndrome
Who? What Symptoms? |
Average age is 73-76 years old
Lightheaded, presyncope, syncope, SOB on exertion, increased angina, palpitations |
|
|
Sick Sinus Syndrome
|
Chronic inappropriate and often severe bradycardia
Sinus pauses, arrest and exit block with and without appropriate atrial or junctional escape rhythms AV node conduction disturbance 50% alternating brady and tachycardia, atrial fib, atrial flutter, PSVT Atrial fib with slow ventricular conduction |
|
|
Sick Sinus Syndrome
Causes |
Tachy-brady syndrome with remodeling of sinus node
Sinus node fibrosis Diseases of SA nodal artery Childhood or familiar diseases Rarely Infiltrative diseases like Sarcoidosis, scleroderma, hemachromatosis or tumor Epicardial or pericardial disease Inflammation: rheumatic fever, Lyme disease, pericarditis Primary SA node dysfunction/ Drugs/Trauma Decreased Thyroid, temp, O2 |
|
|
Sick Sinus Syndrome
Treatment |
Pacemakers
Remove causes such as if it is causes by a drug |
|
|
Pathogenesis of Hypertension
Causes: |
Poorly understood. May be caused by:
Increased Peripheral Vascular Resistance *4 Prolonged increase in Cardiac Output Hyperthyroidism, Beriberi (B1 deficiency) Increased Blood Volume Mineralcorticoid excess Renal Failure Increased Blood Viscosity Increased sympathetic neural activity *2 Increased angiotensin II activity and mineralcorticoid excess Genetics Reduced adult nephron mass |
|
|
Complications of Hypertension
|
Premature cardiovascular disease
Heart Failure Left Ventricular Hypertrophy Stroke Intracerebral Hemorrhage Chronic Renal Insufficiency Acute life threatening emergencies Hypertensive encephalopathy, strokes, hemorrhages, aortic dissection, glomerulonnephritis, cocaine, severe body burns, severe epistaxis, sudden stop of hypertensive meds, etc |
|
|
Malignant hypertension
|
severe hypertension that runs a rapid course, causing necrosis of arteriolar walls in kidney, retina, etc; hemorrhages occur and death most frequently is caused by uremia or rupture of cerebral blood vessels
|
|
|
Blood Pressure Classification***
|
Normal blood pressure: < 120/80
Prehypertension: 120-139/80-89 Stage 1 hypertension: 140-159/90-99 Stage 2 hypertension: 160+/100+ (BP should be kept < 130/80 in diabetics or renal disease patients) |
|
|
Factors that contribute to Hypertension
|
Smoking
Obesity Stress Old Age Family History Genetics Thyroid Disorders Adrenal Disorders Kidney Disorders Dietary Salt 73% of blacks are salt-sensitive hypertensives compared to 55% of whites |
|
|
Symptoms of Hypertension
|
In over 1/3 of all individuals with hypertension, there are no symptoms.
With severe hypertension, a patient may feel: Fatigued Palpitations Chest pain Headache Blurred vision Shortness of breath Swelling Blood in urine |
|
|
Testing for Hypertension
|
Blood pressure is measured with a sphygmomanometer (blood pressure cuff)
|
|
|
Physical Exam for hypertension
-Minimum- |
Minimum components of exam
Check BP in both arms. BMI = wt (kg)/ ht (m2) Funduscopic Exam Palpate thyroid Auscultation for carotid, abdominal, femoral bruits Complete examination of heart Complete examination of lungs Examine abdomen for enlarged kidneys, masses and abnormal pulsations Check lower extremities for edema and pulses Neurological assessment |
|
|
Initial Workup for Hypertension
|
EKG
Chest X-ray (heart size, rib notching, lungs) Chemistry Panel Electrolytes: Na, K, Cl, CO2, Liver Function: SGOT, SGPT, Total Protein, albumin, billirubin, alkaline phosphatase Kidney Function: BUN, Creatinine Glucose, Calcium Fasting Cholesterol Panel Complete Blood Count (CBC) Thyroid Stimulating Hormone (TSH) |
|
|
Etiologies of Hypertension
Frequency of Hypertension Types |
Essential 88%
Renal Renovascular 2% Parenchymal 3% Endocrine Primary aldosteronism 5% (1.5-15%) Cushing’s Syndrome 0.1% Pheochromocytoma 0.1% Other adrenal forms 0.2% Estrogen treatment 1% Misc. Coarctation, etc 0.6% |
|
|
Hypertension Treatment
|
Lifestyle
Reduce stress Exercise, especially aerobic Stop smoking Low sodium, well balance diet-http://dashdiet.org/ DASH Diet (Diet Approaches to Stop Hypertension) Loose weight Moderate consumption of alcohol Medication Diuretics Ace Inhibitors Angiotension Receptor Blockers (ARBs) Patient should be initially seen monthly, and K+ and Creatinine checked 1-2x year for the above meds Beta-blockers Calcium Channel Blockers, etc |
|
|
Coarctation of the Aorta
|
Congenital narrowing of the aorta that usually is found just distal to the left subclavian artery
Increased blood pressure is found prior to the narrowing in the arms and head, and lower in the lower extremities Treatment Removal of the narrowed part of the aorta |
|
|
Pheochromocytoma
|
Patient usually has palpitations, headache, diaphoresis, paroxysms of hypertension
Occurs in less than 0.5% of population Abnormal urinary catecholamine excretion Norepinephrine >80 micrograms/24h VMA (Vanillylmandelic acid) >5 mg/24h Increased plasma metanephrines CT or MRI of adrenals Tx: alpha-adrenergic inhibitors, beta-blockers, surgery |
|
|
Hyperaldosteronism
|
Condition where patient secretes too much aldosterone and retains sodium and looses potassium. Excess sodium retains excess water, increasing blood volume and blood pressure.
Patient usually presents with fatigue. Initial studies show hypokalemia (low potassium) and it does not respond to potassium supplements. Further testing shows abnormal ratio of aldosterone to renin (>25.1), abnormal response to sodium loading, imaging with CT or MRI shows adrenal adenoma. May occur between 1.5 and 15% of hypertension. |
|
|
Cushing’s Syndrome
|
Overexposure to cortisol
Testing will find increased levels of urinary cortisol (>55micrograms/24 hours) Positive results on dexamethasone suppression test. CT or MRI to look for pituitary adenomas or adrenal tumors Treatment is with Surgical Intervention |
|
|
Types of Hypertension in Pregnancy
|
Chronic Hypertension
>140/90 2x prior to 20 weeks gestation Gestational Hypertension New onset hypertension w/o proteinuria after 20 weeks gestation Preeclampsia New onset hypertension w proteinuria after 20 weeks gestation |
|
|
Gestational Hypertension
|
New onset hypertension w/o proteinuria after 20 weeks gestation
|
|
|
Preeclampsia
|
New onset hypertension with proteinuria after 20 weeks gestation
Severe- HELLP Syndrome Hemolysis, elevated liver enzymes, low platelets Need to deliver High rates of maternal and fetal morbidity |
|
|
Eclampsia-
|
seizures w or w/o hypertension
|
|
|
Preeclampsia
treatment |
Occurs after 20th week of pregnancy
New onset or worsening Hypertension Albuminuria Hyperuricemia Coagulation abnormalities Treatment may include Hospitalization Early fetal delivery Antihypertensives and anticonvulsants |
|
|
Hypertensive Urgency and Crisis
|
1% of hypertensives; Sudden increase in blood pressure over 180/110 mmHg.
Urgency may include: Elevated blood pressure Severe headache Severe anxiety Shortness of breath Crisis may include Fluid in your lungs (pulmonary edema) Brain swelling or bleeding A tear in your aorta (aortic dissection) Heart attack Stroke Eclampsia, if you are pregnant. Treatment may include IV Nitroprusside; lower BP 25% then lower BP slowly to 160/100 over 2-6 hours |
|
|
Secondary Hypertension= ABCDE
|
Accuracy of dx, sleep Apnea, Aldosteronism,
renal artery Bruits (renal artery stenosis), renal parenchymal disease (Bad kidneys) Coarctation of the aorta, excess Catecholamines, Cushing’s syndrome Drugs, Diet excess Erythropoietin, Endocrine disorders |
|
|
Carbon monoxide
in cigarettes |
attaches to the hemoglobin of the blood.
Hemoglobin is responsible for the transport of oxygen throughout the body. Carbon monoxide replaces the oxygen, thus reducing the ability of hemoglobin to transport oxygen to the heart and throughout the rest of the body. |
|
|
Health Impact Data
Cigarettes |
A smoker loses 15 years of life from smoking
One third of all smokers will die from tobacco related conditions Smokers are 3x more likely to die from cardiac arrest, 20x from lung cancer Smoking is responsible for one in five deaths in the United States (4.9 million lives a year) Smoking is the world’s single biggest preventable cause of death Accounts for one-third of all cancers, including 90% of lung cancer cases |
|
|
Nicotine
|
stimulates adrenaline production, which causes the heart to beat faster and thus raises blood pressure.
It constricts arteries through out the body. This is the chemical to which people become addicted. |
|
|
Smoking
heart- cholesterol? |
impact on the production of cholesterol. Cigarette smoke increases the production of LDL cholesterol (the bad cholesterol) while at the same time decreasing the production of HDL (the good cholesterol).
|
|
|
Stages of Patient Readiness
|
Pre-contemplation
Contemplation Preparation Action Maintenance Relapse |
|
|
Cardiovascular Disease
Epidemiology |
Cardiovascular Disease Prevalence 2006
80 Million, 36.6% of population 38.7 Million men, 37.6% of men 41.3 Million females, 34.9% of women |
|
|
Cardiovascular Disease
Risk Factors |
Disease People Percent
HTN 73.6 M 33.3% Tobacco 47.1 M 20.8% Cholesterol 98.6 M 45.1% No Exercise 69.2% Overweight 145.0 M 67% Diabetes 23.4 M 10.6 |
|
|
artery walls consist of three layers
|
Tunica Adventitia: This is the strong outer covering of arteries and veins which consists of connective tissues, collagen and elastic fibers.
Tunica Media: This is the middle layer and consists of smooth muscle and elastic fibres. This layer is thicker in arteries than veins. Tunica Intima: This is the inner layer which is in direct contact with the blood flowing through the artery. It consists of an elastic membrane and smooth endothelial cells. The hollow centre through which blood flows is called the lumen |
|
|
Fatty Streak formation
|
Fatty Streak formation (by 20 y.o.)
Intimal injury from nonlinear arterial flow High concentrations of Low Density Lipoproteins (LDL) permeate the damaged intima LDL is oxidized and in Diabetes, glycation These modified LDL attract leukocytes into the intima and are scavenged by macrophages leading to foam cells. This is visualized as a fatty streak. |
|
|
Fibrous Plaque
|
Smooth muscle cells are then recruited and migrate to the site of the foamy cells were they proliferate and manufacture extracellular matrix.
A large volume of the plaque is occupied by extracellular matrix (collagen and proteoglycan) secreted by the smooth muscle cells. The lesion begins to encroach on the lumen of the vessel. Small blood vessels form in these plaques (angiogenesis) and these plaques can subsequently calcify. Inflammation plays an important role in promoting smooth muscle cell migration and proliferation. The final lesion is a fibrous cap overlying a lipid rich core which also contains necrotic material, which is all highly thrombogenic |
|
|
Atheroma
|
White, elevated, and partially occludes the lumen
The core then becomes necrotic, hemorrhages and calcifies. Thrombosis on or around the plaque |
|
|
Plaque formation
Occurs ... |
Occurs at artery:
Bifurcations Curvatures Taperings Right and left main arteries (they branch sharply off the aorta) |
|
|
Ischemia Occurs with what % reduction in lumen...
|
With exercise?
Only need 50-60% reduction in lumen size With normal activity? Only need 75% reduction in lumen size With rest? Need 90% reduction in lumen size |
|
|
Risk Factors for CAD
Actual numbers... |
Dyslipidemias
particularly high LDL and low HDL LDL: Optimal < 100 mg/dL, Near or above optimal 100-139 mg/dL, Borderline high 140-159 mg/dL, High > 160 mg/dL. Total cholesterol: Desirable < 200, Borderline high 200-239 mg./dL, High > 240 mg./dL. HDL: Low < 40 mg./dL Hypertension Normal BP: systolic < 120 mmHg AND diastolic < 80 mmHg Prehypertension: systolic 120-139 OR diastolic 80-89 mmHg Hypertension: systolic > 140 OR diastolic > 90 mmHg Diabetes mellitus Normal fasting glucose < 110 mg/dL Impaired 110-≤ 126 mg/dL Diabetes > 126 mg/dL Family history of premature coronary artery disease (CAD); First degree male relatives < 55 years or females < 65 years. |
|
|
CVD risk with hypertension...
with each ___ ___, risk ____ |
CVD risk doubles with each 20/10 BP increase over 115/75
|
|
|
Anaerobic metabolism
in Ischemia produces ... |
Produces adenosine triphosphate during low oxygen
Resulting lactic acid impairs LV function Causing decreased contraction strength, and impaired wall motion |
|
|
Angina Pectoris
|
The blood flow to the heart muscle decreases, providing less oxygen, causing myocardial ishemia.
Pain is substernal or radiating to the back, neck, arm or across chest Usually described as an “elephant sitting on the chest” \Thought to be due to lactic acid release that stimulates nerves Conducting through sympathetic nerves to middle cervical ganglia, to thoracic ganglia to spinal chord Referred pain is probably from the interconnections between the sympathetic nerves that enter the spinal chord from C3 to T5 |
|
|
Acuteness of an infarction
EKG Limb leads... Chest leads... Q wave... |
ST segment elevation
Elevated 1mm in limb leads and 2 mm in chest leads Significant Q wave One small square wide or one-third of the entire QRS amplitude |
|
|
Anterior MI
treatment |
In office
ASA, oxygen, nitroglycerin, transport to ER, start IV In hospital Cardiologist consult – catheterization, echo IV, morphine for pain, nitroglycerin, hypertension medicine – beta-blocker (for example) |
|
|
Lab Biomarkers
Cardiac troponin I (cTnI) and T (cTnT) |
cardiac regulatory proteins that control the calcium-mediated interaction of actin and myosin
concentrations usually begin to rise two to three hours after the onset of acute MI. By two to three hours after presentation, up to 80 percent of patients with AMI will have elevations. Elevations in cTnT and cTnI after an acute MI persist for up to 10 days thus permitting late diagnosis Preferred over CK and CK-MB since better Sensitivity and Specificity |
|
|
Lab Biomarkers
diagnosis of Troponin elevation |
acute infarction
moderate to severe pulmonary embolism with acute right heart overload heart failure myocarditis trauma, as occurs during cardiopulmonary resuscitation, electrical cardioversion, or implantable cardioverter defibrillator (ICD) firings |
|
|
Lab Biomarkers
Creatinine Kinase |
dimers of M and B chains and exist in three combinations: MM, MB, and BB
These isoenzymes reside in the cytosol and facilitate the egress of high energy phosphates into and out of mitochondria. CK-MB fraction found in the heart is higher than in most other tissues, but up to 10% in muscle tissue CK-MB has high specificity for cardiac tissue and was the preferred marker of cardiac injury for many years. CK-MB typically begins to rise four to six hours after the onset of infarction but is not elevated in all patients until about 12 hours. Elevations return to baseline within 36 to 48 hours Skeletal muscle damage can confound the diagnosis of an MI, as CK-MB can be released. Eg CPR |
|
|
Lab Biomarkers
Myoglobin |
Released after Troponins, not specific for heart, rapid release and metabolism
|
|
|
Lab Biomarkers
Heart-type fatty acid binding protein (H-FABP) |
molecular weight protein that behaves similarly to myoglobin in its kinetics and release
more fatty acid binding protein in heart compared to skeletal muscle = more specific Not approved in US |
|
|
Lactate dehydrogenase (LD, formerly abbreviated LDH)
|
commonly used in the past in combination with aspartate aminotransferase (AST or SGOT) and CK-MB to diagnose an acute MI.
LD consists of M (muscle) and H (heart) subunits that give rise to five isoenzymes. The heart primarily contains LD1 and some LD2. Red cells, kidney, stomach, and pancreas are other important sources of LD1. LD5 predominates in skeletal muscle and liver LD activity rises to abnormal levels approximately 10 hours after the onset of MI, peaks at 24 to 48 hours, and remains elevated for six to eight days Not used much anymore since Troponins are more specific. |
|
|
Gold standard tests
For Cardial Infarction |
Coronary angiography
This is the gold standard |
|
|
Exercise Stress Testing
When can't it be done? |
Can’t be done if resting ST segment changes, LVH, LBBB, a ventricular paced rhythm, WPW
Patient must be able to exercise to 85% of predicted maximal heart rate |
|
|
Cardial Infarction tests
approx (relative) sensitivity and specificity |
Exercise ECG testing — 68 and 77 percent
Radionucleotide scan Planar thallium rMPI — 79 and 73 percent SPECT rMPI — 88 and 77 percent Stress echocardiography — 76 and 88 percent PET scanning — 91 and 82 percent Not widely available |
|
|
MI Management
At the ER: steps |
Assessment of the hemodynamic state and correction of abnormalities that are present (ABCs)
(hypotension; tachycardia; impaired cognition; cool, clammy, pale, ashen skin) Initiation of reperfusion therapy with primary percutaneous coronary intervention (PCI) or fibrinolysis (within 30 min of arrival) Antithrombotic therapy to prevent rethrombosis or subtotal stenosis at the site of an ulcerated plaque Aspirin, heparin Relief of ischemic pain Nitrites, morphine |
|
|
MI Management
administration of different drugs that may improve the long-term prognosis: |
Antiplatelet therapy to reduce the risk of recurrent coronary artery thrombosis or, with PCI, coronary artery stent thrombosis
ACE inhibitor to prevent remodeling of the left ventricle Beta blockers to prevent recurrent ischemia /life-threatening ventricular arrhythmias Statins to lower cholesterol and to prevent or slow disease progression; Anticoagulation in the presence of left ventricular thrombus or chronic atrial fibrillation to prevent embolization |
|
|
MI EKG findings for...
Posterior Lateral Anterior Inferior |
1) Large R in V1, V2. Maybe Q in V6. Mirror test.
2) Q in LeadI, AVL 3) Q in V1, V2, V3, or V4 4) Q in II, III, AVF |
|
|
Epidemiology
Peripheral Artery Disease (PAD) |
one of the types of Peripheral Vascular Disease
PAD affects about 8 million Americans and is associated with significant morbidity and mortality. PAD prevalence increases dramatically with age and disproportionately affects blacks. Most studies suggest that PAD prevalence is similar between men and women. PAD affects 12–20 percent of Americans age 65 and older. |
|
|
Risk Factors for PAD
metals? |
High blood levels of lead and cadmium may increase the risk of PAD,
Exposure to these two metals is possible through cigarette smoke. |
|
|
Claudication
|
only about 10 percent of persons with PAD have the classic symptoms of intermittent claudication (intermittent leg pain).
About 40 percent do not complain of leg pain the remaining 50 percent have a variety of leg symptoms different from classic claudication. |
|
|
Ankle Brachial Index (ABI)
|
Measure systolic blood pressure with doppler ultrasound in:
Each arm DP and PT pulses ABI = higher ankle pressure/arm pressure Range 0.9-1.3 = normal Range 0.41-0.9= mild to mod PVD Range 0-0.41= severe PVD with critical leg ischemia 95 percent sensitive and specific for angiographic PAD |
|
|
Peripheral Artery Disease
Treatment |
Angiography
Revascularization Surgery Percutaneous Transluminal Angiography Femoropopliteal Bypass (a portion of the saphenous vein can be removed and used to bypass a portion of a diseased artery. To accomplish this, an incision is made down the inside of the leg (A). The saphenous vein is tied off from its tributaries and removed (B). An incision is made in the recipient artery (C), and the vein is stitched to it at the top and bottom of the leg ) |
|
|
Buerger’s Disease
|
Thrombangiitis obliterans
An inflammatory condition of small and medium-sized arteries that may affect the upper or lower extremities Arteries swell and can become blocked with thrombi Found almost exclusively in smokers, especially males under age of 40 |
|
|
Fibromuscular Dysplasia
|
Affects small and medium arteries in women
Usually seen in renal and carotid arteries Can be in limbs and can look identically to PAD Treatment is based upon arteriograms and usually includes percutaneous transluminal angioplasty. |
|
|
young female, unequal pulses and blood pressure in her arms. history of pain in her arms with activity, improves with rest. She had had fatigue, night sweats, weight loss, muscle or joint pain and fever for 1 week. unequal pulses and blood pressure in her arms
|
Takayasu's Arteritis
|
|
|
Takayasu's Arteritis
|
the inflammation damages the aorta — the large artery that carries blood from your heart to the rest of your body — and the aorta's main branches. This can lead to arm or chest pain, high blood pressure, and eventually to heart failure or stroke.
Takayasu's arteritis mainly affects young girls and women under 40. Although the exact cause isn't known, it's possible that an infection triggers Takayasu's arteritis in people with a genetic predisposition. The goal of treatment is to relieve inflammation in the arteries and prevent potential complications. Even with early detection and treatment, however, Takayasu's arteritis can be challenging to manage. In Takayasu's arteritis, the aorta and other major arteries, including those leading to your head and kidneys, become inflamed. Over time, the inflammation causes changes in these arteries, including thickening, narrowing and scarring. The result is reduced blood flow to vital tissues and organs, which can lead to serious complications and even death. Just what causes the initial inflammation in Takayasu's arteritis isn't known. Some experts believe infection plays a role in the disease, particularly because people who have Takayasu's arteritis often have or have had tuberculosis, but the association between these two illnesses isn't clear. In the United States, most people with Takayasu's arteritis have no history of tuberculosis. Another theory is that it is an autoimmune disease |
|
|
Patient is a 31 year-old smoker mechanic with a history of a wound on his foot. It just has not healed over 3 months. He also notes pain in his legs while at rest especially while lying down.
PE: Significant only for decreased pulses in his feet bilaterally and a 2 cm ulcer located on the sole of his foot |
Buerger’s Disease
Thrombangiitis obliterans An inflammatory condition of small and medium-sized arteries that may affect the upper or lower extremities Arteries swell and can become blocked with thrombi Found almost exclusively in smokers, especially males under age of 40 |
|
|
Patient is a 35 year –old woman who noticed an increasing amount of pain in her feet while walking around waiting for her sailor to return to port. This gets better with rest. She has also had more headaches lately.
PE: Is normal except for a BP of 148/90, a right carotid bruit, a left renal artery bruit and decreased pulses in her feet bilaterally |
Fibromuscular Dysplasia
Affects small and medium arteries in women Usually seen in renal and carotid arteries Can be in limbs and can look identically to PAD |
|
|
Patient is a 25 year-old female with history of pain in her arms with horseback riding and other activities that improves with rest, and cold blue fingers on occasion. She had had fatigue, night sweats, weight loss, muscle or joint pain and fever for 1 week.
PE: unequal pulses and blood pressure in her arms |
Takayasu's Arteritis
inflammation damages the aorta — the large artery that carries blood from your heart to the rest of your body — and the aorta's main branches. This can lead to arm or chest pain, high blood pressure, and eventually to heart failure or stroke. mainly affects young girls and women under 40. |
|
|
Patient is an elderly male who present to your office with a swollen left calf and foot. He came as soon as his plane from India landed. He was asleep most of the flight but the pain woke him up with one hour left to fly.
Patient has a history of colon cancer from when he was fifty and a history of a broken leg when he slipped on a loose carpet in his house last year. PE: Normal except for a 2 cm larger left > right calf with tenderness and a palpable chord running along the back of the calf. |
Deep Venous Thrombosis
|
|
|
What are the veins of the legs?
|
femoral vein, sometimes called the superficial femoral vein, which is a source of confusion.
profunda femoris vein popliteal vein peroneal vein anterior tibial vein posterior tibial vein |
|
|
Thrombophlebitis
|
Thrombosis with inflammation
|
|
|
Phlebothrombosis
|
Thrombosis without inflammation
|
|
|
Superficial Thrombophlebitis
|
Local Swelling
Redness Warmth A subcutaneous chord |
|
|
Virchow’s Triad
|
Venous stasis
Vein wall changes Hypercoaguable state May result from inflammation or trauma to vein wall, but frequently there is no cause noted |
|
|
Pathophysiology of Thrombosis
|
Venous flow slows and platelets aggregate
Several days later, a secondary reaction in the wall of the vein causes a sudden proximal extension from the end of the clot Emboli may develop or the clot may become organized This is when it becomes organized into fibrous tissue. Plasminogen becomes entrapped within the clot when it formed; as it is slowly activated, it breaks down the fibrin mesh The vessel becomes recanalized. Venous blood backs up behind the thrombosis Collateral circulation may compensate and so one does not see any edema If there is no compensatory circulation, pressure builds up distally Causing venous distension, and congestion, and pressure changes inhibit fluid reabsorption and this is how edema is formed. |
|
|
Thrombosis
Clinically |
Superficial Veins
Redness, pain, tenderness, local edema, and maybe even fever Lower Extremity Veins Calf pain, tenderness, calf enlargment, + Homan’s sign Impaired or absent pulses, pitting edema, cyanosis Chronic edema may be brawny edema = thick, hard, infiltrated with plasma proteins and looks like an “orange peel” |
|
|
Deep Vein Thrombosis
Clinically |
Venous distention, clot
Swollen, tense, hot, painful, calf or ankle with sudden onset Palpable chord posteriorly (only 50% of patients) >2cm difference is calves circumference Homan’s sign The sign is present where pain in the calf is produced by passive dorsiflexion of the foot. The test has fallen into disfavor because of the risk of precipitating a pulmonary embolism and is highly non-specific |
|
|
Venous Insufficiency and Stasis
|
Old thrombophlebitis damaged valves and walls that become inelastic.
Damaged valves are no longer able to move blood caudally when leg muscles pump because of valvular incompetence resulting in retrograde flow. Venous pressure in the legs becomes high, and which decreases capillary fluid exchange resulting in edema. The valves in the veins have become damaged. Theses valves normally keep blood flowing toward the heart, but damaged valves allow some blood to flow backward, causing the veins to become overfilled. Fluid seeps out of the engorged veins into surrounding tissues, resulting in tissue breakdown and venous skin ulcers. |
|
|
Venous Insufficiency and Stasis
Clinical signs |
Stasis also is present and seen by skin changes around the distal third of the leg and ankle.
Clinically Edema Hyperpigmentation Induration (firm hard area) Stasis cellulitis Venostasis ulcers Pain (dull ache worse with standing, better with reclining) |
|
|
Venous Peripheral Vascular Disease
|
Swelling of feet and legs
Ulcers on lower legs, often near ankles Hyperpigmentation, edema, and possible cyanosis when legs are dependent occur with venous stasis ulcers Inflammation May be from cellulitis, superficial thrombophlebitis, and erythema nodosum |
|
|
Patient is a petite female who has developed large painful veins on her lower legs. They are gone and painless in the morning when she awakes and more uncomfortable as she get up and around.
|
Varicose Veins
|
|
|
Varicose Veins
History |
History
symptoms of aching, cramping, itching, fatigue, and swelling Worse with standing and better with lying down age at onset of varicosities, family history of varicose veins, prior trauma or deep venous thrombosis, number of prior pregnancies, prior lower extremity surgery, associated symptoms of chronic venous insufficiency including edema, skin changes, or prior ulcer |
|
|
Varicose Veins
Exam |
Dilated elongated and tortuous superficial veins of the lower extremities
Produced by incompetent valves and increased intraluminal pressure Develop 2nd to Inherent weakness in vein structure Hereditary Predisposition Pregnancy Prolonged standing Marked obesity |
|
|
Varicose Veins
Treatment |
Liquid and foam sclerotherapy
Liquid injection sclerotherapy is typically reserved for patients with small non-saphenous varicose veins (less than 5 mm), perforator veins, and residual or recurrent varicosities following surgery Endovenous catheter ablation Endovenous laser ablation (EVLA) and radiofrequency ablation (RFA) are minimally invasive catheter based percutaneous techniques. They are used primarily to treat saphenous insufficiency (great or small), however, special probes have been designed for the radiofrequency device to manage non-saphenous and perforator veins. Surgery Saphenous vein stripping |
|
|
Lymphatic Sysytem
|
Drains excess fluids and proteins from interstitial space
Dumps back into heart to recirculate in blood When fluid leaks into interstitial space from venous obstruction or heart failure, the lymph system can initially compensate. |
|
|
Lymphedema
|
a collection of fluid that causes swelling (edema) in the arms/legs.
Primary lymphedema can be present at birth or develop during puberty or adulthood. Primary lymphadema- rare |
|
|
Milroy’s Disease
|
Primary lymphadema- rare
faulty development of lymphatic channels |
|
|
Lymphedema praecox
|
females 9-25 yr old – swelling of feet
|
|
|
Lymphedema
Treatment |
Treatments
Meticulous skin and nail care, ROM exercises, manual massage Elevation of affected limb Exercise is not harmful after initial stages Compression bandages and garments Early antibiotic use in infections No drugs work (diuretics, coumadin, etc) Surgery (no good studies to support this) |
|
|
“brawny skin”
Thick, hard, filled with plasma proteins and looks like an “orange peel”, does NOT pit on pressure |
Lymphedema
Results from stasis |
|
|
Patient is a 22 year-old male who had injured his right shoulder falling of a bike. Three days later he noticed redness, warmth and a red streak on his skin.
|
Lymphangitis
Inflammation of the lymph vessels usually from bacterial infection Painful red streaks Elevated temperature, malaise, chills Lymphadenitis Inflammation of the lymph nodes |
|
|
Raynaud’s Disease
|
Distal portion of fingers
Episodic spasm of small arteries Digital ischemia changes of blanching, followed by cyanosis with cold exposure (or emotional upset) and then rubor with rewarming Numbness tingling and some pain No vascular occlusion Raynaud’s Phenomenon Second to condition: collagen vascular disease, arterial occlusion, trauma, drugs |
|
|
Chronic Insufficiency
Artery |
Intermittent claudication
Pain at Rest Pale with elevation Dusky red when down Cool Edema absent or mild Thin shiny atrophic skin Loss of hair over foot Nails thickened and ridged Ulcers can be on toes Gangrene possible |
|
|
Chronic Insufficiency
Vein |
No pain to achy when dependent
Normal Pulses Normal Color or cyanotic when down Petechia then brown pigment when chronic Temp is normal Edema is present Stasis dermatitis and thickened skin Ulcers can be at ankles, medially especially |
|
|
Patient is an 18 year-old Caucasian male who reports that he has been passing out while running around with his dog. He thinks it is just because he gets scared a lot. He states that when he exerts himself, he vision starts to black out and he gets lightheaded. He awakes lying on the ground with his dog licking his face. He does not get SOB while running.
CV: Regular rate and rhythm with 2/6 crescendo-decrescendo mid-systolic murmur hear best at the right sternal border at the 2nd intercostal space. |
Bicuspid Aortic Valve with Stenosis
|
|
|
Etiology of Aortic Valve Stenosis
|
There are three primary causes of valvular AS:
A congenitally abnormal valve with superimposed calcification (unicuspid or bicuspid) = 38% Calcific disease of a trileaflet valve (also seem with chronic kidney diease) = 33% Rheumatic valve disease = 24%; more common worldwide than in US. Rare causes include metabolic diseases (eg, Fabry's disease), systemic lupus erythematosus, Paget disease, and alkaptonuria. |
|
|
Aortic Stenosis Pathophysiology
|
Valve becomes obstruction to ventricular ejection gradually over time
Increased systolic pressure in left ventricle Concentric left ventricular hypertrophy Compensated ventricle keeps cardiac output and left-ventricular end-diastolic volume are maintained Stenosis and hypertrophy progress creating less compliant ventricle and greater end-diastolic pressure = symptoms This can lead to dyscoordination of ventricular contraction, resulting from regional wall motion abnormalities, fibrosis, or subendocardial ischemia. |
|
|
Pathophysiology – Calcific Valve
|
Characterized by aortic valve leaflet thickening and calcification in patients with a congenital bicuspid valve or an anatomically normal trileaflet valve.
At the tissue level, the valve leaflets show lipid accumulation, inflammation, and calcification Accumulation of LDL and Lp(a) with evidence of lipoprotein oxidation; An inflammatory cell infiltrate with T-lymphocytes and macrophages; Local production of proteins that promote tissue calcification, suggesting that valve calcification is actively regulated rather than being an unregulated degenerative process; Production and activity of angiotensin converting enzyme; Other inflammatory mediators such as interleukin-1-beta and transforming growth factor beta-1; Upregulation of adhesion molecules and alterations in matrix metalloproteinase activity; Late in the disease process, active cartilage and bone formation are present |
|
|
Aortic Regurgitation
|
Due to inadequate closure of the aortic valve leaflets.
It can be induced either by damage to and dysfunction of the aortic valve leaflets distortion or dilatation of the aortic root and ascending aorta. Causes Aortic valve disease – 43% Bicuspid Aortic Valve (62%) and Infective Endocarditis (20%) Nonvalvular Unclear- 74% - possibly due to hypertension and altered elasticity/diameter of aortic root that caused valve incompetence Marfan’s – 12% |
|
|
Aortic Regurgitation
Pathophysiology |
AR causes ventricular stroke to leak back from the aorta into the left ventricle.
The added volume of regurgitant blood produces an increase in left ventricular end-diastolic volume; According to Laplace's law, the increase in left ventricular end-diastolic volume causes and an elevation in wall stress The heart responds with compensatory myocardial hypertrophy., which returns wall stress toward normal The combination of hypertrophy and chamber enlargement raises the total stroke volume. The net effect is that forward stroke volume and hence cardiac output are initially maintained despite the regurgitant lesion. Although left ventricular volume is increased, end-diastolic pressure remains normal due to an increase in ventricular compliance. Thus, the heart initially adapts well to chronic AR, functioning as a very efficient and compliant high output pump. |
|
|
Aortic Regurgitation
Clinical Manifestations |
A sense of pounding and an uncomfortable awareness of the heartbeat.
These symptoms are especially pronounced when lying down or lying on the left side which brings the left ventricular apex closer to the chest wall, augmenting the sensation during systolic contraction. Atypical chest pain induced by a mechanical interaction between the heart and the chest wall. Palpitations due to tachycardia or premature beats. Symptoms of left-sided heart failure (dyspnea on exertion, orthopnea, paroxysmal nocturnal dyspnea, and eventual pulmonary edema) occur in the presence of left ventricular dysfunction. Angina pectoris is uncommon with isolated AR, since the coronary arteries are typically dilated large. |
|
|
Wide pulse pressure
|
Aortic Regurgitation
Systolic – diastolic pressure The increased stroke volume results in abrupt distension of the peripheral arteries and an elevation in systolic pressure. Regurgitation back into the left ventricle then leads to a rapid fall in pressure with quick collapse of the arteries and a low diastolic pressure which often may approaches zero in severe disease. |
|
|
Aortic Regurgitation
Cardiac Auscultation |
S1 may be soft, often reflecting a long PR interval
S2 is variable; it may be soft, absent, or single A2 is often soft or absent while P2 may be normal, but obscured by the diastolic murmur A systolic ejection sound may be due to abrupt aortic distension caused by the large stroke volume A third heart sound (S3 gallop) is heard when left ventricular function is severely depressed early diastolic murmur – high pitched and “blowing” Best heard when the patient is sitting up, leaning forward, and holding his or her breath in expiration. The site at which the murmur is best heard varies with the cause. The murmur is heard best along the left sternal border, at the third and fourth intercostal space, when AR is due to valvular disease. In contrast, abnormalities of the aortic root produce murmurs that are best heard at the right sternal border and apex. |
|
|
Aortic Regurgitation
Testing |
EKG
LVH concurrent ST and T wave changes, indicative of underlying chronic ischemia LAH Left axis deviation CXR Cardiomegally, dilated ascending aorta Echo Valvular disease, dilated aortic root, increased left end sys and end diast volumes |
|
|
Aortic Regurgitation
Treatment |
Med
Vasodilators (Nifedipine, ACE) Surgery To replace damaged aortic valve To repair dilated aortic root (eg. Marfan’s) |
|
|
Patient is a brainy 25 year-old female grad student majoring in criminal science She is American Samoa. She comes in today for a check-up. She has no complaints.
PMHx: Rheumatic fever as a child only. FMHx: HTN in father ROS: significant only for dyspnea on exertion, fatigue which she attributes to being out of shape studying so much. Denies CP, palpitations, systemic symptoms, PND or orthopnea. CV: RRR w 4/6 crescendo diastolic murmur heard at apex Ext: No cyanosis, clubbing or edema. Pulses: +2/3 in radial and PT/DP bilat |
Mitral Stenosis secondary to Rheumatic Heart Disease
|
|
|
Rheumatic Valve Disease
|
fusion of the commissures between the leaflets, with a small central orifice.
The rheumatic process typically involves the mitral valve as well; as a result, most patients with rheumatic aortic stenosis also have mitral stenosis and/or mitral regurgitation. |
|
|
Mitral Stenosis secondary
Treatment |
Medical Therapy – treats the symptoms not the cause
Diuretics – for congestion Digoxin, Beta and Ca Channel Blockers for Afib rate control Anticoagulation – for AFib and LA clots Medical Therapy – treats the symptoms not the cause Diuretics – for congestion Digoxin, Beta and Ca Channel Blockers for Afib rate control Anticoagulation – for AFib and LA clots Open Commisurotomy – valve repair Mitral Valve Replacement |
|
|
Mitral Valve Prolapse
|
Prolapse of the mitral valve refers to systolic billowing of one or both mitral valve leaflets across the plane of the mitral valve annulus into the left atrium
Occurs in about 2.4% of the population May be primary, secondary or functional |
|
|
Mitral Valve Prolapse
Primary |
idiopathic myxomatous degeneration of the mitral valve leaflets and subvalvular apparatus in the absence of any recognizable systemic connective tissue disorder.
|
|
|
Mitral Valve Prolapse
Secondary |
myxomatous degeneration of the mitral valve leaflets in the context of a recognizable connective tissue disorders including Marfan syndrome, Ehlers-Danlos syndrome, adult polycystic kidney disease, osteogenesis imperfecta, and pseudoxanthoma elasticium
|
|
|
Mitral Valve Prolapse
Functional |
Prolapse of anatomically normal mitral valve leaflets can occur in the following conditions:
Papillary muscle displacement (previously known as papillary muscle dysfunction) due to myocardial ischemia. Dilated mitral annulus secondary to dilated cardiomyopathy. A left ventricular cavity that is too small to accommodate the mitral valve. This condition is frequently observed in patients with hypertrophic cardiomyopathy or in some patients with decreased blood volume due to anorexia nervosa or a secundum atrial septal defect. |
|
|
Mitral Valve Prolapse
Ascultation |
A midsystolic click or multiple clicks followed by a midsystolic to late systolic murmur at the apex of the left ventricle over the mitral area
Physiologic maneuvers (such as standing from a squatting position) to show that the nonejection click moves closer to the first heart sound with decreased left ventricular volumes. This change can easily be missed by an examiner not used to performing these maneuvers. |
|
|
Mitral Regurgitation
Etiologies |
lterations of the Leaflets, Commissures, Annulus
Rheumatic MVP Endocarditis Alterations of LV or LA size and Function Papillary Muscle (Ischemic, MI, Myocarditis, DCM) Hypertrophic Obstructive Cardiomyopathy LV Enlargement – Cardiomyopathies - LA Enlargement from MR |
|
|
Mitral Regurgitation
Symptoms |
Fatigue and weakness
Dyspnea and orthopnea Right sided HF MVP Syndrome |
|
|
Mitral Regurgitation
Physical Exam |
Holosystolic Apical Blowing Murmur
Laterally displaced apical impulse Split S2 (but is obscured by the murmur) S3 Gallop (increased volume during diastole) Radiation depends on the etiology |
|
|
Pulmonary Stenosis
|
Pulmonic stenosis can occur at three locations:
Valvular A trileaflet valve is present in patients with typical valvular pulmonic stenosis, with varying degrees of fibrous thickening and fusion of the commissures. The restricted leaflets typically have a conical or dome-shaped appearance during systole, with an orifice in a shape similar to a "fish-mouth." Calcification of the stenotic valve is rare Subvalvular - rare Supravalvular – rare, like pulmonary artery stenosis Stenosis of the pulmonary valve is a relatively common congenital defect, occurring in up to 10 percent of children. There is a slight female predominance, and familial occurrence has been reported in 2 percent of cases. More unusual causes of pulmonic stenosis include: Tetralogy of Fallot. Congenital rubella syndrome Secondary pulmonic stenosis is most often due to carcinoid syndrome Noonan syndrome. Isolated stenoses at both supravalvular and subvalvular positions also occur but are rare. |
|
|
Pulmonary Stenosis
Symptoms |
The patient who is initially asymptomatic may begin to experience symptoms that vary from mild exertional dyspnea to signs and symptoms of right heart failure, depending upon the severity of obstruction and the degree of myocardial compensation.
Moderate to severe obstruction may lead to an inability to augment pulmonary blood flow during exertion, resulting in exercise-induced fatigue, syncope, or chest pain. |
|
|
Pulmonary Stenosis
Exam |
Prominent right ventricular systolic impulse with a left para-sternal lift.
A crescendo-decrescendo midsystolic ejection murmur with maximal intensity at the 2nd and 3rd ICS Pulmonary ejection click Split S2 S4 heard over left sternal border Signs of tricuspid regurgitation Cyanosis in extreme cases with right-left shunts through patent foramen ovale or septal defect |
|
|
Pulmonary Stenosis
Treatment |
Balloon Valvotomy
|
|
|
Pulmonary Regurgitation
|
A small amount of pulmonic regurgitation is normal and occasionally can be heard in thin subjects.
Etiologies pulmonic hypertension-most common residual after Tetralogy of Fallot repair in adults Infective Endocarditis pulmonary artery and ring dilation Rheumatic heart disease: Pulmonary valve affected following mitral, aortic, and tricuspid valve involvement. Carcinoid heart disease |
|
|
Pulmonary Regurgitation
Symptoms |
Right Heart Failure Symptoms
Dyspnea on exertion is the most common complaint. Easy fatigability, light-headedness, peripheral edema, chest pain, palpitations, Syncope More advanced presentations of right-sided heart failure, abdominal distension secondary to ascites, right upper quadrant pain secondary to hepatic distension, and early satiety may occur. |
|
|
Pulmonary Regurgitation
Signs |
High pitched and “blowing” murmur
Accented P2 of the S2 (may be delayed in pulmonary hypertension – A2….P2) Early decrescendo diastolic murmur Hard to tell apart from AR Heard best of left 2nd and 3rd ICS Called Graham Steell murmur of pulmonary hypertension |
|
|
Pulmonary Regurgitation
Testing |
Testing
EKG: RV hypertrophy Chest x-ray typically shows evidence of conditions underlying pulmonary hypertension, RV hypertrophy Echo |
|
|
Pulmonary Regurgitation
Treatment |
management of the condition causing PR.
Pulmonic valve replacement is an option if symptoms and signs of RV dysfunction–induced HF develop, but outcomes and risks are unclear because the need for replacement is so infrequent |
|
|
Tricuspid Stenosis
|
Most commonly of rheumatic etiology; the majority of cases present with tricuspid regurgitation or a combination of regurgitation and stenosis
Rheumatic tricuspid stenosis almost never occurs as an isolated lesion, but is generally associated with mitral valve disease and, in some cases, the aortic |
|
|
Tricuspid Stenosis
Physical Examination |
Similar to those of mitral stenosis.
lungs are usually clear jugular venous distension, hepatomegaly and hepatic pulsations, ascites, peripheral edema, occasionally, anasarca (extreme general edema). A right ventricular parasternal lift is usually not obvious |
|
|
Tricuspid Stenosis
Auscultation |
An opening snap of the tricuspid valve may be heard and is localized to the lower left sternal border.
A low frequency diastolic murmur is heard at the lower left sternal border in the fourth intercostal space; it is usually softer, higher pitched, and shorter in duration than the murmur of mitral stenosis. The intensity of the murmur and opening snap in tricuspid stenosis increase with maneuvers that increase blood flow across the tricuspid valve, especially with inspiration (Carvallo sign) and also with leg raising, inhalation of amyl nitrate, squatting, or isotonic exercise. |
|
|
Tricuspid Stenosis
|
Patients with signs and symptoms of systemic venous hypertension and congestion should be considered for balloon valvotomy.
Tumor masses, vegetations, and thrombi are contraindications to valvotomy. |
|
|
Tricuspid Regurgitation
Normal |
A small degree of tricuspid regurgitation is present in approximately 70 percent of normal adults. On echocardiography, this "normal" degree of regurgitation is localized to a small region adjacent to valve closure, often does not extend throughout systole, and has a low signal strength
|
|
|
Tricuspid Regurgitation
Functional |
Tricuspid regurgitation is most commonly functional, being caused by dilatation of the right ventricular and the tricuspid annulus.
|
|
|
Tricuspid Regurgitation
Causes |
Left sided heart failure
Mitral stenosis or regurgitation Primary pulmonary disease — cor pulmonale, pulmonary embolism, pulmonary hypertension of any cause Left to right shunt — atrial septal defect, ventricular septal defect, anomalous pulmonary venous return Eisenmenger syndrome Stenosis of the pulmonic valve or pulmonary artery Hyperthyroidism Right ventricular dilatation may result from any condition that directly involves the right ventricle or causes pulmonary hypertension and an elevation in right ventricular systolic pressure, leading to dilatation of the right ventricle and tricuspid annulus |
|
|
Tricuspid regurgitation
Pathophysiology |
Tricuspid regurgitation is characterized by the backflow of blood into the right atrium during systole.
Since the right atrium is relatively compliant, there are often no major hemodynamic consequences with mild or moderately severe TR. However, when TR is severe, right atrial and venous pressure rise and can result in the signs and symptoms of right sided heart failure. In such patients, right ventricular pressure and/or volume overload frequently lead to right ventricular systolic dysfunction and a low forward cardiac output |
|
|
Special Maneuvers for Systolic Murmurs
Standing and Squatting Valsava Maneuver |
Standing and Squatting
Standing decreases venous return, PVR, arterial BP, SV, and volume of blood in left ventricle Valsava Maneuver Straining down decreases venous return to right heart, left ventricular volume and arterial BP Both Helps identify a mitral valve prolapse Helps to tell difference between hypertrophic cardiomyopathy and aortic stenosis |
|
|
Standing; Straining Valsalva
|
Decrease left ventricular volume and arterial BP
Hypertrophic cardiomyopathy Increased outflow obstruction = increased murmur Aortic stenosis Decreased blood volume into aorta = decreased murmur Squatting; Releasing Valsalva Opposite of above occurs |
|
|
Patient is a elderly white male who presents to your office with ankle swelling that comes and goes for 3 months. Swelling goes away when he stops eating popcorn and elevates his legs. Episodes occur for 3-5 days, and had 7 episodes in 7 months. Denies pain, trauma, redness, warmth of legs or joints.
CAD with anterior MI 3 years ago. History of HTN, high cholesterol, alcohol use and smokes pipe. Meds: Atenolol, Simvastatin, Accupril, ASA urinates 3x each night +S4 Left ventricular and septal wall motion abnormalities Moderate concentric LVH Left ventricular dysfunction with an estimated LVEF of 35% Normal valves |
Heart Failure
|
|
|
Causes of Heart Failure
|
Ischemic heart disease — 40%
Dilated cardiomyopathy — 32% Primary valvular heart disease — 12% Hypertensive heart disease — 11% Other Causes Idiopathic — 50% Myocarditis — 9% Ischemic heart disease — 7% Infiltrative disease — 5% Peripartum cardiomyopathy – 4% Hypertension — 4% HIV infection — 4% Connective tissue disease — 3% Substance abuse (alcohol) — 3% Doxorubicin — 1% Other — 10% |
|
|
Systolic Dysfunction
|
low cardiac output caused by impaired systolic function (low ejection fraction)
Types High Output Heart Failure Low Cardiac Output Syndrome Right Heart Failure Left Heart Failure Biventricular Failure |
|
|
High Output Heart Failure
|
Demand for blood exceeds capacity for normal heart to meet demand; occurs in severe anemia, AV malformations with blood shunts, hyperthyroidism
|
|
|
Low Cardiac Output Syndrome
|
Seen w fatigue, loss of lean muscle, dyspnea, impaired renal function, altered mental status
|
|
|
Right Heart Failure:
|
Has peripheral edema
|
|
|
Left Heart Failure
|
Has pulmonary congestion
|
|
|
Forward Failure
|
Caused by low cardiac output or systolic dysfunction
Symptoms include fatigue, lethargy, hypotension |
|
|
Backward Failure
|
Caused by increased filling pressure or diastolic dysfunction
Symptoms include dyspnea, peripheral edema, ascites |
|
|
Heart Failure Classification
|
Class I: No limitations of physical activity
Class II: Slight limitation of physical actiivity. Develops fatigue or dyspnea with moderate exertion Class III: Marked limitation of physical activity. Even light activity produces symptoms. Class IV: Symptoms at rest. Any activity causes worsening. |
|
|
Patient is an elderly African-American female who has SOB and fatigue for several days. She thinks she is getting fatter and more out of shape. Her clothes are tighter around her middle and her feet are swelling.
Significant for rheumatic heart fever as a child Lungs: Bibasilar rales CV: RRR w right sided heave, 3/6 diastolic murmur heard lateral to the 5th ICS MCL |
Left Ventricular Failure
EKG with R axis deviation and bilateral atrial hypertrophy Chest Xray with pulmonary congestion and enlarged right heart Echo: Mitral valve stenosis with mild right ventricular hypertrophy |
|
|
Left Ventricular Failure***
Hemodynamics |
Systolic dysfunction leads to decreased stroke volume thus decreased cardiac output
Heart responds by: Increased preload (blood returning to heart) can lead to increased contractions of sarcomeres (Frank-Starling Relationship) Increased catecholamine release can increase cardiac output by increasing HR Cardiac muscle hypertrophies and ventricular volume and elasticity can increase Diastolic Dysfunction Increase in left end-diastolic pressure Present in any disease that causes decreased relaxation, decreased elastic recoil, or increased stiffness of ventricle eg Hypertension (all three) eg Ischemia (decreased relaxation) eg MI (myocytes replaced with fibrosis) |
|
|
Left Ventricular Failure: Neurohumoral
|
After injury, increased endogenous neurohormones and cytokines released
Compensated for by increased adrenergic system and renin-angiotensin systems until overtaxed Increased sympathetic activity w elevated norepinephrine caused increased cardiac contractility and HR which given increased cardiac output Over time get increased preload from venous vasoconstriction, and afterload from arterial vasoconstriction HF causes reduced renal blood pressure that stimulates the release of renin and Angiotension II. Angiotensin II and sympathetic activation cause efferent glomerular artery vasoconstriction. This maintains renal blood flow despite decreased cardiac output. Angiotensin II stimulates aldosterone which resorbs Na+ and excretes K+ Continued hyperactivity of renin-angiotensin system leads to severe vasoconstriction, increased afterload, and further reduced cardiac output and GFR |
|
|
vasopressin
|
Left Ventricular Failure: Neurohumoral:
Increased release of vasopressin from the posterior pituitary gland Powerful vasoconstrictor Promotes reabsorption of water in renal tubules |
|
|
Left Ventricular Failure: Cellular Changes
|
Left ventricular remodeling: increased rate of myocyte’s natural cell death (apoptosis) (causes stress on remaining myocytes leading to hypertrophy which further increased rate of cell death, etc.
Increased interstitial collagen deposition Gradual dilation of ventricle second to collagenases that disrupt myocytes’ proximity |
|
|
Mr. Sparrow is a middle aged man who has worsening shortness of breath for several weeks. He thought it was just because he is on the run.
He props himself up in his hammock to sleep at night. He sometimes wakes up SOB, but feels better when he sits up and dangles his legs off the side of the boat. His feet are more swollen. He denies CP. Regular Rhythm, split S2, S4 at apex, PMI 5th ICS at MCL, late peak systolic murmur at R upper sternal border that radiates to carotids. Bilateral pedal edema |
Congestive Heart Failure
Aortic Stenosis ? Dyspnea present? Yes EKG (LVH, MI, anterior Q waves, LBBB) If normal, 94% chance not heart failure CXR ( enlarged heart, pulmonary vascular congestion, Kerley B lines) Abnormal EKG Echocardiogram with doppler flow studies Left Ventricular Ejection Fraction (LVEF) of 55-70 % is normal. Lab Testing B-type natriuretic peptide (>150pg/ml abnormal) |
|
|
Dyspnea
|
Elevated left atrial pressures cause increaased pulmonary venous and capillary pressure, leading to pulmonary edema
Pulmonary edema causes activation of interstitial or J receptors in the lung that leads to shallow rapid breathing Initially only with exertion; Exercise tolerance decreases over time until it finally occurs at rest |
|
|
Orthopnea
|
Dyspnea seen in the lying down position.
Often see patients sleeping in a recliner or with extra pillows |
|
|
Paroxysmal Nocturnal Dyspnea
|
Patient wakes up 2-3 hours of sleep with “air hunger” cough and wheezing; resolves with sitting up and taking deep breaths.
Lying down causes more venous return from legs leading to worse pulmonary congestion Diaphragm is also pushed up by viscera Respiratory center is depressed during sleep; Sympathetic drive is diminished |
|
|
Brain Natriuretic Peptide
|
The brain natriuretic peptide (BNP) test is used to:
Check for heart failure. Especially helpful in ER setting. Find out how severe heart failure is. Check the response to treatment for heart failure. |
|
|
as Kerley "B" or "A" lines.
|
Patients with congestive heart failure commonly will have increased density of the interstitial markings of the lung fields. Very specific patterns have been described as Kerley "B" or "A" lines. They are commonly accompanied by other signs of interstitial edema such as bronchial cuffing and a blurring of the margins of the pulmonary vasculature at the hila.
Kerley A lines are straight, long lines in lung parenchyma mostly midway between hilum and pleura. Presence of these lines depend on the accumulation of abnormal amounts of edema or other tissue within the perilymphatic connective tissue but are not due to distention of the lymphatics themselves. They are reversible in pulmonary edema, but irreversible when caused by pneumoconiosis or lymphangitic carcinoma. |
|
|
Treatment of chronic CHF
|
General Principles
Correct systemic factors (hyperthyroidism, DM, infection) Lifestyle modification Smoking, aldohol, obesity, salt restriction (2-3g max per day) Review Rx that contribute to heart failure Treat cause of heart disease Rx treatment to control symptoms, slow progression and improve survival In select patients, implantable cardiovertor-defibrillator (ICD) or cardiac resynchronization therapy (CRT) with biventricular pacing. Standard Loop Diuretics then Ace Inhibitors or ARBs then Beta Blockers In select patients: Hydralazine with Nitrates (work well for blacks) ARBs added with an Ace Inhibitor Spirolactone- blocks aldosterone Digoxin- with systolic dysfunction and/or a fib |
|
|
Cardiomyopathy
|
A heterogeneous group of diseases of the myocardium, usually with inappropriate ventricular hypertrophy or dilation
Various causes May be part of systemic disorder Primary Genetic, mixed (genetic and nongenetic) or acquired Secondary Infiltrative, toxic, inflammatory, etc |
|
|
Cardiomyopathy
Types |
Dilated cardiomyopathy
Hypertrophic cardiomyopathy Restrictive cardiomyopathy Arrhythmogenic right ventricular cardiomyopathy (ARVC) Unclassified cardiomyopathy |
|
|
Dilated Cardiomyopathy
Hypertrophic Cardiomyopathy rates... |
Dilated Cardiomyopathy
Most Common Affects 5 in 100,000 adults Third leading cause of heart failure Behind CAD and hypertension Hypertrophic Cardiomyopathy Leading cause of death in athletes 1 in 500 people Autosomal dominant Restrictive and ARVC are very rare |
|
|
Cardiomyopathy
Presentation |
May be asymptomatic in the early stages
Typical Heart Failure Symptoms Shortness of breath (SOB) Fatigue Cough Orthopnea - dyspnea while lying flat Paroxysmal nocturnal dyspnea (PND) – sudden onset of SOB at night while sleeping, often with cough or wheeze Edema |
|
|
Arrhythmogenic right ventricular cardiomyopathy (ARVC)
Presentation |
Heart Failure Symptoms uncommon
Syncope, atypical chest pain, ventricular tachycardia, skin signs (extremely curly-kinked hair, and palmarplantar keratoderma such as in Naxos disease) |
|
|
Restrictive Cardiomyopathy
Presentation |
Diastolic Heart Failure
Classical heart failure symptoms Syncope may occur Rare sudden cardiac death |
|
|
Concentric hypertrophy
Eccentric hypertrophy |
Hypertrophic growth of a hollow organ without overall enlargement, in which the walls of the organ are thickened and its capacity or volume is diminished.
Hypertrophic growth of the walls of a hollow organ, especially the heart, in which the overall size and volume are enlarged. |
|
|
found to have an abnormal heartbeat (exercise-induced ventricular tachycardia), and was prescribed a beta blocker. However, Gathers felt that the medication adversely affected his play, and he soon cut back on his dosage.
On Sunday, March 4, 1990, he collapsed again with 13:34 left in the first half of a West Coast Conference tournament quarterfinal game against Portland, just after scoring on an alley-oop dunk that put the Lions up 25–13. He was declared dead on arrival at a nearby hospital at the age of 23. |
An autopsy found that he suffered from a heart-muscle disorder, hypertrophic cardiomyopathy
|
|
|
Stage B
Structural Heart Disease w/o signs of heart failure Example, patient with MI, left ventricular remodeling including LVH and low ejection fraction or asymptomatic valvular heart disease |
Treat: all stage A measures
Rx: Ace Inhibitor, ARBs or beta-blockers in appropriate patients Implantable cardiac defibrillators |
|
|
Stage A
High risk for heart failure but w/o structural heart disease Example, pt with HTN, CAD, DM, obesity, Metabolic Syndrome, using cardiotoxins, FMHx of cardiomyopathy |
Treat HTN, Cholesterol, stop smoking, exercise, decrease Etoh/drug use
Rx: Ace inhibitor or ARB in DM or vascular pts |
|
|
Stage C
Structural heart disease with symptoms of heart failure |
All Stage A and B measures
ACE Inhibitors, beta-blockers, diuretics for fluid retention Selected pts: ARBS, Aldosterone antagonists, digitalis, hydralazine or nitrates Biventricular pacing, implantable defibrillators |
|
|
Stage D
Refractory Heart Failure requiring special intervention Marked symptoms despite maximal treatments |
Stage ABC measures
End of life care/hospice Heart transplant, permanent mechanical support, experimental surgery or drugs |
|
|
Peripartum Cardiomyopathy
|
The onset of cardiac failure with no identifiable cause in the last month of pregnancy or within five months after delivery.
The absence of heart disease before the last month of pregnancy. Presence of specific echocardiographic criteria which include a left ventricular systolic dysfunction with a left ventricular ejection fraction of less than 45 percent, fractional shortening of less than 30 percent on an M-mode echocardiographic scan, or both, and a left ventricular end-diastolic dimension of more than 2.7 cm per square meter of body-surface area. |
|
|
Dilated Cardiomyopathy
|
Characterized by dilation and impaired contraction of one or both ventricles.
Affected patients have impaired systolic function and may or may not develop overt heart failure. left ventricular ejection fraction <40 percent The presenting manifestations can include atrial and/or ventricular arrhythmias, and sudden death can occur at any stage of the disease |
|
|
Dilated Cardiomyopathy
Causes: |
Ischemia- 50-75% in US
Stress-induced Infectious Viral: Coxsackievirus, influenza, adenovirus, echovirus, CMV, and HIV Chagas' disease protozoan infection due to Trypanosoma cruzi Leading cause in Central and South America Lyme Disease Autoimmune Toxic Alcohol Cocaine accumulation (cobalt, arsenic) or deficiency (selenium) Familial Dilated Inherited disorders muscular dystrophies and myotonic dystrophy, hereditary hemochromatosis, the hereditary sideroblastic anemias and thalassemias Sarcoid, SLE, Celiac Disease End-stage renal disease |
|
|
Dilated Cardiomyopathy
Presentation |
between the ages of 20 and 60
progressive dyspnea with exertion impaired exercise capacity orthopnea paroxysmal nocturnal dyspnea peripheral edema |
|
|
Dilated Cardiomyopathy
Treatment |
Treat underlying conditions first
Treat signs and symptoms of heart failure Cardiac transplant Most common cause of cardiac transplant in age group of 20-40 year-olds is dilated cardiomyopathy |
|
|
Restrictive Cardiomyopathy
|
A nondilated ventricle with normal wall thickness
Ventricular walls that are rigid, resulting in severe diastolic dysfunction and restrictive filling that produces elevated filling pressures and dilated atria Normal left ventricular systolic function in the vast majority of patients |
|
|
Restrictive Cardiomyopathy
History |
Pulmonary and systemic congestion
The most common symptoms include dyspnea, peripheral edema, palpitations, fatigue, weakness, and exercise intolerance due to failure of the cardiac output to increase with an increase in heart rate without further compromising ventricular filling. In advanced cases, there may be a marked elevation in central venous pressure, resulting in hepatosplenomegaly, ascites, and anasarca |
|
|
Restrictive Cardiomyopathy
Ascultation |
The first and second heart sounds are usually normal.
A third heart sound (S3 gallop) is frequently present because of the abrupt cessation of the rapid ventricular filling. Soft systolic murmurs of functional mitral and tricuspid valve regurgitation are also common. |
|
|
Restrictive Cardiomyopathy
Treatment |
Treat secondary causes
Loop Diuretics- relieve venous congestion Ca++ Channel Blockers- control rate to optimize filling Beta Blockers- control rate and improve ventricular contraction Ace Inhibitors-improve diastolic filling Pacemaker- to control rate Anticoagulants- in select patients with a fib Transplant |
|
|
Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)
|
ARVC is characterized macroscopically by a fatty appearance of the RV free wall.
The fibrofatty replacement of the RV myocardium initially produces typical regional wall motion abnormalities that later become global, producing RV dilation. The tissue replacement can also involve areas of the left ventricle (LV) with relative sparing of the septum |
|
|
- ARVC
History and examination |
Arrhythmogenic Right Ventricular Cardiomyopathy
The principle symptoms associated with ARVC are dizziness, palpitations, and syncope. Atypical chest pain — 27 percent Dyspnea — 11 percent |
|
|
ARVC
Risk of exercise |
Can cause ventricular arrhythmias including ventricular tachycardia and sudden cardiac death (scd)
risk of exercise may be due in part to increased stress on the right ventricle Supraventricular arrhythmias, including atrial fibrillation, atrial tachycardia, and atrial flutter, are present in approximately 25 percent of patients with ARVC |
|
|
Patient is a 46 year-old woman who has used IV heroin for 4 years. She began feeling ill 2 weeks ago with malaise, decreased appetite and muscle soreness. She has been having fevers up to 103 F. And night sweeats. She has also had mild headaches, neck stiffness and back pain.
She denies any ST, cough, chest or abdominal pain, dysuria or diarrhea. Her back pain has worsened over last two days with radiation in to her buttocks bilat. She has bilat thigh numbness, and anal and vaginal numbness. She has not been incontinent to urine or stool. CV: tachycardiac, normal rhythm, soft ejection murmur just to right of sternum. |
CBC, Blood Cultures, Chem 20, UA C&S
Echocardiogram Found vegetation on tricuspid valves MRI Spine Spinal epidural abscess causing caudal equina syndrome |
|
|
Infectious Endocarditis**
Microbiology |
Staph: 42%
Strep: 40% |
|
|
Q Fever Endocarditis
|
Coxiella burnetii
|
|
|
Infectious Endocarditis
Risk Factors |
Intravenous drug use
Right-sided > left-sided More likely with cocaine and heroine Prosthetic heart valve 100,000 heart valves placed each year Structural heart disease Rheumatic heart disease Mitral valve prolapse with mitral regurgitation Aortic valve disease Congenital heart disease Bicuspid aortic valve PDA Coarctation of Aorta VSD Tetralogy of Fallot Nosocomial Infective Endocarditis Diagnosed within 72 hours of hospital admission Within 60 days of invasive procedure Hemodialysis HIV: Salmonella, Listeria Pregnancy Shunts: for ascites or hydrocephalus Colon Ulcers: strep bovine (poorly understood) |
|
|
Dukes Criteria: Definite IE
Dukes Criteria: Possible IE Dukes Criteria: Rejected IE |
Direct evidence of endocarditis based upon histological findings (a pathological criterion)
Positive Gram stain results or cultures of specimens obtained from surgery or autopsy (a pathological criterion) Two major clinical criteria One major and any three minor clinical criteria, or Five minor clinical criteria. Possible endocarditis is defined as the presence of one major and one or two minor clinical criteria or the presence of three minor clinical criteria The diagnosis of endocarditis is considered rejected if any of the following are present: A firm alternate diagnosis is made Resolution of clinical manifestations occurs after four days of antibiotic therapy or less No pathological evidence of infective endocarditis is found at surgery or autopsy after antibiotic therapy for four days or less Clinical criteria for possible or definite infective endocarditis not met |
|
|
IE: Major Criteria
|
Persistently positive blood cultures for organisms that are typical causes of endocarditis
Vegetations or other typical findings of endocarditis present on echocardiography; these other typical findings include new or partial dehiscence of a prosthetic valve or an abscess in the tissues surrounding a heart valve Evidence of endocardial damage such as a new regurgitant murmur Serological or culture evidence of infection with Coxiella burnetii |
|
|
IE: Minor Criteria
|
Fever
The presence of a predisposing valvular condition or intravenous drug abuse; a predisposing valvular condition is defined as a prosthetic heart valve or a valve lesion that leads to significant regurgitation or turbulence of blood flow "Vascular phenomenon" emboli to organs or the brain, hemorrhages in the mucous membranes around the eyes "Immunologic phenomenon" glomerulonephritis, or lesions such as Roth's spots (in the retina of the eyes) or "Osler's nodes (nodules on the fingers or toes) Positive blood cultures that do not meet the strict definitions of a major criterion |
|
|
Petechiae
|
Petechiae are not specific for IE but are its most common skin manifestation.
They may be present on the skin, usually on the extremities, or on mucous membranes such as the palate or conjunctivae, the latter usually as hemorrhages best seen with eversion of either upper or lower eyelids |
|
|
Splinter Hemorrhages
|
Splinter hemorrhages
nonspecific for endocarditis nonblanching linear reddish-brown lesions found under the nail bed |
|
|
Janeway Lesions
|
macular, blanching, nonpainful, erythematous lesions on the palms and soles
|
|
|
Osler's Nodes
|
Painful
Violaceous nodules found in the pulp of fingers and toes Are seen more often in subacute than acute cases of IE |
|
|
Roth Spots
|
exudative
edematous hemorrhagic lesions of the retina |
|
|
Infective Endocarditis
Empirical Therapy |
While awaiting cultures, empirical therapy should cover
staphylococci (methicillin-susceptible and resistant), streptococci enterococci. Vancomycin (30 mg/kg per 24 h IV in 2 divided doses) is appropriate choice for initial therapy in most patients. |
|
|
Q Fever
Treatment |
Doxycycline 100mg po bid + hydrocloroquine 600mg qd x 1.5-3 years
|
|
|
Congenital Heart Defects
Maternal factors |
Diabetes (TGA, VSD, hypertrophic cardiomyopathy)
Connective tissue diseases (Heart block) Congenital Infections (CMV, Herpes, Coxsackie, Rubella) Alcohol use (ASD, VSD) Dilantin, Lithium use |
|
|
7 pound 0 ounce 19 in newborn female born vaginally to a 24 G1P1 female with a normal pregnancy
Patient turned blue with crying. Patient was tube fed from start 2nd to fatigue. General: Patient has mottled skin and very sleepy. She reacts to stimulus weakly. She only feeds for 5-6cc until she falls back asleep. Feeding also causes cyanosis. Patient has facial features of Down’s Syndrome. A holosystolic murmur is heard. |
Echo revealed complete AVSD and PDA.
Patient was sent home on feeding tube but never gained weight (why?) 2 months later pt started to gain weight and looked fuller, but developed a hacky cough which made her turn blue. Heart Failure was diagnosed and patient put on Digoxin, Lasix and Prevacid. Surgery was moved up and included two patches and reattachment of mitral valve to a patch. PDA resolved on own. |
|
|
AVSD
|
When the septum and valves do not grow together properly, a large hole occurs in the middle of the heart.
There are several types of AV septal defects depending on how abnormal the septum and valves are. In a complete AVSD instead of two valves, there is only one "common" AV valve over a large hole between all four chambers. |
|
|
Complete AVSD: The Shunt
|
In complete AV septal defect, blood can mix in all four chambers.
"Red blood" which has already been through the lungs, passes from the left to right side, going back to the lungs again. Some "blue blood" also goes to the left side. Both sides of the heart work hard. With time, blood vessels in the lungs can be damaged from all the extra blood. |
|
|
Tetralogy of Fallot
|
Ventricular septal defect (VSD) - an opening in the ventricular septum, or dividing wall between the two lower chambers of the heart known as the right and left ventricles.
Pulmonary (or right ventricular outflow tract) obstruction - a muscular obstruction in the right ventricle, just below the pulmonary valve, that decreases the normal flow of blood. The pulmonary valve may also be small. Overriding aorta - the aorta is shifted towards the right side of the heart so that it sits over the ventricular septal defect. Right ventricle becomes enlarged as it tries to pump blood past the obstruction into the pulmonary artery. |
|
|
Tetralogy of Fallot
Pink baby Blue Baby |
Pink baby
Lower O2 sat than normal but mild right ventricular outflow obstruction causes only a small amount of deoxygenated blood to mix with oxygenated blood in the left heart before going to the body Might see temporary blue color when cries when increased lung pressure is present Blue Baby Lower O2 sat but significant right ventricular outflow obstruction causing a higher level of deox blood to mix with ox blood before going systemic |
|
|
Tetralogy of Fallot
treatment |
Surgical repair is made at around 6 months of age, or even a little earlier
|
|
|
Transposition of Great Vessels
|
"Red blood" pumped continually through the left side of the heart to the lungs and back, without entering the rest of the body.
"Blue blood" pumped continually through the right side of the heart to the body and back, without entering the lungs. Babies born with transposition are cyanotic (bluish color of skin, lips, and nail beds) shortly after birth because of the low oxygen in their blood. Two normal connections in the newborn heart and blood vessels help some "red blood" and "blue blood" to mix, keeping babies alive. foramen ovale is an opening between the two atria (upper chambers). This can be stretched open more with balloon. patent ductus arteriosus In addition, medicine can be given to keep this second connection open. This second connection is a blood vessel between the aorta and pulmonary artery, which usually closes after the first few days of life. Requires Surgery to survive. |
|
|
Patent Ductus Arteriosis
|
A patent ductus arteriosus (PDA) is a blood vessel, which connects the aorta to the pulmonary artery. This is normally present in the fetus and allows blood to bypass the lungs. The PDA usually closes within a few days in a full term infant. In premature infants, the closure may take longer.
Mothers should not take NSAIDS in the 3rd Trimester since they inhibit prostaglandins which would normally keep PDA open. |
|
|
Patent Ductus Arteriosis
Pathophysiology |
When a PDA fails to close, "red blood" from the aorta mixes with "blue blood" in the pulmonary artery. This extra blood in the pulmonary artery travels to the lungs and left side of the heart.
Over time, this extra blood may stress and damage the blood vessels in the lungs. The left side of the heart may enlarge as it works harder. |
|
|
PDA
ascultation |
Commonly has a “machine-like” late systolic murmur heard at left-sternal edge.
|
|
|
Coarctation of the Aorta
|
A constriction (narrowing) of a part of the aorta, the main artery carrying "red blood" to the body.
Occurs close to the region where arteries to the head and neck arise. The constriction obstructs blood flow to the lower parts of the body. It causes blood pressure to increase above the coarctation, resulting in higher blood pressure in the upper part of the body compared with the lower part of the body. Depending on the location of the coarctation, the left and right arm may have different blood pressures. Thus it is important to always check BP in both arms!!! The left side of the heart works hard as it tries to pump blood past the coarctation. This may cause the left ventricle to enlarge. If the coarctation is very severe, an infant's heart may fail, resulting in rapid heart rate, rapid breathing and poor feeding. In less severe narrowing, the child may have no noticeable side effects except increased blood pressure. If the high blood pressure continues, damage results to other blood vessels in the body. The age when the coarctation is repaired depends on the severity of the constriction and the patient's symptoms. Usually, surgical ligation is needed very early in infancy. NOTE: There is no shunt! |
|
|
Hypoplastic Left Heart Syndrome
|
A very small (hypoplastic) left ventricle (the lower chamber which normally pumps blood out to the body): too small to pump enough blood throughout the body.
Small aorta Aortic valve atresia (absence): When atresia is present, there is no connection between the left ventricle and aorta, and no forward blood flow. Mitral valve stenosis or atresia: This valve normally opens and closes to let blood flow between the left atrium and left ventricle. Stenosis causes little blood flow; atresia causes no blood flow. Either atresia or stenosis may be present. This very serious combination of heart defects results in little red blood (blood high in oxygen) getting to the body. Two normal connections that infants are born with, PFO and PDA provide some blood flow. These connections allow the infant to appear healthy at birth. However, as these connections begin to close, the infant quickly becomes critically ill. Surgery for this defect may be performed in stages or cardiac transplantation may be considered. Successful surgery has only been accomplished in the last few years and long term results remain unknown. |
|
|
Hypoplastic Left Heart Syndrome
HLHS: The Shunt |
Oxygenated blood travels from the left atrium into the right atrium through the patent foramen ovale.
Semi-oxygenated blood goes through the pulmonary artery and lung to become oxygenated ending in the left atrium Through the PDA to the rest of the body and back to the left atrium Deoxygenated blood travels from the body back to the right atrium. |
|
|
Ebstein's Anomaly
|
A downward displacement of the tricuspid valve into the right ventricle, due to anomalous attachment of the tricuspid leaflets, the Ebstein tricuspid valve tissue is dysplastic and results in tricuspid regurgitation
The abnormally situated tricuspid orifice produces an "atrialized" portion of the right ventricle Often the right ventricle is hypoplastic |
|
|
Patient is a 45 year-old Caucasian who was in great health until approximately 1 week ago. He developed a cold with low grade fever, fatigue, and muscle aches. Today he states that he awoke with left-sided chest pain worse with breathing. It radiates to his left jaw and arm. Rated 6/10 and is sharp and constant. He feels better with leaning forward but worse when lying down.
VS: BP 145/80, temp 100.2 F, pulse 87, Respirations 20 CV: RRR with a tri-phasic friction rub heard best with the diaphragm along the left sternal border with the patient sitting up and leaning forward. It is heard best at end expiration and resembles a rasping or creaking sound like leather rubbing together. Increase in cardiac panel markers Eg. Troponin I with or without CK-MB Inflammation Increased WBC Increased Sedimentation Rate C-Reactive Protein |
Pericardial Rub
large transmural myocardial infarction? |
|
|
Rub
|
Pericardial Friction rub is present in 85% of patients
triphasic in 50% of patients The three phases correspond with the movement of the heart against the pericardial sac during atrial systole, ventricular systoli, and rapid ventricular filling. Superficial scratchy or squeaking sound that is best heard with the diaphragm of the stethoscope. Localized or widespread, but are usually best heard over the left sternal border The intensity of the rub frequently increases after application of firm pressure with the diaphragm, during suspended respiration, and with the patient leaning forward or resting on elbows and knees. This maneuver is designed to increase contact between visceral and parietal pericardium, but is seldom used in practice since it is cumbersome for the patient. Suspension of respiration during auscultation permits distinction from a pleural or pleuropericardial rub. A pleuropericardial rub results from the friction between the inflamed pleura and the parietal pericardium; it can be heard only during the inspiratory phase of respiration. |
|
|
EKG
Pericarditis |
Stage 1
seen in the first hours to days, is characterized by diffuse ST elevation (typically concave up) with reciprocal ST depression in leads aVR and V1. There is also an atrial current of injury, reflected by elevation of the PR segment in lead aVR and depression of the PR segment in other limb leads and in the left chest leads, primarily V5 and V6. Thus, the PR and ST segments typically change in opposite directions, although the PR deviations, which are highly specific although not sensitive, are frequently overlooked. Stage 2 normalization of the ST and PR segments. Stage 3 development of diffuse T wave inversions, generally after the ST segments have become isoelectric. However, this stage is not seen in some patients. Stage 4 the ECG may become normal or the T wave inversions may persist indefinitely ("chronic" pericarditis |
|
|
CXR
Pericarditis |
May have an enlarged cardiac sillouette
|
|
|
Clinical Criteria for diagnosis
acute pericarditis |
Chest pain (usually sudden onset and ant chest, worse with inspiration)
Pericardial friction rub scratchy or squeaking sound that is best heard with the diaphragm of the stethoscope ECG changes — new widespread ST elevation or PR depression Pericardial effusion At least 2 of the 4 should be present |
|
|
Pericarditis
Treatment |
Outpatient treatment
Aspirin or Ibuprofen (max 800mg every 6 hours) will help to treat the fever, chest pain and friction rub. Treatment may last 3-4 weeks and tapered off slowly. Maybe add colchicine to prevent recurrence. Hospitalization Features of high risk include: Fever (>38ºC [100.4ºF]) and leukocytosis Evidence suggesting cardiac tamponade A large pericardial effusion (ie, an echo-free space of more than 20 mm) Immunosuppressed state A history of oral anticoagulant therapy Acute trauma Failure to respond within seven days to NSAID therapy Elevated cardiac troponin, suggestive of myopericarditis |
|
|
A 69-year-old male was admitted to the hospital for shortness of breath and fever.
White count of 15, 000 leukocytosis Mycoplasma titers and cold agglutinin tests were positive Chest x-ray demonstrating a right middle lobe infiltrate and an enlarged cardiac silhouette. Echocardiogram showed a moderate sized pericardial effusion. |
Mycoplasma pneumonia with associated pericardial effusion
Treatment with intravenous erythromycin, IV fluids, non-steroidal anti-inflammatories (NSAIDs) and prednisone. After significant clinical improvement in his shortness of breath, resolution of his fevers and a follow up echocardiogram demonstrating a stable, moderate sized pericardial effusion he was discharged from the hospital on oral antibiotics and prednisone and scheduled follow appointments for one week. |
|
|
tamponade
|
3 phases of hemodynamic changes in tamponade.
Phase I: The accumulation of pericardial fluid causes increased stiffness of the ventricle, requiring a higher filling pressure. During this phase, the left and right ventricular filling pressures are higher than the intrapericardial pressure. Phase II: With further fluid accumulation, the pericardial pressure increases above the ventricular filling pressure, resulting in reduced cardiac output. Phase III: A further decrease in cardiac output occurs, which is due to equilibration of pericardial and left ventricular (LV) filling pressures. |
|
|
Cardiac Tamponade
|
Cardiac tamponade is characterized by the accumulation of pericardial fluid under pressure and may be acute or subacute.
The primary abnormality is compression of all cardiac chambers due to increased pericardial pressure. The pericardium has some degree of elasticity; but once the elastic limit is reached, the heart must compete with the intrapericardial fluid for the fixed intrapericardial volume. As tamponade progresses, the cardiac chambers become smaller and chamber diastolic compliance is reduced. |
|
|
Cardiac Tamponade
Physical Exam |
Sinus Tachycardia (to help maintain cardiac output)
The jugular venous pressure is almost always elevated in tamponade and may be associated with venous distension in the forehead and scalp A pericardial rub may be heard in patients with inflammatory pericarditis |
|
|
Pulsus paradoxus
|
an abnormally large decrease in systolic blood pressure (>10 mmHg) on inspirations, is a common finding in moderate to severe tamponade and is the direct consequence of ventricular interaction.
The limitation on outward expansion of the right ventricle as blood flows in during inspiration results in bulging of the interventricular septum into the left ventricle, leading to a large reduction in left ventricular filling that contributes to a large decrease in stroke volume. |
|
|
Myopericarditis
|
Inflammation of the muscular wall of the heart and of the enveloping pericardium.
Definite diagnosis of acute pericarditis PLUS 2. Suggestive symptoms (dyspnea, palpitations, or chest pain) and ECG abnormalities not documented previously (ST/T abnormalities, supraventricular or ventricular tachycardia or frequent ectopy, atrioventricular block), OR focal or diffuse depressed LV function of uncertain age by an imaging study 3. Absence of evidence of any other cause 4. One of the following features: evidence of elevated cardiac enzymes (creatine kinase-MB fraction, or troponin I or T), new onset of focal or diffuse depressed LV function by an imaging study, abnormal imaging consistent with myocarditis (MRI with gadolinium, gallium-67 scanning, anti-myosin antibody scanning) |
|
|
Likely diagnosis?
|
Suspected myopericarditis:
criteria 1 plus 2 and 3 Probable myopericarditis: criteria 1,2,3, and 4 Confirmed myopericarditis: histopathologic evidence of myocarditis by endomyocardial biopsy or on autopsy |
|
|
Anemia
|
Concentration of hemoglobin or the number of red blood cells is reduced.
Oxygen-carrying capacity of the blood is decrease. Pt is unable to maintain normal tissue oxygenation. Signs and symptoms are often gradual with significant compensation. |
|
|
Anemia
Symptoms |
Fatigue
Pallor Decreased attention Mood changes Tachycardia Tachypnea Symptoms of Progressive Anemia Irritability Headache Dizziness Nausea Heart Murmur Symptoms of Severe Anemia Chest pain Congestive heart failure Shock Coma Hypoxic Tissue Ascidosis |
|
|
Etiology of Anemia
|
Blood Loss
Blood Destruction Impaired Production |
|
|
Anemia from Blood Loss
|
Acute
Uncompensated anemia Vigorous Reticulocytosis Chronic Anemia indices may be misleading if protein production (albumin and TIBC) is reduced. |
|
|
Anemia
Destruction from Intrinsic Defects: |
Membrane Defects
Hereditary spherocytosis Hereditary eliptocytosis Defects in Hemoglobin Sickle Cell Thalassemias Defects in RBC Metabolism |
|
|
Anemia
Destruction From Extracorpuscular Factors |
Immune Mediated destruction
Auto-immune Rh antibodies Nonimmune Infection agents Chemical Agents Trauma HUS, TTP, DIC Chronic Inflammation Malignancy |
|
|
Anemia
Destruction from an Interaction Between Intra- and Extracorpuscular Factors |
Paroxysmal Nocturnal Hemoglobinuria
Associated enzyme defects G6PD Deficiency Favism |
|
|
Anemia - Impaired Production
|
Nutritional Deficiencies
Iron B12, Folate Bone Marrow Dysfunction Drugs Infection (Parvo) Idiopathic bone marrow failure Marrow replacement Malignancies, myelofibrosis, solid tumors (neuroblastoma, rhabdomyosarcoma) Relative Bone Marrow Failure Infection Chronic inflammatory disease Renal, liver, endocrine diseases Dyserthropoiesis Primary Secondary |
|
|
Microcytic Hypochromic
With reticulocytosis |
Acute Blood Loss
Hemolysis Splenic Pooling |
|
|
Microcytic Hypochromic
Without reticulocytosis |
Iron deficiency
Thalassemia Syndromes Lead Poisoning Copper Deficiency Sideroblastic Pyridoxine-responsive anemia |
|
|
Macrocytic Anemia
|
Folate Deficiency
Goats Milk B12 Deficiency Short gut syndrome Bone Marrow Failure Syndromes Diamond-Blackfan Syndrome Aplastic Anemia Dyserythropoietic Anemia Hypothyroidism, Liver disease |
|
|
Anemia- Newborn
|
Blood loss
Iatrogenic Isoimmunization Hyperbilirubinemia may suggest a congenital hemolytic anemia (HS or G6PD) Infection |
|
|
Anemia-
3-6 months |
Congenital Disorders of hemoglobin synthesis or structure
Almost never iron deficiency in otherwise healthy, term infant |
|
|
Anemia- >6months
Older toddler |
Iron Deficiency
Large volume of Cow’s milk or lactose intolerance. |
|
|
Anemia- males
|
G6PD deficiency
PDK Phosphglycerate Kinase Deficiency |
|
|
Anemia- Diet
|
Pica or other phagia may suggest Iron deficiency
Diets may be low in Iron Toddler on too much cow’s milk may have a mild protein associated colitis with chronic blood loss in the stool |
|
|
anemia:
Race/Ethnic |
Hemoglobins S and C common in African
Beta-thalassemia more common with Mediterranean background Alpha-thalassemia more common in African and Asian ancestry G6PD Deficiency more common in Sephardic Jewish, Filipino, Greek and Kurdish ancestry |
|
|
Iron Distribution
Iron Requirements |
Iron Distribution
70% in hemoglobin 25% in storage (ferritin) 5% in enzyme systems and myoglobin Iron Requirements Preterm: 2 mg/kg/day (max 15 mg/d) Term: 1 mg/kg/day (max 15 mg/d) Age 4-10: 10 mg/day Teenagers: 18 mg/day Adults: Male: 10 mg/day Female: 18 mg/day |
|
|
Iron Deficiency Anemia
|
Still the most common cause of Anemia
Especially during times of rapid growth Infancy Toddlers Adolescence Cow’s milk Almost no bioavailable iron. Large amounts result in colonic inflammation and chronic blood loss. |
|
|
Progression in Iron Deficiency
|
Depletion of Iron Stores
Decrease in serum ferritin and bone marrow iron Decrease in Transport Iron Decrease in serum Iron Increase in TIBC Decreased Hemoglobin Production Decreased Hgb, Proportionately decreased MCV Decreased reticulocytosis |
|
|
Iron Replacement-
response |
12-24 hours -- subjective improvement in mood and appetite
36-48 hours -- marrow erythroid response 48-72 hours -- reticulocytosis peaks Week two -- hemoglobin increased 0.5 to 1 gm/day After Hgb normalizes, treat for an additional 2-3 months to replace iron stores |
|
|
Lead Poisoning
|
Hypochromic Microcytic Anemia
Changes is mood and behavior Abdominal colic Peripheral neuropathy CNS symptoms - seizures followed by cardiorespiratory arrest and coma Blood smear shows hypochromic, microcytic anemia. Only 30% have Basophilic stippling. Always test for Lead when treating for Anemia |
|
|
Hereditary Spherocytosis
|
Red cell membrane defects
Round RBCs prone to hemolysis Reduced RBC life span |
|
|
Congenital Spherocytosis with an aplastic episode.
treatment |
Treated with RBC transfusion and supportive care.
Recovered to baseline Hgb of 8-9 Similar episode 4 months later. Partial splenectomy after pneumovax resulted in baseline Hgb of 12. |
|
|
Aplastic Anemia
treatment |
Pt treated with GCSF, ATG and cyclosporin with slow improvement in counts over the next four months.
Stable on GCSF Off Cyclosporin Will get matched sib BMT if recurs |
|
|
Transient Erythroblastopenia of childhood
|
Bone Marrow showed near absence of erythroid precursors but otherwise normal morphology.
Nml hemoglobin electrophoresis No RBC antibodies Spontaneous resolution |
|
|
Splenic Sequestration and aplastic crisis: (in HbSS)
treatment |
Treatment
Transfusion Fluids Antibiotics after blood culture |
|
|
HUS
presentation: Outcome: |
12 year old present to PMD with 2 weeks of vomiting.
Initially vomited 6 x/day with watery stools for 6 days. Since then still vomiting once or twice per day. Smiling, calm, alert, nml HEENT exam I/VI Systolic ejection murmur Benign exam except a little puffy in the face. UA shows lots of blood and protein BP at 99% for age Legs edematous Hgb 9 with fragmented RBCs BUN 45 / Creatinine 3.2 Outcome: Progression to total renal insufficiency Dialysis the next day Awaiting kidney transplant |
|
|
Clinical Triggers of DIC
|
Gram Neg Sepsis
NEC SGA PIH/HELP Syn Dead Fetal Twin Shock PolyTrauma Endothelial Damage Malignancies APML Neuroblastoma Rhabdo Burns Ascitic Fluid Hypoxia Ascidosis |
|
|
G6PD Deficiency
treatment |
Treatment
Supportive care Withdrawal of offending agent |
|
|
G6PD Deficiency
triggers: |
Antimalarias
Antipyretics Analgesics Sulfa Drugs Misc Fava Beans Naphthalene |
|
|
case: 5 year old well AA boy
Treated 5 days ago with Bactrim for recurrent OM Pale, Irritable, not eating well Exam: Tachycardic, Mild Jaundice Hgb 7, Retic 4 shredded RBCs on Smear |
G6PD Deficiency
|
|
|
Acute Otitis Media
|
80-90% of infants have an ear infection by age 3 y.o.
Most occur between 6-24 months in US. Infrequent in school-aged children, teenagers and adults |
|
|
Acute Otitis Media
Risk Factors |
Age:
Immature anatomy, physiology and immune system changes to decrease OM as one ages Change in skull shape Vectors for eustachian tubes Antibodies following bacterial exposure Daycare Tubes placed 7x more likely in daycare children Breast Feeding: (for 3 months) may decrease likelihood of OM by: Immune or non-immune protective factors in breast milk Facial musculature changes Position maintained while feeding Pacifier Use: slight increase in chance of OM Smoking Exposure Irritant ? Increased carriage of S. pneumonia Ethnicity: Native American, Alaskan and Canadian Eskimoes 40% have a chronic tm perforation by 18m.o. Family History Genetics: more common in identical twins than fraternal twins Underlying disease (e.g., cleft palate, Down syndrome, allergic rhinitis) |
|
|
Otitis Media: Pathogenesis
|
The patient has usually an URI or allergy.
Congestion of the respiratory mucosa of the nose, nasopharynx and eustachian tube. This obstructs the narrowest portion of the tube, the isthmus. Causing negative pressure and secretions accumulate from the mucosa of the middle ear. Viruses and bacteria reach the middle ear via aspiration, reflux, or insufflation. Antibiotic treatment may leave effusion behind for several weeks. |
|
|
Otitis Media: Microbiology
|
Streptococcus pneumoniae
Pneumococcal vaccine hits 60-70% of serotypes Decreased incidence from 48% to 31% Haemophilus influenzae Beta-lactamase producer Increased incidence from 38% to 57% Moxarella catarrhalis Beta-lactamase producer Uncommon: group A strep and staph Virus: rhinovirus-22%, RSV-18%, coronavirus-7% |
|
|
Otitis Media: Clinical Findings
|
Otalgia
Severe-42%, mild-moderate-40% Otorrhea or ear discharge, or swelling about the ear Fever, irritability, headache, apathy, anorexia, vomiting, and diarrhea , conjuctivitis (H. influenza) Abrupt onset of signs and symptoms of middle ear effusion Presence of middle ear infusion Bulging tympanic membrane Limited or absent mobility of tm Air fluid level behind tm otorrhea Inflammation tm erythema Moderate or severe otalgia Fever over 102 F |
|
|
Otitis Media
Complications |
Hearing loss (as long as fluid is present)
Lower test scores of speech, language Vertigo Ruptured TM-usually heals in hours to days Mastoiditis Other: meningitis, epidural abscess, brain abscess, lateral sinus thrombosis, cavernous sinus thrombosis, subdural empyema, and carotid artery thrombosis. |
|
|
Otitis Media- Treatment
|
High dose amoxicillin (80-90mg/kg)
If severe illness (mod/severe pain/temp 102 F) amoxicillin/clavulante “Augmentin” (80-90mg/kg of amoxicillin) PCN-allergic Cephalosporins (eg cefdinir “Omnicef”) azithromycin “Zithromax” or clarithromycin “Biaxin” Fever or Pain Ibuprofen or acetaminophen, topical benzocaine |
|
|
History:
In general, a history of 1-2 days of progressive ear pain Frequently a history of exposure to water Itching Purulent discharge Conductive hearing loss Feeling of fullness or pressure Physical: Pain on gentle traction of the external ear. Periauricular adenitis may occur, but it is not necessary for the diagnosis. Erythema, edema of the epithelium, and an accumulation of moist debris in the canal. Other The tympanic membrane may be difficult to see but normally mobile on insufflation. Spores and hyphae may be seen if fungal Eczema of the pinna may be present. By definition, cranial nerve (CN) involvement is not associated with simple otitis externa. |
Otitis Externa:
|
|
|
Otitis Externa
Bacteriology |
Common is children especially in the summer when they are swimming a lot.
Common in adults when they use Q-tips to clean out their ears or pierce ears. Bacteriology Acute infection = Staph. aureus Pseudomonas (38%), gram negative rods, rarely Fungi |
|
|
Otitis Externa: Treatment
|
Antibiotic Ear Drops
Ofloxicilin 0.3% solution Polymyxin B+neomycin+hydrocortizone Ciprofloxin + hydrocortizone Oral: Dicloxicillin QID Analgesics: Drops: Auralgan NSAIDS, Tylenol, heat Ear Wick |
|
|
Patient is a middle-aged short obese African male with a chief complaint of runny nose for 2 weeks. He usually has “no worries” but he is now developing focal facial pressure, mucopurulent nasal discharge, and right sided tooth pain.
|
Rhinosinusitis
Definition Inflammation or infection of the mucosa of the nasal passages and at least one of the paranasal sinuses. One of the ten most common illnesses seen in the office setting-25 million/year Fifth most common medical diagnosis for which antibiotics prescribed |
|
|
Acute Bacterial Rhinosinusitis (ABRS)
|
Only 1 in 8 patients have ABRS
Antibiotics prescribed 98% of the time Patients actually want reassurance, a careful exam, symptom relief. And the ability to resume their activities more than they want antibiotics. Caused by swelling and obstruction of ostiomeatal complexes |
|
|
Acute Bacterial Rhinosinusitis (ABRS)
ABRS: Pathology |
Outpatient
Streptococcus pneumoniae Haemophilus influenzae Inpatient (nosocomial) Gram negative Anaerobic- associated with dental infections Immucompromised-fungal |
|
|
Acute Bacterial Rhinosinusitis (ABRS)
Helpful Signs and Symptoms |
Purulent nasal discharge
Maxillary tooth or facial pain Especially unilateral Unilateral maxillary sinus tenderness Worsening symptoms after initial improvement |
|
|
Acute Bacterial Rhinosinusitis (ABRS)
Treatment |
When to treat?
Have symptoms for >7d, or 2+ symptoms (purulent discharge, maxillary tooth or facial pain, unilateral max sinus tenderness, or worsening symptoms after initial improvement Amoxicillin x 10-14 days High doses in areas with PCN-resistant S. pneumoniae Augmentin, fluroquinilones |
|
|
Acute Bacterial Rhinosinusitis
ARBS Complications |
Periorbital Cellulitis
Intracranial abscess Meningitis Cavernous Sinus Thrombosis Pott’s puffy tumor (infectious erosion of the ethmoid or frontal sinus) |
|
|
Pharyngitis
|
a beefy, red, swollen uvula; petechiae on the palate; excoriated nares (especially in infants); and a scarlatiniform rash.
Viral: the absence of fever conjunctivitis, cough, hoarseness, coryza, anterior stomatitis, discrete ulcerative lesions, viral exanthems, and diarrhea |
|
|
Pharyngitis
Severe Symptoms |
Symptoms
difficulty swallowing secretions, drooling, dysphonia, "hot potato" voice neck swelling Watch for: Parapharyngeal space infections, peritonsillar abscess ("quinsy"), and submandibular space infection (Ludwig's angina) |
|
|
Pharyngitis and Tonsillitis
Organisms |
Pathology
Group A, C, G Strep Only 10% group A in adults Viral Infectious mononucleosis Coxsackie Other C. diphtheria, mycoplasma, gonococcal, Candida |
|
|
Why treat Group A Strep (GAS) Pharyngitis?
|
To prevent rheumatic fever —nearly disappeared in North America.
To prevent peritonsillar abscess —a vanishing complication To reduce symptoms —there is a modest (approximately one day) reduction in symptoms with early treatment To prevent transmission — while this is important in pediatrics, due to extensive exposures, it is considered far less important in adults. |
|
|
Pharyngitis and Tonsilitis
Treatment |
Treatment
Penicillin for 10 days Oral 2nd Cephalosporins Clindamycin Azithromycin x 5 days “Zithromax” Clarithromycin x 10 days “Biaxin” Erthromycin x 10 days Dirithromycin x 10d |
|
|
Complications: Rheumatic Fever
|
An inflammatory reaction to certain Group A Streptococcus bacteria.
The body produces antibodies to fight the bacteria, but instead the antibodies attack a different target: the body's own tissues. Begin with the joints and often move on to the heart and surrounding tissues. heart valves become inflamed, the leaflets stick together and become scarred, rigid, thickened and shortened = leads to mitral regurgitation. Fewer than 0.3% of people with strep ever contract rheumatic fever |
|
|
Mononucleosis
|
systemic illness
pharyngitis and tonsillar exudate may be prominent splenomegaly, lymphadenopathy, persistent fatigue, weight loss, and hepatitis. tender anterior cervical adenopathy often have enlarged tender posterior cervical nodes. |
|
|
Epiglotitis
|
Since 1985, with the widespread vaccination against Haemophilus influenzae type b (or Hib), which was the most common organism related to epiglottitis, the overall incidence of the disease among children has dropped dramatically.
Epiglottitis caused by Hib has a unique distribution in that it typically occurs among children aged 2-7 years and has not been reported among Navajo Indians and Alaskan Eskimos. Epiglottitis occurs with different peaks in both children and adults. In children, generally epiglottitis typically peaks in children aged 2-4 years. In adults, it peaks between ages 20-40 years. |
|
|
Epiglottitis: Causes
|
Infectious
H influenzae type b Streptococcus pneumoniae, Haemophilus parainfluenzae, Varicella-zoster, Herpes simplex virus type 1, Staphylococcus aureus, among others. Non-infectious |
|
|
Epiglottitis: Exam
|
Mild Distress
Sore throat muffling or changes in the voice difficulty speaking fever difficulty swallowing fast heart rate difficulties in breathing Respiratory Distress drooling, leaning forward to breathe, taking rapid shallow breaths, Accessory muscle retractions high-pitched whistling sound when breathing (stridor) trouble speaking |
|
|
Epiglottitis: Treatment
|
Keep child calm
anxiety may lead to an acute airway obstruction Humidified oxygen/IVs Laryngoscopy in the operating room Cricothyrotomy (cutting the neck to insert a breathing tube directly into the windpipe). IV antibiotics Corticosteroids and epinephrine have been used in the past. However, there is no good proof that these medications are helpful in cases of epiglottitis. |
|
|
Laryngitis
|
Inflammation of the larynx
voice is raspy or hoarse acute or chronic can last as long as two weeks. Causes An upper respiratory infection, especially a cold or flu. Straining or overusing the voice Allergies. Exposure to irritants, such as smoke or chemicals. Gastroesophageal reflux disease (GERD). |
|
|
Laryngotracheitis (Croup)
|
Respiratory illness characterized by inspiratory stridor, cough, and hoarseness
Symptoms result from inflammation in the larynx and subglottic airway. Barking cough in infants and young children Croup usually in 3-36 month age, up to 6 years old Hoarseness in older children and adults. Usually mild and self-limited illness Significant upper airway obstruction, respiratory distress, and, rarely, death, can occur. |
|
|
Bronchitis
|
Inflammation of the bronchi and clinically expressed as cough, usually with sputum production, and evidence of concurrent upper airway infection.
The absence of abnormalities on chest radiography distinguishes acute bronchitis from pneumonitis. American College of Physicians and the Centers for Disease Control and Prevention: Both state that the only form of bronchitis that should be treated with antibacterial agents is pertussis |
|
|
Bronchitis: Microbiology
|
influenza A and B
parainfluenza coronavirus (types 1-3) rhinovirus respiratory syncytial virus human metapneumovirus Mycoplasma pneumoniae (5%) Chlamydophila (formerly Chlamydia) pneumoniae (5%) Bordetella pertussis (12%) |
|
|
Bronchitis: Diagnosis
|
Cough
Disappears by day 14 in 75% of common colds If sever paroxysmal cough or posttussic vomiting Check for pertussis Fever is unusual in bronchitis Presence means pneumonia or influenza When you need Chest X-Ray? abnormal vital signs (pulse >100/min, respiratory rate >24, or temperature >38 ºC) or crackles on chest examination In adults, testing for Mycoplasma, Chlamydia or pertussis is not indicated do to poor availability, no consensus evidence by experts (Mycoplasma), and equal sensitivity compared to clinical diagnosis alone (influenza) |
|
|
Bronchitis: Treatment
|
Symptomatic Treatment
Ipratropium (Atrovent) Beta2 agonists if airway obstruction present Pertussis Azithromycin (Zithromax) Clarithromycin (Biaxin) Influenza influenza A infections amantadine or rimantadine but only if begun within 48 hours of the inception of symptoms. influenza A and B Neuraminidase inhibitors are active against both. Zanamivir (inhaled) and oseltamivir (oral) appear to be as effective as amantadine or rimantadine against influenza A and are also active against influenza B |
|
|
Tuberculosis
Systemic Manifestations |
Fever, weight loss, malaise – related to TNF release
• Anemia of chronic disease: 10% • WBC: usually modest elevation, rarely leukemoid reaction or pancytopenia • Hyponatremia:11% |
|
|
Pott’s Disease
|
Skeletal TB
|
|
|
Management: Latent TB infection
(+PPD, no symptoms, negative CXR) |
• History and physical exam, CXR, HIV • If obtainable: sputum cultures and smears x 3 • 9 month INH 300 mg/day for adults • Consider 50 mg B6 daily (pyridoxine)
|
|
|
anagement of TB disease
(+PPD usually, +symptoms, usually +CXR) |
Hospitalize,isolateseriouslyillpatients
• PPDskintest • Confirmdiagnosis:3-5sputumspecimensfor smear and culture – Bronchoscopy if necessary • If high probability of disease and patient gravely ill: start Rx immediately • Start 4 drug Rx (INH, Rif, PZA, Ethambutal) • Long-term:DOT |
|
|
Chikungunya
|
"that which bends up”
Mosquito-borne: Aedes aegypti, Aedes albopictus |
|
|
|
|
|
|
Cutaneous Larva migrans
|
“creeping eruption”
|
|
|
Leishmaniasis
|
Protozoan parasite
|
|
|
Myiasis
|
botfly, tumbu fly larvae
|
|
|
Ascaris lumbricoides
|
25% world population infected
|
|
|
Schistosomiasis
|
|
|
|
Systemic Febrile Illness: DDx
|
Malaria, malaria, malaria
|
|
|
Clues: time elapsed since travel,
|
< 14 days: malaria, dengue, rickettsiae, typhoid (chikungunya)
|
|
|
most common cause of pneumonia worldwide.
|
Streptococcus pneumoniae
|
|
|
Pneumonia
|
an inflammation of the lung most often caused by infection with bacteria, viruses, and other organisms although there are also non-infectious causes.
Pneumonia is often a complication of a pre-existing condition/infection and triggered when a patient's defense system is weakened, most often by a simple viral respiratory tract infection or a case of influenza, especially in the elderly. |
|
|
Pneumonia
Epidemiology |
Pneumonia and influenza together are ranked as the eighth leading cause of death in the United States.
Pneumonia consistently accounts for the overwhelming majority of deaths between the two. In 2004, 60,207 people died of pneumonia. There were an estimated 651,000 hospital discharges in males (44.9 per 10,000) and 717,000 discharges in females (47.7 per 10,000) all attributable to pneumonia in 2005. The highest pneumonia discharge rate that year was seen in those 65 and over at 221.3 per 10,000. |
|
|
Chlamydophila pneumoniae
|
produces a ciliostatic factor
|
|
|
Mycoplasma pneumoniae
|
shear off cilia
|
|
|
Influenza virus
|
reduces tracheal mucus velocity within hours of onset of infection and for up to 12 weeks postinfection.
|
|
|
Pneumococcus produces other virulence factors including:
|
the capsule that inhibits phagocytosis, pneumolysin
Thiol-activated cytolysin that interacts with cholesterol in host cell membranes Neuraminidase Hyaluronidase |
|
|
Streptococcus pneumoniae and Neisseria meningitidis produce...
|
proteases that can split secretory IgA.
|
|
|
Mycoplasma
|
The smallest free-living agents of disease in man,
Characteristics of both bacteria and viruses. Cause a mild and widespread pneumonia. Cough that tends to come in violent attacks, but produces only sparse whitish mucus. Mycoplasma is responsible for approximately 15-50 percent of all adult cases of pneumonia and an even higher rate in school-aged children. |
|
|
Radiographic appearances of CAP
|
lobar consolidation
interstitial infiltrates cavitation “Gold standard" for diagnosing pneumonia |
|
|
Pneumococcal Vaccine
|
Immunocompromised persons aged 19 years, including those with HIV infection, malignancy, chronic renal disease, nephrotic syndrome, congenital immunodeficiency;
those receiving immunosuppressive chemotherapy (including glucocorticoids); asplenia; post organ or bone marrow transplantation. Immunocompetent persons Persons aged 65 years Persons aged 19-64 years with chronic cardiovascular disease, chronic pulmonary disease (including asthma), or diabetes mellitus Persons aged 19-64 years who smoke cigarettes, or who have alcoholism, chronic liver disease, cerebrospinal fluid leaks, or cochlear implants Persons aged 19-64 years living in special environments or social settings such as chronic care facilities |
|
|
Bronchiolitis obliterans organizing pneumonia (BOOP)
|
an inflammation of the bronchioles and surrounding tissue in the lungs.
often caused by a pre-existing chronic inflammatory disease like rheumatoi arthritis. BOOP can also be a side effect of certain medicinal drugs, e.g. amiodarone. clinical features and radiological imaging resemble infectious pneumonia. However, diagnosis is suspected after there is no response to multiple antibiotics, and blood and sputum cultures are negative for organisms. May need biopsy for diagnosis Treatment is with steroids |
|
|
Restrictive lung disease
|
Diseases or conditions that result in the inhibition of normal expansion of the lung
Difficulties experienced in inspiration |
|
|
Restrictive lung disease
Causes |
Respiratory Center Depression
Narcotics/barbiturates Neuromuscular Guillain-Barre Duchenne MD Thoracic Excursion Restriction Deformed Thorax Flail Chest Obesity Pleural Effusion Pneumothorax Lung Parenchyma Disorders Pulmonary Fibrosis TB Atelectasis ARDS Pulmonary Edema Aspiration Pneumonia Pneumoconiosis Bacterial Pneumonia Viral Pneumonia Interstitial Lung Disease Pulmonary Fibrosis |
|
|
Pneumothorax
|
Air leaks into the intrapleural space
This causes: Intrapleural pressure to rise Chest wall moves out Diaphragm moves out Pulmonary blood flow to decrease Alveolar pressure to decrease Most spontaneously resolve, but larger ones may require chest tube placement Repeated pneumothorax may require obliteration of the space |
|
|
Flail Chest
|
Flail chest is a serious, life-threatening chest injury and is most commonly seen in cases of significant blunt trauma. In ER, approximately 30% of patients with extensive thoracic trauma have a flail chest.
Three or more adjacent ribs are fractured in two or more places Allows that segment of the thoracic wall to displace and move independently of the rest of the chest wall. Flail chest can also occur when ribs are fractured proximally in conjunction with disarticulation of costochondral cartilages distally. For the condition to occur, generally there must be a significant force applied over a large surface of the thorax to create the multiple anterior and posterior rib fractures. |
|
|
Interstitial Lung Disease
|
Some ILD’s can cause of obstructive patterns
Lymphangioleiomyomatosis (LAM) Tuberous Sclerosis Sarcoidosis (uncommon) Hypersensitivity Pneumonitis (uncommon) Most cause restrictive pattern from either inflammation and fibrosis, or granulamatous reactions |
|
|
Atopy
|
considered present when there was a mean wheal size ≥2 mm in response four antigens — house dust, mixed grasses, mixed trees, and ragweed
|
|
|
Physical Examination**
Presence of emphysema |
Presence of emphysema (only when severe) is indicated by:
Overdistention of the lungs in the stable state (chest held near full inspiratory position at end of normal expiration, low diaphragmatic position) Decreased intensity of breath and heart sounds Prolonged expiratory phase Evidence of airflow obstruction: wheezes during auscultation on slow or forced breathing prolongation of forced expiratory time Frequently observed with severe disease (characteristic, but not diagnostic): pursed-lip breathing use of accessory respiratory muscles retraction of lower interspaces. Other Unusual positions to relieve dyspnea at rest. Digital clubbing suggests the possibility of lung cancer or bronchiectasis. Mild dependent edema may be seen in the absence of right heart failure. |
