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;
180 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 |
|
|
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 |
|
|
QT Interval
|
Ventricular contraction or “systole” |
|
|
What is VO2 |
Oxygen Consumption = (Arterial oxygen content - venous oxygen content) x Cardiac Output |
|
|
What is Oxygen Delivery |
DO2 = Arterial oxygen content x cardiac output |
|
|
What is oxygen extraction ratio? |
VO2/DO2 |
|
|
For each molecule of glucose that is metabolized, how many molecules of ATP are produced? |
36 molecules of ATP (32 aerobic and 4 anarobic) |
|
|
What is heart afterload? |
Afterload is the tension or stress developed in the wall of the left ventricle during ejection. |
|
|
What is Oxygen Debt? |
Tissue Oxygen Debt or recovery oxygen consumption is the difference between oxygen debt and oxygen consumption. In healthy individuals - it happens during intense workout. In sick - it is correlated with survival. |
|
|
What is hematocrit? |
Percent of volume of RBC in blood. Normal values - 42-46% |
|
|
What is diffusion? |
Measure of how well the lungs exchange gas |
|
|
What is perfusion |
The blood that reaches the alveoli |
|
|
What is the V/Q ratio? |
Ventilation/perfusion ration is v/q the air that reaches the alveoli/blood that reach the alveoli. |
|
|
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 |
|
|
What process require a continuous source of ATP? |
Muscle contraction and nerve impulse transmission |
|
|
What is the major source of energy? |
ATP |
|
|
Hypertrophy
|
An increase in size or muscle mass |
|
|
What can be caused by lactic acid accumulation? |
Metabolic Acidosis |
|
|
P wave is diphasic |
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 |
|
|
What is convection? |
? |
|
|
What is normal Ph range? |
Normal range of ph is 7.35 - 7.45, if less then it is acidosis. |
|
|
Right shift of dissociation curve? |
Increase temp, 2-3 DPG, p(Co2) pH decreases |
|
|
Pyruvic Acid is? |
An intermediate product formed when the body uses glucose |
|
|
Cellular Oxidation |
Another name for respiration |
|
|
Sick Sinus Syndrome |
Chronic inappropriate and often severe bradycardia |
|
|
What happens to O2 affinity with a left shift? |
Increases |
|
|
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: |
|
|
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 |
|
|
Factors that contribute to Hypertension
|
Smoking |
|
|
Symptoms of Hypertension
|
In over 1/3 of all individuals with hypertension, there are no symptoms. |
|
|
Testing for Hypertension
|
Blood pressure is measured with a sphygmomanometer (blood pressure cuff) |
|
|
Physical Exam for hypertension
-Minimum- |
Minimum components of exam |
|
|
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 |
|
|
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 |
|
|
In the first 10 seconds of exercise what does your body use for energy? |
ATP and CP (creatin phosphate) |
|
|
Your body will use what for 30 - 60 seconds? |
Glycolysis |
|
|
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 |
|
|
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 |
|
|
Gold standard tests
For Cardial Infarction |
Coronary angiography
This is the gold standard |
|
|
MI Management |
Assessment of the hemodynamic state and correction of abnormalities that are present (ABCs) |
|
|
In a muscle contraction what moves off of binding sites on actin so myosin can bind? (cross bridge) |
Tropomyosin |
|
|
What causes tropomyosin to roll? |
Calcium |
|
|
Thrombophlebitis
|
Thrombosis with inflammation |
|
|
Phlebothrombosis
|
Thrombosis without inflammation
|
|
|
Superficial Thrombophlebitis |
Local Swelling |
|
|
Virchow’s Triad |
Venous stasis |
|
|
Virchow's Node |
Left supraclavicular fossa, if inlarged sign of abdominal cancer. |
|
|
Thrombosis |
Superficial Veins |
|
|
Deep Vein Thrombosis |
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. |
|
|
Fast twitch muscle fibers are: |
fast, fatigue quickly anaerobic |
|
|
Venous Peripheral Vascular Disease
|
Swelling of feet and legs |
|
|
What valve do you listen to on R side of body? |
Aortic |
|
|
What valve do you listen to on 2nd intercostal space on Right? |
|
|
|
What would you categorize a sound over mitral valve after S1? |
Systole regurgatant |
|
|
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 |
|
|
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) |
|
|
Raynaud’s Disease
|
Distal portion of fingers |
|
|
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 |
|
|
Etiology of Aortic Valve Stenosis
|
There are three primary causes of valvular AS: |
|
|
Aortic Stenosis Pathophysiology
|
Valve becomes obstruction to ventricular ejection gradually over time |
|
|
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 |
|
|
Mitral Regurgitation
Etiologies |
lterations of the Leaflets, Commissures, Annulus |
|
|
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. |
|
|
Tricuspid Stenosis
Auscultation |
An opening snap of the tricuspid valve may be heard and is localized to the lower left sternal border. |
|
|
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 |
|
|
tamponade
|
3 phases of hemodynamic changes in tamponade. |
|
|
Etiology of Anemia
|
Blood Loss |
|
|
Anemia from Blood Loss
|
Acute |
|
|
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. |
|
|
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 |
|
|
What is a primary determinant of DO2 |
CO (Cardiac Output) = SV x HR |
|
|
Cutaneous Larva migrans
|
“creeping eruption”
|
|
|
Leishmaniasis
|
Protozoan parasite
|
|
|
Myiasis
|
botfly, tumbu fly larvae
|
|
|
Ascaris lumbricoides |
25% world population infected |
|
|
What is preload? |
Preload is end diastolic muscle fiber length of the ventricles before systolic ejection |
|
|
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 |
