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;
163 Cards in this Set
- Front
- Back
|
What is myocarditis?
|
inflammation of myocardium
|
|
|
What do all the causes of myocarditis have in common (ie infectious microorganisms, toxins, autoimmune stuff)
|
inflammation
|
|
|
Whats the rang of outcomes wit myocarditis?
|
BROAD
Asymtopmatic (full recovery) -> heart failure/arrhythmias (death) |
|
|
T/F: Myocarditis may be acute, subacute or chronic
|
TRUE
|
|
|
Myocarditis may be responsible for up to what percent of unexplained sudden cardiac death?
|
20%
|
|
|
Who is affected more by myocarditis, males or females?
|
males
|
|
|
Whats the incidence of mycarditis?
|
8-10/100,000 TO 1-5/100
= There COULD be a LOT of it, kinda unknown |
|
|
How do most babies acquire myocarditis?
|
mother (60-70%)
Hospital staff (30-40%) |
|
|
What do virus causes the most myocarditis in babies?
|
Adenovirus
(Onset usually in 1st 7 days) |
|
|
If the pt. lives through the acute phase of myocarditis, what are the possible outcomes?
|
Resolve (no residual changes)
OR Inflammatory lesions healed via progressive fibrosis |
|
|
Whats the most common cause of myocarditis?
|
Viral
THEN: Drugs (ex. = cocaine) and Autoimmunity |
|
|
Myocarditis kills what percent of infants who get it?
|
50-70% with death within 1 week
BUT Survivors usually fully recover |
|
|
Whats the KEY FEATURE of myocarditis?
|
Inflammatory infiltrate (=inflammatory cells etc)
= purple dots = Lymphocytes myocyte damage necrosis |
|
|
Whats the most common cause of Myocarditis in ADULTS?
|
Adults = Coxsackie (enterovirus)
Infants = Adenovirus (also parvovirus B19 and HHV 6 = human herpes virus 6 can cause it) |
|
|
Whats the most common PROTOZOAL cause of myocarditis?
|
Trypanosoma cruzi
= symptoms will be different than if a virus, like adenovirus or coxsackie caused it. |
|
|
Whats the most common cause of myocarditis in HIV or CMV (or immuno-compromised) pts?
|
Picornovirus (=small RNA viruses)
|
|
|
Clinical presentation of myocarditis in adults? (infants?)
|
adults = cold, flu-like, respiratory, GI symptoms
infants = listless, anorexc, respiratory, tachypnea, diaphoresis |
|
|
What are the non-viral causes of myocarditis?
|
Two in AIDS pts:
Unknown Caused by HIV directly Non-infectious causes: 1. hypersensitivity rxns (drugs like antibiotics, diuretics) 2. systemic immune disease (rheumatoid arthritis, SLE, polymyositis) |
|
|
How does Diptheria toxin cause myocardal damage?
|
Inhibits elongation factor II = inhibits protein synthesis
|
|
|
Whats are the 3 steps in pathophysiology of viral myocarditis?
|
1. viral phase = enters GI or respiratory via CAR receptor
2. immune response = virus or immune response cause injury --> cardiac damage 3. cardiac remodeling = cardiac injury and immune response may destroy heart tissue acutely or linger and produce cardiac remodeling leading to cardiomyopathies, HF, or death |
|
|
What receptor does coxsackie and adenovirus bind to in GI to lead to myocarditis?
|
CAR (Coxsackie-Adenovirus Receptor)
|
|
|
Why would you do an EKG in a pt with suspected myocarditis?
|
to rule out other Dxs....
|
|
|
What are the best ways to Dx myocardits?
|
blood work = suggestive, NOT Diagnostic
Inc Creatine kinase, Inc. Tropinin = myocyte necrosis occured Heart biopsy = most suggestive |
|
|
If you were able to do a heart biopsy on a pt. with suspected myocarditis, what would you find if it WAS myocarditis?
|
Presence of inflammatory cells AND myocyte degeneration/necrosis on SAME biopsy specimen
|
|
|
Tx for Myocarditis?
|
fluids, bed rest, supportive care, cardiac monitoring, drugs to tx heart failure
|
|
|
What are the newer diagnostic tools to Dx myocarditis?
|
PCR and in situ hybridization
|
|
|
What are the newer therapeutics to Tx myocarditis?
|
Type-1 interferons, immunoglobulins, anti-viral agents. Maybe immunosuppressants
|
|
|
How do Coxsackie virus and Adenovirus, two totally unrelated viruses, cause viral myocarditis?
|
they both bind the same receptor, CAR
|
|
|
Whats the infectious agent of Chagas disease?
|
Trypanosoma crizi (=SAME as myocarditis protozoal cause)
|
|
|
What insect transmits Chagas disease?
|
Triatomid = kissing bug
|
|
|
How does Triatomid spread chagas disease?
|
it poops on your face, trypanosoma cruzi then enters via skin lesion (b/c of scratching) or around eyes.
|
|
|
What does the Parasite that causes chagas do once inside body?
|
changes shape
|
|
|
What are the signs, symptoms, epidemiologic clues that might lead you to believe chagas disease is occuring in a pt?
|
ACUTE:
Chagoma (=the site of entry) Romana's sign = eye swollen shut) fever fatigue rash S. or Central American origin/travel myocarditis (rarely) Arrhythmia cardiac failure CHRONIC: megaesophagus palpitations megacolon dypsnea mexicans syncope arrhythmia cardiac failure |
|
|
Whats the difference between SIRS and Sepsis?
|
SIRS = systemic inflammatory Response Syndrome
Sepsis = SIRS due to INFECTION |
|
|
What defines SIRS?
|
Two or more of the following:
Temp above 38 or below 36 heart rate above 90 resp. rate more than 20 breaths/min (OR PACO2 less than 32 mmHg) WBC more than 12,000 (OR less than 4000 cells/mL OR greater than 10% band PMN) |
|
|
Whats the difference between Sepsis and Sepsis Syndrome?
|
Sepsis syndrome = Sepsis PLUS:
HyPOperfusion (of organs) OR Organ dysfunction With at least one of these: "POMMELED-CH" Platelets Low Oliguria Mental Status Change Mottled Skin EEG Lung Injury (acute) Elevated Lactate Disseminated Intravascular Coagulation Cardiac Dysfunction Hypoxemia |
|
|
Whats the difference between Sepsis Syndrome and Septic Shock?
|
All the requirements of Sepsis Syndrome PLUS
HypOtension (despite adequate fluid) Resuscitation that may require vasopressors |
|
|
Likely setting for development of sepsis caused by staph. aureus?
|
Nosocomial (=hospital acquired)
ICU pts Intravascular Devices |
|
|
Likely setting for development of sepsis caused by pseudomonas?
|
Burn victims
ICU pts Neutropenia |
|
|
Likely setting for development of sepsis caused by E. coli/ Klebsiella (othe rgram neg. bac.)?
|
vagina ie UTI's
|
|
|
Likely setting for development of sepsis caused by Coagulase-neg staph?
|
post-surgical (someones laying in bed after surgery, don't want clots = coagulase NEG. staph)
intravascular devices |
|
|
Likely setting for development of sepsis caused by strep. pneumoniae?
|
community-acquired pneumonia
|
|
|
Likely setting for development of sepsis caused by bacteriodes, clostridium, other anaerobes?
|
Deep wounds, abcesses
|
|
|
Likely setting for development of sepsis caused by Group B strep.?
|
B = Babies
|
|
|
Likely setting for development of sepsis caused by Listeria?
|
Immunosuppressed pts (HIV etc.)
|
|
|
What are some of the cardiovascular alterations found in pts with septic shock?
|
Dec. SVR
Inc. CO HypOperfusion |
|
|
A Community acquired pneimonia. Whats the most likely causative organism of their sepsis ?
|
strep. pneumoniae
|
|
|
A pt. suffered a deep tissue wound. whats the most likely causative organism of their sepsis?
|
Bacteroides, clostridium, other anaerobes
|
|
|
A pt. has a UTI, whats the most likely causative organism of their sepsis?
|
E. coli, Klebsella, other gram neg. bacilli
|
|
|
A pt. suffers an infection from an intravascular device. Whats the most likely organism of their sepsis?
|
the "staphs"
staph aureus, coag. neg. staph |
|
|
A pt, suffers a severe burn, whats the most likely causative organism of their sepsis?
|
Pseudomonas
|
|
|
T/F: the most likely infection leading to septic shock is a wound infection.
|
FALSE
resp. tract infection then UTI |
|
|
Unique characteristics of pseudomonas aeruginosa?
|
MICRO;
Gram neg. bacilli Oxidase Pos. Pigments and toxins Pt: Immunocompromised Neutropenic higher mortality rate LESION: Seen in minority of pts... Ecthyma gangrenosum lesion = a black looking thing. |
|
|
A pt comes in with a black lesion in his leg. Whats the most likely causative organism?
|
pseudomonas aeruginosa
Its an ecthyma gangrenosum |
|
|
What HOST activities are thought to play a significant role in the development of sepsis syndrome?
|
"NIT - PICK"
Nitric Oxide IL-1 TLR-4/ TNF-alpha PAF/ Prostaglandins IL-6 Complement (=C5A)/ Coag. factors Kinins |
|
|
What HOST factors in Sepsis Syndrome cause vasodilation, inc. permeability, and dec. perfusion?
|
NO
PAF IL-6 |
|
|
What is the hallmark of Shock?
|
Tissue HypOperfusion
|
|
|
What are the Coagulation abnormalities seen in sepsis?
|
1. Vasodilation --> leakage
2. HypOtension (responsive to volume replacement) abd Dec. myocardial Activity 3. CV insifficiency due to vascular and myocardial abnormalities from: Maldistributuion of blood Endothelial damage HypOperfusion 4. Coagulation Abnormalities w/organ damage |
|
|
What are the Cardiac and Pulmonary changes in septic shock?
|
1. Tissue Hypoperfusion
2. Dec. myocardial activity 3. Clotting and bleeding can occur simultaneously in same pt. 4. Acute Respiratory Distress Syndrome (ARDS) = "Shock Lung" |
|
|
How do you manage a pt. with sepsis or sepsis syndrome?
|
Shock/organ failure: stabilize, reverse CV probs, fluids, vaso/cardio reactive drugs
Antimicrobial therapy: give a general anti-microbial first until we know what caused infection Invasive: Drain abcess, debride necrotis tissue, Remove colonized prosthesis or catheters |
|
|
What are the three main categories of pt. management in a pt. with sepsis or sepsis syndrome?
|
Shock and organ failure
Antimicrobial therapy Invasive procedures |
|
|
What are the most important considerations and general pt. management steps needed to inc. the likelihood of a pos. outcome for pt. with severe sepsis?
|
supportive measures: O2, fluids
Anti-microbial therapy Surgical drainage THEN: re-evaluate and focus anti-microbial therapy THEN... did fluid replacement inc. BP? If NO, vasopressor and ionotropic agent and other treatments (corticosteroids, insulin) |
|
|
Define Syncope
|
Global hypoperfusion characterized by:
Rapid Onset Short Duration Spontaneous Complete Recovery Non-traumatic |
|
|
What are some the the differntial diagnoses of syncope?
|
Epileptic seizure
psychogenic pseudosyncope rare causes (cataplexy, drop attacks, TIA) |
|
|
Whats the most frequent cause of syncope?
|
Reflex syncope
-vasovagal -situational -carotid sinus syncope |
|
|
What are some of the types of syncope secondary to orthostatic hypotension?
|
primary autonomic failure
secondary autonomic failure drug-induced volume depletion |
|
|
What are the types of cardiac syncope?
|
Arrhythmia
structural disease |
|
|
what are the 3 classifications for syncope?
|
Reflex
Secondary to orthostatic hypotension Cardiac |
|
|
Whats the formula for understanding why syncope occurs?
|
BP = TRP x CO
|
|
|
Alternations in what effect syncope? CO and TPR
|
Dec. Co
Dec. TPR |
|
|
If relfex syncope is the most common cause of syncope, whats the second most common cause?
|
Cardiac
|
|
|
Prognosis after a syncope event is related to what?
|
The underlying cause of the syncope, not the syncope itself
|
|
|
What 3 questions should you ask on your initial evaluation of a pt. with syncope?
|
1. did pt have true syncopal event? (for ex., seizure= NOT syncope)
2. What is the CAUSE (etiology) of the pts. presentation? 3.Is the pt. at HIGH RISK for cardiovascular events or sudden cardiac death? |
|
|
Initial evaluation can determine the cause of syncope is what percent of cases?
|
23-50%
|
|
|
What included in the initial evaluation of syncope?
|
Hx
Physical Orthostatic BP EKG THEN Additional stuff based on Hx and PE |
|
|
What should the History portion of a syncope workup focus on?
|
CARDIAC CAUSES (because these are the most severe ie sudden death
|
|
|
What are some questions you shuld ask during history portion of the workup of a syncope pt. to determine if the even is cardiac in origin?
|
Palpitations?
Chest pain? What activity was the pt. engaged in prior to episode? Position of the pt.? Prodromal symptoms? |
|
|
Whats one of the causes of sudden death in young pts, that can present with syncope?
|
Hypertrophic cardiomyopathy
|
|
|
What is the San Francisco Syncope Rule?
|
Predicts risk for serous outcomes related to syncope
|
|
|
What are the risk factors examined in the San Francisco Syncope rule?
|
systolic less than 90
shortness of breath EKG: non-sinus rhythm Hx. of CHF Hematocrit less than 30% LOW RISK = NO risk factors HIGH RISK = one or MORE risk factors |
|
|
HIGH risk of adverse outcomes with syncope are defined in what pts?
|
HIGH Risk of adverse outcomes = Over 60 with cardiovascular Dx
OR Young pts Exercising with OUT a benign cause |
|
|
LOW Risk of adverse outcomes with syncope are defined in what pts?
|
Less than 45 with OUT cardiovascular disease (or other risk factors)
Reflex syncope (=of no concern) |
|
|
A pt. presents with syncope and upon PE you find an outflow obstruction. Is this pt at high or low risk for adverse outcomes?
|
HIGH
Any pt with outflow obstruction (via echo) or CHD = high risk ie EKG abnormalities |
|
|
Risk of sudden death associated with syncopal event is directly related to what?
|
severity of left ventricular dysfunction
|
|
|
Whats the major goal in evaluating a pt with syncope?
|
ID a potentially life-threatening Dx.
Ischemia, Arrhythmias, underlying heart disease |
|
|
A pt. presents to your office after a syncope event, and after examination you find this pt. to have Non-ischemic dilated cardiomyopathy. Whats your Differnetial Dx?
|
Brady
Tachy Orthostatic hypotension Pulm. embolism |
|
|
Whats one of the causes of sudden cardiac death in young pts?
|
Hypertrophic Cardiomyopathy
|
|
|
A young pt. presents with syncope with physical exercise. How are you going to evaluate this pt?
|
Echo
Exercise stress test (Rule OUT Brady and Tachy and underlying cardiac disease) |
|
|
A pt presents after a syncopal even with a murmur and you conjecture there may be an outflow obstruction. Should you admit this pt?
|
Yes, consider admitting, depending on presence of other risk factors
|
|
|
A pt presents to your office after a syncopal event. Apon PE, you notice lateral lesions on the tongue. Is this event due to syncope or something else?
|
something else, most likely seizure.
Lateral tongue lesions = Seizure Lesions on the end of the tongue (anterior lesions) = syncope |
|
|
Define stable angina
|
Occurs upon exertion
Relieved by rest or nitroglycerin |
|
|
Define unstable angina
|
Occurs at rest
|
|
|
What are the TIMI risk factors for stable and unstable angina?
|
Inc. Risk factors = Worse outcome so more aggressive Tx needed:
Age over 65 Greater than 3 risk factors for CAD Documented CAD ST Deviation greater than 0.5mm More than 2 angina episodes in last 24 hrs. Elevated cardiac markers Aspirin use within last week |
|
|
73 y/o Pt comes into office having had 3 anginal episodes the previous night. He had CAD last year for which he is taking meds. His EKG shows ST elevtions, and his las show elevated Myoglobin and CK isoforms. what should you do?
|
His TIMI Score is really high. Treat him aggressively
|
|
|
What are some of the high risk physical exam findings for Stable and usntable angina?
|
Pulm edema
New/worsening murmur New S3 or S4 rales Hypotension, Brady, Tachy Age greater than 75 |
|
|
If a pt. has an intermediate or high TIMI score, how should you treat them?
|
Intermediate = 3-4
High = 5-7 Treat INVASIVELY |
|
|
If a pt has a low TIMI score (0-2) how should you treat them?
|
Conservatively OR Invasively, either were shown to provide similar outcomes for LOW risk pts.
|
|
|
Pt comes in complaining of chest pain, and you Dx Stable angina. Cardiac markers are negative, and EKG is normal. How do you Tx?
|
Aspirin
Clopidogrel (Plavix) UFH/LMWH Anti-iscemic therapy Early Conservative Rx |
|
|
A pts walks into your office and you Dx Stable angina. Since he is a low risk pt, what do you give him as you send him away until he can return to do the stress test in invoke ischemia?
|
Aspirin
sublingual nitro B-Blocker |
|
|
Whats the standard EKG stress test used for pts of low risk unstable (or stable) angina?
|
Standard EKG stress test
(No extra echo etc. are needed UNLESS the EKG shows ABNORMALITIES, then we bring out the big boys...echo etc.) |
|
|
What Cardiac biomarker do you see peaking the earliest when evaluating a pt. for unstable or stable angina?
|
Myoglobin and CK isoforms
|
|
|
What biomarkers peaks the highest is a LARGE MI? (small MI?)
|
Large MI = Troponin
Small MI = myoglobin or CK isoforms, with CKMB coming in second. ie, Tropinin is NOT elevated in a SMALL MI*** |
|
|
Whats the advantage of looking for Tropnin as a cardiac biomarker in stable and unstable angina?
|
Troponin can help you catch the fac tthat an MI occurred up to TWO WEEKS after it happened.
|
|
|
How does aspirin work?
|
Inhibits COX1 = Blocks synth of Thromboxane A = diminishes platelet aggregation
|
|
|
What dose of aspirin should be used by pts with acute MI?
|
160 mg/day = 2 baby aspirins
|
|
|
A pt. had bleeding prior to presenting with angina. To thin the blood, do we give Low Molecular Weight Heparin or Unfractionated Heparin?
|
Unfractionated
|
|
|
A pt. is Dx'ed with a percutaneous coronary block of 50% of the artery. Is Stenting an option?
|
NOPERS.
Has to be at least 70% blocked. you gonna die, son. |
|
|
When do you do CABG (Coronary Artery Bypass Graft) OVER STENT (Percutaneous Coronary Intervention)?
|
If pt has:
L. Main coronary artery more than 50% stenosed 2-3 vessels diseased with Proximal LAD stenosis DM (treated) L. Ventricular Dysfunction |
|
|
T/F: Statins, part of the adjuctive therapy for stable and unstable Agnina, should be given to all pts. regardless of LDL Lipid levels
|
TRUE
|
|
|
T/F: O2 is useful in all pts. with stable or unstable angina and should be given to everyone.
|
FALSE
|
|
|
How likely are you to DIE within 30 days from Unstable angina, NSTEMI or STEMI?
|
Unstable Angina = 1.7%
NSTEMI = 7.4% STEMI = 11.1% |
|
|
T/F: The risk of dying within 30 days after onset of symptoms increases in this order: STEMI, NSTEMI, Unstable Angina
|
FALSE
Risk Increases from = Unstable Angina, NSTEMI, STEMI |
|
|
Why are ACE inhibs used in pts with Unstable Angina?
|
Used in all pts, stable and unstable to reduce mortality and pulm. edema if present
|
|
|
Why do we use anti-thrombitic therapy in pts with unstable angina, NSTEMI and STEMI?
|
Inc. blood supply to tissues
|
|
|
What are the most common findings in Unstable Angina and NSTEMI pts when a surgeon does cardiac catheterization?
|
Critical Obstruction (greater than 50% stenosis) of THREE vessels = 38% of the time
Two vessels = 28% One vessel = 26% NO stenosis greater than 50% = 13% (so you're gonna find stenosis...) Left Main Artery stenosis greater than 50% = 5-10% = NOT very likely to find |
|
|
Whats the MOST Common finding when a surgeon does cardiac catheterization of a pt. w/ unstable or NSTEMI?
|
greater than 50% stenosis of 3 vessels
|
|
|
What are the goals of reperfusion therapy?
|
1. Get needle in pt. in less than 30 min (after pt. is found)
2. Get balloon in pt. within 90 min (after pt is found) |
|
|
How do Fibrinolytic agents help with acute MIs?
|
Fibrinolytic agent = activate Plasminogen = Plasminogen --> plasmin so it can dissolve fibrin = clot dissolved
|
|
|
What is the appropriate presentation of a pt in whom fibrinolytic agents should be used?
|
Early presentation (3 hours or LESS from onset of symptoms)
Can't do invasive stuff (no cath lab, can't access vessel) DELAY in getting pt to cath lab (ie its OVER 3 hrs. since symptoms started) Door to balloon - Door to needle is GREATER than 1 hr. Greater than 90 min post event occured |
|
|
A pt. with acute MI falls at home in rural Lewisburg, WV, and it not found until 2 hours later. The nearest cath lab is the sprawling metropolis of Charleston, WV, 1.5 hrs. away. What do you do for this pt.?
|
Fibrinolytics
|
|
|
What types of complications can occur after an Acute MI?
|
Free wall rupture
VSD Papillary muscle rupture Right Ventricular infarction |
|
|
Pt presents in the first 24 hours after an acute MI with dypsnea and hypotension. On exam you note No murmur, but right ventricular dilation. Whats your DX?
|
Right Ventricular Infarction
|
|
|
Pt presents 5 days post acute MI with no murmur, clear lung sounds, but pericaridal effusion, intrapericaridal blood clots, and tamponade. Whats your DX?
|
Free wall rupture
|
|
|
Pt presents 1, OR 3-5 days post acute MI with shock, dyspnea, and a LOUD holostystolic murmur. Whats your DX?
|
VSD
|
|
|
Pt. presents 2-7 days post acute MI with a soft or barely audible holosystolic murmur denoting mitral regurgitation, Whats your DX?
|
papillary muscle rupture
|
|
|
Whats the most common initial presentation of CHD in women?
|
chest pain
|
|
|
Whats the leading cause of mortality in women in US?
|
CHD
|
|
|
T/F: CHD affects women of average 10 years later than men, and MI's occur as much as 20 years later
|
TRUE
|
|
|
T/F: Women have better outcomes following MI and CABG than men
|
FALSE. women have WORSE outcomes following MI and CABG than men
|
|
|
What are the 3 phases of cardiac arrest?
|
Electrical - to 4 min post collapse. Defibrillate
Circulatory - 4-10 min post collapse. CPR before defibrillate Metabolic - 10 min after collapse. They gon' die. |
|
|
A pt falls over in Wal-Mart, and you are not alerted about the situation until 8 minutes after they've fallen. THey are having a cardiac arrest - whats the most appropriate step here?
|
GIVE GOOD CPR before Defibrillation
|
|
|
T/F: Early defibrillation (within 2 min) can restore a rhythm 80% of the time
|
TRUE
(if its after 4 min, go directly to CPR) |
|
|
After 10 minutes of a cardiac arrest, the success rate of CPR/Defibrillation falls to what percent?
|
5%
|
|
|
What subsets of pts get defibrillators implanted?
|
Cause of MI NOT reversible
Structural Heart disease (stable OR unstable) Syncope of unknown cause and VF or VT Left. Vent. Ejection fraction less than 35% 40 days post MI in NYHA class II or III Left. Vent. dysfunction dur t oMI 40 days post MI with less than 30% NMHT class I Non-sustained VF due to prior MI with less tan 40% inducible VF or sustained VT |
|
|
Whats a Life Vest?
|
Defibrillator pts can wear until they qualify (over 90 days) for getting a defibrillator implanted
|
|
|
What are the currents in the AP of a myocyte?
|
0 = Na+ out
1 = K+ in 2 = Ca2+ and Na+ IN, K+ out 3 = K+ out 4 = resting potential |
|
|
What are the currents in the SA and AV node AP?
|
4 = resting potential
0 = Ca2+ in 3 = K+ out (repolarization) |
|
|
Triggered Arrythmias are seen in what states?
|
Intracellular Ca2+ overload (ex = digitalis intox or depletion of ryanidine receptor stabilizing protein calstabin 2)
|
|
|
VF and Torsades are examples of what type of Arrhythmia?
|
Triggered
|
|
|
What causes Triggered arrythmias?
|
Early after Depolarizations because of Inc. Ca2+ Intracellularly
|
|
|
What causes Reentry arrhythmias?
|
Slow Conduction or Uni-directional block
|
|
|
What are some examples of Reentry?
|
AV node reentry, AV reentry, Atrial Tachy
|
|
|
What causes Automatic arrhythmias?
|
Spontaneous diastolic depolarization
|
|
|
Whats an example of Automatic spontaneous diastolic depolarization?
|
FOCAL Atrial Tachy (vs Atrial Tachy seen with reentry arrhythmias)
|
|
|
How do you treat Triggered (=caused by early after depolarizations) arrhythmias?
|
Inc HR
|
|
|
What is the leading cause of sinus node dysfunction?
|
idiopathic degeneration of sinus node
|
|
|
What are some diseases that can lead to sinus node dysfunction?
|
Hypertension
Ischemia Infiltrative/Inflammatory processes (ex. = amyloidosis) Normal Aging process |
|
|
What are some causes of AV node Block?
|
Atherosclerotic Heart Disease with acute or healed MI
Calcific valvular heart disease infiltrative, inflammatory, and collagen vascular diseases Aortic valve replavement/Sx Drugs that depress function |
|
|
All of the following will cause Sinus node dysfunction EXCEPT: B-Blockers, CCBs, Digoxin
|
Digoxin
|
|
|
Stuff that causes AV Node Block?
|
Atherosclerosis
Calcified valves inflamm.infiltrative vascular diseases Aortic valve replaced Congenital septal defect repair Drugs that depress SA node ALSO depress AV node |
|
|
What are some things that might lead you to believe the pt has A-fib?
|
Heart Disease
Hypertension CAD AF episodes (at night, after stopping exercise, after meals) Pericarditis Pulm. embolism Thyrotoxicosis |
|
|
What do you look for on EKG that helps you Dx mechanism of the tachycardia?
|
P waves inside S waves
P wave neg. = pseudo S wave |
|
|
Whats the goal of AV node ablation therapy?
|
To ablate (burn) the SLOW pathway of the AV node
|
|
|
What are the three dif. types of SVT (=Supraventricular Tachy)?
|
AV Node Reentry
Atrioventricular reentry (Orthodromic) Atrial Tachy |
|
|
Whats the most common cardiac abnormality?
|
A-Fib
|
|
|
Define "Lone" AF
|
Patients with AF over 60 withOUT any underlying cause for the abnormality
|
|
|
Whats the cause of A-Fib in most patients?
|
A rapidly firing focus (driver)
Often its in the: atrial sleeves of pulm. vein, (ALSO: Sup, Vena Cava, Crista terminalis, coronary sinus, or Left. Post. Free Wall) |
|
|
What is the CHAD's score used to determine?
|
"CHAD's Lung is at risk of Thromboembolism in A-fib"
Thromboembolism risk if a pt. has A-fib. |
|
|
What is the CHAD's score point system?
How do you use it to assess risk of thromboembolism in A-fib? |
1 POINT:
Congestive HF Hypertension Age over 75 Diabetes 2 POINTS Stroke If CHAD's score 1 or less, give aspirin b/c thromboembolism risk LOW If CHAD's score 2 or more, give Warfarin/Dabigatran (Pradaxa) because risk of thromboembolism HIGH |
|
|
An 82 y/o Pt comes in with a history of congestive HF with A-fib. What drug are you going to give them, if anything at all?
|
their CHAD's score is 2 (age over 75, CHF)
so give Warfarin/ Dabigatran (Pradaxa) |
|
|
A 47 y/o pt. comes in with a history of hypertension and A-fib. What drug are you going to give them based on CHAD's score?
|
Aspirin
b/c their CHAD's score is only 1 (hypertension) |
|
|
Whats a non-pharmacologic Tx option for A-fib?
|
A-Fib Ablation
|
|
|
How do you treat Ventricular arrhythmias?
|
ACE inhibs, ARBs, Aspirin, Statins, B-Blockers
|
