Cardio Flashcards
Prevalence of PAD
4% of people 40 years and older
15-20% of those 65+
Greater in men than women
Greater in black patients
Prognosis for PAD
risk of death from cardiovascular causes increases 2.5-6x and their annual mortality rate is 4.3-4.9%
50% 10-year mortality
What percent of people with PAD are asymptomatic
50%
15% have classic claudication
33% have atypical leg pain (functionally limited)
1-2% present with critical limb ischemia
Clinical manifestations of PAD
intermittent claudication (discomfort, ache, cramping in leg with exercise–resolves with rest), functional impairment (slow walking speed, gait disorder), rest pain (pain or paresthesias in foot or toes, worsened by leg elevation and improved by dependence), ischemic ulceration and gangrene
Associated arterial occlusion sites with the related claudication areas for patients with PAD
Aortic/iliac occlusion–gluteal and thigh claudication
Femoral occlusion–calf claudication
Popliteal/tibial occlusion–calf claudication or foot pain
Distinct Syndromes that PAD patients present with
Critical Limb Ischemia: ischemic rest pain, non-healing wounds, or gangrene and symptoms for more than 2 weeks
Acute Limb Ischemia: 5Ps defined by the clinical symptoms and signs for less than two weeks (pain, pulselessness, pallor, parasthesias, paralysis)
Differential Diagnoses for exertional leg pain
Lumbosacral radiculopathy: may see reduced DTR but normal pedal pulses
Describe pseudoclaudication vs claudication
Pseudoclaudication: cramping, tightness, aching, and fatigue with tingling, burning and numbess, location of buttock, hip, thigh, calf, or foot, may or may not be exercise-induced, pain occurs with standing, they sit/lean forward/change position to feel relief, and relief from symptoms occurs in less than 30 minutes
Claudication: cramping, tightness, aching, fatigue in the buttock, hip, thigh, calf, or food, pain is exercise-induced and the distance one must walk for symptoms to begin is consistent, pain does not occur with standing, patients stand or stop walking for symptoms relief, and symptoms improve within 5 minutes
Physical exam for PAD
Do complete CV exam with palpation of all pulses and auscultation of accessible arteries for bruits
Pulse abnormalities and bruits increase the likelihood of PAD
Decreased or absent pulse provides insight into the location of arterial stenoses
Physical findings in PAD physical exam
Arterial ulcers: pale base with irregular borders, usually involve tips of toes or heel of foot, develop at pressure sites
Diagnostic tests for PAD
Ankle- brachial index, PVR, segmental pressures, treadmill test, duplex US, CTA, MRA, angiography
Ankle-brachial index
Ankle systolic pressure/brachial systolic pressure
Normal: 1.00-1.40
Borderline: 0.91-0.99
PAD: less than or equal to 0.9
Pain/ulceration: less than or equal to 0.4
Non-compressible: more than or equal to 1.40
Limits to ABI testing
Calcified vessels can give falsely elevated pressure
Don’t know where stenotic arteries are
Solution: segmental pressures, waveform analysis
Goals for PAD treatment
Reduction in cardiovascular morbidity and mortality (discontinue tobacco use, SUPERVISED walking program, control BP to goal, high-dose statin therapy, antiplatelet therapy)
improve quality of life
maintain limb viability (good foot care, revascularization, cilostazol)
Factors of exercise that gives the best results for PAD patients
Duration of more than 30 minutes per session
at least 3 sessions per week for more than 6 months
walking used as the mode of exercise
Reach maximal claudication pain endpoint each session
When is revascularization considered?
If the patient has lifestyle-limiting claudication with an inadequate response to GDMT (guideline directed medical therapy)
Percutaneous transluminal angioplasty and stents
Peripheral catheter-based interventions are indicated for
- lifestyle limiting claudication despite trial of exercise rehab or pharm therapy
- symptomatic patients and clinical evidence of inflow disease as manifested by buttock or thigh claudication and diminished femoral pulses
- critical limb ischemia whose anatomy is amenable to catheter based therapy
What is the most frequent operation for patients with aortoiliac disease
Aorta-bifemoral bypass
What is the operative mortality rate for extra-anatomic bypass procedures
2-5%
*reflects in part the serious comorbid conditions and advanced atherosclerosis of many of the patients who undergo these procedures
Compare open and endovascular approaches for aortoiliac occlusive disease
Open surgical: excellent long-term patency rate, 85-90% for 5 years, requires general anesthesia, 1-3% mortality rate
Endovascular: high procedural success rates (90%), excellent long-term patency (more than 80-90% at 5 years), less morbidity/mortality
Endovascular procedures are done first in Type A and Type B lesions
Surgery may be considered first in Type D lesions
When do you treat a patient that presents with critical leg ischemia
ASAP ASAP ASAP
localize the lesion and then do revascularization as soon as possible to prevent loss of the limb
What is Dressler Syndrome
Pericarditis that occurs after an MI
What can occur 5-7 days after an MI
Cardiac tamponade (most likely time for the heart to rupture)
cor pulmonale
lung problems causing right heart failure
what are heart failure cells
alveolar macrophages filled with hemosideran
What body systems does Chagas disease affect?
esophagus, colon, heart
Describe Pericardial effusion types
Serous (transudate): low protein and no cells
Purulent (exudate): infectious, high protein, many WBCs
Malignant: metastatic disease
What are the causes of hemopericardium
Ruptured myocardium (from MI or trauma)
Aortic Dissection (hypertension or Marfan)
What is a severe hemopericardium and what can be the consequence?
more than 500 mL of blood
can cause tamponade, leading to sudden death
Causes of pericarditis
infectious agents (viruses, pyogenic bacteria, tuberculosis, fungi, parasites), immunological mediated (Rh fever, SLE, scleroderma, postcardiotomy, Dressler syndrome, drug hypersensitivity reaction), miscellaneous (uremia, trauma, radiation, etc)
** viral, TB, fibrinous, and SLE/scleroderma
Acute Serous Pericarditis
causes: infectious, usually autoimmune diseases, malignancy
Morphology: volume 50-200mL, scant inflammatory cells
3 causes of fibrinous pericarditis
post MI (dressler), uremia, rheumatic fever
causes of hemorrhagic pericarditis
malignancy, bacterial infections, following cardiac surgery
Chronic pericarditis
disabling because of adhesive scar formation
Adhesive Mediastino pericarditis
type of chronic pericarditis
follows suppurative inflammation or TB
sac obliterated and adhered to adjacent structures
increased strain on heart–>hypertrophy and/or dilation
Constrictive pericarditis
type of chronic pericarditis
results from suppurative or hemorrhagic pericarditis (staph or TB)
pericardial space obliterated by scar and/or calcification*
severe cardiac dysfunction (tamponade)
heart encased in dense fibrocalcific scar that limits diastolic expansion
HEART SOUNDS ARE DISTANT AND MUFFLED
ONLY TYPE OF PERICARDITIS ASSOCIATED WITH CALCIFICATION
what are telangiectasis
dilated capillaries that create small focal red lesions usually in skin and mucous membranes of body
Spider telangiectasis: associated with hyperestrogenism (pregnancy, live cirrhosis)
Hemangiomas
benign neoplasm of capillary or cavernous (can be in brain, very problematic if this ruptures)
usually in skin, can occur in liver, spleen, and kidney
usually occur early in life and fade
Glomus tumors
Painful, modified smooth muscle cell tumors on distal digits (ex/ under nails)
arises from glomus body
Painful but benign
Hemangiosarcoma
malignant atypical endothelial cells
associated with known carcinogens (polyvinyl chloride)
Kaposi Sarcoma
Types: classic or European(chronic)–not HIV associated; Immunosuppression or transplant-associated–AIDS-associated
Associated with HHV8–causes proliferation of blood vessels and angiogenesis
can occur in heart, lung, brain, skin, stomach, etc..
Carney syndrome
AD myxomas of skin and hyperpigmentation cardiac myxomas endocrinopathies mutation of some tumor suppressor gene
Myxoma
benign tumor of the atria (usually left)–blocks blood flow out of mitral (or tricuspid) valve (ball valve effect)
Dx: Echocardiography
rhabdomyoma
associated with tuberous sclerosis (hamartomas in CNS, skin, heart, and kidney)
benign
Angiosarcoma
Malignant tumor
where do metastatic tumors of the heart usually originate?
breast or lung
Cardiac transplantation complications
Rejections: cellular (t cells), or humoral (antibodies)
Infections: CMV, toxoplasmosis
Lymphoproliferative disease post-transplant: EBV mediated
Clinical presentation of acute pericarditis
flu-like sx or GI sx (viral prodome is common)
sharp, pleuritic chest pain precipitated by lying flat dt inflammation being placed on posteriorly located nerves, relieved by leaning forward, pain radiates to shoulder
EKG changes (diffuse ST elevations)
Friction rub best heard over left sternal border
pericardial effusion
EKG changes with pericarditis?
diffuse ST elevations and PR segment changes
What will a chest xray look like in most cases of acute pericarditis?
Normal
Diagnosis of acute pericarditis
at least two of the following:
- Characteristic chest discomfort (persistent, pleuritic, and positional)
- Suggestive ECG changes (diffuse ST elevation)
- Pericardial Friction Rub
- New or worsening pericardial effusion
Treatment of Acute Pericarditis
NSAIDs/Salicylates
Colchicine (3 months)
AVOID: glucocorticoids and pericardiectomy
Most cases of pericarditis can be treated outpatient. When is hospitalization (inpatient) required?
High fever (>38) Subacute onset large pericardial effusion trauma evidence of myocarditis immunosupressed pt concominant use of anticoags evidence of cardiac tamponade
Goals of pericarditis treatment
symptom relief, decrease inflammation
Pericardial Effusion
usually serous effusion
if Hemorrhagic: malignant, surgery/procedure complication, post-pericardiotomy syndrome, complications of MI, idiopathic, aortic dissection, infection (TB)
Biggest risk factor for pericardial tamponade
rate of fluid accumulation
*fluid causes compression of all cardiac chambers due to increased pericardial pressure
pericardium has a degree of elasticity but once that limit is reached–>potential for tamponade
Symptoms and PE of cardiac tamponade
symptoms: dyspnea, chest discomfort/fullness, peripheral edema, fatigability
PE: sinus tach, JVD, pulsus paradoxus
what is electrical alternans
beat-to-beat alteration in QRS appearance (best seen in leads V2 to V4)
What is electical alternans suggestive of
Strongly suggestive of pericardial effusion (usually with cardiac tamonade)
the alternating ECG pattern in electrical alternans is related to what?
the back-and-forth swinging motion of the heart in the pericardial fluid
Clinical presentation of tamponade
hypotension with pulsus paradoxus (more than 10 mmHg fall with inspiration)
elevated venous pressure with blunted or absent y descent
distant heart sounds
clear lung fields
Causes of pulsus paradoxus
respiratory: severe bronchial asthma, tension pneumothorax, COPD
Cardiac: cardiac tamponade, constrictive pericarditis, pericardial effusion, restrictive cardiomyopathy
Others: anaphylactic shock, obesity
Treatment for cardiac tamponade
URGENT PERICARDIOCENTESIS (only definitive therapy for cardiac tamponade) usually done percutaneously IV fluids may improve cardiac output (esp in hypotensive pt)
DO NOT GIVE DIURETICS
Constritive pericarditis
thickened, rigid pericardium
Which types of pericarditis are most likely to advance into constrictive pericarditis
TB pericarditis and purulent pericarditis
Clinical presentation of constrictive pericarditis
symptoms related to fluid overload (peripheral edema to anasarca)
symptoms related to diminished cardiac output in response to exertion (fatigability and dyspnea on extertion)
PE findings with constrictive pericarditis
JVP, pulsus paradoxus, Kussmaul’s sign (lack of inspiratory decline in JVP), pericardial knock (accentuated heart sound occurring slightly earlier than S3)
Echo/Doppler results with constrictive pericarditis
accentuated respirophasic effects on transvalvular velocities; septal bounce (ventricular interdependence), pericardial thickening
What is the anatomic imaging modality of choice in constrictive pericarditis?
CT/MR
tx for constrictive pericarditis
diurectics
surgery: results are often limited
* pericardiectomy
* surgical risk factors: age, NYHA class, organ failure, XRT, other cardiac disease
Effusive-Constrictive disease
clinical and hemodynamic manifestations of tamponade on presentation
After pericardiocentesis, residual clinical and hemodynamic manifestations of constriction
(High RAP despite reduction of pericardial pressure to as low as 0)
Cardiac arrest
the abrupt cessation of heart functiong
Causes of sudden cardiac death?
over 35: Coronary artery disease
Under 35: congenital and acquired abnormalities
Hypertrophic obstructive cardiomyopathy
Autosomal Dominant
ECG: QRS waves are very tall
Echo: hypertrophy is in the septum (not symmetrical like in hypertension)
Beta blockers help treat the SYMPTOMS (doesnt prevent SCD)
What is the most common coronary artery anomalous origin in HOCM
the origin of the right coronary artery from the left sinus of Valsalva
Marfan’s Syndrome signs
Wrist sign and thumb sign
Myopic with lens subluxation
Symmetric pectus excavatus
What is a concerning health risk in Marfan’s Syndrome?
Risk of aortic tear or aneurysm
Dysarrythmias that can cause SCD
Long QT syndrome (more than 440 mms)
Brugada’s Syndrome
Wolff-Parkinson White
Commotio Cortis
Vfib and SCD that is triggered by a blunt, non-penetrating, innocent-appearing blow to the chest during ventricular repolarization without any damage to the chest wall or heart
*most common in male baseball players
Pacemaker vein placement
placed in subclavian vein usually (specialists can do axillary or cephalic)
How does a pacemaker work
battery generates electricity and insulated wire has an extendable/retractable corkscrew tip (actively penetrates into myocardium) or a tyne tip (causes reaction at endocardial level)
pacing pulses are delivered to myocardium via the lead
What kind of battery does a pacemaker have?
lithium iodide battery that lasts about 15 years
What arrhythmia requires just a ventricular lead?
Afib
Function of pacemakers
Pace and sense the myocardium
Inhibits when pacing not needed
Algorithm to increase heart rate with activity
How is a lead inserted into the left ventricle
via the coronary sinus
What is a standard lead
goes to atria and right ventricle
corkscrew tip that extends 1.8 mm
How does a HIS bundle lead work?
does not directly stimulate the myocardium
gets the electrical activity to travel down the HIS bundle
How can pacemakers increase heart rate with activity?
Most use an accelerometer to identify postural changes and body movements related to physical activity (only enabled as needed)
Some use Minute Ventilation sensory to drive the pacing rate–measures resistance between an electrode on cardiac pacing lead and the metal housing of the device (changes with respiratory rate and chest excursion)–more natural heart rate response to exercise
DDD tracking mode
pacing and sensing in atrium and ventricle
inhibited by intrinsic P wave and QRS
In DDD mode, the pacemaker can truly adapt to what the heart is doing and mimics normal conduction as closely as possible
what is VOO mode
Pacing in ventricle, sensing is off, response to sensing is off
*paces at a programmed rate regardless of intrinsic activity
What is VVI mode
Pacing in ventricle, sensing in ventricle, inhibit
Pacemaker is capable of sensing the heart’s intrinsic activity and inhibiting pacing when it is unnecessary
When would you use VOO mode?
in surgery that uses cauterization (mimics heart’s electrical activity) or meds that might affect blood pressure
Defibrillation
pulseless VT or VF can be converted to sinus rhythm but delivering sudden electrical massive depolariation–>causes all myocardium to depolarize, then after phase 3 the pacemaker signal gets through the AV node depolarizing the ventricles and sinus rhythm is restored
what is an ICD
implantable cardiovertor defibrillator
electricity delivered to endocardium
Which device does not have pacing programming?
Subcutaneous ICD
How does subq ICD minimize infection risk?
Avoids transvenous access
How effective are ICDs
97-98% effective
One of the most successful treatments in medicine today
Why is drug therapy still indicated after ICD implantation
to suppress ventricular arrhythmias, minimize the frequency of ICD shocks, improve patients’ tolerance, and decrease energy use
*multiple shocks associated with shorter life
Chlorthalidone
thiazide diuretic (preferred for black patients with isolated hypertension) Side Effects: hyperglycemia, hypercalcemia, hypokalemia
What causes ischemic heart disease?
due to reduced blood flow due to obstructive atherosclerosis of the coronary arteries (CAD)
Clinical manifestations of ischemic heart disease
- myocardial infarction
- angina pectoris (ischemia is not severe enough to cause infarction)
- chronic ischemic heart disease with heart failure
- sudden cardiac death
what are some causes of ischemic heart disease
reduced coronary flow
increased myocardial demand (hypertrophy)
reduced availability of O2 in the blood
What inflammatory marker predicts the risk of coronary heart disease
C reactive protein
Pathogenesis of ischemic heart disease
Acute plaque change
Inflammation
Thrombosis
vasoconstriction
Describe unstable angina
plaque disruption causes thrombosis and vasoconstriction, leads to a severe but transient reduction in blood flow
Describe sudden cardiac death
regional myocardial ischemia that leads to a fatal ventricular arrhythmia
Stable angina
caused by chronic coronary stenosis of an atheroscleroting coronary artery
pain on exertion
Prinzmetal angina
caused by coronary artery spasm
effect is pain at REST
Where is the most common place for ischemic heart disease?
anterior septum resulting from occlusion of the LAD (45% of all cases)
Transmural infarction
necrosis of full thickness of ventricular wall, perfused by a single coronary artery–>coronary atherosclerosis–>plaque disruption–>thrombus
Subendocardial infarction
necrosis of 1/3 to 1/2 of the ventricular wall–>perfused by more than one coronary artery–>shock, hypertension or transient thrombus
What changes are present in the heart after MI? 0-4 hr 4-12 hr 12-24 hr 1-3 days 3-7 days 7-10 days 10-14 days 2-8 weeks more than 2 months
0-4: no changes
4-12: dark mottling, early coag necrosis, edema, hemorrhage
12-24 hr: dark mottling, ongoing coag necrosis, myocyte hypereosinophilia, early neutrophilic infiltrate
1-3 days: mottling with yellow-tan infarct center, coag necrosis, interstitial infiltrate of neutrophils
3-7 days: hyperemic border, central yellow-tan softening, macrophages at infarct border
7-10 days: yellow-tan with depressed red-tan margins, granulation tissue at margins
10-14 days: red-gray depressed infarct borders, well-established granulation tissue with new blood vessels and collagen deposition
2-8 weeks: gray-white scar with increased collagen deposition and decreased cellularity
more than 2 months:dense collagenous scar
What is the earliest histological change seen in acute MI
contraction band necrosis
myocardial fibers lose cross striations and the nuclei are not clearly visible
many irregular darker pink wavy contraction bands extending across the fibers
What molecules can be used as biomarkers for acute MI?
troponin I (best option, elevates 4-6 hours after MI, lasts 7-10 days)
CK-MB (peaks at 12 hours, back to baseline by 72 hours post-MI)
myoglobin (increased at 2-4 hours, peaks 9-12 hours, back to baseline by 24-36 hours)
Which markers is cardiac specific
troponin-i (99.4% specific)
will not show elevation in trauma or other disease states
What troponin range indicates MI
anything more than 0.5
When is a rupture of the myocardium most likely to occur?
3-5 days post-MI (this is when the myocardium is the softest)
What is chronic ischemic heart disease?
(aka ischemic cardiomyopathy) a condition of elderly who develop progressive heart failure as a result of ischemic myocardial
predisposing factors: post-infarction, severe atherosclerosis without infarction but myocardial dysfunction is present
What can cause sudden cardiac death
acute MI, congenital anomalies, aortic stenosis, mitral prolapse, myocarditis, myopathies, hypertensive heart, cocaine
What are common infectious causes of myocarditis?
coxsackie, lyme, chagas
Common immune-mediated reactions that cause myocarditis
poststreptococcal (rheumatic fever), transplant rejection
Clinical presentation of myocarditis
asymptomatic
fever, malaise, pericardial pain
sudden onset of acute heart failure
Gross findings in myocarditis
dilated ventricles, flabby heart, minute hemorrhages, mural thrombi may be present
What chemotherapeutic agent can cause myocardial disease
doxorubicin (causes lipid peroxidation in myocytes)–>dilated cardiomyopathy
What other drugs can cause myocardial disease
anthracyclin, lithium, chloroquine
Describe the morphology of myocarditis with drug toxicity
myofibers swelling, cytoplasmic vacuolization, fatty change
Name some causes of myocarditis
drug toxicity, amyloidosis (transthyretin), hemochromatosis, hyper/hypothyroidism
Congestive Heart Failure
mechanical failure of the heart to maintain systemic perfusion commensurate with the requirements of metabolizing tissues
what is forward heart failure?
decreased cardiac output
what is backward heart failure
damming back of blood in the venous system
Left-sided heart failure causes
ischemic heart diseases, hypertension, aortic/mitral valve diseases, myocardial diseases
Clinical presentation of left sided heart failure
dyspnea, orthopnea, paroxysmal nocturnal dyspnea
What are heart failure cells and when are they found?
alveolar nuclei with hemosideran inside of them
found in LEFT sided heart failure
What happens to the kidneys in left sided heart failure? the brain?
decreased renal perfusion (activation of RAAS–>retention of salt and water–>increased blood volume)
Brain: hypoxic encephalopathy
what can systolic heart failure cause?
ischemic diseases, valvular diseases
what can diastolic heart failure cause?
defective filling causes amyloidosis, fibrosis, severe hypertrophy
What is the most common cause of right-sided heart failure
left sided heart failure
Signs of right sided heart failure
liver congestion (may cause cardiac cirrhosis)(elevated LDH5, necrosis of hepatocytes around the central vein) congestive splenomegaly pleural effusion ascites peripheral edema brain congestion and edema JVD
What does elevated BNP indicate
values more than 100 indicate congestive heart failure
Where does ANP come from? BNP?
ANP comes from the atria
BNP comes from the ventricles
both increase in response to stretching of atria/ventricles
How are cardiomyopathies diagnosed
cardiac biopsy
Causes of dilated cardiomyopathy
alcohol (may be direct toxicity or thiamine deficiency), peripartum, genetic (dystrophin gene mutation, other sarcomere mutations), myocarditis (coxsackie virus), adriamycin toxicity
What mutations are associated with genetic hypertrophic cardiomyopathy
Cardiac troponin T
Myosin binding protein C
beta myosin heavy chain
what is disproportionately thickened in HCM
the septum
Is dilated cardiomyopathy systolic or diastolic dysfunction?
systolic
Is hypertrophic cardiomyopathy systolic or diastolic dysfunction?
diastolic
Describe the microscopic appearance of HCM
hypertrophy, disarray, fibrosis
What kind of murmur is associated with HCM
harsh systolic ejection murmur
Causes of restrictive/infiltrative CMP?
amyloidosis, hemochromatosis, hyper/hypothyroidism
what protein is associated with cardiac amyloidosis
transerythin
What is cor pulmonale
right ventricular enlargement resulting from structural or functional lung disorders (ex/ PE,, COPD)
explain the pathogenesis of hypertrophy in long-standing hypertension
increase BP–>accelerated aortic stenosis–>decreased large vessel compliance–>thickening of small arteries and arterioles–>increased peripheral resistance–>hypertrophy–>increased O2 demand and decreased heart compliance
What is the goal during adaption to insult to the heart?
maintain perfusion
Wall stress
Frank-Starling (initially helpful)
Hypertrophy (eventually maladaptive)
Molecular, cellular, structural changes=ventricular remodeling (maladaptive)
Activation of neuro-hormonal systems
What is the problem hypertrophy?
increases metabolic demands of the heart, but no increase in capillary volume–>supply and demand mismatch that increases the risk of ischemia
What happens in ventricular remodeling
shift of gene expression to upregulation of early response and fetal genes (in absence of DNA synthesis)
what does a non compressible vein indicate
DVT
Afib EKG findings
absent P waves and irregularly irregular RR interval
what drug is most effective for lowering triglycerides?
Fibrates
How do fibrates work?
activate PPAR-alpha and increase lipoprotein lipase activity–>lowers LDL and SIGNIFICANTLY lowers triglycerides, increases HDL
Side effect of fibrates
increased risk of cholesterol gallstones bc they inhibit CYP450; also hepatotoxicity and myopathy
What murmur is heard in mitral stenosis
diastolic murmur best heard at apex
opening snap after S2
**shorter interval between S2 and opening snap indicates more severe disease
What valve defect is often seen in Marfan syndrome?
Mitral valve prolapse
Describe mitral valve prolapse murmur
late systolic crescendo murmur with a midsystolic click
What is Beck Triad
Muffled heart sounds, distended neck veins, hypotension
describe electrical alternans
low voltage QRS complex with fluctuating R wave amplitude
what happens to the stroke volume is diastolic heart failure
narrow stroke volume
What happens to aortic stenosis murmur with maneuvers that increase the afterload (Ex/ handgrip)
decrease intensity of the murmur
test of choice for diagnosing DVT
compression ultrasonography
which holosystolic murmur increases with inspiration
tricuspid regurgitation
what is amplodipine
dihydropyridine calcium channel blocker
causes vasodilation and decreases BP
Common side effects: peripheral edema, headaches, dizziness, flushing, reflex tachycardia
Antidote for norepinephrine extravasation
phentolamine
Most common congenital cardiac anomaly in down syndrome
Atrioventricular septal defects (aka endocardial cushion defects)
Prinzmetal angina
symptoms occur at rest
triggers include stress, smoking, alcohol, drugs, triptan use
anterior ST elevations
What is the effect of PDGF from platelets and macrophages in atherosclerotic plaques?
intimal migration of smooth muscle cells, which mediates the transformation of fibroblasts into myofibroblasts (necessary for fibrous cap formation)
Infants born to diabetic mothers are at increased risk for which congenital heart defect?
transposition of the great vessels
What medication inhibits cholesterol absorption in the intestines and what is a side effect of this medication
Ezetimibe, elevated liver function tests (hepatotoxicity)
Pressure and volume overload occurs when frank-starling mechanisms fail…this leads to what?
concentric hypertrophy in response to pressure overload
eccentric hypertrophy in response to volume overload
overall, increase in size and mass of the heart
What happens to myocardial metabolism in heart failure?
begins to use glucose (like is a fetal heart) with downregulation of FA metabolism machinery
What causes interstitial fibrosis in heart failure
oxidative stress of cardiac fibroblasts (decrease collagen synthesis and activate fibroblast degradation) and NOX2 (activates fibroblast degradation)
Which adrenergic receptor does NE selectively bind?
beta 1 (more than beta 2 or alpha 1)
What happens in response to decreased cardiac output?
increased RAAS
Increased ADH
Increased SNS activity (increase contractility and HR)
Harmful effects of adrenergic receptors in human heart
cardiac myocyte growth, fibroblast hyperplasia, myocyte damage/myopathy, fetal gene induction, myocyte apoptosis, proarrhythmia, vasoconstriction
Compare the beta receptors in normal hearts and hearts in heart failure
Normal: 70-80% are beta1 agonist receptors
Heart failure: downregulation of beta1 so beta1:beta2 ratio is 60% to 40%
What drug can be used in heart failure
beta blockers
block effects of NE beta1 stimulation to re-establish normal autonomic nervous system homeostasis, also upregulates beta1 receptors slightly (improve exercise tolerance)
What is the effect of natriuretic peptides
vasodilation (also natriuresis and diuresis, antihypertrophy, antifibrosis, inhibition of SNS)
What secretes CNP
vascular endothelial cells, in response to inflammatory mediators
What is sacubitril (entresto)
inhibits neprilysin (normally cleaves ANP, BNP, CNP)
Factors associated with lower than expected BNP or NT-proBNP
obesity, flash pulmonary edema, heart failure causes upstream from left ventricle, cardiac tamponade, pericardial constriction
Factors associated with elevated BNP
left ventricular dysfunction, previous heart failure, arrhythmia, acute coronary syndromes, cardiotoxic drugs, significant pulmonary disease, advanced age, renal dysfunction, anemia, critical illness, high output states (sepsis, cirrhosis, hyperthyroidism)
what type of dysfunction is seen in HFrEF
Systolic dysfunction
what type of dysfunction is seen in HFpEF
diastolic dysfunction (abnormal relaxation)
List some causes of systolic dysfunction
coronary artery disease (MI), chronic volume overload (mitral or aortic regurg), dilated cardiomyopathies, advanced aortic stenosis, uncontrolled severe hypertension
List some causes of diastolic dysfunction
left ventricular hypertrophy, restrictive cardiomyopathy, myocardial fibrosis, transient MI, pericardial constriction or tamponade
describe the PV loop in HFpEF
LV pressure will be higher for any given volume
ESV will be lower due to stiffness
What worses diastolic dysfunction
exercise
Use exercise echo to evaluate diastolic dysfunction
Causes of acute HF
nonadherence with medication regimen, recent addition of negative inotropic drugs, initiation of drugs that increase salt retention, excessive alcohol or illicit drug use, endocrine abnormalities, concurrent infections
When do you administer ACEI/ARB or HF beta blockers to patients who were not previously on these drugs?
wait until after the IV heart failure meds (diuretics and vasopressors) are given
Describe the dose of IV loop diuretics given for acute HF. What if the patient does not respond?
usually about 2X the home dose, either bolus or infusion
no response=increase loop diuretic dose or add metolazone
What are some signs of low perfusion
cool extremities, low urine output, altered mental status, inadequate response to IV diuretic, prerenal azotemia
What are some signs of congestion
increase JVD, peripheral edema, S3, DOE/SOA, orthopnea/PND, rales, recent weight gain
treatments for patients with HFrEF that are
wet and warm
dry and cold
wet and cold
WW: watch for decreased perfusion, BP, mental status changes, decreased urine/kidney function with diuretics
DC: give inotropes to improve perfusion
WC: diuretics and inotropes
what increases risk for in-hospital mortality in acute HF presentation?
Hypotension (SBP less 115 mmHg)
BUN>43
Creatinine >2.75 mg/dL
What treatment is given for HFrEF patient with decreased perfusion
inotropes (beta 1 agonists)
What is milrinone
a PDE3 inhibitor that increases cAMP to cause vasodilation
can be used in acute decompensated HF
What is a common medication used in chronic HFrEF
digoxin (usually oral)
What drug is added for patient with HFrEF if beta blocker therapy is not sufficient
ivabradine (inhibits funny current in SA node)–>reduced persistently elevated HR and does not affect contractility
What are treatment options for ventricular arrhythmias in stage C HFrEF
muscle scar is arrhythmogenic for ventricular arrhythmias
tx=amidarone or sotalol
*mexilitine if they are resistant to the others
What happens to the SVR in cardiogenic shock
SVR is increased to compensate for loss of CO
Describe changes in preload, afterload, and cardiac output in different types of shock
Distributive: preload decreased, afterload decreased, CO increased
Hypovolemic: preload decreased, afterload increased, CO decreased
Cardiogenic: preload increased, afterload increased, CO decreased
Obstructive pulmonary: preload increased in RV and decreased in LV, afterload increased, CO decreased
Obstructive mechanical: preload decreased, afterload increased, CO decreased
Treatment for cardiogenic shock?
IV positive inotropes (dobutamine)
what is the number one cause of SCD in athletes
HYPERTROPHIC CARDIOMYOPATHY
Mutations coding for what can be the cause of genetic heart disease?
sarcomeres (more than 1400 mutations have been identified)
Common sequelae of HCM
LV outflow tract obstruction, diastolic dysfunction, myocardial ischemia, mitral regurg, systolic dysfunction
what are the 3 broad symtom categories of HCM
heart failure, chest pain, arrhythmias
what percentage of px with HCM present with a murmur
53%
What is the most common symptom of HCM in px less than 1 year old
murmur
mortality is high for infants with HCM, what is the cause of death
heart failure (as opposed to arrhythmia)
What causes LV outflow tract obstruction
combo of septal hypertrophy and systolic anterior motion of mitral valve–>this causes a murmur
Describe the murmur in HCM
loudest at apex/LLSB, may radiate to axilla, murmur increases with valsalva and standing (decreased preload), murmur decreases with handgrip and squatting (increased afterload)
Name some causes of restrictive cardiomyopathy
hemochromatosis, sarcoidosis, amyloidosis
What kind of heart failure does restrictive cardiomyopathy cause?
diastolic heart failure (HFpEF)
Causes of dilated cardiomyopathy
selenium deficiency, viral myocarditis, alcoholic cardiomyopathy, doxorubicin therapy
Formula for ejection fraction
stroke volume/end diastolic volume
mutations in titin protein will cause what?
dilated cardiomyopathy
describe the pathophysiology of ACS
vulnerable vessel–>acute plaque rupture or erosion–>vascular spasm and in situ thrombosis–>luminal compromise
Signs and symptoms of NSTEMI
chest pain/other ischemic symptoms with abnormal EKG changes (ST depression or T-wave inversions) and elevated troponin levels
How is the unstable angina clinically differentiated from NSTEMI
troponin is negative in unstable angina
Why is ST depression seen in NSTEMI
subendocardial ischemia causes ST vector to be directed toward the inner layer of the affected ventricle and ventricular cavity so the overlying leads record this as ST depression bc the electrical current is traveling away from the leads
Why is ST elevation seen in STEMI
with transmural or epicardial injury, the ST vector is directed outward and toward the overlying leads, so these leads record it as ST elevation (can get reciprocal ST depression in contralateral leads)
How long does it take after an MI to have complete necrosis of the cardiac muscle?
24 hours (wavefront phenomenon)
What biomarker is the gold standard for an MI/ACS
troponin (released from cardiomyocytes when these cells die)
What often causes cardiac arrest in a STEMI
Ventricular fibrillation
Describe treatment for a STEMI
aspirin 325 mg X 1 STAT
Heparin 5000 U bolus
activate STEMI team to fix occluded artery within 90 minutes
Emergency percutaneous coronary intervention
Dual antiplatelet therapy (aspirin plus P2Y12 antagonist)
NSTEMI initial treatment
aspirin and heparin drip, statin and beta blocker, nitroglycerin to receive chest pain, cardiac cath within 2-48 hours, DAPT
Describe EKG changes in an untreated STEMI
Acute: ST elevation
Hours: ST elevation, decreased R wave, Q wave begins
Days 1-2: T wave inversion, Q wave deeper
Days later: ST normalizes, T wave is inverted
Weeks later: ST and T normal, Q wave persists
differentiation between ischemia and infarction
Ischemia: reduced coronary perfusion resulting in myocardium with inadequate oxygen delivery
Infarction: death of cardiomyocytes, usually due to acute coronary syndromes
What is the underlying substrate of ACS
large lipid plaques
list the 3 main platelet activation pathways and the drugs associated with them
COX/thromboxane: aspirin
P2Y12 receptor agonists (ADP agonist): clopidogrel, ticagrelor, prasugrel
GPIIb/IIIa inhibitors: tirofiban, eptifibatide, abciximab
How does heparin work
catalyst for anti-thrombin III–>inhibits thrombin=anticoagulation
When is an ACEI used in ACS patients?
EF less than 40%, Diabetes mellitus, HTN
When are aldosterone blockers used for patients post MI? when are they contraindicated?
if ejection fraction is less than 40%
significant renal disease or hyperkalemia
describe use of anticoag/antiplatelet therapy in ACS
anticoagulation with unfractionated heparin from ER presentation until cardiac cath
STOP anticoag therapy after PCI
DAPT are continued after PCI
Biomarker for acute pulmonary embolism
D-dimer (if positive, then CTA chest PE protocol and V/Q scan)
Treament for PE (esp is patient is not a candidate for t-PA)
surgical embolectomy!
Describe the pain is acute pericarditis
pleuritic chest pain: sharp, worse with deep inspiration
EKG changes seen in acute pericarditis
Diffuse ST elevations, PR segment depression in lead II, PR segment elevation in lead aVR
How is acute pericarditis treated?
NSAIDs or colchicine
common cause of acute pericarditis?
viral
Typical medication treatment for STEMI after PCI
aspirin 81 mg daily, P2Y12 antagonist (clopidogrel or ticagrelor), atorvastatin/rosuvastatin, metoprolol, lisinopril, smoking cessation and therapy, medical therapy for HTN and diabetes as needed
Risk factors for CAD
age, HTN, hyperlipidemia, cigarette smoking, diabetes
What is the major site of resting resistance in the coronary circulation
arterioles
What substance causes max vasodilation of the arterioles which leads to hyperemic blood flow
Adenosine
At what percentage of stenosis do patients experience a drop in coronary flow during exercise (angina symptoms)? at rest?
70% stenosis is when symptoms appear during exertion, 90% stenosis causes symptoms at rest
What is normal resting coronary blood flow?
225 ml/min
When does the coronary blood flow occur?
during diastole (d/t compression during systole)
what should be the effect of exercise on coronary blood flow normally?
about a 4 fold increase in coronary blood flow to match the demand for oxygen
Stable angina
chest pain or tightness + possible dyspnea on exertion and fatigure/exercise intolerance, relieved with rest
Describe primary prevention
prevention of a disease or disease event in a person with no known evidence of this disease
Describe secondary prevention
Prevention of a disease/disease event in a person who has been diagnosed with a disease and/or had a symptomatic event due to disease
What is coronary CTA. what is a requirement to be a candidate for coronary CTA
newer alternative to stress testing to assess patients with chest pain. MUST have creatinine less than 1.5 so they can safely receive IV contrast
Stable angina therapy has two main goals. What are they and what medicines are used to achieve them?
reduce risk of MI and death: aspirin 81 mg daily, high intensity statin therapy
Reduce symptom burden: beta-blockers, long acting nitrates, calcium channel blocker, ranolazine
What are the two methods of revascularization
PCI (stent) and CABG
What are the three options for bypass conduit in CABG
saphenous vein graft, radial artery, or LIMA
Simplistic breakdown of which patients receive which revascularization
Severe, symptomatic CAD with triple vessel CAD or left main disease are treated with CABG; severe, symptomatic CAD with all other CAD anatomy (single vessel, double vessel) are typically treated with PCI
What is the most common method for assessing severity of coronary artery stenosis
visual estimation on coronary angiogram (can have inter-observer variability, over/under estimation of true severity)
What is FFR/intracoronary physiology.
Formula?
a method to determine severity of coronary artery stenosis.
FFR=distal coronary pressure/proximal coronary pressure *measured during maximum hyperemia
what is the FFR cutpoint for significant ischemia
FFR less than or equal to 0.8
what is iFR (instantaneous wave free ratio)
similar to FFR but does not require hyperemia–it is a resting physiologic index
Cutpoint for iFR
less than or equal to 0.89
optimal medical therapy for CAD
antiplatelet therapy (aspirin)
high intensity statin
beta blocker
second anti-anginal med (ex/ nitrate, ranolazine, CCB)
Which medication indicated for CAD is associated with a reduction in the risk for mortality?
Atorvastatin (and aspirin)
What can cause dilated cardiomyopathy?
idiopathic, familial (sarcomere mutations), inflammatory causes (infectious or peripartum) toxic (alcohol, cocaine, chemo), thyrotoxicosis, hypothyroidism, chronic hypocalcemia, tachycardia (afib), myotonic dystrophy
common mutations that cause DCM?
desmin, dystrophin, myosin binding protein C, titin, beta-myosin heavy chain, troponin, lamin A/C (many of these proteins are also mutated in HCM)
pathophysiology of DCM
decreased contractility, decreased stroke volume–>increased ventricular filling pressures (pulmonary and systemic congestion results), LV dilation leads to mitral regurg, decreased foward cardiac output (manifests as fatigue and weakness)
what heart sound is heard with DCM
S3 (also a mitral regurg murmur due to left ventrical dilation)
What happens to the PMI in dilated cardiomyopathy
lateral displacement (bc cardiomegaly)
How do you treat peripartum DCM
during pregnany: avoid nonselective beta blockers, use b1 selective (metoprolol succinate at low doses), NO acei, use hydralazine/nitrate combo
If LVEF is less than 25% or LV dysfunction persists for more than 6 months post partum, what are your recommendations
no subsequent pregnancies anticoagulation therapy (high incidence of LV thrombus if LVEF is less than 35%)
Does heparin cross the placenta
no
Other names for stress cardiomyopathy
broken heart syndrome, apical ballooning syndrome
What is stress cardiomyopathy
transient regional systolic dysfunction of LV apex with sparing of the base, presents like an acute MI, cardiac cath shows normal coronaries
Who gets stress cardiomyopathy
females more than males, common in japan, postmenopausal is common, often preceded by a stressor
Pathophysiology of stress cardiomyopathy
excess catecholamines, microvascular disease (NOT classic epicardial CAD)
Stress cardiomyopathy ECG and cardiac biomarkers
ECG: ST elevation in about 45% of patients, ST depression in 7%, QT prolongation is common
Cardiac biomarkers: troponin is positive in most patients, BNP is positive
Treatment for stress cardiomyopathy
Beta-blockers, ACEI/ARB, diuretics
Prognosis is great (most recover in months), recurrences are possible
describe restrictive cardiomyopathy
impaired diastole (active process) due to loss of compliance, fibrosis or scaring of endomyocardial tissue, infiltration of a noncontractile complex/material into myocardium normal ejection fraction until end stage
Examples of restrictive cardiomyopathy
scleroderma, amyloidosis, sarcoidosis, hemochromatosis, glycogen storage diseases (fabry, pompe), hypereosinophilic syndrome (Loefflers), metastatic tumors, radiation therapy
Pathophysiology in restrictive cardiomyopathies
reduced LV filling, normal ejection fraction, reduced cardiac output, increased diastolic pressures, smaller ventricular chambers (decreased cardiac output and higher heart rates)
Symptoms of restrictive cardiomyopathy
DOE, venous congestion, usual heart failure signs and symptoms, exercise intolerance
Increased diastolic ventricular pressure in restrictive cardiomyopathy can cause what?
atrial fibrillation
Physical exam findings for restrictive cardiomyopathy
tachycardia, JVD, Kussmaul sign (inspiratory increase in JVP as stiff RV cannot accommodate more volumes), pulm congestion with rales, irregularly irregular rhythm if Afib is present, TR murmur, ascites, peripheral edema
ECG findings in restrictive cardiomyopathy
nonspecific ST and T wave changes (can be afib rhythm), amyloid heart has low voltage and Q waves, sarcoid has conduction blocks
Echo findings with restrictive cardiomyopathy
dilated atria, left ventricles have normal to small chamber size, left ventricle EF is normal (until end stage), in infiltrative types there is a speckled appearance of LV
How do you differentiate between restrictive CM versus constrictive pericarditis
echo, invasive heart cath (hemodynamic study), CT chest or MRI (thick pericardium), EM biopsy can be helpful too (normal in constriction)
What kind of medical management is appropriate for restrictive cardiomyopathy
overall poor prognosis
Hemochromatosis: iron chelation plus phlebotomy
Primary amyloid AL: chemo plus stem cell transplant
TTR Amyloid: new treatments available
Arrhythmogenic right ventricular dysplasia
Genetic disorder with incomplete penetrance and incomplete expressivity
Genes that code for desmosomes (loss of intercalated discs) replacement of mainly RV free wall by fibrofatty tissues
diagnosis of ARVC
ECG: epsilon waves, RV arrhythmias
Echo is not very helpful, neither is cardiac biopsy (too many false positives)
Cardiac MRI
Genetic testing when a family member is diagnosed
Signs and symptoms of ARVC
family history positive for syncope or SCD, RV arrhythmias (palpitations, syncope, SCD)
Treatment for ARVC
ICD to prevent SCD
Left ventricular noncompaction
prominent trabeculae, deep recesses, contraction abnormalities and relaxation abnormalities that lead to heart failure, conduction abnormality leads to arrhythmias, thrombotic risk
inheritance of left ventricular noncompaction
AD, AR, or X-linked recessive, sarcomere mutation
Treatment for left ventricular noncompaction
anticoagulation and ICD
ultimately transplant is needed
Why is mitral regurg present in HCM
due to abnormal mitral valve, abnormal chordae tendinae, poor coaptation
Other cardiac findings in HCM
S3 or S4, paradoxic splitting of S2 (with severe LVOTO), brisk and bifid arterial pulses, diffuse LV apical impulse on palpation, parasternal lift, signs of CHF
Describe the murmur in HCM
harsh ejection murmur loudest at apex/LLSB due to combo of septal hypertrophy and systolic anterior motion of mitral valve
May radiate to axilla and base (rarely to the neck)
When would you use a cardiac MRI for HCM
if echo diagnosis is undetermined, to evaluate for fibrosis
ECG for HCM
most sensitive but not specific (5% had a normal ECG)
prominent Q waves in inferior and lateral leads, enlarged P waves in lead II suggesting atrial enlargement (byproduct of diastolic dysfunction), left axis deviation, inverted T-waves in lateral leads
Echo is HCM
can determine LV hypertrophy, systolic anterior motion of the mitral valve, and LVOT obstruction
what is considered gray zone for LV thickness?
13-15 mm–hard to distinguish between HCM and athletes heart
Why do we care about thickness of LV in HCM
increasing risk of SCD with increasing wall thickness
Conditions associated with HCM
Fabry disease, noonan syndrome (male version of Turner syndrome), pompe disease, fatty acid oxidation deficiency, mitochondrial
Who should be screened for HCM
all 1st degree relatives of a HCM patient with genetic mutation–should be screened every 12-18 months by eacho and every 5 years after 21
Which arrhythmias are seen in HCM
atrial and ventricular arrhythmias; nonsustained VT associated with significant increase risk of SCD; SVT observed in up to 40% of patients
which type of arrhythmia is rare except for patients with fabry disease
bradyarrhythmias
What is the goal of pharmacologic treatment in HCM
symptoms and improve functional capacity, slow disease progression (NOT prevention of arrhythmias)
What are some factors that are proposed to lead to arrhythmias
myocardiac hypertrophy, disarray, fibrosis, ischemia, and autonomic disturbance
How is myocardial fibrosis detected
late gadolinium enhancement on cardiac MRI
Risk factors for SCD in HCM patients
family history of SCD, unexplained syncope, NSVT (more than 3 beats at a rate of 120), massive left ventricular hypertrophy (more than 33 mm), abnormal blood pressure response to exercise (failure to increase SBP by at least 20 mmHg or fall more than 20 mmHg from peak exercise BP to ongoing exercise)
how many high-risk factors must a HCM patient have to have a drastically increased risk of SCD
at least 3 high-risk factors
Cause of death in young (5-15 years old) HCM patients compared to older HCM patients
younger patients usually die from SCD, older patients have increased chance of dying from heart failure (or stroke)
When is an ICD used in HCM patients
two or more high risk factors (may consider for 1 high risk factor), sudden cardiac arrest, end stage HCM (LVEF less than 50%), or LV apical aneurysm
Side effects of ICD in HCM
25% experience inappropriate ICD discharge, some have lead complications, 4-5% with device infection, 2-3% experience bleeding or thrombosis
What is the goal of treatment for HCM
treat symptoms (if a patient is asymptomatic, treatment is unnecessary)
Common medications given in HCM
beta blockers (reduce LVOTO), calcium channel blockers (usually verapamil), disopyramide, ranolazine, careful use of diuretics (because HCM patients are extremely preload dependent)
How do beta blockers reduce angina symptoms
decrease myocardial oxygen demand
How do CCB reduce angina symptoms
improve microvascular function
Nonpharmacologic treatment of left ventricular outflow tract obstruction
used in pharm fails (heart failure symptoms persist despite max medical therapy or LVOT gradient more than 50 mmHg)
Options include surgical myectomy or alcohol ablation
What is a septal myectomy
direct removal of septal muscle (may also address abnormal mitral valve leaflets at the same time)
Complications associated with septal myectomy
excess septal tissue removed causing a ventricular septal defect; LBBB; CHB
What is alcohol ablation? what is one drawback?
creates localized infarction in basal septum (performed through coronary artery. Alcohol ablation does not offer the ability to address mitral valve issues
Compare septal myectomy and alcohol ablations
no difference in long term mortality or rates of aborted sudden cardiac death
Need for pacemaker is much higher in alcohol ablation
Compare sports restrictions in europe and america
Europe allows recreational activities (no competitive sports), American does not allow any sports
Name two drugs that we learned in cardio that result in tachyphylaxis (rapid diminished response to a drug due to depletion of endogenous receptors)
nitroglycerine, phenylephrine
describe the effects of calcium channel blockers (verapamil)
negative inotropic, negative dromotropic, negative chronotropic, vasodilation
what is the underlying mechanism for mitral valve prolapse?
myxomatous degeneration
what is a prominent side effect of amiodarone?
pulmonary fibrosis (may see blue-grey skin discoloration too but this isnt dangerous)
An increase in which metabolites can lead to local vasodilation in exercising muscle
adenosine, lactate, H+, K+, CO2
Indications for cardiac stress testing
diagnosis of coronary artery disease, prognosis of coronary artery disease, efficacy of treatment of CAD; chest pain; angina in CAD pt; post MI; exercise prescription for cardiac rehab; pre op eval for noncardiac surg; new cardiomyopathy
Contraindications of stress testing
acute MI; 100% pacing or patient with chronotropic incompetence with a pacemaker; unstable angina; uncontrolled cardiac arrhythmias causing sx or hemodynamic compromise; symptomatic severe aortic stenosis; uncontrolled symptomatic heart failure; acute PE or pulm infection; acute myocarditis or pericarditis; acute aortic dissection
Relative contraindications to stress testing
left main coronary stenosis, moderate stenotic valvular heart disease, electrolyte abnormalities, severe arterial hypertension, tachy or bradyarrhythmias, HCM/outflow tract obstruction, mental or physical impairment leading to inability to exercise, high-degree AV block, LVH with repolarization changes
Compare development of CAD in men and women
women are delayed in developing CAD by about 1 decade compared to men
ECG treadmill stress test goals
HR=(220-age)*0.85
BRUCE protocol
treadmill starts flat x 3min
Q3 min treadmill increases speed and angle
Naughton slower and lower treadmill angle for CHF px and modified BRUCE for less conditioned patients
ECG criteria for positive stress test
measure ST depression 80ms from the J point
- 2mm horizontal or downsloping ST depression in anterior or lateral leads=ischemia
- 1mm horizontal or downsloping ST depression in inferior leads=ischemia
What is myocardial perfusion imaging
images of tissue perfusion of isotope after exercise compared to rest images (imaging can occur up to 4-6 hours after injection)
How do we do stress testing in patients unable to do treadmill
nuclear/echo/PET imaging ONLY (ecg not helpful bc there is no target heart rate)
How is regadenosine used in nuclear stress testing
it is a coronary vasodilator–>blocked artery wont be able to vasodilate to caliber of normal artery and will not change with readenosine administration (already max vasodilated due to endogenous vasodilators)–>evaluate for lack of tissue perfusion to identify ischemic areas
Dosage of regadenosine is stress testing
LOW DOSE (bc higher doses can also block the AV node)
what can you do if patient is unable to reach target HR with treadmill test
add regadenosine dose to treatmill test patient and then do usual post stress imaging
Why do we add echo to stress tests?
to determine wall motion abnormalities and determine culprit coronary artery
what is the advantage to using echo over MPI
evaluates for CAD and/or valve function, pulmonary pressures, and LV outflow tract obstruction during exercise
when is dobutamine stress echo indicated
nonCAD dyspnea, diastolic dysfunction, mitral valve disease, aortic valve disease, prosthetic valve eval
Dobutamine protocol
start infusion at 2.5 micrograms/kg/min and increase at 3 minute intervals
What does a biphasic response (improvement then worsening) in a dobutamine stress test indicate?
ischemia
What patient population is likely to receive a dobutamine stress test?
severe COPD patients
*cannot walk on treadmill and cannot tolerate regadenosine
Indications for Holter monitor
symptoms occur daily (monitor duration is 24-72 hours)
indications for event recorder
symptoms occur less than daily, more than 1-2 events per month, Afib burden (monitor duration 2 weeks to 4 weeks)
indications for internal loop recorder
symptoms less than monthly, cryptogenic stroke, AF burden (monitor duration is 3 years)
Chest radiography findings in congestive heart failure
cephalization of vessels, interstitial edema, alveolar edema, pleural effusions
