CV Final Flashcards
What is Virchow’s Triad?
Endothelial damage
Venous stasis
Hypercoagulability
According to wells Criteria what do you do for a DVT risk of 3 or more?
Less than 3?
Do the D-dimer test, and if positive you get imaging
Get imaging immediately.
According to Well’s criteria, when do you get immediate imaging for a suspected PE?
A number 5 or higher.
Anything 4 or lower you do a D-dimer test.
What is the gold standard of DVT diagnosis?
What is the most common and practical?
Contrast Venography
Compression ultrasound
What is the gold standard of PE imaging?
What is the most common, and what is another option?
Conventional Pulmonary angiography
Most common is CT angiography
Other is a V/Q scan
What are the treatment options of a DVT?
DOAC: direct oral anticoagulants
Thromboectomy
Vena Cava Filter
What is the treatment for a PE?
Catheter based thrombolysis
Pulmonary embolectomy
What is the most common and preventable cause of death among hospitalized patients?
VTE: Venous thromboembolism
What is the Levine Sign?
Clenched fist to the chest
Describe Stable Angina
Predictable episode of pain based on exertion
Less than 20 min total. That has gradual onset and decline
Associated w/ stable fixed plaques.
What is different when women present with heart Dz?
Usually 5-10 yrs older at presentation
Will have more Prinzmeta angina: cardiospasm
What is the exercise stress test, and how effective is it?
What is an abnormal test?
Treadmill test to 85% max HR
They are connected to EKG
75% sensitive
Abnormal: decrease of SBP by 10, ST depression of 2 mm, chest pain or SOB
***Can’t do test if pt has starting abnormal EKG
What is a Stress Echo, when are they used?
It is an US that looks at wall motion abnormalities.
Used when a patient can’t exercise or uses dobutamine or adenosine
What are 4 tests used to check Angina?
Exercise Stress test
Stress echo
Stress radionuclide Myocardial Perfusion Scan
Angiography: Coronary angiography is invasive. CT angiography non invasive. Calcium score.
What is the treatment for Stable Angina
Reassurance Treat aggravating conditions Treat Risk Factors Revascularization Medication
What medications can you used to treat stable angina?
Which medication should be avoided?
Beta blockers 1st
CCB if BB not tolerated
Nitrates
Antiplatelts: Aspirin, P2Y12 inhibitors
***Avoid NSAIDS
What are the 2 types of Revascularization, and when should you use each?
Percutaneous Coronary Intervention PCI: Balloon angioplasty with stent to open artery
Coronary Artery Bypass Graft (CABG): Graft of Artery (better than veins.
Use PCI unless you have stenosis of the LAD, 3vessel disease w/ diabetes, or impaired LV function
Explain what Unstable Angina is
Chest pain that is less from exertion and happens at rest, and increasingly frequent. Associated w/ plaque disruption and thrombus.
What is Acute Coronary Syndrome
Blanket term for Unstable angina, NSTEMI, and STEMI
How can you diagnose an MI?
Cardiac biomarkers: TnT or TnI
Early phase hyperacute T waves in 2 or more leads
ST elevations in two contiguous leads. 1 mm in 1,2,3,aVL,aVF,aVR. 2mm in V1,V4,V5,V6.
***NOT V2 or V3
Which artery always needs a bypass if there is stenosis?
Left main artery before split to circumflex and LAD
What is the difference between unstable angina and NSTEMI?
They present the same, even the EKG. There are Elevated enzymes in a NSTEMI.
What are the differences between NSTEMI and STEMI?
STEMIs will have EKG-ST elevation. They are also treated with reperfusion instead of anitplatelet therapy or heparin
When would you see Q waves on an EKG?
After a past untreated MI
Which artery leads to Inferior STEMIs, and which leads do you see elevation and depression?
Right coronary A.
ST elevation in 2, 3, and AVF
Reciprocal depression in V2, V3, AVL and 1
Which artery do you see Anterior STEMIs, and where do you see elevation and depression?
LAD
ST elevation in V1 through B5
Reciprocal Depression in 2, 3, and AVF
Which artery leads to Lateral Wall MI, where do you find elevation and depression?
Circumflex A
ST elevation in 1, AVL, V5, and V6
Reciprocal Depression in 3, AVF, V2, and V3
What is the primary treatment of symptoms in Unstable Angina?
MOAN
Morphine, O2, Aspirin, Nitro
Heparin if unresolved.
What circumstances lead to a STEMI vs a NSTEMI?
STEMIs will classically be transmural, complete occlusion, and give Q-waves
Giving treatment to an MI patient within 3 hours leads to how much decrease in mortality?
50%
What is Fibrinolysis and when is it used?
Used only in STEMIs.
Use of plasminogen activators tPA, TNk, or rPA to break up clots.
What are contraindications of Fibrinolysis?
History of any bleed in brain Suspicion of aortic dissection Stroke within 3 months Head trauma in 3 months Active bleeding Uncontrolled HTN
When would you do PCI instead of Fibrinolysis?
You would always try to PCI first. Use Fibrinolysis when PCI can’t be done within 90 minutes.
Remember: Must use dual antiplatelet therapy. ASA drugs (aspirin) and P2Y12 inhibitors
What are some of the complication of MI?
Arrhythmias
AV blocks: may need pacemaker
LBBB caused by Anterior MI. *****If pt. Presents with this always treat as acute MI.
Pericarditis: Pain decreases when sitting up.
If a patient comes in with a new LBBB how would you treat them?
As if they are having an acute MI because they probably are.
What is Dressler Syndrome?
Pericardial and Pleural effusions.
From immune related causes. Will present with fever.
What do you do to treat a LV aneurysm?
Coumadin (Warfarin)
In right ventricular failure where does the blood back up?
In left ventricular failure where does blood back up?
Systemic flow
Lungs
How do you treat a right ventricular infarct?
Fluid bolous
Don’t give morphine or nitrates as that will decrease preload.
What is post-myocardial infarction treatment?
Lifelong aspirin and/or P2Y12 inhibitor
Lifelong high intensity statin
If a stent is placed, only need meds for 1 year.
How many patients are sent home from ER with missed MI?
2-4%
Where do the majority of Artery Emboli originate?
The LV. If not the LV it is from the proximal aorta.
What are the 6 p’s of acute Ischemia?
Pain Pallor Parathesias Paralysis Pulselessness Poiporithermia
What change in extremity vasculature is an automatic emergency?
Loss of pulse in the extremity.
What is the most common complication of an AAA?
Aortoenteric Fistula
What are the normal and abonormal sizes of an AAA?
Less than 3 cm is normal
More than 5 cm is worry
What is the best emergency option of imaging with a suspected Thoracic Aortic Dissection?
TEE
What meds do you use to prep for surgery in a TAA?
BB: Labetalol which is a B blocker and a1 blocker. Or Esmolol which is just a short acting B blocker.
Nitroprusside: usually used with esmolol to help bring the HR under 60 and SBP under 120 (100 is better).
What causes varicose veins?
Failing valves that can cause pain, edema, or thrombosis.
Cause dilated and tortuous veins.
The thrombi form, but do not leave the superficial veins
What is Trousseau Syndrome?
It is procoagulation from malignancy.
Causes thrombophlebitis
What is Peau d’orange?
Chronic edema that leads to superficial fibrosis. Usually can’t see the edema.
What is Lymphangitis?
Acute inflammation caused by bacterial seeding in lymph vessels.
What are the two causes of Primary Lymphedema?
Congenital isolated defect or Milroy disease (familial passed)
What is secondary lymphedema?
Obstruction of the lymph vessels by a physical blockage
What is Monckeberg medial sclerosis?
Calcification in muscular arteries. Lumen stays open.
What are the pathogenic causes of aneurysms and dissections of the aorta?
Inadequate connective tissue: TGF-B making defective elastin and collagen
Excessive connective tissue degradation: Increased matrix metalloprotease
Loss of SMC: Atherosclerotic thickening, systemic hypertension narrows lumen.
What are the percentages of chance of rupture at which size in abdominal aneurysms?
Less than 4 never
4-5 at 1%/yr
5-6 at 11%/yr
More than 6 at 25%/yr
What is the largest reason for aortic dissection?
More than 90% due to HRN in men 40-60
What percentage of occlusion lead to problems in arteries?
Less than 70% asymptomatic
More than 70 is critical stenosis, stable angina
More than 90 will be unstable angina.
What is usually the cause of unstable angina?
Plaque disruption
When in an MI, when is the greatest risk to develop an arrhythmia?
In the 1st hour
When would pericarditis occur in an MI?
After 2 or 3 days, and following a transmural infarct DVT to inflammation.
When and where would a myocardial rupture happen after an MI?
Usually in the LV or septum after 3-7 days after MI.
What are the risks after a subendocardial MI?
Thrombus formation.
No pericarditis, rupture, or aneurysm
What are the first steps after ischemia in the heart?
Aerobic pathways slow down or stop.
ATP is in short supply
Anaerobic glycolysis increased, increased Lactate, Decreased pH
What is the ROS quenching of Oxygen to Water?
O2 takes an oxygen to become superoxide and then is quenched by superoxide dismutase (SOD). 2 H and 1 e added to make H2O2 by catalase. 1 H and 1 e added to give an H20 and Hydroxyl radical.
Explain acute myocardial ischemia-reperfusion injury
In ischemia anaerobic glycolysis makes more lactate and lower pH
Na H pump tries to move H out but fills cell with Na
Na Ca exchanger takes Na in but increase Ca
The acid also opens the Mitochondrial Permeability Transition Pore MPTP killing the mitochondria.
Reperfusion generates ROS from restarted ETC which opens the MPTP more
The damage attracts neutrophils, damages SR, and mtDNA
The increased Ca from above and the hurt SR increases Myocyte contractility.
Restoration of membrane potential lets more Ca in which keeps the MPTP open
Over time the neutrophils accumulate and the cells die causing necrosis.
What is the gold standard in the diagnosis of an MI?
Elevated cTn and clinical presentation, with ECG changes.
Aspirin
MOA Indications ADR Considerations Use
Irreversibly COX1 and 2 inhibitors in platelets. Also inhibits production of TxA2
Thromboembolic disorder, OA, RA, fever, MI, stroke
GI ulcers
Minimum dosage 81 mg Max 325 mg, avoid use with other anticoagulants.
Irreversible effects may inhibit platelets up to 1 week
Platelet Inhibitors
ADP Receptor Antagonists
MOA Indications ADR Considerations Use
Clopidogrel, Prasugrel, Ticagrelar
Irreversibly inhibit ADP receptor on platelets to block aggregation
Prevent thrombotic events, acute unstable angina
Considerations: Non-reversible, Omeprazole interactions
GPllb/lllA
MOA Indications ADR Considerations Use
Abciximab, Eptifibatide, Tirofiban
Block the gpllb-llla receptor that is necessary for platelet aggregation.
Used for recent MI, stroke, PCI
Hemorrhage, thrombocytopenia
Bleeding disorders increase risk of major bleeding events. DON’T use throbolytics, NSAIDs, DOACs
What are some of the risk factors of contracting Endocarditis?
Prior Infective endocarditis (IE), prosthetic valve, cardiac device, IV drug use, indwelling catheter, immunosuppressive, resent surgery
What are the signs of Endocarditis?
Fever in 90% New murmurs Petechiae Splenomegaly Splinter hemorrhage, Roth Spots Jane way Lesions Osler Nodes
Which bacteria leads to the most IE infections?
Staph Aureus
What is the difference between acute and subacute IE?
The virulence of the organism.
Which valves are most commonly infected in IE? Which group of people may also include the tricuspid valve?
The aortic and Mitral valves.
IV drug users.
What two factors dictate an IE diagnosis?
Echo findings
Blood cuture
What are non-infected vegetation’s?
From deposition of sterile thrombi.
Non destructive lesions. That can lead to embolism.
The damage acts as a place that bacteria can start an IE
Which organism causes myocarditis?
Virus
Trypanosoma Cruz’s
Borrelia Burgdoferi: Lyme disease
What is the treatment for myocarditis?
Treat the underlying cause. Usually a virus.
Which criteria is used to diagnose myocarditis?
Dallas Criteria
What are the major criteria for endocarditis? Minor? How many are needed for diagnosis?
Major:
- 2 separate blood cultures or persistently positive cultures.
- Echo positive for vegetation, abscess or prosthetic valve
- New valvular mumur
Minor:
- Predisoposition
- Fever
- Vascular phenomena
- Positive culture that doesn’t meet major criteria
- Immunological phenomena (Osler node, Roth spots etc)
2 major, 5 minor, 1 major and 3 minor
What are the clinical signs of Pericarditis?
Chest pain on trapezius ridge. Improves leaning forward, worse lying down and on inspiration.
Friction rub
Widespread ST elevation
Pericardial Effusion
What is Polyangitis?
Small vessel
What is Cryoglobulinemic Vasculitis?
Small vessel, Hep B associated
Serum proteins leak out in the cold “cold agglutinins”
Microscopic Polyangitis (MPA)
Lower Hb
Higher Creatine, ESR, and CRP
Urine: +Blood, +++Protein, +Leukocytes
Normal Kidney Ultrasound
+pANCA/anti-MPO*****
Affects skin, joints, kidneys, lungs, eyes. Immunosuppression will usually induce remission.
Will see blue neutrophil fragments in stain.
Granulomatous w/ Polyangitis
Wegeners
Small vessel
Presentation: Couging up blood, blood in urine, feverish
Clinical: Nodules in Chest X-ray, splinter hemorrhages, cANCA/PR3*****
Granulomas forming in lungs, kidney, skin, etc.
Crescent shape in glomerulus
Eosinophilic Granulomatosis w/ Polyangiitis
Churg-Strauss Syndrome
Small Vessel
Eosinophils greater than 10%
Asthma, URT, gut
Mononeuritis Multiplex- peripheral neuropathy
Thromboangitis Obliterans
Buerger Disease
Sm-Medium Vessels
Heavy Smokers
Causes Raymond’s, intermittent claudication, and gangrene.
Giant Cell (Temporal) Arteritis
Med-Large Vessel
Only over 50
Flu-like and girdle weakness may= polymyalgia Rheumatica.
Will lead to sudden irreversible blindness through Opthalmic artery if untreated. Immediately give corticosteroid or anti-TNF therapy. T-cell mediated
Do biopsy of temporal A. to diagnose
Polyarteritis Nodosa
Urine: +++Protein, +++RBC
Renal failure, increased Creatine, anemia, need to biopsy affected organ. NOT LUNGS
Will cause nodules in the arteries of affected organ in angiography.
Due to Hep or idiopathic
Will increase BP in previously healthy person if in the kidneys due to renal A. Involvement.
IgA Vasculitis
Henoch-Scholein
Sm-Med vessels
Palpable purpura, Arthralgia, GI, and kidney.
Mostly in children 4-7, but can affect adults.
Kawasaki Disease
Cause of MI in kids
Fever, lymphadenopathy, oral/lip erythema, rash on feet, cervical node enlargement, edema
Viral disease may trigger the B-cells to make auto AB.
Tx: Intravenous immunoglobulin infusions and aspirin.
Takayasu Arteritis
Pulseless disease of upper extremities due to narrowing of aorta.
Md-Lg
Over 50 is giant cell Aortitis, lower 50 is this.
Affects the aortic arch and its branches.
Transmural scarring and thickening of aorta that narrows the lumen.
Low BP in extremities. Fatigue, fever. Faint Carotid Pulse
What do ANCAs do?
Activate Neutrophils, that releases ROA and Proteolytic enzymes leading to EC injury.
What is the most common form of Cardiomyopathy?
Dilated Cardiomyopathy
Dilated Cardiomyopathy
Usually in 40-60 years old
Will see enlarged ventricles, normal wall thickness, systolic dysfunction
SS: Arrhythmias and Thromboembolic events
Eianoses confirmed with Echo
EKG: Septal Q-waves, Tachyarrhythmias, BBB
Tx: Follow Heart Failure guidelines
Hypertrophic Cardiomyopathy
Often asymptomatic, but diagnosed by murmur, incidental EKG, or family screening
SS: Atypical Chest pain (after meals, exercise, dehydration)
Normal S1, S2, but can hear S4***
Hear Systolic murmur that increases with Valsalva maneuver
EKG: Abnormal Q waves, LVH, Left axis, Deeply inverted T-waves in V2-V4
Echo: See thickened septum
Tx: BB 1st line, CCB if BB aren’t tolerated (verapamil), May use surgical or alcohol septal ablation, dual pacing or transplant.
Arrhythmogenic RV Dysplasia/Cardiomyopathy
Disease of the Desmosomes proteins that leads to fat infiltration of RV. Thin RV wall
SS: Palpitations, syncope, occasionally SCD
EKG: inverted T-waves and Epsilon waves in right precordial leads
Tx: BB, antiarrhytmic drugs, catheter ablation, transplant.
Restrictive Cardiomyopathy
Nondilated V. W/ impaired V. Filling (diastole) due to fibrosis.
More common in the tropics.
3 kinds
1. Amyloidosis: deposition of protein in B-pleated sheets
2. Endomyocardial Fibrosis: Diffuse fibrosis of V. Linked to nutritional deficiencies. Most common
Loeffler Endomyocarditis: Hyper-eosinophilic infiltrates
SS: Dyspnea, peripheral edema, fatigue from decreased preload.
C-X-ray: Shows pulmonary congestion with normal cardiac silhouette
EKG: Prolonged PR, decreased voltage
Echo: A. Enlargement, LV appears normal
TX: Manage volume w/ diruetics or ARDs. May use pacemaker.
Peripartum Cardiomyopathy
LV systolic dysfunction in last trimester up to 6 months postpartum.
Associated w/ age, Multiple gestation, black, preclampsia, HTN. Iron Overload
Will reoccur frequently in with multiple gestation.
SS: CHF
Echo: LV dilation, LV systolic dysfunction
Tx: No ACEI or ARBs, Avoid hypotension. Half recover spontaneously
Takatsubo Cardiomyopathy
Broken Heart Syndrome- LV dysfunction in response to emotional stress.
Mostly in postmenopausal Women
Echo: Ballooning of LV
TX: Anticoagulation w/ loss of wall motion. Will usually last 1 month until symptoms resolve.
Myxomatosis Mitral Valve
One or both leaflets are floppy. Causing prolapse back into the atria.
Morphology: Thickening of proteoglycan spongiosa layer
Clinical: Palpitations, midsystolic click, sometimes a regurgitant murmur. Increases risk for IE or SCD
What percentage of valve disease is acquired stenosis of aortic and mitral valve?
66%
Rheumatic Valvular Disease
Inflammatory disease from B-hemolytic strep infection.
Deforming and scarring of mitral valve causing stenosis.
Will see Plump activated macrophages (antischkow cells). In Aschoff Bodies.
Auto AB against the M proteins in certain strep bind the myocardium and cardiac valves. It takes 2-3 weeks to start.
Will cause pancarditis. Will cause fusion at the edge of the mitral valve causing fishmouth stenosis.
Mural thrombi is common due to dilation and fibrosis. Cultures are negative for strep when symptoms appear.
Each infection worsens the disease.
To: Valve replacement and treat symptoms
2 jones criteria and previous strep infection proven through serology for diagnosis.
What are the 5 Jones Criteria, and how many do you need to diagnose which disease?
You need 2 of 5 to diagnose rheumatic valvular disease.
- Carditis
- Migratory arthritis to the large joints
- Subcutaneous nodules
- Erythematous annular skin rash
- Sydenham Chorea: Purposeless rapid movements
Calcification Aortic Stenosis
Usually asymptomatic
Anatomically normal on valves in age 70-80. It may be due to a bicuspid aortic valve in the 40-50 range.
Get calcified heaped-up masses on cusps.
Clinical: Will cause LVH and Angina. May lead to dyspnea and CHF
What causes systolic dysfunction?
Inadequate contractile function from HTN or ischemia
Diastolic Dysfunction
Inability to relax and fill.
Causes LVH, fibrosis, amyloid deposition, or constrictive pericarditis.
What will cause valve dysfunction?
Endocarditis, or rapid increase of Blood volume or pressure
What is forward failure?
Decrease of CO
What is Backward Failure
Increase congestion of venous circulation
What does a pressure increase do to myocytes
Adds number of myocytes in parallel. Increases the number without increasing chamber size.
What does Volume overload do to myocytes?
They are added in series. Fiber length increases.
Heart Weight is best measure of hypertrophy.
What will compensatory Hypertrophy lead to?
The extra thickness will lead to ischemic injury.
What are the 3 mechanisms of compensation?
Frank-Starling Mechanism
Activation of Neurohumoral Systems
Myocardial Structural Changes
Left Sided Heart Failure
cause?
Morphology?
Clinical?
Tx?
Causes: HTN, Ischemic Heart Disease, Mitral or aortic valve disease, and amyloidosis (primary myocardial disease)
Morphology: LVH and possible dilation
Causes increase pressure in pulmonary veins
Clinical: Edema, congestion, cardiomegaly, 3rd heart sound, pleural effusion, tachycardia, dilated LV, mitral regurgitation, dilated LA: causing A. Fib
To: Correct underlying cause, increase contractility, decrease Na, Decrease afterload w/ ACEI, Decrease volume (diuretic)
Right-Sided HF
Cause
Morphology
Clinical
Usually consequence of left sided HF. Any isolated right HF comes with disorders of lungs
Hepatic congestion will cause Ascities. Produces a fluid with decreased fluid, and no inflammatory cells.
Clinical: LL peripheral edema, No respiratory symptoms, Venous congestion, hepatic and splenic enlargement, bluish tinge, pleural effusion.
Aortic Regurgitation
Murmur
SS
PE
Increases afterload
SS: HF, Dyspnea, Flash pulmonary edema, lowers BP
PE: Soft early diastolic decresendo, Carotid pulse, Will hear 3rd and 4th heart sounds.
Aortic Stenosis
Murmur
SS
PE
Classic Triad of Dyspnea, Syncope, Angina
High pitched dimmed crescendo decresendo, splitting of S2
Pulsus Parvus et tardus
Flow slowed in carotid
What is an Austin Flint Murmur?
Jet of aortic regurgitation hits mitral valve.
What can you use to treat Aortic Valve, and what should you avoid?
Inoperable Cases: Digoxin, Diuretics, Nitro
Don’t use BB, CCB, or vasodilators
What is the Ross Procedure?
Autologous Pulmonic Valve. Use a cadaver to replace your own pulmonic valve.
TAVR
Transcatheter Aortic Valve Replacement
Used for those w/ calcium and considered inoperable.
What is the leading cause of Mitral stenosis?
Rheumatic Fever
What murmur will you get in Early MS
S1 accentuated, will get low pitched rumbling diastolic murmur.
What is the most common congenital heart disease?
Ventricular Septal Defects
When do embryologic developmental issues appear?
3-8 weeks
What are 3 of the defined environmental factors that influence congenital heart disease?
Rubella, Teratogens, Maternal diabetes
Which shunt is cyanotic?
Right to left Shunt
Explain Ostium Secundum?
Ostium Primum
Sinus Venosus
Are they tolerated well?
Defect in atrial septum in the middle. Usually no associated defects.
Towards the bottom. No related valve abnormalities
Towards the top. Usually has pulmonary vein drainage back into RA.
Well tolerated with holes less than 1 cm. Overtime they will get pulmonary HTN.
Ventricular Septal Defects
Left-Right shunt. Most common defect.
Membrane may close spontaneously.
Will cause RV hypertrophy and increase the Pulmonary Artery diameter.
Pulmonary HTN will reverse the shunt and may cause jets of blood that produce lesions and lead to IE
Patent Ductus Arteriosus
Used to Bypass the lungs. Within 1 to 2 days after birth it will close.
-the closure happens due to increase arterial O2, and decreased prostaglandin E2, and Pulmonary resistance.
There will be a high pressure left to right shunt that will lead to R to L shunts.
Eisenmenger Syndrome
Cyanotic condition related to R-L shunts.
What is HFpEF
What is HFrEF
HF w/ preserved EF (diastolic HF)
HF w/ reduced EF (systolic HF)
What are the stages of HF?A
A: High risk of HF, no Symptoms or structural changes
B: Sturcture changes with no symptoms
C: Structural changes with prior or current symptoms
D: Refractory HF requiring specialized interventions.
What are the classifications of HF?
1: Pts w/ HF, but no limitations on Physical activity
2: Pts w/ HF. Slight limitations of PA, and exercise induces symptoms
3: Pts w/ HF and marked PA limitations. Symptoms develop with less than ordainary PA
4: Pts w/ HF resulting in inability to carry out PA. Symptoms may occur at rest
What are the major and minor criteria of HF?
How many of each do you need for diagnosis?
Major: PND, Orthopedics, Elevated JVP, Pulmonary Rales, Third heart sound, cardiomegaly, weight loss more than 10 lbs in 5 days under treatment
Minor: Lung edema, Dyspnea on exertion, hepatomegaly, pleural effusion, tachycardia, weight loss more than 10 lbs in 5 days.
2 major or 1 major and 2 minor
What is Pulsus Alternans?
Pathognomonic of Severe LV systolic failure.
Evenly spaced strong and weak peripheral pulses.
What is a BNP, and what are normal limits?
Brain Naturemic Protein
Less than 100 no HF
100-400 unsure
Over 400 is HF
What will almost always be abnormal in HFrEF?
The EKG
When should you use BB to treat HF and which ones are used?
BB for all cases except during acute symptoms.
Use Carvedilol, metoprolol succinct, bisoprolol
What can be done to manage HF with lifestyle?
Watch weight, exercise, limit Na+ to 3g/day, with class D type 4 can limit fluids to 1.5-2 L/day, no drinking, no smoking.
What treatments are used in Acute Decompensation?
Typical?
Pulmonary Edema?
Low Output?
Cardio genie Shock?
Typical: Vasodilators w/ HTN. Diuretics w/o HTN
PE: Opiates, Vasodilators, Diuretics, and O2 ventilation
Low Output: Vasodilators, Hemodynamics monitoring, inotropic therapy
Shock: Inotropic therapy (catecholamines), Mecanical circulatory support
What are the symptoms of Left HF vs Right HF
Left:
Fluid Backup from heart to lungs
Dyspnea
Bilateral Basilar Crackles
Right: Fluid backup in body Peripheral edema Ascites RUQ discomfort with hepatic congestion JVD
Explain first exposure vs second exposure anaphylaxis.
You won’t get a reaction the first time you are exposed. Your body makes the IgE, forms memory B-cells for IgE, and IgE binds mast cells.
The second exposure will cause instant degranulation by mast cells bound with IgE
Secondary Anaphylaxis?
A reaction that may take 2-48 hours after the first exposure.
Take home Epi pen!
What is Anaphylaxis treatment?
Epi and O2
Albuterol (B-agonist) open airway, antihistamines to reduce inflammation
What is the Mayo Clinic way to stop anaphylaxis
Seek Support
Allergen
Follow up
Epinephrine
SAFE
What are the effects of Histamine in the body?
Rapid dilation of blood vessels that decrease BP.
May cause dysrhythmia, AV Block, Tachycardia, or edema. ST elevation may occur
Where does histamine affect the body?
Cysteinyl Leukotrienes?
Platelet Activating Factor? (PAF)
Anaphylatoxins
Histamine: Upper Resp, Resp, CV, Digestive, Skin
CysLT: Resp CV, Skin
PAF: CV, Skin
Anaphylatoxins: Skin
What are the steps of anaphylaxis?
- Allergen exposure
- Activation of TH2 cells and IgE class switch
- Production of IgE
- Binding of IgE to mast cells
- Rep[eat exposure to antigen
- Activation of mast cells and release of mediators
- Immediate hypersensitivity reaction vs late phase reaction (2-48 hrs)
What makes up the Tetralogy of Fallot?
VSD
RV outflow tract obstruction (subpulmonic stenosis)
Overriding of the VSD by the aorta
RV Hypertrophy
What is the morphology and clinical factors of tetralogy of fallot?
Proximal aorta dilated, pulmonary trunk is hypoplastic.
RV is hypertrophied
VSD is large and in the membranous portion of the septum.
Aorta is major exit of blood for both ventricles
Increases aortic flow, decrease pulmonary flow.
Usually Right to left shunt, and will cause hypertrophic osteoarthropathy.
BOOT CHEST X-RAY
Transposition of Great Arteries
Incompatible with postnatal life.
Aorta from RV and Pulmonary Trunk from LV
Marked RV Hypertrophy and LV is hypoplastic.
Cyanotic and needs surgery or pt will die
Aortic Coarction
2 types
Narrowing of the aorta
Infantile: Preductal: early cyanosis in lower half of body. Needs correction. RV hypertrophied.
Adult: Postductal: usually asymptomatic, but will cause HTN in UE and hypotension and weak pulse in LE.
- LV hypertrophy
- Systolic murmur and palpable thrill
- Balloon dilation and stent or surgical resection
What are the criteria for Circulatory Shock?
- Ill appearing
- HR more than 100
- RR more than 20/min
- Lactate more than 4 mM/L
- Urine Output less than .5 mL/kg/h
- Hypotension more than 30 min duration
What is the difference between heart failure and cardiac shock?
Failure is loss of forward flow
Shock: end organ damage.
At least 40% of myocardium is dysfunctional
What is SIRS
Systemic inflammatory Response Syndrome
More than 38 or less than 36 deg C
HR over 90, RR over 20, WBC over 12k or under 4K
What is the best vasopressin for cardiac shock?
Norepinephrine
Sometimes Dobutamine w/ NE but the dobutamine will lower BP too much
Which medications should be avoided in shock?
Steroids
Volume expanders: Hespan and Albumin
Familial Hyperchylomicronemia
Burger-Gratz syndrome
Monogenic disorder
Deficiency of LPL Lipoprotein lipase
Autosomal R
SS: elevated plasma TAGs even in fasting, Xanthomas, pancreatitis
Familial Hypercholesterolemia
Defect in the LDL receptor
Autosomal D
INCOMPLETE DOMINANCE
Homozygous: extremely high levels of LDL adn death happens in 20s.
Heterozygous: onset is later with mid-high range of LDL
Familial Defective apoB-100
Defect in the ApoB-100 affecting binding to LDLR
Autosomal D
R3500Q is affected altering the binding ability
Hypercholesterolemia
Defect in the PCK9 protein (gains function)
Enhances degradation of LDLR
Autosomal Dominant
Hyperlipoproteinemia type 3
Broad Beta Disease
Caused by homozygosity for ApoEe2, a genetic variant that does not bind to hepatic apoE receptors
Autosomal Recessive
Symptoms: Chylomicron remnants and IDLs remain in the blood. Elevates both, TAGs, and Cholesterol. Early CVD and xantomas are seen
Tangier Disease
Defect in the ABCA1 protein
Autosomal recessive
Significantly reduced HDL, mild hypertriglyceridemia. Causes Neuropathy, and enlarged orange-colored tonsils
Abetalipoproteinemia
Bassein-Kornzweig syndrome
Defect in the Microsomal TAG-transfer protein
Autosomal R
Near complete absence of the Apo B containing lipoproteins.
Affects the absorption of dietary fats, cholesterol, and fat-soluble vit. A,D,E,K
Symptoms: happens in first months. Failure to gain weight and grow. Diarrhea, star shaped RBC. Fatty stool. Later CNS impairment, and retina degeneration due to lack of vitamin A.
What is Stokes-Adams Attack?
Syncope from a heart block
What is Jarvell and Lange-Nielsen Syndrome
A hereditary prolonged QT interval that may lead to Syncope and deafness
What is Romano Ward syndrome?
A long QT interval without other symptoms
What is always the 3 things agreed upon by physicians when someone presents with syncope?
Get great history
Do great PE
Get ECG
Are seizures a form of syncope?
NO
What is HOCM syncope and what is the treatment?
Hypertrophic Obstructive Cardiomyopathy
Hypertrophy and fibrosis of myocardium that don’t allow CO to increase with exercise. This condition causes Angina upon exertion
Use Myomectomy, Ethanol Septal ablation, ICD
What is Carotid Sinus Hypersensitivity?
Reflex-mediated syncope from external pressure at the carotid.
From cough, swallow, defecation, turning head
