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CV Final Flashcards

1
Q

What is Virchow’s Triad?

A

Endothelial damage
Venous stasis
Hypercoagulability

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2
Q

According to wells Criteria what do you do for a DVT risk of 3 or more?

Less than 3?

A

Do the D-dimer test, and if positive you get imaging

Get imaging immediately.

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3
Q

According to Well’s criteria, when do you get immediate imaging for a suspected PE?

A

A number 5 or higher.

Anything 4 or lower you do a D-dimer test.

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4
Q

What is the gold standard of DVT diagnosis?

What is the most common and practical?

A

Contrast Venography

Compression ultrasound

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5
Q

What is the gold standard of PE imaging?

What is the most common, and what is another option?

A

Conventional Pulmonary angiography

Most common is CT angiography

Other is a V/Q scan

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6
Q

What are the treatment options of a DVT?

A

DOAC: direct oral anticoagulants

Thromboectomy

Vena Cava Filter

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7
Q

What is the treatment for a PE?

A

Catheter based thrombolysis

Pulmonary embolectomy

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8
Q

What is the most common and preventable cause of death among hospitalized patients?

A

VTE: Venous thromboembolism

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9
Q

What is the Levine Sign?

A

Clenched fist to the chest

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10
Q

Describe Stable Angina

A

Predictable episode of pain based on exertion

Less than 20 min total. That has gradual onset and decline

Associated w/ stable fixed plaques.

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11
Q

What is different when women present with heart Dz?

A

Usually 5-10 yrs older at presentation

Will have more Prinzmeta angina: cardiospasm

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12
Q

What is the exercise stress test, and how effective is it?

What is an abnormal test?

A

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

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13
Q

What is a Stress Echo, when are they used?

A

It is an US that looks at wall motion abnormalities.

Used when a patient can’t exercise or uses dobutamine or adenosine

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14
Q

What are 4 tests used to check Angina?

A

Exercise Stress test

Stress echo

Stress radionuclide Myocardial Perfusion Scan

Angiography: Coronary angiography is invasive. CT angiography non invasive. Calcium score.

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15
Q

What is the treatment for Stable Angina

A 
Reassurance
Treat aggravating conditions
Treat Risk Factors
Revascularization
Medication
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16
Q

What medications can you used to treat stable angina?

Which medication should be avoided?

A

Beta blockers 1st
CCB if BB not tolerated
Nitrates
Antiplatelts: Aspirin, P2Y12 inhibitors

***Avoid NSAIDS

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17
Q

What are the 2 types of Revascularization, and when should you use each?

A

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

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18
Q

Explain what Unstable Angina is

A

Chest pain that is less from exertion and happens at rest, and increasingly frequent. Associated w/ plaque disruption and thrombus.

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19
Q

What is Acute Coronary Syndrome

A

Blanket term for Unstable angina, NSTEMI, and STEMI

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20
Q

How can you diagnose an MI?

A

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

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21
Q

Which artery always needs a bypass if there is stenosis?

A

Left main artery before split to circumflex and LAD

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22
Q

What is the difference between unstable angina and NSTEMI?

A

They present the same, even the EKG. There are Elevated enzymes in a NSTEMI.

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23
Q

What are the differences between NSTEMI and STEMI?

A

STEMIs will have EKG-ST elevation. They are also treated with reperfusion instead of anitplatelet therapy or heparin

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24
Q

When would you see Q waves on an EKG?

A

After a past untreated MI

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25
Q

Which artery leads to Inferior STEMIs, and which leads do you see elevation and depression?

A

Right coronary A.

ST elevation in 2, 3, and AVF

Reciprocal depression in V2, V3, AVL and 1

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26
Q

Which artery do you see Anterior STEMIs, and where do you see elevation and depression?

A

LAD

ST elevation in V1 through B5

Reciprocal Depression in 2, 3, and AVF

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27
Q

Which artery leads to Lateral Wall MI, where do you find elevation and depression?

A

Circumflex A

ST elevation in 1, AVL, V5, and V6

Reciprocal Depression in 3, AVF, V2, and V3

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28
Q

What is the primary treatment of symptoms in Unstable Angina?

A

MOAN

Morphine, O2, Aspirin, Nitro

Heparin if unresolved.

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29
Q

What circumstances lead to a STEMI vs a NSTEMI?

A

STEMIs will classically be transmural, complete occlusion, and give Q-waves

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30
Q

Giving treatment to an MI patient within 3 hours leads to how much decrease in mortality?

A

50%

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31
Q

What is Fibrinolysis and when is it used?

A

Used only in STEMIs.

Use of plasminogen activators tPA, TNk, or rPA to break up clots.

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32
Q

What are contraindications of Fibrinolysis?

A 
History of any bleed in brain
Suspicion of aortic dissection
Stroke within 3 months
Head trauma in 3 months
Active bleeding
Uncontrolled HTN
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33
Q

When would you do PCI instead of Fibrinolysis?

A

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

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34
Q

What are some of the complication of MI?

A

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.

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35
Q

If a patient comes in with a new LBBB how would you treat them?

A

As if they are having an acute MI because they probably are.

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36
Q

What is Dressler Syndrome?

A

Pericardial and Pleural effusions.

From immune related causes. Will present with fever.

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37
Q

What do you do to treat a LV aneurysm?

A

Coumadin (Warfarin)

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38
Q

In right ventricular failure where does the blood back up?

In left ventricular failure where does blood back up?

A

Systemic flow

Lungs

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39
Q

How do you treat a right ventricular infarct?

A

Fluid bolous

Don’t give morphine or nitrates as that will decrease preload.

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40
Q

What is post-myocardial infarction treatment?

A

Lifelong aspirin and/or P2Y12 inhibitor
Lifelong high intensity statin
If a stent is placed, only need meds for 1 year.

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41
Q

How many patients are sent home from ER with missed MI?

A

2-4%

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42
Q

Where do the majority of Artery Emboli originate?

A

The LV. If not the LV it is from the proximal aorta.

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43
Q

What are the 6 p’s of acute Ischemia?

A 
Pain
Pallor
Parathesias
Paralysis
Pulselessness
Poiporithermia
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44
Q

What change in extremity vasculature is an automatic emergency?

A

Loss of pulse in the extremity.

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45
Q

What is the most common complication of an AAA?

A

Aortoenteric Fistula

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46
Q

What are the normal and abonormal sizes of an AAA?

A

Less than 3 cm is normal

More than 5 cm is worry

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47
Q

What is the best emergency option of imaging with a suspected Thoracic Aortic Dissection?

A

TEE

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48
Q

What meds do you use to prep for surgery in a TAA?

A

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).

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49
Q

What causes varicose veins?

A

Failing valves that can cause pain, edema, or thrombosis.

Cause dilated and tortuous veins.

The thrombi form, but do not leave the superficial veins

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50
Q

What is Trousseau Syndrome?

A

It is procoagulation from malignancy.

Causes thrombophlebitis

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51
Q

What is Peau d’orange?

A

Chronic edema that leads to superficial fibrosis. Usually can’t see the edema.

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52
Q

What is Lymphangitis?

A

Acute inflammation caused by bacterial seeding in lymph vessels.

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53
Q

What are the two causes of Primary Lymphedema?

A

Congenital isolated defect or Milroy disease (familial passed)

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54
Q

What is secondary lymphedema?

A

Obstruction of the lymph vessels by a physical blockage

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55
Q

What is Monckeberg medial sclerosis?

A

Calcification in muscular arteries. Lumen stays open.

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56
Q

What are the pathogenic causes of aneurysms and dissections of the aorta?

A

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.

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57
Q

What are the percentages of chance of rupture at which size in abdominal aneurysms?

A

Less than 4 never
4-5 at 1%/yr
5-6 at 11%/yr
More than 6 at 25%/yr

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58
Q

What is the largest reason for aortic dissection?

A

More than 90% due to HRN in men 40-60

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59
Q

What percentage of occlusion lead to problems in arteries?

A

Less than 70% asymptomatic
More than 70 is critical stenosis, stable angina
More than 90 will be unstable angina.

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60
Q

What is usually the cause of unstable angina?

A

Plaque disruption

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61
Q

When in an MI, when is the greatest risk to develop an arrhythmia?

A

In the 1st hour

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62
Q

When would pericarditis occur in an MI?

A

After 2 or 3 days, and following a transmural infarct DVT to inflammation.

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63
Q

When and where would a myocardial rupture happen after an MI?

A

Usually in the LV or septum after 3-7 days after MI.

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64
Q

What are the risks after a subendocardial MI?

A

Thrombus formation.

No pericarditis, rupture, or aneurysm

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65
Q

What are the first steps after ischemia in the heart?

A

Aerobic pathways slow down or stop.

ATP is in short supply

Anaerobic glycolysis increased, increased Lactate, Decreased pH

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66
Q

What is the ROS quenching of Oxygen to Water?

A

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.

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67
Q

Explain acute myocardial ischemia-reperfusion injury

A

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.

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68
Q

What is the gold standard in the diagnosis of an MI?

A

Elevated cTn and clinical presentation, with ECG changes.

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69
Q

Aspirin

MOA
Indications
ADR
Considerations 
Use
A

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

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70
Q

ADP Receptor Antagonists

MOA
Indications
ADR
Considerations 
Use
A

Clopidogrel, Prasugrel, Ticagrelar

Irreversibly inhibit ADP receptor on platelets to block aggregation

Prevent thrombotic events, acute unstable angina

Considerations: Non-reversible, Omeprazole interactions

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71
Q

GPllb/lllA

MOA
Indications
ADR
Considerations 
Use
A

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

72
Q

What are some of the risk factors of contracting Endocarditis?

A

Prior Infective endocarditis (IE), prosthetic valve, cardiac device, IV drug use, indwelling catheter, immunosuppressive, resent surgery

73
Q

What are the signs of Endocarditis?

A 
Fever in 90%
New murmurs
Petechiae
Splenomegaly
Splinter hemorrhage,
Roth Spots
Jane way Lesions
Osler Nodes
74
Q

Which bacteria leads to the most IE infections?

A

Staph Aureus

75
Q

What is the difference between acute and subacute IE?

A

The virulence of the organism.

76
Q

Which valves are most commonly infected in IE? Which group of people may also include the tricuspid valve?

A

The aortic and Mitral valves.

IV drug users.

77
Q

What two factors dictate an IE diagnosis?

A

Echo findings

Blood cuture

78
Q

What are non-infected vegetation’s?

A

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

79
Q

Which organism causes myocarditis?

A

Virus
Trypanosoma Cruz’s
Borrelia Burgdoferi: Lyme disease

80
Q

What is the treatment for myocarditis?

A

Treat the underlying cause. Usually a virus.

81
Q

Which criteria is used to diagnose myocarditis?

A

Dallas Criteria

82
Q

What are the major criteria for endocarditis? Minor? How many are needed for diagnosis?

A

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

83
Q

What are the clinical signs of Pericarditis?

A

Chest pain on trapezius ridge. Improves leaning forward, worse lying down and on inspiration.

Friction rub

Widespread ST elevation

Pericardial Effusion

84
Q

What is Polyangitis?

A

Small vessel

85
Q

What is Cryoglobulinemic Vasculitis?

A

Small vessel, Hep B associated

Serum proteins leak out in the cold “cold agglutinins”

86
Q

Microscopic Polyangitis (MPA)

A

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.

87
Q

Granulomatous w/ Polyangitis

A

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

88
Q

Eosinophilic Granulomatosis w/ Polyangiitis

A

Churg-Strauss Syndrome
Small Vessel

Eosinophils greater than 10%

Asthma, URT, gut

Mononeuritis Multiplex- peripheral neuropathy

89
Q

Thromboangitis Obliterans

A

Buerger Disease
Sm-Medium Vessels

Heavy Smokers

Causes Raymond’s, intermittent claudication, and gangrene.

90
Q

Giant Cell (Temporal) Arteritis

A

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

91
Q

Polyarteritis Nodosa

A

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.

92
Q

IgA Vasculitis

A

Henoch-Scholein
Sm-Med vessels

Palpable purpura, Arthralgia, GI, and kidney.

Mostly in children 4-7, but can affect adults.

93
Q

Kawasaki Disease

A

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.

94
Q

Takayasu Arteritis

A

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

95
Q

What do ANCAs do?

A

Activate Neutrophils, that releases ROA and Proteolytic enzymes leading to EC injury.

96
Q

What is the most common form of Cardiomyopathy?

A

Dilated Cardiomyopathy

97
Q

Dilated Cardiomyopathy

A

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

98
Q

Hypertrophic Cardiomyopathy

A

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.

99
Q

Arrhythmogenic RV Dysplasia/Cardiomyopathy

A

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.

100
Q

Restrictive Cardiomyopathy

A

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.

101
Q

Peripartum Cardiomyopathy

A

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

102
Q

Takatsubo Cardiomyopathy

A

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.

103
Q

Myxomatosis Mitral Valve

A

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

104
Q

What percentage of valve disease is acquired stenosis of aortic and mitral valve?

A

66%

105
Q

Rheumatic Valvular Disease

A

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.

106
Q

What are the 5 Jones Criteria, and how many do you need to diagnose which disease?

A

You need 2 of 5 to diagnose rheumatic valvular disease.

  1. Carditis
  2. Migratory arthritis to the large joints
  3. Subcutaneous nodules
  4. Erythematous annular skin rash
  5. Sydenham Chorea: Purposeless rapid movements
107
Q

Calcification Aortic Stenosis

A

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

108
Q

What causes systolic dysfunction?

A

Inadequate contractile function from HTN or ischemia

109
Q

Diastolic Dysfunction

A

Inability to relax and fill.

Causes LVH, fibrosis, amyloid deposition, or constrictive pericarditis.

110
Q

What will cause valve dysfunction?

A

Endocarditis, or rapid increase of Blood volume or pressure

111
Q

What is forward failure?

A

Decrease of CO

112
Q

What is Backward Failure

A

Increase congestion of venous circulation

113
Q

What does a pressure increase do to myocytes

A

Adds number of myocytes in parallel. Increases the number without increasing chamber size.

114
Q

What does Volume overload do to myocytes?

A

They are added in series. Fiber length increases.

Heart Weight is best measure of hypertrophy.

115
Q

What will compensatory Hypertrophy lead to?

A

The extra thickness will lead to ischemic injury.

116
Q

What are the 3 mechanisms of compensation?

A

Frank-Starling Mechanism

Activation of Neurohumoral Systems

Myocardial Structural Changes

117
Q

Left Sided Heart Failure

cause?
Morphology?
Clinical?
Tx?

A

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)

118
Q

Right-Sided HF

Cause
Morphology
Clinical

A

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.

119
Q

Aortic Regurgitation

Murmur
SS
PE

A

Increases afterload

SS: HF, Dyspnea, Flash pulmonary edema, lowers BP

PE: Soft early diastolic decresendo, Carotid pulse, Will hear 3rd and 4th heart sounds.

120
Q

Aortic Stenosis

Murmur
SS
PE

A

Classic Triad of Dyspnea, Syncope, Angina

High pitched dimmed crescendo decresendo, splitting of S2

Pulsus Parvus et tardus
Flow slowed in carotid

121
Q

What is an Austin Flint Murmur?

A

Jet of aortic regurgitation hits mitral valve.

122
Q

What can you use to treat Aortic Valve, and what should you avoid?

A

Inoperable Cases: Digoxin, Diuretics, Nitro

Don’t use BB, CCB, or vasodilators

123
Q

What is the Ross Procedure?

A

Autologous Pulmonic Valve. Use a cadaver to replace your own pulmonic valve.

124
Q

TAVR

Transcatheter Aortic Valve Replacement

A

Used for those w/ calcium and considered inoperable.

125
Q

What is the leading cause of Mitral stenosis?

A

Rheumatic Fever

126
Q

What murmur will you get in Early MS

A

S1 accentuated, will get low pitched rumbling diastolic murmur.

127
Q

What is the most common congenital heart disease?

A

Ventricular Septal Defects

128
Q

When do embryologic developmental issues appear?

A

3-8 weeks

129
Q

What are 3 of the defined environmental factors that influence congenital heart disease?

A

Rubella, Teratogens, Maternal diabetes

130
Q

Which shunt is cyanotic?

A

Right to left Shunt

131
Q

Explain Ostium Secundum?

Ostium Primum

Sinus Venosus

Are they tolerated well?

A

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.

132
Q

Ventricular Septal Defects

A

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

133
Q

Patent Ductus Arteriosus

A

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.

134
Q

Eisenmenger Syndrome

A

Cyanotic condition related to R-L shunts.

135
Q

What is HFpEF

What is HFrEF

A

HF w/ preserved EF (diastolic HF)

HF w/ reduced EF (systolic HF)

136
Q

What are the stages of HF?A

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.

137
Q

What are the classifications of HF?

A

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

138
Q

What are the major and minor criteria of HF?

How many of each do you need for diagnosis?

A

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

139
Q

What is Pulsus Alternans?

A

Pathognomonic of Severe LV systolic failure.

Evenly spaced strong and weak peripheral pulses.

140
Q

What is a BNP, and what are normal limits?

A

Brain Naturemic Protein

Less than 100 no HF
100-400 unsure
Over 400 is HF

141
Q

What will almost always be abnormal in HFrEF?

A

The EKG

142
Q

When should you use BB to treat HF and which ones are used?

A

BB for all cases except during acute symptoms.

Use Carvedilol, metoprolol succinct, bisoprolol

143
Q

What can be done to manage HF with lifestyle?

A

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.

144
Q

What treatments are used in Acute Decompensation?

Typical?

Pulmonary Edema?

Low Output?

Cardio genie Shock?

A

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

145
Q

What are the symptoms of Left HF vs Right HF

A

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
146
Q

Explain first exposure vs second exposure anaphylaxis.

A

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

147
Q

Secondary Anaphylaxis?

A

A reaction that may take 2-48 hours after the first exposure.

Take home Epi pen!

148
Q

What is Anaphylaxis treatment?

A

Epi and O2

Albuterol (B-agonist) open airway, antihistamines to reduce inflammation

149
Q

What is the Mayo Clinic way to stop anaphylaxis

A

Seek Support
Allergen
Follow up
Epinephrine

SAFE

150
Q

What are the effects of Histamine in the body?

A

Rapid dilation of blood vessels that decrease BP.

May cause dysrhythmia, AV Block, Tachycardia, or edema. ST elevation may occur

151
Q

Where does histamine affect the body?

Cysteinyl Leukotrienes?

Platelet Activating Factor? (PAF)

Anaphylatoxins

A

Histamine: Upper Resp, Resp, CV, Digestive, Skin

CysLT: Resp CV, Skin

PAF: CV, Skin

Anaphylatoxins: Skin

152
Q

What are the steps of anaphylaxis?

A
  1. Allergen exposure
  2. Activation of TH2 cells and IgE class switch
  3. Production of IgE
  4. Binding of IgE to mast cells
  5. Rep[eat exposure to antigen
  6. Activation of mast cells and release of mediators
  7. Immediate hypersensitivity reaction vs late phase reaction (2-48 hrs)
153
Q

What makes up the Tetralogy of Fallot?

A

VSD

RV outflow tract obstruction (subpulmonic stenosis)

Overriding of the VSD by the aorta

RV Hypertrophy

154
Q

What is the morphology and clinical factors of tetralogy of fallot?

A

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

155
Q

Transposition of Great Arteries

A

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

156
Q

Aortic Coarction

2 types

A

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
157
Q

What are the criteria for Circulatory Shock?

A
  1. Ill appearing
  2. HR more than 100
  3. RR more than 20/min
  4. Lactate more than 4 mM/L
  5. Urine Output less than .5 mL/kg/h
  6. Hypotension more than 30 min duration
158
Q

What is the difference between heart failure and cardiac shock?

A

Failure is loss of forward flow

Shock: end organ damage.
At least 40% of myocardium is dysfunctional

159
Q

What is SIRS

A

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

160
Q

What is the best vasopressin for cardiac shock?

A

Norepinephrine

Sometimes Dobutamine w/ NE but the dobutamine will lower BP too much

161
Q

Which medications should be avoided in shock?

A

Steroids

Volume expanders: Hespan and Albumin

162
Q

Familial Hyperchylomicronemia

A

Burger-Gratz syndrome
Monogenic disorder

Deficiency of LPL Lipoprotein lipase

Autosomal R

SS: elevated plasma TAGs even in fasting, Xanthomas, pancreatitis

163
Q

Familial Hypercholesterolemia

A

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

164
Q

Familial Defective apoB-100

A

Defect in the ApoB-100 affecting binding to LDLR

Autosomal D

R3500Q is affected altering the binding ability

165
Q

Hypercholesterolemia

A

Defect in the PCK9 protein (gains function)

Enhances degradation of LDLR

Autosomal Dominant

166
Q

Hyperlipoproteinemia type 3

A

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

167
Q

Tangier Disease

A

Defect in the ABCA1 protein

Autosomal recessive

Significantly reduced HDL, mild hypertriglyceridemia. Causes Neuropathy, and enlarged orange-colored tonsils

168
Q

Abetalipoproteinemia

A

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.

169
Q

What is Stokes-Adams Attack?

A

Syncope from a heart block

170
Q

What is Jarvell and Lange-Nielsen Syndrome

A

A hereditary prolonged QT interval that may lead to Syncope and deafness

171
Q

What is Romano Ward syndrome?

A

A long QT interval without other symptoms

172
Q

What is always the 3 things agreed upon by physicians when someone presents with syncope?

A

Get great history

Do great PE

Get ECG

173
Q

Are seizures a form of syncope?

A

NO

174
Q

What is HOCM syncope and what is the treatment?

A

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

175
Q

What is Carotid Sinus Hypersensitivity?

A

Reflex-mediated syncope from external pressure at the carotid.

From cough, swallow, defecation, turning head

CV (3 decks)

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