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Bloc C - Exam 2 > Clinical > Flashcards

Clinical Flashcards

1
Q

What are the types of acyanosis (O2 not compromised)?

A
  1. Atrial Septal defect (ASD)
  2. Ventricular Septal defect
  3. Coartation aorta
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2
Q

What’s the most common type of cyanosis (02 affected)?

A

Tetralogy of Fallot:

  1. Malalignment VSD
  2. Subvalvular +/- valvular pulmonary stenosis
  3. Right ventricular hypertrophy (RVH)
  4. Overriding aorta
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3
Q

True or false: Patent Foramen Ovalis is a type of ASD?

A

Fasle.

Patent Foramen Ovalis is neither a CHD nor an ASD and usually has no clinical significance. It is problematic when patient has a stroke, when severe desaturation or when scuba diving/space travel.

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4
Q

CLinical presentaiton of Atrial septal defect (ASD)?

A
  • Fixed split S2 on auscultation
  • Normal saturation
  • JVP
  • 2/6 mid-systolic pulmonary flow murmur heard at 2nd LICS
  • Seen later in adults with arrhythmias
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5
Q

Types of Atrial Septal Defects (ASD)?

A
  1. Secundum (most common, area of foramen ovalis, absent radius bone)
  2. Primum (associated with endorcardial cushion defect)
  3. Sinus venosus defect (not a “true” ASD)
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6
Q

Treatment of ASD?

A

Closure is only necessary if shunt is significant:

  1. Symptomatic arrhythmias: Palpitations and ¯ exercise tolerance
  2. Right-sided chamber enlargement
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7
Q

Clinical presentation of Ventricular septal defect?

A
  • Thrill, displaced apex, Harsh, high-frequency holosystolic murmur (3-4/6).
  • The smaller the hole the bigger the murmur. Small lesions do not result in volume or pressure overload of the ventricle but big lesions results in LV enlargement and failure
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8
Q

Types of Ventricular Septal defects?

A
  1. Infundibular septum
  2. Membranous septum
  3. Atrioventricular/Inlet septum
  4. Trabecular/muscular septum
  5. OTHER: Eisenmenger Syndrome
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9
Q

What is Eisenmenger Syndrome?

A

A type of VSD:

Irreversible pulmonary vascular obstructive disease as a result of a LARGE, uncorrected, longstanding acyanotic LàR shunt, can lead to pulmonary atrial hypertension

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10
Q

Treatments of VSD?

A

The degree of shunting and hemodynamic effect is related to size of VSD and pulmonary and systemic vascular resistance. Surgical closure if not closed by the age of 2 with catheter for some patients.

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11
Q

Clinical presentation of Coartation of aorta?

A
  • Associated with Bicuspid aortic valve (BAV) and Turner’s Syndrome
  • The body creates collateral aortic vessels + LVH + high BP in the arms (difference of > 30 mmHg with the legs)
  • Bleeding nose
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12
Q

Types of Coartation of aorta?

A

Narrowing of the aorta usually in the region of the ligamentum arteriosum:

  1. Post-ductal
  2. Preductal
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13
Q

Treatment of Coartation of aorta?

A

Surgery, percutaneous or trans-catheter

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14
Q

Clinical presentation of tetralogy of Fallot?

A
  • Most case sporadic, 15% of cases associated with 22q11 deletion
  • NO PHT nor Eisenmendger
  • Squating children to compensate (Tet Spells)
  • Clubbing
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15
Q

What is called tetralogy of Fallot + Coexistant ASD?

A

Pentalogy of Fallot

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16
Q

How is normally treated tetralogy of Fallot?

A

Surgical repair during neonatal period

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17
Q

True or false: Small acyanotic lesions result in volume or pressure overload of the ventricle

A

NON. Just the big ones.

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18
Q

What are the types of Genetic disorders affecting the structure of the heart – presenting as malformations?

A
  1. Trisomy 21
  2. Syndrome of 22q11 deletion
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19
Q

What’s the management of heart disease in trisomy 21?

A
  • 40% have congenital cardiac malformation (atrial and ventricular septal defects, common atrioventricular canal, patent ductus arteriousus).
  • Management and counselling include specific guidelines for evaluation and follow-up
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20
Q

What’s the treatment of heart diseases in Syndrome of 22q11 deletion?

A
  • 75% have heart malformations; also have , parthyroid hypoplasia, thymus hypoplasia, and
  • We do a chromosome microarray and there are specific guidelines for evaluation and follow-up
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21
Q

What are the types of genetic disorders affecting the muscle of the heart – presenting as cardiomyopathy?

A
  1. Mitochondrial DNA disorder
  2. Fabry Disease (metabolic cardiomyopathy)
  3. Noonan Syndrome
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22
Q

What’s the management of heart diseases in mitochondrial DNA disorder?

A
  • Cause: (1) heteroplasmy (80-09% are mutant DNA, same muration) (2) mitotic segregation (pleiotropy, different mutations) (3) maternal inheritance
  • Can affect at any age, any organ, any symptoms, and any inheritance
  • We investigate with general biochemical work-up; evaluate the organs involved, specific mitochondrial evaluation (biopsy) and molecular tests (nuclear DNA). Management include specific follow-up, symptomatic treatment, specific vitamins and medication
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23
Q

What is the management of heart diseases in Fabry disease?

A
  • Males more affected than female (X linked), Heart murmur, angiokeratoma, and corneal opacities
  • Evaluation include cardiology, nephrology, neurology, ophthalmology
  • Due to lysosomal storage disorder
  • Management include enzyme therapy and specific surveillance
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24
Q

What is the management of heart disease in Noonan Syndrome?

A
  • 50-80% have cardiac defect; also have dysmorphic features, short stature, hearing and vision problems
  • Due to a genetic defect-RAS-opathy, locus heterogeneity, the genetic cause of this cardiomyopathy is diverse (could be neuromuscular). They can be classified as dilatatice CM, hypertrophic CM and arrhythmogenic right ventricle dysplasia
  • Evaluation: (1) Clinical cardiovascular features (2) Detailed medical history (3) Cumulative phenotype information WE DON’T ALWAYS TEST FOR GENETIC BECAUSE NOT ALWAYS CONCLUSIVE
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25
Q

Name a Genetic disorders affecting the vascular system.

A

Marfan’s syndrome

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26
Q

What is the management of Marfan’s syndrome?

A
  • Autosomal dominant, manifectations include long thin arms and legs, asymmetric chest and scoliosis, arachnodactyly, dilatation/dissection of the ascending aorta, or descending thoracic or abdominal aorta
  • Evaluations: Ophthalmology, Cardiology, Respirology and gene testing for
  • Management and follow-up include guidelines, avoidance of contact sport and cardiac stimulant (coffee) and cascade testing for family
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27
Q

What mechanisms can cause heart malformation?

A
  • Abnormal # of chromosome
  • Mocrodeletion/duplication
  • Single gene mutation
  • Storage Lysosomal
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28
Q

What mechanisms can cause Hypertrophic cardiomyopathy?

A
  • Mocrodeletion/duplication
  • Single gene mutation
  • Energy dysfunction (mitochondrial)
  • Storage Lysosomal
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29
Q

What mechanisms can cause vascular disease?

A
  • Mocrodeletion/duplication
  • Single gene mutation
  • Energy dysfunction (mitochondrial)
  • Storage Lysosonal
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30
Q

What is ischemia?

A

An imbalance between myocardial O2 supply and demand

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31
Q

How does ischemia manifests?

A

It manifest in different ways:

  1. Angina Pectoris (pain in the chest)
    1. Stable Angina: fixed obstruction CAD (>70%), with exertion HR, BP, contractility and myocardial O2 demand ↑
    2. Unstable Angina: sudden ↑ in tempo and duration of the ischemic episode, precursor to acute MI
    3. Variant Angina: at rest, caused by coronary vasospasm, ST-Elevation, endothelial/sympathetic activity problems
  2. Silent ischemia
    Common in diabetic, woman and elderly
  3. Myocardial Infarction (MI)
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32
Q

How do patients describe their symptoms when they have angina?

A
  • “Pressure, elephant sitting on chest, discomfort or burning” NOT “stabbing, sharp, pleuritic (increases with inspiration) or worst with palpation”
  • Usually diffuse, radiates to chest, shoulder, neck, lower face and back
  • Associated with dyspnea, fatigue, weakness, SNS or PNS (nausea, tachycardia, sweats)
  • Precipitated by anything ↑ myocardial O2 demand (activity, large meal, cold, emotions)
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33
Q

What are the 2 principal ways to dx angina?

A
  1. ECG (transient ischemia: ST depression and Y wave flat or inversion)
  2. Stress Testing (EST): exercise on a treadmill and they are CLINICALLY (pain) and/or ELECTRIALLY positive (1 mm ST depression)
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34
Q

Treatment of CAD?

A
  1. Nitrates
    Oral, patches
    Drug tolerance: we need a nitro-free interval for several hours (resets receptors)
    They don’t save life, they make patients feel better
    Side effects: headache, lightheadedness, and palpitations
  2. Beta-adrenergic blockers
    First line chronic therapy
    ↓ MVO2 (↓ contractility and HR)
    Contraindication with asthma (bronchospasm) and decompensated LV failure
    Side effects: fatigue and erectile dysfunction
  3. Calcium channel blockers
    Potent vasodilators:
    ​↓ MVO2
    ↑ myocardial O2 supply
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35
Q

Preventing complications of CAD?

A
  1. Antiplatelet therapy
    1. Aspirin (all patients for life)
    2. Clopidogrel
  2. Lipid-lowering therapy
    1. Statins: lower MI and death rates in patients with established CAD
  3. ACE-I and ARBs
    Reduce rates of death, MI, and CVA in patients with CAD
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36
Q

What are the indications for revascularization therapy?

A

When to consider

  1. Symptoms of angina do not respond adequately to anti-anginal drug therapy
  2. Unacceptable side-effects of medications
  3. Non-invasive testing suggests high risk CAD for which revascularization is expected to improve survival

Techniques

  1. Percutaneous Coronary Intervention (PCI) STENTS

Need anti-proliferative medication (prevents scaring down)

  1. Coronary Artery Bypass Graft (CABG) surgery (better for diabetics)
  2. Veins: saphenous vein, vulnerable to accelerated atherosclerosis
  3. Arteries (IMA): internal mammary artery, better (used for the LAD)
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37
Q

Features of unstable angina?

A

Symptoms:

Crescendo, rest, new onset severe angina, no response to nitro

Myocardial Biomarkers:

None

ECG:

ST depression and or T-wave inversion

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38
Q

Features of NSTEMI?

A

Symptoms:

Prolonged crushing chest pain, wider radiation, more severe

Myocardial Biomarkers:

Troponin I and T, starts after 3-4 hours, Peak 18-36 hours, can be seen for 10 days ish

ECG:

ST depression and or T-wave inversion

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39
Q

Feartures of STEMI?

A

Symptoms:

Prolonged crushing chest pain, wider radiation, more severe

Myocardial Biomarkers:

Troponin I and T, starts after 3-4 hours, Peak 18-36 hours, can be seen for 10 days ish

ECG:

ST elevation and Q wave later

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40
Q

Treatment of unstable angina and NSTEMI MI?

A

FIRST:

  • Admission to an intensive care setting: continuous ECG monitoring for arrhythmias
  • Bed rest to minimize myocardial oxygen demand
  • Supplemental oxygen if hypoxemia to improve oxygen supply
  • Analgesics (e.g. morphine) to reduce chest pain and anxiety

THEN:

  1. Anti-ischemic:
    1. Nitrates: venodilation, vasodilation, IV, are helpful with heart failure and hypertension
    2. Calcium channel blockers: used when contraindication of beta-blockers, should NOT be prescribed to patients with severe LV dysfunction
    3. Beta-blockers: ↓ sympathetic drive, ↓ MVO2, ↓ mortality

venodilation, vasodilation, intravenous, CCB

  1. Anti-thrombotic therapy to prevent further growth and facilitating resolution of the partially occlusive thrombus
  2. Antiplatelet (aspirin + P2Y12 antagonist such as clopidogrel, prasugrel or ticagrelor + Glycoprotein (GP) IIb/IIIa receptor antagonists)
  3. Anticoagulant (unfractionated heparin, LMWHs)

We start with conservative treatment and then we do invasive (angiogram) decided by TIMI score ≥3

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41
Q

Treatment of STEMI?

A

FIRST:​

  • Admission to an intensive care setting: continuous ECG monitoring for arrhythmias
  • Bed rest to minimize myocardial oxygen demand
  • Supplemental oxygen if hypoxemia to improve oxygen supply
  • Analgesics (e.g. morphine) to reduce chest pain and anxiety

THEN:

  1. Fibrinolytic drugs (NSTEMI and U/A patients DO NOT BENEFIT from fibrinolytic therapy) 2 first hours, not if bleeding
  2. Percutaneous coronary mechanical revascularization (best option if 90 minutes) + dual antiplatelet therapy (aspirin + P2Y12 antagonist)
  3. Aspirin, Heparin, Beta-blockers, Nitrates

+ Adjunctive therapies

  1. ACE inhibitors
  2. Cholesterol-lowering statins
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42
Q

What are the elements of the TIMI score?

A
  1. Age > 65
  2. > 3 CAD risk factors
  3. Prior stenosis > 50%
  4. ST deviation
  5. > 2 anginal events in < 24 h
  6. ASA in last 7 days
  7. Elevated cardiac markers
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43
Q

What’s the post-discharge therapy after an MI?

A
  • Aspirin + Second antiplatelet drug (clopidogrel/ticagrelor/prasugrel)
  • Beta-blocker
  • HMG-CoA reductase inhibitor (statin)
  • ACE-inhibitors (or ARBs if intolerant)
  • Nitroglycerine puffer (to be used as needed for angina)
  • Risk factor modification
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44
Q

What is Bernoulli equation?

A

It measures the pressure gradient between two chambers

Bernoulli ∆P = 4V2

45
Q

What is the Continuity equation?

A

It is used to estimate the effective area of a region of interest, most commonly the effective area of a stenotic valve orifice

Continuity A1V1=A2V2

V is velocity

46
Q

What are the basic principles of Doppler Echocardiography?

A

Doppler shift is used to interrogate regions in the heart, especially valves, to obtain quantitative information about the velocity and direction of blood flow. Color Doppler is used to depict Doppler measures of blood flow velocity, direction and turbulence according to a color scale; image shows case of aortic regurgitation (AR). Red is moving toward the probe and blue away from and the color is the velocity.

47
Q

What is Transesophageal echography (TEE)?

A

High frequency echo used for small structures such as valvular vegetations, left atrial appendage thrombi, PFO and aortic dissection flaps.

48
Q

What is Nuclear perfusion imaging?

A

Gamma waves, injected into the body and are amost proportional to blood flow (plateau). We can see it on a camera because of the principle of Flow = ∆P/R. We can identify fixed defects (MI, scar) and reversible defects (ischemia at stress but not rest).

49
Q

Why are PET scans used?

A

To evaluate metabolism (glycogen consumsion)

50
Q

What is cardiac Catheterization?

A

Based on continuous X-RAYs. We go through the radial artery, trace back to the aorta, inject iodine and take pictures of the arteries. We can do it while we to a PCI (stents) and valve replacements (TAVR).

  • Complications: death, MI, stroke (1/1000), arrhythmia, anaphylaxis, neuropathy (1/25), and minor bleeding + infections (1/100)
  • Coronary Flow reserve (CFR): flow at maximal vasodilation/flow at rest (4-5X)

** THO: We can diagnose mitral stenosis and regurgitation with ECG.

51
Q

What are the advantages of Cardiac magnetic resonance (CMR)?

A
  1. High spatial and contract resolution
  2. Accurate measurements
  3. Tissue characterization
  4. No radiation or iodinated contrast
52
Q

What are the limitations of What are the limitations of Cardiac magnetic resonance (CMR)??

A
  1. Time consuming
  2. Not always feasible
  3. Susceptible to artefacts
  4. Very rare risk with severe renal dysfunction patients
53
Q

Why are used Cardiac magnetic resonance (CMR)?

A

We can change the sequence and highlight different things (fat, water, late gadolinium enhancement). It measures: volume, perfusion, function, blood flow, oedema, fibrosis, ischemia and scars (late gadolinium). Therefore, they are used for myocarditis, pericarditis, cardiac masses, myocardial viability in ischemic cardiomyopathies, aortic pathologies, RV pathologies, congenital heart disease… Reference are mostly for weak or thick hearts.

54
Q

What’s the difference between calcium CT and and coronary CT?

A

Not the gold standard, a lot of artefacts because of movements (slow HR needed). Calcium in the arteries is usually in the wall and is not the same as stenosis of the arteries, which is in the lumen. A coronary CT calcium scan is a risk classification test to know if the patient is at risk of CAD (low radiation, low contrast, low resolution). The angiogram on the other hand is high resolution, radiation and contrast to visualize the patency of the coronary artery lumen.

55
Q

What are aneurysms?

A

Focal increase in vessel size by 50% compared with normal. True aneurysm includes dilatation of all three layers of aorta.

They are associated to cystic medical degeneration (congenital syndromes), artherosclerosis, infections of arterial wall and vasculitis.

56
Q

What’s the clinica presentation of Aortic aneurysm?

A

Most often asymptomatic and incidental discovery. Possible symptoms are awareness of pulsatile mass, compression of adjacent structures, congestive heart failure and back pain or GI symptoms.

57
Q

What’s the management of aortic aneurysm?

A
  1. Optimization of risk factors
  2. Medication (beta-blocker and ACE-inhibitors)
  3. Interventions (surgery, percutaneous endovascular repair)
58
Q

What are the different types of Aortic dissection?

A
  • Dissection: tear in the intima into the media
  • Acute intraumural hematoma: haemorrhage in the wall without intimal tear
  • Penetrating artherosclerotic ulcer: erosion of a plaque into the aortic wall
  • Aortic rupture: a cause of any of the above and in blows
59
Q

Management of aortic dissection?

A
  • Classification: type A (ascending) and type B (does not include ascending)
  • Complications: pericardial tamponade, hemothorax, stroke, MI, renal failure, aortic regurgitation
  • Diagnostic: CT, transesophageal, echo, resonance angiography
  • Treatment: reduce BP (beta-blockers and nitroprusside), surgery for type A and medical therapy for type B if stable
60
Q

Describe Chronic peripheral artery disease

A
  • Most common cause is atherosclerosis, increases with age.
  • Symptoms: claudication, bruit, ulcerations (DIABETICS), infections, necrosis, atrophy, cyanotic, hair lost.
  • Diagnosis: ankle-brachial index higher sBP of PT or DP / higher sBP Brachial, should be >1
  • Treatment: risk factors, antiplatelet and anticoagulants, supportive care, exercise, revascularization, amputation
61
Q

How do we recognize Acute Arterial Occlusion?

A
  • 6 “P”:
    Pain;
    Pallor;
    Paralysis;
    Parasthesia;
    Pulselessness;
    Poikilothermia (aka cold)
  • Caused by an emboli
  • Treatment includes re-establishment of flow
62
Q

What are the 3 types of Vasculitic Syndromes?

A
  1. Takayasu Arteritis: Affects aorta and its major branches
  2. Giant Cell Arteritis: (Temporal Arteritis): Medium to large arteries, commonly involves cranial vessels
  3. Thromboangiitis Obliterans: (Buerger disease): Inflammation of small and medium arteries, as well as veins and nerves involving distal vessels of upper and lower extremities. CAUSED BY SMOCKING.
63
Q

What’s Raynaud’s syndrome?

A
  • Vasospastic disease of the digital arteries
  • Benign, affect more woman
  • It can be primary or secondary (more severe, arterial occlusive disease)
  • Avoid clod, calcium channel blockers, other medications
64
Q

What is the pericardium?

A

3 layered sac that encircles the heart

  1. Visceral pericardium:
  2. Parietal pericardium
  3. Fibrous pericardium

A thin layer of pericardial fluid decreases the friction between the visceral and parietal layers

65
Q

What is pericarditis?

A

Most common affection of pericarditis, is an inflammation of the pericardial layers

Etiology:

  • Infectious (tuberculosis)
  • Viral (most common, sometimes idiopathic)
  • Bacterial (ex. Trauma)
  • Post MI (early or late)
  • Uremic (complication of renal failure)
  • Neoplastic
  • Radiation-induced
  • Associated with connective tissue disease
  • Drug-induced
66
Q

What is the clinical presentaion of pericarditis?

A
  • Sharp, pleuritic, retrosternal and left-sided pain, radiates to the back, worst when lying down, dyspnea and fever
  • Scratchy pericardial friction rub leaning forward during exhalation
  • Dyspnea
  • Fever
67
Q

How do we diagnose pericarditis?

A
  • ECG: Diffuse ST segment elevation and PR segment depression
  • Increased White blood cell count (WBC)
  • Elevated inflammatory markers
  • Elevated cardiac biomarkers (myoperdicarditis)
  • Visible on an echocardiogram: visible when fluid
68
Q

How do we treat pericarditis?

A

Rest, pain relief, oral steroids, colchicine, analgesics

  • Post MI Pericarditis

High dose aspirin + Avoid other anti-inflammatory agents as they may impair healing of the infarcted myocardium

  • Viral pericarditis

Self-limited but can use anti-inflammatory and colchicine

  • Purulent Pericarditis

Catheter drainage, intensive antibiotic therapy, high mortality rate even when treated

  • Tuberculous Pericarditis

Prolonged multidrug anti-tuberculous therapy

  • Uremic Pericarditis
    Intensive therapy
  • Malignant Pericarditis
    Palliative therapy, indicates advanced metastatic disease
69
Q

What is a pericardial effusion?

A

A complication of pericarditis.

Etiology

Non-inflammatory serous effusions may results from

  1. Increased capillary permeability (e.g. severe hypothyroidism)
  2. Increased capillary hydrostatic pressure (e.g. congestive heart failure)
  3. Decreased plasma oncotic pressure (e.g. cirrhosis or nephrotic syndrome)
70
Q

On what factors depends the level compression of the heart in a pericardial effusioN?

A
  1. Fluid volume
  2. Rate of accumulation
  3. Pericardium compliance
71
Q

What is the clinical presentation of a pericadial effusion?

A
  • Asymptomatic
  • Dull ache on the left side of the chest
  • Effusion may compress adjacent structures
  • Soft heart sounds
  • Reduced intensity of friction rub
  • Ewart sigh (dullness over posterior lung) on percussion
72
Q

How do we diagnose pericardial effusion?

A
  • CXR
  • Reduced QRS or beat to beat variation in the height of the QRS complex
  • Visible on an echocardiogram
73
Q

How do we treat pericardial effusion?

A

We treat the underlying cause.

74
Q

What is pericardial tamponade?

A

Condition in which pericardial fluid accumulates under high-pressure and compressed the heart

Etiology

Any etiology of acute pericarditis can progress to tamponade (even a benign viral), but it happens with cancer

75
Q

What is the clinical presentation of cardiac tamponade?

A

Beck’s triad

  1. JVP
  2. Hypotension with Pulsus Paradoxus (decrease of systolic BP of > 10 mmHg during inspiration)
  3. Quiet pericardium on auscultation (quiet heart sounds)
76
Q

How do we diagnose cardiac tamponade?

A
  • Visible on an echocardiogram
  • Cardiac catheterization with measurement of intracardiac and intrapericardial pressures
  • ‘y’ descent is blunted because the high intrapericardial pressure presses on the RV
77
Q

How do we treat cardiac tamponade?

A

Pericardiocentesis under ultrasound guidance most of the time

78
Q

What is Constrictive Pericarditis?

A

Fluid organization, fibrous scar formation and calcification

Etiology: Idiopathic

79
Q

What is the clinical presentation of constrictive pericarditis?

A
  • Abnormalities occur during diastole
  • Reduced cardiac output (fatigue, hypotension, reflex tachycardia)
  • Elevated systemic venous pressures (JVC moves up in inspiration aka Kussmaul’s sign, peripheral oedema, hepatomegaly)
  • Early diastolic “knock” may follow the second heart sound
80
Q

How do we diagnose constrictive pericarditis?

A
  • Calcification on CXR (sometimes)
  • Visible on an echocardiogram (thickened)
  • CT or MRI (thickened)
  • Cardiac Catheterization: prominent y descent in the right atrial pressure tracing
81
Q

What is the treatment of constrictive pericarditis?

A

Surgical removal of pericardium

82
Q

What is heart failure?

A

The heart is unable to pump blood forward at a sufficient rate to meet the metabolic demands of the body OR is able to do so only if the cardiac filling pressures are abnormally high.

83
Q

What are the 2 main categories of heart failure ?

A
  1. Heart failure with REDUCED ejection fraction HFrEF (EF < 40%) EF px
  2. Loss of contractility (weak pump): ↑ end-diastolic volume and ↑ end-systolic volume, leads to pulmonary edema
  3. Pressure overload (high afterload): ↑ end-systolic volume, leads to pulmonary edema
  4. Heart Failure with PRESERVED EF HFpEF (EF ≥ 50%) dysatolic function px
    1. Impaired early diastolic relaxation
    2. Increased stiffness of the ventricular wall
84
Q

What are the symptoms of left-sided HF?

A
  • Dyspnea
  • Congestive symptoms: orthopnea, paroxysmal nocturnal dyspnea (PND)
  • Low CO: dull mental status, impaired urine output, fatigue and weakness
85
Q

What are the symptoms of right-sided HF?

A
  • Weight gain
  • Peripheral edema
  • Hepatic enlargement
  • Abdominal discomfort
86
Q

What are the non-specific to a side symptoms of HF?

A
  • Cheyne-Stokes respiration (advanced heart failure)
  • Tachypnea
  • Sinus tachycardia
  • Pulsus alternans (weak and strong pulse, advanced heart failure)
  • Cachexia (fail, wasted appearance)
  • Diaphoresis
  • Pleural effusion (more right-sided)
87
Q

What are the left-sided HF physical signs?

A
  • Abnormalities of the cardiac apex (enlarged, sustained of lifting)
  • Pulmonary rales or crackles
  • S3 and S4
  • Mitral regurgitation murmur
88
Q

What are the righ-sided HF physical signs?

A
  • Palpable parasternal right ventricular “heave” (RB enlargement)
  • Distension of the jugular veins
  • Peripheral oedema
  • Hepatic enlargement with abdominal tenderness
  • Murmur of tricuspid regurgitation
  • Right-sided S3 and S4 gallops
89
Q

What is the NYHA Symptom Classification (I-IV)?

A
90
Q

What are the stages of HF?

A
91
Q

What are the diagnosis tests for HF?

A
  • B-Type Natriuretic Peptide (blood test): biomarkers that correlates with LV dysfunction
  • Echocardiography: to distinguish between systolic and diastolic dysfunction
92
Q

What are the precipiting factors of HF? Aka why is the patient coming back to the hospital when he was compensated?

A

Things that increase the cardiac workload.

93
Q

What are the treatments for reduced ejection fraction HF?

A
  1. Identification and correction of the underlying condition causing heart failure
  2. Elimination of the acute precipitating cause of symptoms in a previously compensated patient
  3. Management of heart failure symptoms
  4. Treatment of pulmonary and systemic vascular congestion (salt and loop diuretics)
  5. Measures to increase forward CO and perfusion of vital organs (vasodilators)
  6. Modulation of the neurohormonal response
  7. Prolongation of long-term survival

Treat preferentially with drugs/devices that have been proven to reduce mortality

  1. ACE inhibitor (or ARB if ACE intolerant)
  2. β-blockers
  3. Aldosterone antagonists (MRA)
  4. Spironolactone or Eplerenone
  5. Sacubitril-valsartan (instead of ACE/ARB in selected pts)
  6. Implantable Defibrillator +/-Resynchronization therapy
  7. HF with reduced EF < 35%: implantable cardioverter defibrillator (reduces mortality)
  8. Cardiac Resynchronization Therapy (reduces mortality) for conduction problems (EF < 35% and bundle branch)
  9. Cardiac transplantation or mechanical assist device (refractory patients)
94
Q

What are the treatments of Preserved ejection fraction HF?

A
  • Diuretics reduce pulmonary congestion and peripheral edema
  • For patients with normal EF, NO mortality benefit demonstrated for
  1. Beta-blockers
  2. ACEI/ARBs
  3. ARNIs being studied for this indication
  • Only drug showing potential benefit = spironolactone
  • Inotropic drugs not indicated (contractility is normal)
95
Q

What are the profiles of acute HF?

A
  • Warm and Dry Profile: Normal hemodynamics

Not a HR problem

Warm and Wet Profile

“Wet” lungs but preserved tissue perfusion (“warm” extremities)

Cold and Wet Profile

  • Congestive findings + impaired forward cardiac output
  • Marked systemic vasoconstriction

Cold and Dry Profile

May arise in volume-depleted pts or in pts with very limited cardiac reserve in the absence of volume overload

96
Q

What are the treatments of acutre HF?

A

Warm and Dry Profile

Treatment: Look for alternate explanations for symptoms

Warm and Wet Profile

Treatment: Diuretic and/or vasodilator

Cold and Wet Profile

Treatment: Diuretic and/or vasodilator + Inotrope

Cold and Dry Profile

Treatment: Volume expansion

97
Q

What is acute HF?

A

May develop in a previously asymptomatic patient with acute MI, SEVERE uncontrolled HTN and acute valvular regurgitation

98
Q

What are the 2 classifications of HF?

A
  1. Volume overload (wet) as a reflection of elevated LV filling pressures CONGESTION
  2. Signs of decreased cardiac output with reduced tissue perfusion COLD
99
Q

What are the prognostic indicators suggesting a patient is endstage?

A

Clinical Evaluation

  • Etiology (reversible potential)
  • Symptomatic NYHA III or IV with maximum therapy
  • Intolerance to therapy (hypotension)
  • Frailty & comorbidities
  • 2 or more hospitalisations in past 6 months (most important one)

Labs

  • Hyponatremia
  • BNP (higher)
  • Organ function (renal (worsening cardio-renal syndrome), hepatic, thyroid)
  • Anemia
  • Low albumin

Hemodynamics

  • Hypotension;
  • Tachycardia;
  • RV failure;
  • Pulmonary hypertension;
  • Low output symptoms (SOB & fatigue when euvolemic, mental status changes, anorexia/cachexia).
100
Q

What are the adjustments in medical therapy for end stage patients?

A

End-of-life considerations

  1. Reassurance that periodic re-evaluation of preferences and treatment goals will occur
  2. Potential treatment plan for sudden increase in symptoms while at home
  3. Planning for anticipated death (e.g. normalizing, DNR in home)
  4. Withdrawal of therapies (turning off ICD)
  5. Active withdrawal of therapies when patients are dependent on them (pacemakers)
  6. Living wills, goals of care and advanced directives
  7. Preferences for CPR
  8. Identification of surrogate decision-maker
  9. Exploration of nontraditional symptoms of heart failure (insomnia, nausea, hopelessness)
  10. The role of comorbidities and frailty in the patient’s prognosis

Trajectory and intervention

  • Investigations and diagnosis
  • Referrals for device therapy (ICD, resynchronization)
  • Bridge to recovery or transplant
  • Symptom control with outpatient therapy as needed (IV lasix, NTG, and inotropes)
  • Teaching, counseling, support
  • Accompany patients in the end stage of their life
  • Adjusting to limitations and future course of illness
  • Pharmacology changes
  • Helping the patients cope with the “uncertainty” of their illness
101
Q

What are the 2 types of cholesterol?

A
  1. High-density lipoprotein (HDL)
  2. Low-density lipoprotein (LDL)
102
Q

What is the mahor composition of plasma?

A

Lipids

103
Q

What are Low-Density Lipoproteins (LDL) pathologies?

A
  • Familial Hypercholesterolemia (FOUNDER EFFECT)
  • Most frequent genetic disorder associated with premature CAD (3-5%) of patients.
  • LDL-receptor defects underlie the majority of cases
  • CAD develops in men 35-55 years, in women 45-65 years.
  • Respond to statins (+ bile acid binding resins) (+ intestinal cholesterol absorption inhibitors ezetimibe)
  • If a patient has a bypass at 30, we test all the family in prevention (cascade screening)
  • Heterozygous or homozygous
  • Frequency 1:250 (up to 1:80 in Lac St-Jean)
  • Tendinous xanthomas
  • LDL-Receptor gene defect
  • LDL-C 2x ULN

One type of LDL is a Lp(a), which is a heterogeneous macromolecule associated with early myocardial infarction, coronary artery disease, and stroke. The level of Lp(a) is genetically controlled.

104
Q

What are the Secondary Causes of Dyslipoproteinemias?

A
  • Metabolic Diabetes: lipodystrophy and glycogen storage disorders
  • Renal Chronic renal failure: glomerulonephritis with nephritic syndrome
  • Hepatic Cirrhosis: biliary obstruction and porphyria
  • Hormonal Estrogens: progesterones, growth hormone, thyroid disorders (hypothyroidism) and corticosteroids
  • Lifestyle Physical inactivity: obesity, diet rich in fats, saturated fats, alcohol intake, smoking
  • Medications
105
Q

What do we take into consideration when treating patients with high LDL?

A
  • Will this medication save his/her life?
  • Will it prevent a heart attack or a stroke?
  • Will the patient feel better?
  1. Dyslipidemias are asymptomatic
  2. Evaluate cardiovascular risk
  3. Apply therapies based on evidence
  • Dont’t treat the lab test !!!!
106
Q

How do we assess ischemic pain?

A
  • Onset
  • Provocation/palliation
  • Quality
  • Region and radiation
  • Severity
  • Time
107
Q

What is one of the major factors of chronic pain?

A

Pain after surgery

108
Q

Differentiate between acute and chronic pain.

A

Bloc C - Exam 2 (7 decks)

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