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6th year subjects > Internal cardio topics > Flashcards

Internal cardio topics Flashcards

1
Q

what is S3

A

Rapid ventricular filling due to overload

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2
Q

Physiological S3

A

Pregnancy
Young children
Athletes

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3
Q

S4 heart sound

A

Atrial contrasction in ventricular hyperthrophy

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4
Q

what is heart murmurs

A

sound prduced by turbulent bloodflow

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5
Q

classificatrion of murmurs

A

Functional: infants, children, pregnancy
Pathological: structural defect

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6
Q

Diastolic murmurs

A

Mitral stenosis
Tricuspid stenosis
Aortic regurgitation
Pulmonary regurgitation

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7
Q

Aortic regurgitation type of murmur

A

High pitched - Blowing - Early diastyolic - Decresendo murmur

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8
Q

Etiology of aortic regurgitation

A

BEAR

Bicuspiod aortic vavle
Endocarditis
Aortic root dilation
Rheumatic fever

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9
Q

Pulmonary regurgitation

A

Rar - Early diastolic - Decresendo

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10
Q

Pulmonary regurgitation etiology

A

Pulmonary HTN
Dilated cardiomyopathy

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11
Q

Mitral stenosis

A

Location: Best heard at the apex.
Characteristics: Low-pitched, rumbling diastolic murmur.
Opening snap, loud S1
Mitral face (flushed cheeks, exertional dyspnea).
Causes: Rheumatic heart disease, mitral annular calcification.

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12
Q

Systolig murmurs

A

Aortic stenosis
Pulmonary stenosis
Mitral regurgitation
Mitral valve prolaps
HOCM murmurs

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13
Q

Aortic stenosis

A

Description: Harsh, crescendo-decrescendo systolic murmur.
Location: Best heard at the right upper sternal border.
Radiation: May radiate to the carotids.
Causes: Calcific aortic valve, bicuspid aortic valve.

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14
Q

Mitral regurgitation

A

Description: Holosystolic murmur.
Location: Best heard at the apex, radiating to the axilla.
Associated findings: S3 gallop
Causes: Mitral valve prolapse, rheumatic heart disease.

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15
Q

Pulmonary stenosis

A

Description: Harsh, crescendo-decrescendo systolic murmur.
Location: Best heard at the left upper sternal border.
Associated findings: Pulmonary ejection click.
Causes: Congenital pulmonary valve abnormalities, rheumatic heart disease..

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16
Q

Mitral proiolaps

A

Late systolic crescendo murmur with midsystolic click (MC) due to sudden tensing of chordae tendineae as mitral leaflets prolapse into the LA.

Causes: Idiopathic, connective tissue disorders

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17
Q

HOCM murmur

A

Crescendo-decrescendo systolic ejection murmur

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18
Q

Primary riskfactorsk for CVD divided into?

A

Major non modefiable
Modefiable

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19
Q

What are the primary risk factorsk for CVD

A

Major non-modifiable: (AGG)
o Age (old)
o Gender (males)
o Genetics

Major modifiable:
o Smoking
o HTN
o Hyper/dyslipidemia
o DM
o Obesity (abdominal)

Additional risk factors:
o Alcohol consumption
o Exercise, diet
o Uric acid
o Metabolic syndrome

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20
Q

Primary prevention of CVD

A

Main tools: lifestyle changes, CV risk factor profile modification.
Development of CHD: preclinical phase lasts for years if properly modefied

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21
Q

Secondary prevention in CVD

A

Focuses on slowing the progression of established disease.
Tools: Lifestyle changes, CV risk factor profile modifications, drugs (statins, antiplatelet drugs, ACE-inhibitors, ARB, BB)

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22
Q

CVS effects in DM

A

Altered response to arterial injury
Diminished fibrinolysis
Platelet hypercoagulability
Goal: HbAi1c less than 7%.

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23
Q

CVS effects in smoking

A

Increased HR and BP
Platelet activation: thromboembolism
Vascular plaques
Increased LDL, + Decreased HDL
Goal: complete cessation

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24
Q

Lipid managment in CVD

A

Primary goal: LDL < 1.8 mmol/L
Treatment: Statins

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25
Q

BP control goal in CVD

A

Less than 140/90 mmHg
Less than 130/80 mmHg in DM and CKD

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26
Q

Define ischemic heart disease

A

Plaque building up in coronary arteries.
Ischemia of the heart muscle is usually due to CAD

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27
Q

Define CAD

A

Ischemic heart disease due to narrowing of CA, most commonly due to atherosclerosis, resulting in a mismatch between myocardial oxygen supply and demand

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28
Q

What is Angina

A

chest pain caused by myocardial ischemia due to narrowing of coronary arteries. (necrosis of myocytes has not yet occurred)

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29
Q

What is stable angina

A

occurs upon exertion, mental stress, and/or exposure to cold and usually subsides within 20 minutes of rest or after administration of nitroglycerin

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30
Q

Define significantg stenosis of CA

A

> 50% in the left main and > 70% in other coronaries

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31
Q

Clinical features of ischemic heart disease

A

Asymptomatic/silent MI (in DM)
Angina
Dyspnea
Anxiety
Response to sublingual nitrates (complete, partial, not)
Ischemic ECG changes (in rest)or on a stress ECG
Arrhythmia
Sudden Cardiac Death

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32
Q

Dx of ischemic heart disease

A

Family history, medical history, physical examination
Risk factor evaluation
ECG: ST-depression, Flat/inverse T
Exercise ECG (stress)
CXR
MRI/CT

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33
Q

Define stable CAD

A

Patients are either asymptomatic
Have stable angina
Patients having had a MI but symptomes are under control

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34
Q

Factors reducing oxygen supply to heart muscle

A

Coronary atherosclerosis
Vasospasms
Increased heart rate
Anemia

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35
Q

Factors increasing oxygen demand to heart muscle

A

Increassed Heart rate
Increased Afterload

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36
Q

what is the cardinal symptom of CAD

A

Angina

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37
Q

when does CAD become symptomatic

A

Stenosis > 70%

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38
Q

Pain in angina

A

Typically retrosternal chest pain or pressure that radiates to the left arm, neck, jaw, epigastric region or back

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39
Q

treatment of stable CAD (ABCDE)

A

Aspirin (Clopidogrel if Cl)
Anti-angina treatment (Nit) up to every 30 min or as prophylaxis)
Beta-blockers (or ACEi in proven CVD, or CCB if BB is Cl)
BP control
Cigarette cessation
Cholesterol lowering drugs
Diet
DM control
Education
Exercise

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40
Q

when do you do PCI or CABG in CAD

A

Severe symptoms
Acute change in symptom severity
Failed medical therapy
Worsening left ventricular (LV) dysfunction

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41
Q

what drug to avoid in vasospasm angina

A

Dont give Beta Blockers

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42
Q

What composes ACD

A

Unstable angina, NSTEMI, and STEMI

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43
Q

what happens in the heart in unstable angina

A

Acute myocardial ischemia due to partial occlution of Coronary
No elevation in cardiac markers
Normal ECG

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44
Q

what happens in the heart during NSTEMI and what is seen on ECG

A

Acute myocardial ischemia causing subendocardial infarction
Cardiac markers are seen
ECG: T inversion, ST depression Loss of R

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45
Q

causes of ACS

A

CORONARY ARTERY ATHEROSCLEROSIS
Coronary artery dissection
Coronary artery vasospasm
Coronary artery embolism
Myocarditis
Vasculitis (e.g., polyarteritis nodosa, Kawasaki disease)
Myocardial supply-demand mismatch (e.g, anemia)

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46
Q

Clinical triad in right ventricular infarction:

A

Hypotension, JVD, clear lung fields

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47
Q

ECG in ACS NSTEMI

A

ST depression
Inverted T wave
Loss of R wave

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48
Q

Tx of all patients with ACS

A

Sublingual or IV nitrate (nitroglycerin)
Morphine IV or SC (3-5 mg)
Beta blocker recommended within 24 hours of admission
Early initiation of high statins regardless of baseline chol
Loop diuretic (furosemide) if flash pulmonary edema
Supporitve: IV fluids and oxygen > 90%

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49
Q

Treatment of ACS with STEMI

A

Aspirin (loading dose 300mg)
Clopidogrel or ticagrelor (Loading dose 600mg)
Dual AP therapy should be continued for at least 12 months if PCI with DES was performed
Anticoagulation with heparin or enoxaparin
Continue for the duration of hospitalization or until PCI is performed.

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50
Q

Scoring system to risk stratify patients with diagnosed ACS

A

GRACE SCORE
Age, HR, SBP, Creatinine level, CHF

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51
Q

Recommended coronary angio in NSTE-ACS:

A

Depends on severity of the ACS

  1. Immidiate - Within 2h
  2. Early invasive - within 24h
  3. Delayed invasive - within 72h
  4. Elective - within 1 week 9
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52
Q

STEMI VS NSTEMI

A

Ischemia is severe enough to cause ST elevations
Transmurtal infarct
ECG: ST elevation, LBBB
Elevated cardiac markers

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53
Q

etiology of STEMI

A

Plaque rupture causing thrombosis leading to complete occlution of coronary artery

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54
Q

diagnosis of STEMI

A

ECG
LABS
TTE
Cardiac CT

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55
Q

If ACS symptoms and LBBB on ECG

A

considered an STEMI because ST elevations cannot be
adequately assessed in the setting of an LBBB.

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56
Q

ECG leads corr with infarct location

A

V1-V2 LAD
V3-V4 Distal LAD
V5-V6 Left cirtcumflex
I, aVL Lateral
II, III, aVF Inferior

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57
Q

Important cardiac markers

A

Serum troponin T:
- most important cardiac-specific marker
- may be measured 3-4 hours after the onset of MI.

CK-MB (creatinin kinase)
- values correlate with the size of the infarct
- reach a maximum after approximately 12-24 hours
- normalize after only 2-3 days, making CK-MB a good marker for evaluating reinfarction.

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58
Q

The most commonly occluded coronary arteries

A

LAD > RCA > LCX.

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59
Q

Tx of STEMI interventions

A

Immediate PCI within < 90 min not more then 120 min
Thrombolytic therapy if PCI > 120 min: Alteplase, Reteplase
CABG if PCI unsuccessful
Aspirin 250mg
Clopidogrel 600mg
Dual AP therapy for 12 months after PCI with DES

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60
Q

complications of MI 0-24h

A

Cardiogenic shock
Sudden cardiac death
Arrhythmias
Acute left HF

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61
Q

most likely cause of SCD after MI, can it be prevented?

A

Fatal ventricular arrhythmia is
Prevention: installation of the ICD device

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62
Q

complications of MI 1-3 days

A

Early infarct-associated pericarditis

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63
Q

complications of MI 3-14 days

A

Papillary muscle rupture
Ventricular septal rupture
Left ventricular free wall rupture
Left ventricular pseudoaneurysm

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64
Q

complications of MI weeks to months

A
  1. Atrial and ventricular aneurysms can lead to rupture — cardiac tamponade and mural thrombus formation
  2. Dressler syndrom
    Pericarditis occurring 2-10 weeks post-MI without an infective cause, but thought to be due to Ab against cardiac muscle
  3. Congestive heart failure due to ischemic cardiomyopathy
  4. Arrhythmias
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65
Q

what is the consequence of papillary muscle rupture 2—7 days after MI

A

Signs of acute mitral regurgitation: dyspnea, cough, bilateral crackles, hypotension

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66
Q

In which MI is ventricular septal defect seen?

A

Mostly seen 3-5 days after MI in LAD infarct
Acute-onset right HF (jugular venous distention, peripheral edema) due to shunting of blood from L-R

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67
Q

pathuphysiology of a left ventricular free wall rupture after MI

A

Usually occurs 5-14 days after myocardial infarction
Greatest risk during macrophage-mediated removal of necrotic tissue

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68
Q

Cardiac cycle cardiac phases and duration?

A

Systole (0.27s)
Diastole (0.53s)

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69
Q

Cardiac cycle phases

A

Systole
lsovolumetric contraction
Rapid ejection
Reduced ejection

Diastole
Isovolumetric relaxation
Rapid ventricular filling
Reduced ventricular filling (diastasis)

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70
Q

What happens in isovolumetric contraction?

A

Occurs in early systole, directly after the AV valves close and before the semilunar valves open
Ventricle contracts (i.e., pressure increases) with no volume change

LV volume 120ml
LV P: 8-80 mmHg

RV volume 120ml
RV P: 5-25 mmHg

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71
Q

What happens in systolic ejection

A

From ventricle to aorta and pulm artery
Pressure in RV foes from 80-120 mmHg
Volume: ejection of 70 mL SV (50 mL ESV)

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72
Q

what happens in Isovolumetric relaxation

A

Occurs between aortic valve closing and mitral valve opening, no corresponding ventricular volume change until ventricular pressure is lower than atrial pressure and AV valves open

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73
Q

what is the Dicrotic notch?

A

slight increase of aortic pressure in the early diastole that
corresponds to closure of the aortic valve

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74
Q

what happens during ventricular filling

A

Rapid filling (passive filling of 80%)
Reduced filling (atrial systole of 20%)
LVand RV volume: ventricles fill with ~ 70 mL (50 mL — 120 mL)

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75
Q

Cardiac catheterization

A

Dx and Tx of CVS conditions.
Involves the insertion of a catheter into a cardiac vessel or chamber by way of a suitable vascular access.

Once in position, a cardiac catheter can help evaluate:
The blood supply to the cardiac musculature
Open up narrowed or blocked segments by means of a coronary angioplasty with stenting.

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76
Q

Cardiac catheterization: the process

A

Inserted through the Femoral, Radial artery or Brachial artery.
A contrast dye is injected via the catheter, and is visualized with serial x-ray imaging.

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77
Q

when do we do a coronary angio?

A
  1. Coronary artery disease
  2. Valvular or myocardial diseases with symptoms
  3. Recurring chest pain of unidentified cause
  4. Preoperative evaluation prior to noncardiac and planned cardiac surgery (CABG).
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78
Q

what is right heart catheterization

A

The passing of a balloon-tipped, multi-lumen catheter (Swan-Ganz catheter) into the right side of the heart and the pulmonary artery to monitor pressure within the heart (intracardiac pressure) and pulmonary arterial pressure(PCWP)

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79
Q

indications of a right heart catheterization

A
  1. For patients with heart failure, cardiomyopathy
  2. Pulmonary capillary wedge pressure (PCWP) in LVF and mitral stenosis.
  3. In suspected pulmonary hypertension to measure mPAP
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80
Q

Definitions in cardiology
SV
EF
CO
MAP

A

SV = EDV - ESV
EF = SV / EDV (50-70%)
CO =HRx SV
MAP: MAP = CO x TPR (normal 90-100 mmHg)

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81
Q

heart chamber pressures

A

RA: <5mmHg
LA (PCWP): <12 mmHg
RV (pulmonary a pressure): 25/5 mm Hg
LV: 8-130 mm Hg

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82
Q

what is PCI

A

cardiac catheterization in which a blocked coronary vessel is opened and appropriate blood flow is restored. A balloon catheter is used to dilate the narrowed section, with/without the placement of a stent to keep it patent.

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83
Q

PCI technique

A

Seldinger technique
1. Percutaneous puncture (radial, femoral, brachial artery)
2. Guide wire insertion
3. Sheath introducer
4. Removal of guide wire
5. Guiding catheter - Angioplasty/Balloon catheter
6. Inflation of balloon with or wothout a stent on the outside of it

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84
Q

Indications for CABG

A
  1. High-grade left main coronary artery stenosis
  2. Significant stenosis (> 70%) of the proximal LAD artery, with 2-vessel or 3-vessel disease
  3. Symptomatic 2-vessel or 3-vessel disease
  4. Disabling angina despite maximal medical therapy
  5. Poor left ventricular function with myocardium that can
    return to function on revascularization
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85
Q

Indications for emergency CABAG

A
  1. NSTEMI + ongoing ischemia unresponsive to medical therapy/PC|
  2. STEMI with inadequate response to all nonsurgical therapy
  3. Significant ongoing ischemia after a failed PCI or previous CABG
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86
Q

CI for CABG

A

There are no absolute contraindications for CABG, dont do it if its not needed.

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87
Q

process of CABG

A

Thoracotomy via a midline sternotomy — cardiopulmonary bypass (heart-lung machine) > cardioplegic arrest of the heart anastomosis of the bypass vessels distal to the coronary artery stenosis using autologous vessels

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88
Q

Grafts in CABG

A

Internal thoracic artery (internal mammary artery)
Internal thoracic artery (internal mammary artery)
Radial artery

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89
Q

types of CABG

A

Traditional CABG (on pump)
Off-pump coronary artery bypass (OPCAB) surgery
Minimally invasive direct, or totally endoscopic CABG

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90
Q

result of CABG

A

Successful grafts typically last 8-15 years and provide an improved chance of survival (decreased 5-year mortality, especially in patients with triple vessel disease)

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91
Q

define congestive heart failure

A

A clinical syndrome in which the heart is unable to pump
enough blood to meet the metabolic needs of the body, characterized by ventricular dysfunction that results in low CO.

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92
Q

Types of congestive heart failure

A

Systolic dysfunction
Diastolic dysfunction
Right heart failure (RHF)
Left heart failure (LHF)
Biventricular (global) HF
Chronic compensated CHF
Acute decompensated CHF

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93
Q

Define Systolic dysfunction CHF

A

Reduced SV, reduced EF, increased EDV

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94
Q

Define Diastolic dysfunction CHF

A

Reduced SV, preserved EF, normal/reduced EDV
Characterized by low myocardial compliance (due to compensatory hypertrophy)

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95
Q

Define Right heart failure (RHF)

A

due to right ventricular dysfunction.

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96
Q

Define Left heart failure (LHF)

A

due to left ventricular dysfunction.
Long-standing LHF is the most common cause of RHF.

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97
Q

Define Biventricular (global) CHF

A

both the left and right ventricle are affected.
Results in the development of both RHF and LHF symptoms

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98
Q

Define Chronic compensated CHF

A

patient has signs
of CHF onechocardiography but is asymptomatic

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99
Q

Define Acute decompensated CHF

A

Sudden deterioration of CHF or new onset of severe CHF due to an acute cardiac condition like MI

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100
Q

what type of HF dopes the cardiomyopathies form

A

DCM - Systolic dysfunction
RCM - Diastolic dysfunction
HCM - Diastolic dysfunction

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101
Q

markers in congestive heart failure

A

BNP > 400
NT-pro BNP > 450

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102
Q

gold standard diagnosis of CHF

A

TTE which check
- Atrial and ventricular size
- IV septal size ( > 11mm indicates hyperthrophy)
- Systolic function (EF)
- Diastolic fuinction ( Diastollc filling)
- Investigating etiologies

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103
Q

Define dilated cardiomyopathy L

A

Left or biventricular dilation with strucxtural and functional systolic dysfunction in the ansence of CAD, valvular hearty disease or congenital heart disease

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104
Q

Etiology of DCM

A

Idiopathic (~ 50%)
Genetic predisposition
Coronary heart disease
Arterial hypertension
Coxsackie B virus myocarditis, SLE
ALcohol, cocain
Radiation

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105
Q

Genes in DCM

A

Mutations of TTN gene, encoding for the intrasarcomeric protein titin (connectin)
Mutations of MYH7 gene, encoding for the B-myosin heavy chain

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106
Q

pathophysiology o DCM

A
  1. Causative factors decrease the contractility of myocardium
  2. Compensatory mechanisms (Frank-Starling law) are activated to maintain CO - increased EDV (preload) - myocardial remodeling — eccentric hypertrophy
  3. Sarcomeres added in series and dilation of the ventricle — reduced myocardial contractilitym ans systolic dysfunction
  4. Decreased EF leading to heart failure
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107
Q

General symptoms: gradual development of CHF symptoms

A

Exertional dyspnea
Ankle edema, ascites
Angina pectoris

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108
Q
A

Mitral valve regurgitation or tricuspid valve regurgitation
S3 gallop
Left ventricular impulse displacement
Jugular venous distention
Rales over both lung fields
Palpitations
Diffuse abdominal and peripheral edema

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109
Q

x-ray in DCM

A

Cardiomegaly: left-sided hypertrophy with a balloon appearance
Pulmonary edema: sign of LHF decompensation

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110
Q

Define HCM

A

HCM: without obstruction of the LVOT 30%
HOCM: with LVOT obstruction that is dynamic 70%

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111
Q

HCM etiology

A

Most common hereditary heart disease
AD inheritance with varying penetrance
Most commonly by mutations of the sarcomeric protein genes

Also due to
Chronic hypertension (most common cause of LVH)
Aortic stenosis
Friedreich ataxia, Fabry disease, Noonan syndrome
Amyloidosis

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112
Q

Pathophysiology of HCM and HOCM

A

Hypertrophy of the LV ; most commonly occurs with asymmetrical septal involvement, which leads to diastolic dysfunction (impaired left ventricular relaxation and filling) > reduced SVm > reduced peripheral and myocardial perfusion > cardiac arrhythmia and/or heart failure and increased risk of SCD

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113
Q

what happend in the myocardium in both HCM and HOCM

A
  • Increased LV wall thickness with septal predominance, no dilation of left ventricle
  • Myofibrillar disarray, interstitial fibrosis, and myocyte hypertrophy
  • Concentric hypertrophy: a form of cardiac remodeling characterized by parallel duplication of sarcomeres that leads to thickening of the ventricular wall
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114
Q

what can mimick HCM with consentric HT

A

Hypertension and aortic valve stenosis (due to chronic pressure and volume overload): Chronic hypertension > increased afterload + increased myocardial wall tension > changes in myocardial gene expression > sarcomeres laid down in parallel > increased LV
thickness

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115
Q

HOCM Pathomechanism:

A

LVOT obstruction > increased LV systolic pressure > prolongation of ventricular relaxation > increased LV diastolic pressure exacerbation of HCM with further reduction of CO.

116
Q

cause of murmur in HOCM

A

Venturi effect: accelerated blood flow through ventricular outflow tract creates negative pressure that pulls the mitral valve towards the septum > increeased outflow tract obstruction.

117
Q

symptomes of HCM

A

Frequently asymptomatic (especially the nonobstructive type)
Exertional dyspnea
Angina pectoris
Dizziness, lightheadedness, syncope
Palpitations, cardiac arrhythmias
SCD (particularly during or after intense physical activity)

118
Q

Ecco findings in HCM

A
  1. Asymmetrically thickened left ventricular wall (> 15 mm)
  2. Typically involving the septum
  3. If LV wall thickness > 30 mm high risk of sudden death.
  4. Left atrial enlargement with mitral regurgitation
119
Q

pharma in HCM

A

First-line: Beta blockers
Second-line: Nondihydropyridine CCB - Verapamil

120
Q

when not to give CCB in HCM

A

should be avoided if there is hypotension or dyspnea at rest

121
Q

Pharmacotherapy to avoid in HCM

A

High-dose diuretics
Digoxin
Spironolactone

122
Q

General therapy in HCM

A

Lifestyle modifications
Automated implantable cardioverter defibrillator (AICD)
BB anmd CCB
Surgical septal myectomy if LVOT gradient = 50 mm Hg
Heart transplant: If end-stage non-obstructive HCM + LVEF < 50%.

123
Q

Types of Heart failure

A

Acute heart failure: rapid onset of new or worsening signs
Acute decompensated heart failure: due to decompensation of preexisting disease (most common)
De novo heart failure: acute heart failure occurring for the first time

124
Q

Etiology of De novo heart failure

A

Cardiac ischemia from ACS
Myocarditis
Drug-induced cardiomyopathy
Peripartum cardiomyopathy
Thyroid storm
Tachycardia-induced cardiomyopathy
Acute mitral regurgitation after ACS
Bacterial endocarditis
Pulmonary embolism
Pericardial effusion causing tamponade
Aortic dissection

125
Q

Etiology of ADHF

A

In 40-50% of cases, no trigger is found
Uncontrolled and/or refractory hypertension
New/worsening cardiac ischemia
Arrhythmias (e.g., A.fib with RVR, complete heart block)
Serious infection/sepsis (e.g., pneumoni)
Anemia
Renal failure
Volume overload
Drugs with negative inotropic properties (nondihydropyridine CCBs)

126
Q

Clinical features of acute heart failure are commonly classified as?

A

According to perfusion and the presence of congestion at rest
Warm dry
Warm cold
Cold dry
Cold wet

127
Q

Clinical symptomes of left sided congestive heart failure

A

Acute dyspnea
Flash pulmonary edema: rapid, life-threatening accumulation
Signs of increased WOB
Cough (occasionally with frothy, blood-tinged sputum)
Coarse crackles or wheezing on auscultation
Severe cases: central cyanosis

128
Q

Clinical symptomes of right sided congestive heart failure

A

Peripheral pitting edema
Hepatic venous congestion symptoms: abdominal pain + jaundice
Other symptoms of organ congestion (nausea, loss of appetite)
JVD
Kussmaul sign

129
Q

Non spesific ECG findings in heartfailrue

A

Acute ischemic changes due to ACS
Atrial fibrillation
Left ventricular hypertrophy
Bundle branch block
Non-specific ST-segment changes
Low voltage QRS
ECG findings may be normal.

130
Q

X-ray findings in pulmonary congestion

A

Cardiomegaly
Septal lines/Kerley B lines: visible horizontal interlobular septa
Basilar interstitial edema
Dilated pulmonary vessles
Pulmonary effusion

131
Q

How to decide managment of accute hearty failre?

A

Find out whith type first, and if the patient is hemodydamically stable
Warm dry
Warm cold
Cold dry
Cold wet

132
Q

Cardiogenic shock treatment
DRY+COLD

A
  1. Consider small fluid bolus (250-500 mL) if DRY+COLD
    (in WET+COLD)go traight to inotropic agents)
  2. Assess fluid respons; consider additional bolus if responsive.
  3. If shock persists, start a vasopressor, ideally, norepinephrine.
  4. Administer inotropic if hypoperfusion persists despite fluids and vasopressors: DOBUTAMIN
133
Q

Tx of DRY-WARM AHF

A

Optimize oral therapy.

134
Q

Tx of WET+WARM AHF

A

Start diuretics
Consider a vasodilator

135
Q

Respiratory support in acute heart failure

A

Positioning: Ensure the patient is sitting upright.
Oxygen: indicated if SpO2 < 90% or PaO2 < 60 mm Hg
NIPPV: for patients with respiratory distress despite oxygen

136
Q

Indications of invasive mechanical ventilation in HF patients

A

Hypoxemic respiratory failure unresponsive to NIPPV
Refractory hypoxemia (PaQO2 < 60 mm Hg)
Hypercapnia (PaCO2 > 50 mm Hg)
Acidosis (pH < 7.35)

137
Q

Diuretic treatment in HF patients

A

Diuretic-naive patients: IV furosemide or bumetanide
Patients already taking diuretics: 1-2 times the patient’s usual dose

138
Q

Countinued assesment of diuretic treatment in HF patients

A

If urinary output is < 100 mL/hour : Consider doubling the dose.
If urinary output is > 100-150 mL/hour
- If congestion then continue dose
- If no congestion then lower dose

139
Q

Options for refractory congestion despite high doses loop diuretics:

A

Combination therapy with a thiazide diuretic
Addition of a vasodilator
Low-dose dopamine infusion

140
Q

Indication of vasodilator therapy in acute heart failure

A

Acute heart failure caused by hypertensive emergency
Flash pulmonary edema
Adjuvant to diuretics for symptomatic relief of dyspnea

141
Q

Vasodilator therapy in acute heart failure

A

IV nitroglycerin
e Sodium nitroprusside

142
Q

when not to give vasodiulators in acute HF

A

Avoid the use of vasodilators in patients with acute heart failure and hypotension.

143
Q

Mechanical circulatory support indicated in reversible refractory acute heart failure?

A

ECMO is the most widely used form of mechanical support in AHF
Intra-aortic balloon pump and left ventricular assist device may be useful in certain etiologies like mitral regurgitation.

144
Q

Chronic compensated CHF definition

A

a clinically compensated type of CHF in which the patient has signs of CHF on echocardiography but is asymptomatic or symptomatic and stable.

145
Q

what is the pathyphysiology of compensated chronic heart failure

A
  1. Increased adrenergic activity : increase HR, BP, and contractility
  2. Increase of RAAS: activated following decrease in renal perfusion secondary to reduction of and CO
  3. Secretion of BNP
146
Q

mechanismo of aldosteron

A

Aldosterone secretion incrtease renal Na and H2O resorption > increased preload

147
Q

Mechanism of BNP secretion in HF

A

ventricular myocyte hormone released in response to increased ventricular filling and stretching casuing increased intracellular smooth muscle cGMP —> vasodilation, hypotension and decreased PCWP

148
Q

General features of Chronic herart failure

A

Nocturia
Fatigue
Tachycardia, various arrhythmias
S3/S4 gallop on auscultation
Pulsus alternans
Cachexia

149
Q

Kussmaul sign

A

increased JVP on inspiration and failure of decreased JVP on expiration seen in Right sidedn HF

150
Q

Classification of heart failure

A

NYHA
Class 1: Nosymptoms of CHF
Class 2: Slight limitations of moderate or prolonged physical activity
Class 3: Marked limitations of physical activity
Class 4: Symptoms at rest

151
Q

Medical treatment in chronic heart failure

A

Based on the stage of HF +
Diuretics - in volume overload
ACEI - to reduce preload, afterload and improve CO
BB - added once stable on ACEI, good in HT
Aldosteron antagonists - in EF < 35%
Ivabnradin - decrease HR, if no responce to BB, EF < 35%
Hydralazine - if EF < 40%
Digoxin - in HFrEF and symptomes despite BB, ACEI, diuretic and MRA
ARB - persistans symptomes despite first lione drugs
Nesiritide (BNP derivative) - in Acute decompensated HF

152
Q

Drugs improving prognosis of HF

A

BB, ACEi, and MRA

153
Q

Drugs that improve symptoms of HF

A

Diuretics and digoxin
(significantly reduce the number of hospitalizations)

154
Q

Contraindicated drugs in HF

A

NSAIDs: Worsen renal perfusion, Reduce the effect of diuretics, May trigger acute cardiacb decompensation

CCB (verapamil and diltiazem): Negative inotropic effect, Worsen symptoms and prognosis

Antidepressants (citalopram): causes a dose-dependent QT prolongation

155
Q

Non pharma treatment of HF

A
  • Salt restriction (< 3 g/day) in symptomatic patients
  • Fluid restriction in patients with edema and/or hyponatremia
  • Weight loss and exercise
  • Cessation of smoking and alcohol consumption
  • Immunization: pneumococcal an influenza vaccine
  • Patient education in self-monitoring and symptom recognition
  • Daily weight: gain > 2 kg within 3 days requires consultation
156
Q

invasive treatment of HF

A

Implantable cardiac defibrillator (ICD)
Cardiac resynchronization therapy
Coronary revascularization
Valvular surgery
ECMO
Cardiac transplantation

157
Q

Indication of pacemaker in chronic heart failure

A

Heart failure ‘NYHA class II-IV with EF < 35%
Dilated cardiomyopathy
LBBB with QRS > 150 ms
Can be combined with an ICD

158
Q

Types of bradychardia

A

Respiratory sinus arrhythmia
Sinus bradycardia
Sinus pause or arrest
Tachycardia-bradycardia syndrome
AV blocks

159
Q

Define sinus bradychardia

A

Physiological (athletes)
Sinus node dysfunction (e.g, sick sinus
syndrome}, hypothyroidism,
hypothermia,
Drugs: BB, CCB

160
Q

Define Sinus pause or arrest

A

May occur in healthy individuals
Underlying cardiovascular disease (e.g,
sick sinus syndrome}

161
Q

Define achycardia-bradycardia syndrome

A

Abnormal supraventricular impulse
generation and conduction like in sick sinus syndrome

162
Q

Sick sinus syndrom

A

Degeneration and fibrosis of the SA node and surrounding myocardium (most common cause)
Medication (BB, digoxin, non-dihydropyridine CCB such as verapamil)

163
Q

Symptomes of bradychardia

A

Dizziness, Syncope
Lack of increasing heart rate during physical activity
Adams-Stokes attacks (A sudden loss of consciousness)

164
Q

ECG of SSS

A

Non-respiratory sinus arrhythmia
Bradycardia
Sinus arrest
Sinoatrial pauses
SA block

165
Q

Treatment of SSS

A

Initial therapy for hemodynamically unstable patients
1. First-line: atropine
2. Temporary cardiac pacing
Long-term therapy: lsolated symptoms of bradycardia: pacemaker

166
Q

What is Vagal tone

A

Associated slowing of heart rate and decreased atrioventricular node electrical conduction.

167
Q

two classifications of Atrioventricular block (Heart block)

A

Physiological: when decreased vagal tone
Pathologial

168
Q

Pathophysiology of AV block

A

Idiopathic fibrosis of the conduction system
Ischemic heart disease
Cardiomyopathy (e.g., due to amyloidosis or sarcoidosis)
Infections
Hyperkalemia (> 6.3 mEq/L)

169
Q

Drugs causing AV block

A

BB, CCB, digitalis

170
Q

First-degree AV block

A

PR interval > 200 ms
No interruption in atrial to ventricular conduction
Rate of SA node = heart rate

171
Q

1st degree AV block treatment

A

No treatment, but pacemaker if QRS is wide, if conduction time
from the bundle of His to the ventricles is > 100 ms.

172
Q

2nd degree AV block types of

A

Mobitz I
Mobitz II

173
Q

Mobitz type I/Wenckebach

A

Progressive lengthening of the PR interval until a beat is dropped; regular atrial impulse does not reach the ventricles (a normal P wave is not followed by a QRS-complex)

174
Q

2nd degree AV blocks treatment

A

Monitoring with transcutaneous pacing pads
If asymptomatic, find underlying cause
If symptoms not reversible ~ permanent pacemaker
Hemodynamically unstable give atropine

175
Q

Mobitz type II

A

Single non-conducted P waves without QRS complexes
The PR interval remains constant.
RR interval = x2
Follows regular patterns: 2:1 3:1 3:2 block

176
Q

symptoms of AV blocks

A

Bradycardia > decreased cardiac output
o Fatigue
o Dyspnea
o Chest pain
© Dizziness, syncope

177
Q

Third-degree AV block (complete heart block)

A

Third-degree AV block is a complete block with no conduction between the atria and ventricles.
AV dissociation: on ECG, P waves and QRS complexes have their own regular rhythm but bear no relationship
Aventricular escape mechanism is generated by sites that are usually located near the AV node or near the bundle of His.

178
Q

what happens when theres is a sudden onset of 3rd AV Block

A

Sudden onset of a third-degree AV block results in asystole, which lasts until the ventricular escape mechanism takes over. This asystole may lead to Stokes-Adams attacks.

179
Q

symptoms of 3rd degree AV block

A

Depends on Rate of ventricular escape mechanism and Length of asystole

180
Q

Supraventricular tachycardias

A

Atrial Fibrillation (AF)
Atrial Flutter
Atrioventricular Nodal Reentrant Tachycardia (AVNRT)
Atrioventricular Reentrant Tachycardia (AVRT)
Wolff-Parkinson-White Syndrome (WPW)
Atrial Tachycardia (focal or multifocal)

181
Q

Atrial flutter

A

Regular rhythm
Rate: atrial 250-350: ventricular < 200
P waves: Occur before every QRS complex,
Sawtooth appearance of regular P waves
Narrow QRS complex

182
Q

Atrial fibrillation

A

Rhythm: irregularly irregular
Rate: Atrial: 350-450 bpm: ventricular < 200
No P-waves
Narrow QRS complex

183
Q

Focal atrial tachycardia

A

Very abrupt onset, Regular rhythm
Rate: 150-250
P wave: morphology depends on the site of
the ectopic focus (same morphology)
Occurs before the QRS complex
Narrow QRS complex

184
Q

Multifocal atrial tachycardia (MAT)

A

Very abrupt onset with rate variation
Rhythm: irregularly irregular
Rate: 150-250
P waves with different morphologies; no single morphology
Narrow QRS complex

185
Q

Atrioventricular reentry tachycardia (AVRT)

A

Very abrupt onset, Regular rhythm
Rate: 150-250
P wave
- Inverted (downgoing in II, Ill and aVF and/or upright in aVR)
- Occur after the QRS complex
- RP interval is shorter than PR interval
ORS complex:
- Orthodromic AVRT: narrow QRS complex
- Antidromic AVRT: wide QRS complex with delta waves

186
Q

AV nodal reentry tachycardia

A

Regular rhythm
Rate: 150-250
P waves occur during (are not visible) or after the QRS complex
RP interval is shorter than PR interval
Narrow QRS complex

187
Q

AVNRT etiology

A

AVNRT: tachycardia caused by a dysfunctional AV node that contains two electrical pathways

188
Q

AVRT etiology

A

AVRT: tachycardia caused by an accessory pathway between the atria and ventricles

189
Q

Atrioventricular tachycardia (AVT)

A

Atrial tachycardia (AT): The atria respond to impulses from an atrial pacemaker outside of the SA node.
A common cause of AT includes digoxin poisoning which typically presents with concomitant AV block.

190
Q

WPW in AVRT

A

Wolff-Parkinson-White syndrome (WPW): A congenital condition characterized by intermittent tachycardias and signs of ventricular pre-excitation on ECG, which both arise from an accessory pathway known as the “Bundle of Kent”

The bundle of Kent connects the atria and ventricles, bypassing the AV node and leading to a pre-excitation of the ventricles.

191
Q

acute treatment if PSVT

A
  1. Cardioversion: fastest and most effective treatment
  2. Carotid sinus massage and valsava maneuver
  3. Medical therapy IV adenosine: briefly blocks the AV node
192
Q

Long term treatment if PSVT

A

Catheter radiofrequency ablation
Medical therapy as second line

193
Q

The general principles of treating atrial fibrillation include:

A
  1. Correcting reversible causes and/or treatable conditions
  2. Controlling heart rate and/or rhythm
  3. Providing anticoagulation
194
Q

treatment of unstable afib

A

emergent electrical cardioversion

195
Q

Rate control in afib

A

1st line: BB: metoprolol, propranolol esmolol
2nd line: digoxin
3rd: Amiodorane

196
Q

rythm control in afib

A

1st choice: elective electrical cardioversion
2nd choice: pharmacologic cardioversion with
antiarrhythmic drugs such as propafenone

197
Q

risk assessment in afib

A

CHA2DS2-VASc score

198
Q

anticoagulation in afib when

A

High thromboembolic risk: start anticoagulation immediately before or after cardioversion

Low thromboembolic risk: consider anticoagulation directly before or after cardioversion

IV heparin or LMWH immediately before cardioversion
followed by warfarin for up to 4 weeks after

199
Q

Cardioversion define

A

The restoration of normal heart rhythm in patients with tachycardia or arrhythmia using electric current
(electric cardioversion) or drugs (chemical cardioversion).

200
Q

types of cardioversion

A

Synchronized
Pharmacological

201
Q

Define synchronized cardioversion

A

Synchronized electrical cardioversion is the process by which an abnormally fast heart rate or cardiac
arrhythmia is terminated by the delivery of a therapeutic dose of electrical current to the heart at a specific
moment in the cardiac cycle.

202
Q

Define pharmacological cardioversion

A

Pharmacologic cardioversion uses medication instead of an electrical shock to convert the cardiac
arrhythmia.

203
Q

placement of pads in synchronized cardioversion

A

Place one anteriorly just left to the sternum and one posteriorly
to the left of midline.

204
Q

optimal moment in the cardiac cycle for synchronized cardioversion

A

the R wave of the QRS complex on the ECG.

205
Q

why is it important to time a synchronized cardioversion

A

Timing the shock to the R wave prevents the delivery of the shock during the vulnerable period
(or relative refractory period) of the cardiac cycle, which could induce ventricular fibrillation.

206
Q

when to use synchronized cardioversion

A

SVT, including atrial fibrillation and atrial flutter. It is also used in the emergent treatment of wide complex tachycardias, including ventricular tachycardia, when a pulse is present.

207
Q

when do you use unsynchronized cardioversion

A

Pulseless ventricular tachycardia and ventricular fibrillation are treated with unsynchronized shocks referred to as defibrillation.

208
Q

when not to give electrical shock

A

Electrical therapy is inappropriate for sinus tachycardia, which
should always be a part of the differential diagnosis.

209
Q

before a cardioversion

A

Nothing by mouth: for at least 6 hours
Thyroid function: treat thyrotoxicosis or myxedema first, if the patient is stable.
IV access
Sedation: short general anesthesia (propofol)
Cardioversion: check that no one is in contact with the patient

210
Q

cardioversion in intracardiac devices

A

Pacemakers/AICDs: Position the paddles away from the generator and not in the same
vector as the device.

211
Q

complications of cardioversion

A

Asystole/bradycardia
Ventricular fibrillation
Thromboembolism
Transient hypotension
Skin burns
Aspiration pneumonitis

212
Q

Pharmacologic cardioversion

A

If the patient is stable, Adenosine may be administered first, as the medicine performs a sort of “chemical cardioversion” and may stabilize the heart and let it resume normal function on its own without using electricity.

213
Q

classification of antiarrhythmic drugs

A

Class | - Na-channel blockers — Quinidine, lidocaine
Class Il - BBs
Class Ill - Block outward K-channels — Amiodarone, sotalol
Class IV - CCBs which inhibit AP in AV and SA node

214
Q

Catheter ablation

A

Ablation is the removal of tissue.
Destruction of small areas of cardiac tissue by means of electrical energy delivered through an intracardiac catheter.

215
Q

how is catheter ablation done

A

Cells are destroyed by heating > 50 degrees C.
The radiofrequency (RF) generator delivers an alternating current of 500-750 KHz

216
Q

heating in catheter ablation

A

<50 degrees = transient loss of function
>50 degrees = permanent damage
> 80 degrees = coagulation (thromboembolism!)

217
Q

types of catheter ablation

A

Radiofrequency (RF) energy:
Cryoablation

218
Q

Cryo-catheter ablation

A

Liquid nitrous oxide is released into the tip and removes heat
Tissue temperature falls to -30 degrees C, at which stage there is reversible loss of cell function.

The tissue can be further cooled to -60 degrees for 4 minutes to cause permanent destruction.

219
Q

CRT - Cardiac resynchronization therapy

A

CRT devices pace both the left and right ventricles simultaneously to resynchronize the muscle contraction and improve the efficiency (restore EF) of the weakened heart. Can restore function in e.g. dilative cardiomyopathy. Improves cardiac output and symptoms

220
Q

pacemaker letters

A

First letter is pacing location
Second letter is sensing location
Third letter is respons (inhibit, trigger, both)
Fourth letter is added features

221
Q

implantation of pacemaker

A

Most are implanted transvenously using cephalic or subclavian
The ventricular lead is most commonly placed in the RV apex, RV outflow tract or on the septum.
The atrial lead is placed in the right atrial appendage ideally, but anywhere is acceptable.
Pulse generator is placed subcutaneous

222
Q

Definit indications for pacemaker

A
  1. Symptomatic 3rd degree heart block
  2. Symptomatic advanced 2nd degree heart block
  3. BBB.
  4. After STEMI in the presence of high degree AV block
  5. Symptomatic sinus node dysfunction
  6. Symptomatic chronotropic incompetence.
  7. Conditions requiring drugs that result in symptomatic bradycardia.
223
Q

which type of pacemaker should be used

A

Afib: VVI(R)

224
Q

Define supraventricular tachycardias

A

Supraventricular tachycardias (SVTs) are a group of tachyarrhythmias arising from abnormalities in pacemaker activity and/or conduction involving myocytes of the atria and/or AV node.

A tachycardia originating in the following:
Sinus node
AV node
Atrial myocardium
Bundle of His above the bifurcation

225
Q

AVRT reentry tachycardia typed and their bundle

A

WPW: Kent bundle
LGL: James bundle

226
Q

medical therapy in AVRT

A

Amiodarone

227
Q

medical therapy AVNRT

A

Verapamil, BB

228
Q

Respiratory sinus bradycardia

A

bradycardia on expiration, it is physiological

229
Q

Tachycardia-bradycardia syndrome presents with additional symptoms:

A

Palpitations
Dyspnea
Angina pectoris

230
Q

what are temporary cardiac pacing

A

Involves electrical cardiac stimulation to treat a bradyarrhythmia or tachyarrhythmia until it resolves or until long-term therapy can be initiated.
Patients with temporary pacemakers are hospitalized and continuously monitored.

231
Q

which infection can give a AV block

A

Lyme disease

232
Q

how to treat a hemodynamic stable AV block patient?

A

monitor transcutaneous pacing pads, or pacemaker

233
Q

Hemodynamically unstable

A

Atropine
Temporary cardiac pacing (if not responsive to atropine)

234
Q

When does the patient need a heart transplant

A

Patients with end-stage CHF (NYHA class IV), EF < 20%, and no other viable treatment options

235
Q

when is a ICD used as prophylaxis?

A

Patients with ischemic heart disease and EF < 30%
Heart failure NYHA class IIEIV with EF < 35%

236
Q

Secondary prophylaxis indications for an ICD device

A

History of sudden cardiac arrest
Ventricular flutter or ventricular fibrillation

237
Q

Cardiotoxic drugs

A

Anthracylines:
Doxorucibin
Traztuzumab

238
Q

First line drugs used in heart failure

A

BB
Diuretics
ACEI
(aldosteron inhibitor)

239
Q

pathophys of afib

A

Volume overload, hemodynamic stress > atrial hypertrophy and dilatation
Atrial ischemia
Inflammation of the atrial myocardium atal wyocovay
Altered ion conduction by the atrial myocardium

240
Q

what happens in the heart during afib

A

The atria contract rapidly but ineffectively and in an uncoordinated fashion — stasis of
blood within the atria > risk of thromboembolism and stroke

Irregular activation of the ventricles by conduction through the AV node — tachycardia

241
Q

ECG afib

A

Irregularly irregular RR intervals
No P-waves
Tachycardia
‘Narrow QRS complex (< 0.12 seconds)

242
Q

treatment of unstable afib

A

emergent electrical cardioversion

243
Q

afib cardioversion type?

A

1st choice: elective electrical cardioversion
2na choice: pharmacologic cardioversion with
antiarrhythmic drugs such as flecainide, propafenone,

244
Q

drugs used i ryth control of afib

A

BB
CCB
digoxin
amiodoran

245
Q

pharmacological cardioversion

A

first give amiodarone to slow down heart ryth
then give adenosin as the cardioversion drug

246
Q

ventricular arrhythmia etiology

A

Idiopathic
Cardiovascular disease (CAD, myocarditis)
Electrolyte imbalances (e.g., hypokalemia, hypomagnesemia)
Side effect of certain drugs (digoxin, psychiatric medications)
Caffeine, alcohol

247
Q

ventricular arrhythmias

A

premature ventricular beats
ventricular tachy
torsades de point
Vfib

248
Q

weight of the heart

A

approx. 300-500 g

249
Q

vertebra behind the heart

A

T5-T8

250
Q

posteriormorst part of the heart

A

The left atrium is the posteriormost part of the heart, located directly in front of the esophagus. It can
be visualized using TEE.

251
Q

anterior most part of the heart

A

The right ventricle is the anteriormost part of the heart and is at greatest risk of injury following chest
trauma.

252
Q

Common site for the development of thrombi in patients with atrial fibrillation

A

Right auricle
Left auricle (left atrial appendage)

253
Q

what is the cardiac skeleton

A

e Consists of four fibrous rings (annuli fibrosi cordis) that surround the atrioventricular and arterial
orifices

254
Q

the pappilary muscles

A

(two in the left ventricle; three in the right ventricle)
Derive from the myocardium
Extend from the ventricular walls and the septum
Contract during systole and thereby tighten the chordae tendineae: prevent prolapse of valve leaflets and regurgitation

255
Q

what are the chorda tendinae

A

fibrous cords that support the AV valves and connect them to the papillary muscles

256
Q

Subvalvular apparatus

A

chorda and pappilary muscles

257
Q

does the semilunar valves have subvalvular apparatur?

A

three crescent-shaped cusps without subvalvular apparatus

258
Q

Coronary arterial dominance

A

Right-dominant (85% of the pop): PDA supplied by the RCA
Left-dominant (~ 8% of the pop): PDA supplied by the LCX
e Codominant (balanced; ~ 7% of people): PDA supplied by both RCA and LCX

259
Q

what supplies the conduction system of the heart?

A

The RCA supply the sinus and AV node so that stenosis or
occlusion of this vessel often leads to cardiac arrhythmias!

260
Q

wher does the coronary sinus drain?

A

Drains into the right atrium between the IVC orifice and the right atrioventricular orifice

261
Q

where is the AV node

A

in the Koch triangle

262
Q

conduction branches after the bundle of his`

A

2 Tawara branches

263
Q

Cardiac stress test

A

Stress is applied to the heart either by physical exercise or with pharmacological agents

264
Q

pharma agents in cardio stess test

A

Dobutamine, adenosine

Dobutamine is indicated: COPD/asthma, high grade AV block

Adenosine is indicated: unable to exercise, LBBB, and post MI.

265
Q

imaging modalities in cardiac stress test

A

CG, Echo, and SPECT perfusion imaging.

266
Q

indication of coronary stress test

A

Diagnosis of CAD
Post MI patients treated with thrombolytics (pre-discharge)
Pre- and post-revascularization
Evaluation of arrhythmias; optimizing pacemaker
Preoperative evaluation of selective patients
Cardiopulmonary stress testing to evaluate CHF for transplant.
Evaluate valvular lesions in asymptomatic patients

267
Q

CI of cardiac stress test

A

Fever
Pericarditis or myocarditis
Severe aortic stenosis with symptoms
Aortic dissection
Severe uncontrolled HTN
Decompensated HF, unstable angina or acute phase MI

268
Q

what ECG signs do we look for on a cardio stress test?

A

Max ST increase or decrease
ST-slope
Leads showing ST changes: time of onset, duration of ST deviation into recovery

269
Q

what is a positive cardio stress test

A

Positive stress test is manifested by 2mm ST depression or a decrease in BP (which normally should go up)

270
Q

timing of echo measurements in cardiac stress test?
What do you mesure?

A

Incase of exercise: rest + immediately post-stress.
Incase of dobutamine: rest + low-dose + peak-dose + post administration

you look at wall motion and LVEF
Wall motion index above 2 high = risk for further cardiac events.

271
Q

SPECT perfusion imaging stress test

A

Used to diagnose coronary disease by evaluating perfusion.
Involves administration of radiolabeled perfusion tracers at rest, and during stress.
The radiolabeled perfusion tracer emits gamma photons detected by a gamma camera
Myocardial tracer uptake is proportional to blood flow
Radiolabeled: Thallium — taken up like K* into myocytes.

272
Q

what does Unfractionated
heparin (UFH) do? Antidote

A

activation of anti-thrombin III - decrease thrombin and factor X
Protamine

273
Q

what does LMWH (Enoxaparin) do?
Antidote?
CI?

A

Acts on factor Xa predominantly
Protamine sulfate
Cl: renal insufficiency

274
Q

what does fondaparinux do?
Antidote?

A

Factor X inhibitor
NOT reversible

275
Q

Direct antithrombin inhibitors?
antidote?

A

Dabgatran
AD: Idarusizumab

276
Q

Direct factor X inhibitors
Antidote:

A

Apixaban
Rivaroxaban
AD: Andexanet

277
Q

Antiplatelet drugs?

A

Aspirine
Clopidogrel
Abciximab

278
Q

thrombolytic agents

A

streptokinase
reteplase
Alteplase

279
Q

PE etiology

A

Deep vein thrombosis (most common cause)
Fat embolism
Air embolism
Amniotic fluid embolism
Others: bacterial embolism, pulmonary tumor embolism

280
Q

DD i pulmonary embolism

A

D-dimer levels Normal levels: < 500 ng/mL
If = 500 ng/mL: Further testing is required
If the patient is > 50 years of age, adjust for age: age x 10 ng/mL = cut off value in ng/mL
High sensitivity, Low specificity

281
Q

TX PE

A

Massive PE: thrombolytic therapy or thrombectomy (last resort)
Submassive and nonmassive PE: anticoagulation or IVC filter

282
Q

Localization of aortic dissection

A

Ascending aorta: ~ 65% of cases
Descending aorta, distal to the left subclavian artery: 20%
Aortic arch: 10% of cases
Abdominal aorta: 5% of cases

283
Q

An aortic dissection is..

A

is a tear in the inner layer of the aorta that leads to a progressively growing hematoma in the intima-media space.

284
Q

acquired causes of aortic dissectionn

A

HTN
Trauma
Vasculitis
Pregnancy

285
Q
A

6th year subjects (10 decks)

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