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Clin Med I - Comprehensive > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What coronary artery supplies what part of heart?

A
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2
Q

What are the three categories of criteria for Duke’s?

A

Pathological

Major Clinical

Minor Clinical

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3
Q

If _________of the pathological criteria are met, diagnosis is definite.

A

EITHER

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4
Q

What are the two pathological criteria?

A
  1. Microorganisms in a vegetation - culture or histological exam of a vegetation or intracardiac abscess specimen
  2. Pathologic Lesions - Vegetation or intracardiac abscess confirmed by histologic exam showing active endocarditis.
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5
Q

What are the two major clinical criteria?

A
  1. blood cultures positive for endocarditis - microorganisms consistent with IE from 2 separate cultures; single positive culture for Coxiella burnetti or antiphase IgG ab titer >1:800.
  2. Evidence of endoardial involvement - echo positive for IE, abscess, new valvular regurgitation, dehiscence of a prosthetic valve
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6
Q

How many of the major clinical criteria do you need to make a diagnosis definite?

A

BOTH

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7
Q

How many of the minor clinical criteria alone do you need to make the diagnosis definite?

A

​All 5

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8
Q

What are the 5 minor clinical criteria?

A
  1. predisposing heart condition or IV drug user
  2. Fever
  3. Vascular phenomenon -major arterial emboli; septic pulmonary infarcts; mycotic aneurysm; intracranial hemorrhage; conjunctival hemorrhages; Janeway’s lesions
  4. Immunologic Phenomena - glomurelonephritis, Osler’s nodes, Roth’s spots and rheumatoid factor.
  5. Micro evidence - positive blood culture that does not meet a major criterion or serological evidence of active infection with an organism consistent with IE.
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9
Q

If you have one major criteria and one or two minor criteria, the diagnosis is __________?

A

Possible

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10
Q

If you have one major criteria and three minor criteria, the diagnosis is ___________?

A

Definite

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11
Q

What procedure should you do if Possible?

A

A TEE to see if you can make it definite

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12
Q

IF you have three minor criteria, the diagnosis is ___________?

A

Possible

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13
Q

What are Janeway lesions?

A

They are small, bruise-like spots on the palms of the hands and soles of the feet.

Osler’s nodes are similar but they are tender

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14
Q

How much fluid is in the pericardium?

A

20-30 ml

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15
Q

What is cardiac tamponade and how do you treat it?

A

When blood escapes from the heart due to injury, fills up the pericardium, thereby restricting the heart.

Pericardiocentsis: insert a needle in the left infrasternal angle toward the left shoulder in order to avoid puncturing the left lung, and remove excess pericardial fluid.

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16
Q

What is the difference between a right dominant

and left dominant heart?

A

Right dominant (90%) the posterior descending artery PDA comes from the right coronary artery

Left dominant (10%) the posterior descending artery PDA comes from the circumflex branch of the left coronary artery

NOTE: the PDA runs along the atrioventricular groove

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17
Q

What are the five great vessels of the heart?

A

Superior and Inferior Vena Cava

Pulmonary Artery and Vein

Aorta

(Note: from the aorta come the brachiocephalic, common carotid and subclavian arteries)

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18
Q

What part of the cardiac cycle fills the coronary arteries?

A

Diastole

(During systole the huge flow of blood compresses the intramyocardial branches so that blood cannot get through to the coronary arteries.)

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19
Q

What parts of the heart

do the left and right coronary arteries supply?

A

It can vary a bit from person to person, but…

Right coronary artery supplies the right atrium and most of the right ventricle, with some of the left atrium and ventricle.

Left coronary artery supplies all else, and notably the interventricular septum.

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20
Q

What are the two branches of the left coronary artery?

A

Left Anterior Descending LAD

Circumflex Branch

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21
Q

What is considered normal Ejection Fraction?

A

> 55%

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22
Q

How does a cardiac CT work?

A

It is like a big 3D xray.

They use Gallium via IV for contrast, Metoprolol to decreases heart rate to decrease blurriness of image, dilate blood vessels to see better, and patient must hold breath for 10 seconds.

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23
Q

What is a new development re Cardiac CT?

A

Prospective ECG Triggering: the CT is synched to your heartbeat so it only takes an image at diastole and this also minimizes the amount of radiation exposure.

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24
Q

What are indications for Cardiac CT?

A
  • Noninvasive anatomic assessment of CAD
  • Evaluation of structure of heart
  • Risk stratification using coronary calcium scoring
  • Rapid evaluation re acute chest pain
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25
Q

What are the pros of Cardiac CT?

A

Very fast!

Newer developments have decreased radiation, amount of contrast needed, and enable 3-D rendering.

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26
Q

What are the cons or contraindications of Cardiac CT?

A

Radiation exposure

Patient must have BMI under 35

Patient must have GFR >30 and if 30-45 must evaluate risk/benefit ratio

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27
Q

How does cardiac catheterization work

A

They thread a catheter through an artery in your leg or arm, through aorta and into the coronary arteries to take a look.

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28
Q

What are the indications of cardiac catheterization?

A

Gold standard re Dx of CAD

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29
Q

What are the cons of cardiac catheterization?

A

1/2000 risk of

death, MI, stroke or procedural complications

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30
Q

How does a cardiac MRI work?

A

It uses magnets to line up the spinning, angular momentum of protons and uses “math” to translate this into images.

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31
Q

What are the indications for Cardiac MRI?

A

Assess:

  • Myocardial viability
  • Cardiomyopathy
  • Inflammation/myocarditis
  • Congenital Heart Disease such as septal defects
  • Cardiac Tumors
  • Pericardium
  • Great Vessels
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32
Q

What are Cons/Contraindications of Cardiac MRI?

A

Can cause nephrogenic systemic fibrosis if pt has moderate to mild kidney disease

Danger re metal objects, such as shrapnel in tissues or wheelchair in room.

(Orthopedic implants, stents and valves are usually safe though)

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33
Q

Who are prime candidates for noninvasive cardiac imaging?

A

Those patients in the middle in terms of pretest probability.

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34
Q

What are the Cons/Contraindications of ECHO

A

Not sensitive to small blockages

Need a trained technician

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35
Q

What do you know if your patient has a negative ETT and a negative SPECT?

A

Paitne has a 4-5 year “warranty” in the absense of new Sx

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36
Q

How many heart attack patients had LDL levels at NCEP goal?

A

75%

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37
Q

What are the chances a 40 yo will get CAD?

A

1 in 3 women

1 in 2 men

(1 in 8 women will get breast cancer)

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38
Q

What is the most dangerous part of coronary artery disease/atherosclerosis?

A

If it ruptures and creates a thrombus

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39
Q

What are the two types of vulnerable plaques?

A

Erosion prone

Critically Stenotic

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40
Q

What is Chronic Stable Angina?

A

Stable plaque causing ischemia due to an imbalance of supply and demand

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41
Q

Which population is especially at risk for Stable Angina?

A

Incidence in age groups 45-65 is far higher in African American women.

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42
Q

What re the Sx of Stable Angina?

A
  1. Substernal or left chest pain/tightness/pressure/burning, lasting less than 3 minutes (sometimes up to 15)
  2. That increases with physical activity, stress and/or a big meal, and
  3. Decreases with rest, Nitro.

Typical Angina has all three

Atypical has 2 of 3

Asymptomatic has 1 of 3

NOTE: rarely will a patient refer to angina as “pain”

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43
Q

PE findings in Stable Angina

A
  • Levine Sign (clenched fist to chest)
  • PMI shifted to left
  • Apical systolic murmur at mitral valve
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44
Q

Risk Factors/Hx re Stable Angina

A

Hyperlipidemia

Diabetes

Smoking

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45
Q

How do you diagnos Stable Angina?

A

Hx + Risk Factors + EKG

Then Exercise Tolerance Test for

  • Every patient with “typical” angina
  • Men >40, women >50 60 with atypical
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46
Q

What are the four classifications of Stable Angina?

A

Class 0: Asymptomatic

■ Class 1: Angina with strenuous exercise

■ Class 2: Angina with moderate exertion

■ Class 3: Angina with mild exertion

■ Class 4: Angina at any level of physical exertion

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47
Q

Stable Angina Rx

A

Acute/Active: a dose of Nitro

(.3,.4, .5 mg sublingual tablet or .4 mg buccal spray)

every 3-5 minutes up to 3 doses.

If no releif after 5 minutes call 911

Chronic: Long term Nitroglycerin (patch),

Calcium Channel Blockers or Beta Blockers

NOTE: Nitro can go through the skin so only the patient should handle it and should be seated. Blood pressure can drop suddenly.

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48
Q

What are predictors of the severity of Angina?

A
  • # diseased vessels
  • severity and location of obstruction (LAD is bad)
  • Left Ventricular funtion
  • Hx of arrhythmia
  • Accelerating Angina (more frequent, more severe)
  • Duke Treadmill Score
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49
Q

Secondary prevention of Stable Angina?

A
  • Risk Modification (lower cholesterol and HTN, stop smoking, take statins, wt loss, exercise/cardiac rehab)
  • Long acting nitrates
  • Beta Blockers
  • Calcium Channel Blockers
  • Ranolazine
  • Aspirin or clopidogrel (post PCI, post MI)
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50
Q

What patient education is needed about Stable Angina?

A
  • Give prognosis and explain
  • Lifestyle modifications
  • Information about all meds
  • Instructions on Nitro usage
  • Importance of secondary prevention
  • CPR for family members
  • Resources: online or hard copy
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51
Q

What is follow up for a patient with Stable Angina?

A

Every 4-6 months 1st year, then annually.

EKG when change in Sx severity/frequency.

ETT every 1-3 years depending on risk category and/or change in Sx.

Inquire about:

  1. Changes in physical activity
  2. Changes in frequency/severity of angina
  3. Adverse effects of Tx
  4. Adherence to meds and lifestyle changes
  5. Knowledge about CAD
  6. Changes in comorbidities
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52
Q

The coronary arteries can compenstate for atherosclerosis until they are ___% occluded

A

75%

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53
Q

What is the sequence of atherosclerosis?

A

○ Fatty streak formation

○ Leukocyte recruitment

○ Macrophages → Foam cells

○ Development of lipid rich core

○ Accumulation of smooth muscle cells

○ Large atheroma with fibrous surface cap

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54
Q

What is the progression of atherosclerosis?

A

Chronic: slowly encroaches on lumen

Acute: suddenly encroaches on lumen due to plaque destabilization and clot formation.

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55
Q

What are the Coronary Artery Risk Factors?

Which are modifiable?

A

Major Risk Factors: Advanced age, Family history of CAD , Male gender, Hypertension Lipid abnormality, Diabetes mellitus, Cigarette smoking

Other Risk Factors: Physical inactivity, Abdominal obesity, Emotional stress, Low intake of fruits and vegetables , Excessive alcohol intake

Modifiable in italics.

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56
Q

What is the difference between

Ischemia, Injury and Infarction?

A

Ischemia: Insufficient blood flow, cytokine release (“pain”), tissue can survive

Injury: occurs with sustained ischemia, release of initial cardiac biomarkers,

Infarction: irreversible cell death and necrosis, decrease in cardiac funtion, release of later biomarkers

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57
Q

What are the EKG findings for

Ischemia, Injury and Infarction?

A

Ischemia: ST depression +/- T wave inversion

Injury: ST elevation +/- hyperacute T waves,

T wave inversions, new LBBB

Infarction: ST elevation +/- pathologic Q waves

(2.5 deep, 2 wide in 2 contiguous leads)

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58
Q

Who automatically gets and EKG?

A

Every patient with a Hx of chest pain

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59
Q

What are EKG indictions of current infarction or increased risk of infarction?

A

○ Evidence of ischemia, injury, or infarction

○ LV Hypertrophy → hypertension → increased risk for infarction

○ Atrial fibrillation → previous infarct vs. increased risk of infarction

○ Bundle Branch Blocks → if new LBBB, increased risk of infarction, masked ischemia, injury, and infarct

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60
Q

What can an ambulatory EKG/Holter Monitor tell you?

A

Paroxysmal dysrhythmias (SVT, Afib)

Periods of Ischemia (in conjuntion with angina journal, detecting silent ischemia) (NOT ideal for this)

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61
Q

What is the Duke Treadmill Score?

A

Assessment based on Bruce Protocol time in minutes, amount of ST depression on EKG, and degree of angina. Used for insurance purposes.

Low Risk > or = +5

High risk: < or = -11

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62
Q

What are the cons of a Nuclear Study (Myocardial Perfusion Scan)?

A

Takes 4 hours

Expensive so not all centers have it

Hard to read so inter-reader variability

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63
Q

What are the indications and risks of

Coronary Angiography?

A

Definitive Dx of CAD but…

Contraindictions: invasive, contrast media allergy/anaphylaxis, kidney damage

Thus: indicated ONLY if PTCA/stenting or CABG is a consideration

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64
Q

Which cardiac biomarkers appear first and how long do they last?

A

Myoglobin rises first and peaks at 5 hours

Creatine Kinase rises second and peaks at about 15 hours

Troponin rises slowly until about 15 hours, then shoots up and peaks at about 25 hours and declines slowly.

Note: these enzymes are not specific to MI, but WITH chest pain, they are!

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65
Q

What is Percutaneous Coronary Intervention PCI?

A

Stenting and angioplasty

to reduce Sx (Recently disproven by a double blind study with 200 pts)

NO improvement in lifespan

Metal stents can cause clots or inflammatory response

Drug Alluding Stents have endothelial cells growing on them so they are hidden from the immune system

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66
Q

What is Coronary Artery Bypass Grafting CABG?

A

Internal mammary or saphenous vein used to bypass occluded coronary arteries. Only done if multiple vessel disease.

Mortality: 1-8% depending on health of pt

Will add years to life

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67
Q

What are complications of PCI?

A

Intimal dissection

Stent thrombosis

MI (esp if not on anticoag)

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68
Q

What is accelerating angina?

A

Change in pattern such as

  • Greater ease of provocation
  • Longer episodes
  • Greater severity
  • Longer recovery
  • More frequent use of Nitro

May be unstable angina or acute coronary syndrome such as MI.

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69
Q

What do you give in the office if you realize a patient is having a STEMI?

A

MONA:

Morphine, oxygen, Nitro. aspirin

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70
Q

What is a coronary vasospasm?

AKA Prinzmetal Angina

AKA Variant Angina

A

Atherosclerotic arteries plus parasympathetic innervation

leads to coronary vasocontriction

(usually parasympathetic leads to nitric oxide to vasodilation)

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71
Q

What are the risk factors for Coronary Vasospasm?

A

Smoking

Cocaine

Hyperventilation

Provocative Agents (ACh, Ergotovine, Histamine, Serotonin)

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72
Q

What are the Signs/Sx of Coronary Vasospasm? q

A

Typical Anginal Sx BUT

  • Occur at REST, not exertion
  • Perhaps only a small lesion (25%)

May also have CAD so may also have typical angina Sx

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73
Q

What is the treatment for acute Coronary Vasospasm?

A
  • Treat as Acute Coronary Syndrome until R/O significant atherosclerosis: Nitro, Aspirin, Statins, +/- Heparin/Integrillin, Beta 1 selective beta blockers
  • Avoid nonselective Beta Blockers re risk of unopposed alpha receptor mediated coronary vasoconstriction
  • Monitor with serial biomarkers (Troponin, CK), telemetry until vasospasm ends.
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74
Q

How do you treat chronic Coronary Vasospasm?

A

Eliminate causes (smoking, cocaine)

Vasodilators: Calcium Channel Blockers

+/- Long acting Nitrates

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75
Q

What is heart failure?

A
  • Inability of heart to pump at sufficient rate to meet needs without abnormally high filling pressure
  • Abnormality of cardiac function and neurohormonal regulation
  • Effort intolerance, fluid retention and reduced longevity
  • Impairment of ventricles to fill with or to eject blood
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76
Q

How common is heart failure?

A

Prevalence: 1% of those 50-59, 10% of those 80+ in US

Incidence: 550K per year in US

Most common caudse of hospitalization in those 65+

(1/3 are readmitted in 6 mos, 24% in 1 mo)

50% 5-year mortality

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77
Q

What are some diseases that are risk factors for heart failure?

A

HTN, DM, Ischemia, CAD (most common), Valve Disease, Toxins (ETOH, chemo)

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78
Q

What are the three key problems

with heart failure and what causes each one?

A
  1. Myocardial (pump) failure: myocardial loss, increased pressure/work load, increased volume load
  2. LV inflow obstruction (filling problem): mitral stenosis, decrease LV compliance (eg concentric hypertrophy)
  3. Increased cardiac output: due to acute (transfusions) or chronic (eg: anemia) volume overload
  4. Other: thryrotoxicosis, arrhythmias
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79
Q

What are some ways of classifying heart failure?

A

Right vs Left Side

Systolic vs Diastolic

Acute vs Chronic

Compensated vs Decompensated

Dilated vs Hypertrophic vs Restrictive

High Output vs Low Output

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80
Q

What are the three key mechanisms of heart failure and what is their result?

A
  1. Increased Preload (blood volume)
  2. Increased Afterload (resistance)
  3. Decreased Contractility

Leading to increased stroke volume

leading to cardiac remodeling.

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81
Q

What causes Increased Afterload?

A

Resistance in the arterial tree that the ventricle must overcome.

AKA: Systemic Vascular Resistance

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82
Q

What causes increased preload?

A

Total blood volume

Skeletal Muscle exercise (venous return)

Venous Tone (volume storage)

Intrapericardial pressure

Body Position

Intrathoracic pressure

Atrial Function (CHF, HTN, Aortic Stenosis)

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83
Q

What affects Contractility?

A

Increased by: # of cardiomyocytes, strength of stimulation (Ca++), Sympathetic impulses, Circulating catecholamines, Inotropic Agents (digoxin)

Decreased by: Cardiomyopathy (-), MI, Anoxia, Acidosis, Hypercapnia, Medications

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84
Q

How are the four classes of heart failure patients?

A

I: No Sx

II. Sx during ordinary activity

III. Sx during sligh activity

IV: Sx at rest

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85
Q

What are the four stages of heart failure?

A

A. Risk factors but not Sx

B. Structural changes but no Sx

C. Structural changes with Sx

D. Decompensated, end stage

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86
Q

What are the goals of treatment for heart failure?

A

Decrease Symptoms

Prevent/Slow disease progression

Increase survival

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87
Q

What are Hemodynamic Profiles?

A

A simple way of classifying patients

in order to guide treatment options.

Based on level of perfusion and level of congestion/pressure:

I. Normal (Dry and Warm)

II. Congestion (Wet and Warm)

III. Hypoperfusion (Dry and Cool)

IV. Hypoperfusion and Congestion (Wet and Cool)

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88
Q

What is Left Ventricular Failure?

A

When the left ventricle fails and fluid backs up into the lungs

Sx: SOB, DOE, tachypnea, rales, pulmonary edema,

orthopnea, paroxysmal noctural dyspnea,

S3, Mitral Regurgitation, fatigue

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89
Q

What is Right Ventricular Heart Failure?

A

When the right ventricle fails and fluid backs up into the veins/body.

Signs/Sx: increased JVP (FIRST SIGN!!),

pitting, dependent edema (legs, ankles, sacrum), ascites,

hepatomegaly and hepatojugular reflex sign

parasternal heave

nocturia

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90
Q

What causes Right Side Heart Failure?

A
  1. Left Side Heart Failure

or

  1. Pulmonary HTN or Pulm Stenosis –> Cor Pulmonale
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91
Q

What are the two kinds of Left Ventricular Heart Failure?

A
  1. Systolic (aka Heart Failure reduced Ejection Fraction - HFrEF)
  2. Diastolic: (aka Heart Failure preserved Ejection Fraction HFpEF)
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92
Q

What is HFrEF?

A

Systolic Heart Failure = pump failure

More common in men

Signs: large, dilated heart, low ejection fraction, S3, Normal or low BP

Tx: Well established

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93
Q

What is HFpEF

A

Diastolic Heart Failure = filling problem

More common in post-menopausal women

Signs: Concentric LV hypertrophy leading to small LV cavity, HTN, normal/increased ejection fraction, S4

Tx: not well established

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94
Q

What is Acute Decompensated Heart Failure?

A

When a heart failure patient gets rapidly worse due to:

Medications that worsen HF: CCBs, BBs, NSAIDs, Antiarrhythmics, Anti-TNF antibodies,

Other Changes that worsen HF: Pregnancy, alcohol, increased HTN, acute valvular insufficiency, MI, ischemia, arrhythmia, infection (pneumonia), anemia, stopping HF Tx

NOTE: the point is that HF patients are very fragile

and can easily go downhill rapidly!

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95
Q

How do you diagnose Heart Failure?

A

Signs/Sx: elevated JVP, edema, rales, S3

2D Echo with Doppler: decreased LV ejection fraction, LV structural problems, other structural abnormalities (valves, pericardium, RV)

CXR: cardiomegaly (2/3 thoracic cage), pleural effusion, enlarged pulmonary artery, engorged upper lobe veins

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96
Q

What labs help with Heart Failure Dx?

A
  • Initial: CBC, UA, electrolytes (Ca++, Mg++), BUN, Creatinine, Glucose, Lipid Panel, Liver Function, TSH (treatable ETX!), ANP/BNP (best re R/O)
  • Serial Monitoring: Electrolytes and Renal

Also depending on your location and suspicion:

HIV, hemochromatosis, pheochromocytoma,

rheumatoid diseases, amyloidosis, Chagas

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97
Q

What is Invasive Hemodynamic Monitoring

and when is it used?

A

Threading a catheter up to the mitral valve to measure pressure.

Used for: respiratory distress, impaired perfusion, decreased systolic pressure, decreased renal function,

persistent Sx despite Tx

Consideration for revascularization or transplant

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98
Q

When is an endocardial biopsy called for?

A

If you suspect an inflammatory process

and it would change treatment.

(this is invasive)

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99
Q

What is the pharmacological Tx for Heart Failure?

A

For Sx, but do not decrease mortality:

  • Inotropics: (to increase contractility): digoxin, sympathomimetics, phosphodiesterase inhibs

To decrease mortality:

  • Vasodilators (decrease afterload): Nitro, ACEi, ARBs, Nitro, Hydralazine,
  • Aldosterone inhibitors (spironolactone) (10%)
  • Beta Blockers (carvedilol): effective for severe HF (30%+)
  • Neprilysin Inhibitors (LCZ696) esp w ACEi (30%+)
  • Ivabradine re I(f) channels in pacemaker cells
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100
Q

What are some nonpharmacologic treatments for HF?

A

Weight loss, exercise

biventricular pacemakers

ventricular assist devices as bridge to transplantation

heart transplant

hospice and palliative care

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101
Q

What happens during Phase 0 of the ventricular AP?

A

Na+ channels open

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102
Q

What happens during Phase 1 of the ventricular AP?

A

K1 channels open (between -90 mv and -50 mv)

Ca2+ channels open

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103
Q

What happens during Phase 2?

A

Na+ channels and Ca 2+ channels

(Plateau)

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104
Q

CO X TPR =

A

BP

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105
Q

HR x SR =

A

CO

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106
Q

SV is proportional to ___ and _____?

A

contractility and preload

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107
Q

Preload is proportional to _______ and ________?

A

Venous tone and blood volume

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108
Q

76 yo Pt with mechanical mitral valve presents with new onset palpitations.

EKG shows irregular R-R intervals without a distinct P wave, along with fibrillatory waves

A

Atrial Fibrillation: irregularly irregular

Tx Goal: decrease progression, tachy-mediated cardiomyopathy

Tx:

  • Beta Blockers,
  • Aspirin, Warfarin or novel anticoags like Dabigitran;
  • Antiarrhythmics (amiotarone) to prevent cardiomyopathy in younger patients.
  • Chemical or electrical cardioversion
  • Catheter ablation
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109
Q

30 yo man with new onset palpitations

ECHO: normal

EKG: irregularly irregular tachycardia with wide, variable QRS with Delta Wave

A

Atrial Fibrillation with Pre-Excitation

(due to accessory pathway)

Caution: can give rise to Vtach or Vfib

Tx:

  • Stable: procainamide
  • Unstable: electric or chemical (abutalide) cardioversion (60% success) and catheter ablation (95% success)
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110
Q

37 yo man with presyncope/fainting

EKG: PP interval is greater than 1.6 - 2 seconds and pause is not a multiple of PP interval

A

Sinus Pause (aka Sinus Arrest):

SA failure of automaticity followed by SA note impulse or escape rhythm

Note: can lead to tachy brady syndrome

ETX: genetic if younger, or aging to fibrosis to pause

TX: pacemaker

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111
Q

71 yo man with intermittent lightheadedness, syncope and palpitations

EKG: combination of bradyarrhythmia, tachyarrhythmia, sinus pauses, exit blocks and/or junctional escape rhythm

A

Sick Sinus Syndrome aka Tachy Brady Syndrome

ETX: SA node dysfunction seen in elderly

TX: monitoring if Sx (Holter, Zeopatch), pacemaker if syncope

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112
Q

76 y o woman with lightheadedness and weakness

EKG: regular RR interval, P waves are all over the place (before, during and after QRS), HR 40-60 bpm, QRS is narrow

A

Juncional Escape Rhythm

Rhythmn originating from the AV junction

Risk Factors/ETX: athletes with increased vagal tone, sick sinus, acute rheumatic fever, Lyme, digitalis, poast cardiac or valve surgery, isoproterenol IV, during MI

Note: Junctional rhythms can be brady <40, accelerated 60-100, tachy >60

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113
Q

55 y o man with prior A-fib ablation in hospital with palpitations

EKG: narrow complex tachycardia with P waves that all look different, isoelectric baseline, long R-P intervals, atrial rate of 100-240

A

(multifocal) Atrial Tachycardia

SVT originating in atria but outside SA node

ETX:

  • Unifocal: Digitalis
  • Multifocal: COPD, asthma due to hypoxia and irritation of SA node
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114
Q

57 yo man with new onset tachycardia

EKG: narrow and wide QRS,

long RR interval followed by short RR interval

A

Atrial Tachycardia with Aberrancy

Atrial Tach w wide QRS due to depolarization during long refractory period (refractory period influenced by rate and preceding cycle length)

Ashman Phenomenon: long R-R, then short R-R, then aberrant QRS waves

NOTE: can tell it is not Vtach because some of the QRS are narrow.

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115
Q

46 yo woman who drinks lots of coffee presents with sudden onset palpiations

EKG: Narrow complex tachycardia at 150 bpm with short RP interval (less than 1/2 R-R)

A

AV Nodal Re-Entry Tachycardia AVNRT

aka Supraventricular Tachy SVT

ETX: genetic abnormality having dual node pluse exposure + coffee/stress –> PACs or PVCs –> AV node loop

Tx:

  • Acute: vagal maneuver + IV adenosine or diltiazam pill to stop AV node
  • Recurrent: catheter ablation of slow pathway of dual node
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116
Q

50 yo woman with palpitations

EKG: narrow complex tachycardia

with inverted P wave in aVF, long R-P interval.

A

AV Re-Entry Tachycardia AVRT

Re-entrant tachicardia involving the AV node and an accessory pathway

  • Orthodromic: narrow QRS with anterograde conduction via VA node and His-Perkinje system to ventricle
  • Antridromic: wide QRS with anterograde conduction via a bypass tract and retrograde vis AV node

TX: interrupt AV nodal conduction to end tachy (diltiazem CCB or beta blocker) but with crashcart nearby bc can lead to Vfib via accessory pathway in 3/100.

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117
Q

48 yo woman with episodes of sustained tachycardia

EKG: normal P wave axis and morphology, short PR interval (

A

Wolff-Parkinson-White pattern

pre-excitation of ventricles by bypassing AV node

via Bundle of Kent accessory pathway

Tx: catheter ablation if Sx due to risk of sudden death

Can locate accessory tract based upon

where delta waves are seen on EKG

118
Q

53 yo man with aortic stenosis

EKG: narrow complex tachycardia with regular R-R intervals and uniform sawtooth P waves (4:1 rato of P:R)

A

Atrial Flutter

Macro-re-entrant atrial tachycardia originating in the rightr atrium aroung the cavo-tricuspid isthmus

  • Typical/ Counterclockwise (90%): Inverted F waves in inferior leads, everted in V1
  • Atypical/Clockwise (10%): Everted F waves in inferior leads, inverted in V1

Tx: rate control and anticoags; Catheter ablatio in typical

Ratio of P:R tends to be 2:1 or 4:1

119
Q

53 yo woman with non-ischemic cardiomyopathy

EKG: broad complex tachycardia >100 bpm

A

Ventricular Tachycardia

Sustained (.30 sec) vs Non-sustained (3+ beats, <30 secs)

Tx:

  • Stable (re pulse, BP, Sx): amiodarone to control arrhythmia or lidocaine if CAD or cannot take amiodarone
  • Unstable: defibrillation
120
Q

57 yo ma with recent MI

EKG: polymorphic ventricular tachycardia with characteristic twisting beat-by-beat QRS changes

A

Torsades de Pointes

ETX: long QT (often caused by medications) + PVS (prolonged repolarization leads to early after depolarization EADs)

Tx:

  • Avoid provocative agents (meds, ETOH, electrolytes)
  • Suppress long QT using magnesium sulfate
  • Emergency: defibrillation
121
Q

598 yo alcoholic woman with hypocalcemia and hypomagnesemia

EKG: QTc interval > 460 ms

A

Long QT Interval

QTc>440 in men, 460 in women

ETX: genetic +/- hypocalcemia, hypothyroid, meducations (mathodone, haloperidol, etc)

TX:

  • Low Risk of sudden death: avoid provocative agents
  • Sx/Med risk: BB, Na+ channel blockers
  • Hi risk: implanted cardio defibrillator (ICD)
122
Q

66 yo man with CAD presents with syncope and collapse, BP = 0, unresponsive, no previous heart disease

EKG: chaotic, irregular waves without identifiable P, QRS or T

Amplitude decreases with duration (course to fine)

A

Ventricular Fibrillation

ETX: R on T PVC (at vulnerable period), baseball to the chest during T wave, often preceded by Vtach

TX: chest compressions and defribrillation with antiarrhythmics (amiodarone, lidocaine)

123
Q

79 yo asymptomatic man comes into the office for a checkup.

EKG: Long PR (>.2), every P followed by QRS, narrow QRS

A

1st Degree AV Block

Abnormal prolongation of PR interval

ETX: excess CCB or BB, age, AV or aortic valve surgery

TX: none

124
Q

46 yo man with sleep apnea comes in for check up

EKG: progressive prolongation of PR interval along with shortening RR interval until P wave is blocked (no QRS)

A

2nd Degree AV Block Mobitz Type I (Wenckebach)

ETX: Digitalis, CCD, BB, AMI, Rheumatic Fever, Myocarditis, Sleep Apnea

TX: none

125
Q

72 yo man with chest pain for 3 hours

EKG: sinus rhythm with intermittent nonconductant P waves and consistent PR interval, wide QRS

A

2nd Degree AV Block: Mobitz II

TX: pacemaker because it can turn into

3rd degree complete heart block or MI

126
Q

89 yo woman with lightheadedness

EKG: two P waves for every QRS

A

2:1 AV Block

Cannot know whether it is 2nd degree type II or 3rd degree

127
Q

63 yo woman presents with lightheadedness

EKG: complete absense of AV conduction resulting in independent atrial and ventricular rhythms, PR interval varies but PP and RR intervals are constant

A

3rd Degree/Complete Heart Block

ETX: Lyme (treatable!), infiltration (amyloid, sarcoid), digitalis, endocarditis, advanced hyperkalemia

TX: permanent pacemaker

128
Q

What are the major complications associated with anticoagulant therapy?

A

Blow to the head

Cannot stop bleeding

Internal bleeding

129
Q

What are the absolute contra-indications for anticoagulant therapy?

A

Intracranial bleeding

Severe active bleeds

Recent (<72 hrs) surgery, especially eye, brain, spine

pregnancy or <48 hrs post partum

malignant HTN

Esophageal varices

Severe Renal Disease

Thrombocytopenia

130
Q

What are the three key types of cardiomyopathy?

A

DilatedHypertrophicRestrictive

131
Q

What kind of cardiomyopathy involves increased left ventricular volume, decreased ejection fraction and systolic dysfunction?

A

Dilated Cardiomyopathy aka Congestive Heart Failure

132
Q

What type of cardiomyopathy involves thick cardiac muscle, decreased ventricular volume and decreased compliance?

A

Hypertrophic Cardiomyopathy

133
Q

What type of cardiomyopathy involves myocardial and/or pericardial stiffness and decreased compliance?

A

Restrictive Cardiomyopathy

134
Q

What is the pathophysiology of dilated cardiomyopathy?

A
  • Genetic factors which can lead to DNA mutation and Altered immune system
  • Viral infection which can lead to myocarditis
  • The above factors can lead to altered myocardial function
  • Which leads to dilated cardiomyopathy
135
Q

What are some causes of dilated cardiomyopathy?

A
  • Idiopathic
  • Infections such as myocarditis, coxsackie, parvo
  • Ischemia: MI leading to scar tissue
  • Toxins from alcohol, uremia, cobalt, chemo
  • Peripartum (7th month of preg to 3 mos after)
  • Metabolic Ds: Diabetes, Beriberi
  • Arrhythmogenic RV Dysplasia
136
Q

What are the Signs/Sx of dilated cardiomyopathy?

A

SOB and exercise intolerance, rales

tachycardia, S3, holosystolic murmur, JVD, displaced PMI, precordial heave

pallor, cyanosis, cachexia

ascites, hepatomegaly

Decreased cardiac output

137
Q

What do you see on a CXR re dilated cardiomyopathy?

A

Bilateral pulmonary edema

Large heart silhouette

Enlarged ventricles

138
Q

How do you treat dilated cardiomyopathy (CHF)?

A

Diuretics (Sx only, no increased survival)

Inotropes to increase contractility

ACEi and ARBs to decrease afterload to decrease work

Beta Blockers to increase LV systolic fcn and increase survival

Hydralazine + Nitrates for African Americans

NOTE: No beta blockers if in decompensated heart failure!!

139
Q

What is hypertrophic cardiomyopathy?

A

Genetic form of hypertrophy of the heart

that is without an underlying cause.

Due to mutation of sarcomeric proteins

Prevalence: .26%

140
Q

What is the most common cause

of sudden death in athletes?

A

Hypertrophic cardiomyopathy (44%)

141
Q

How do you Dx hypertrophic cardiomyopathy?

A

Heart has thick muscle, decreased volume and decreased compliance

Myocardial fiber disarray

Asymmetrical LV hypertrophy (large septum)

LV outflow obstruction

142
Q

What are the Signs/Sx of hypertrophic cardiomyopathy?

A

Often no Sx but FHx of sudden death at young age

Syncopy, chest pain, dyspnea

Prominent apical pulse

Grade 2/6 midsystolic murmur at left sternal border

Possible arrhythmia

143
Q

What would you find in an Echocardiogram of

hypertrophic cardiomyopathy?

A

Thick muscle

Large septum

Tiny heart chamber

Possible valve problems

High velocity of blood

144
Q

How do you treat hypertrophic cardiomyopathy?

A

NO inotropes or diuretics!

CCB and B blockers to increase size of ventricle and decrease obstruction

Septal myotomy/myectomy or nonsurgical septal ablation

Implanted defibrillator

145
Q

What is the pathophysiology

of restrictive cardiomyopathy?

A
  • Myocardial infiltration or hypertrophy leading to decrease myocardial compliance
  • Pericardial effusion leading to increased intrapericardial pressure
  • Pericardial constriction leading to decreased pericardial compliance
  • All of the above leading to increased ventricular diastolic pressure
  • Leading to elevated diastolic pressure and suboptimal ventricular filling
146
Q

What are some causes of myocardial infiltration?

A

Idiopathic

Amyloidosis, Sarcoidosis

Fibrosis

Tumor(s)

Radiation

Heart transplant

147
Q

What are two causes of pericardial stiffness?

A

Pericardial effusion

Pericardial constriction

148
Q

How do myocardial infiltration and myocardial hypertrophy differ in terms of voltage?

A

Both conditions result in a large, stiff heart but…

Myocardial hypertrophy causes high voltage on an EKG (high amplitude) because the increased size is muscle

Myocardial infiltration causes low voltage because the increased size is due to infiltrates like sarcoid.

149
Q

What is Tako-Tsubo Cardiomyopathy?

A

aka Broken Heart Syndrome

Temporary condition where the heart muscle is suddenly weakend or stunned resulting in apical ballooning

It is a form of stress cardiomyopathy

150
Q

What are Epidemiology, Sx, Dx, Tx

of Tako-Tsubo Cardiomyopathy?

A

Epidemiology: 90% women, thought to be due to estrogen conversion to catecholamines and glucocorticoids

Sx: chest pain, SOB, collapse (palpitations, N/V)

Dx: EKG, blood test, angiogram, Echo, cardiac MRI

Tx: just monitor w serial echos

151
Q

What are the ETX, Sx, Dx and Tx

of infectious myocarditis?

A

ETX: viruses, URI, Lyme

SX: SOB upon exertion 7-10 days post infection, nocturnal dyspnea, fatigue, palpitations, chest pain/pressure, edema, (lightheadedness, arrhythmias, loss of consciousness)

Can lead to dilated cardiomyopathy

DX: EKG, CXR, Echo, cardiac MRI, heart biopsy

Tx: rest, decreased salt, steriods,

If severe: pacemaker, defibrillation

152
Q

What are the Signs/Sx, ETX and Tx of

Acute Pericarditis?

A

Signs/Sx: sudden onset, sharp, anterior chest pain (<6 wks), worse with inspiration and coughing or lying down,

better if sit forward

Pericardial friction rub at Left sternal border (“squeaky”)

ETX: idiopathic/viral (90%), CT dz (SLE), cancer

Tx: NSAIDs, colchicine, corticosteriods

Pericardiocentesis is severe

153
Q

What are two complications of acute pericarditis?

A

Cardiac Tamonade

Constrictive Pericarditis

154
Q

What are the ETX of

Pericardial Effusion?

A

ETX: idiopathic or infectious pericarditis, trauma,

neoplasm (breast, lung, lymphoma, melanoma),

metabolic dz (uremia, hemorrhagic states, myxedema)

problems from contiguous areas (aortic dissection, myocardial rupture, hemopericardium from anticoags)

155
Q

What are the Sx, Dx and TX of

Pericardial Effusion?

A

Sx: chest pain/pressure

(Dyspnea, decreased BP and muffled heart sounds

if moving toward cardiac tamponade)

Dx: waterbottle sign (looks like a flask on CXR)

Tx: NSAIDs, colchicine, corticosteriods

Pericardiocentesis if severe

156
Q

What is pericardial/cardiac tamponade?

A

Hemodynamic compromise of diastolic filling due to compressive intrapericardial pressue from pericardial effusion

157
Q

What are the Sx, Etx, and Tx of cardiac tamponade?

A

Sx: JVD, muffled heart sounds, decreased BP

pulsus paradoxus, tachycardia, tachypnea,

patient looks terrified!

EKG: ST elevation on nearly every lead

CXR: HUGE pericardium

Echo: dark space around heart with collapsing chambers

Tx: pericardiocentesis

(or pericardiotomy/pericardial window or pericardiectomy)

158
Q

What are some causes of constrictive pericarditis

aka pericardial constriction?

A

Idiopathic

Infectious (viral, TB)

CT diseases (RA, SLE, scleroderma)

Neoplasm: Primary (mesothelioma, sarcoma), or secondary

Trauma (penetrating or not)

Radiation

Post Pericardiotomy from CABG

Uremia

159
Q

What are some Sx and Tx of Constrictive Pericarditis?

A

Sx: fatigue, dyspnea, JVD, ascites, peripheral edema, hepatomegaly, Kussmaul’s sign, pleural effusion,

pericardial knock

EKG: low voltage

Chest CT: thick pericardium

CXR: pericardial calcification, small heart, pleural effusion

Tx: Pericardial stripping (entire pericardium removed)

160
Q

What is bacterial/infective endocarditis?

A

Bacteria enter the blood stream

and settle in the heart lining, valves or blood vessels

Bacteria comes mainly from the mouth re poor dental hygeine

Acute: (days) sudden, life threat

Subacute/chronic: (months) less serious

161
Q

What are Sx of bacterial endocarditis?

A

Fever, chills, night sweats, fatigue, tachycardia,

aching muscles and joints,

cough, pedal edema, ascites, weight loss, anemia

162
Q

What are the risk factors for bacterial endocarditis?

A

Cardiac birth defects such malformed valves or septal defect

Valve surgery

Dental or medical procedures

Narcotics

163
Q

What are the longterm sequelae of acute bacterial endocarditis?

A

Vegetations break loose and travel to the

brain, lungs, abdominal organs, kidneys, limbs

causing heart murmur, valve damage, HF,

stroke, seizure

PE, kidney damage, splenomegaly

paralysis

abscesses in heart, brain, lungs

Can cause hypertrophic cardiomyopathy

164
Q

How do you treat bacterial endocarditis?

A

2-6 weeks of IV antibiotics!

165
Q

What is the similarities and differences

between hypertrophic cardiomyopathy

and hypertensive heart disease?

A

Both: ventricular hypertrophy and decreased chamber size

Hypertrophic cardiomyopathy is genetic and causes asymmetrical hypertrophy with a large septum

Hypertensive heart disease is caused by long-standing hypertension and causes symmetrical hypertrophy. Associated with Heart Failure with preserved Ejection Fraction HFpEF

166
Q

What is the difference between

intrinsic and extrinsic causes

of sinus node dysfunction?

A

Intrinsic: (problem within the heart )ideopathic, ischemic, infiltrative, inflammatory, CT disease, post op, genetic

Extrinsic: (problem outside of the heart, part of another system): medications, drugs, electrolyte imbalance, hypothyroid, neural reflexes, neural syncope, intracranial HTN, hypothermia

167
Q

What is the resting membrane potential in cardomyocytes compared to pacemaker cells?

A

Cardiomyocytes: -90 mV

Pacemakers: -60 mV

168
Q

What feature allows pacemaker cells to continually fire at a consistent rate?

A

If channel slowly leaks Na+ so it gradually increases from -60 resting membrane potential to -40 threshold at which point slow Ca++ channels open and begin to depolarize.

It is the If channels that are the “clock” that never stops ticking and keeps the pacemaker in a consistent loop.

169
Q

What are the inherent rates of the SA node, AV node, and His-Purkinje system? Why are they different from one another?

A

SA node: 60-100

AV node: 40-60

His-Purkinje system: 30-40

They are different so that the AV node can serve as a back-up or fail-safe for the SA node

and the His-Purkinje as a backup for the AV node

170
Q

What are the key mechanisms of arrhythmia?

A

Problems with Automaticity:

  • Abnormal impulse formation: more or less frequently than normal
  • Abnormal impulse conduction: slowed or blocked such as in heart block

Problems with Triggered Activity

  • Early AfterDepolarization (EAD): think Long QT or Torsades
  • Delayed AfterDepolarization (DAD): think Digitalis or hypercalcemia
171
Q

What are some causes of Bradycardia?

A

Failure of SA node

Conduction block (permanent or transient)

Uni or bidirectional

Drugs/medications

Ischemia

Fibrosis (eg: calcification in elderly)

Electrolyte imbalance (Na+, K+, Ca++)

Trauma

172
Q

What mechanism causes Re-Entry Tachycardia?

A
  1. Two pathways, either due to an accessory pathway or damage to atrial cardiomyocytes
  2. Each pathway has different electrical properties pertaining to rate of depolarization and repolarization
  3. One side is momentarily blocked

This creates a continuous loop and is the MOST important mechanism of tachy arrhythmias!

173
Q

In a nutshell how do you treat Bradycardia?

A

Reverse the cause, such as fixing electrolyte imbalances

If this does not work, then pacemaker.

174
Q

In a nutshell, how do you treat tachycardia?

A

Reverse the cause

Try vagal maneuvers to control SVT

Cardioversion/defibrillation

Medications

Catheter ablation

Implanted defibrillator

Surgery

175
Q

What are two kinds of Superventricular Tachycardia SVT and how do they affect treatment?

A

Automatic: treat the cause

Re-Entrant: need to fix with meds, catheter, cardioversion

176
Q

What forms of tachycardia do not require heart medications or treatment?

A

Automatic problems:

  • Sinus tachy: it is normal to be tachycardic in response to pain, infection, blood less, etc. If you fix the problems (with pain meds, antibiotics, etc), the tachy stops
  • Atrial tachy and Multifocal Atrial Tachy (MAT): usually in response to hypoxia from lung disease. Treat the lungs and the tachy will stop.
  • Junctional Tachy: usually due to ischemia, acid-base, electrolytes. Correct the problem and the tachy will stop.
177
Q

What is the difference between stable and unstable tachycardia and how does that affect Tx?

A

Stable: no Sx, so you can take your time

Unstable: Serious Sx such as chest pain, altered mental status, hypotension, so do electrical cardioversion (defibrillation)

178
Q

What is syncope?

A

A symtom, not a disease

Sudden temporary loss of consciousness, loss of postural tone, with variable onset (some with warning) and spontaneous, complete recovery.

Caused by abrupt reduction in cerebral blood flow.

1-6% of all hospital admissions

179
Q

What affect does syncope have on a patient?

A

Anxiety

Decrease in activities of daily living

Driving restrictions

Loss or change of employment/profession

180
Q

What are common causes of Syncope?

A

34%: unknown cause

24%: Neurally-Mediated (vasovagal, carotid sinus, situational)

11%: Orthostatic (drug induced, autonomic nervous system fail)

14%: Cardiac Arrhythmia (brady, tachy, long QT)

12%: Non-cardiovascular: psychogenic, metabolic, neurological

4%: Structural Cardiac: (aortic stenosis, hypertrophic cardiomyopathy, pulm HTN, PE, tamonade)

181
Q

What are the more likely causes for younger patients as compared to older patients?

A

Younger: vasovagal, situational, psychiatric, genetic heart conditions such as Long QT, Brugada, WPW, hypertrophic cardiomyopathy

Older: mechanical or arrhythmic cardiac conditions, orthostatic hypotension, medications, neural, multifactorial

182
Q

What is the most serious/deadly cause of syncope?

A

Cardiac

183
Q

What are the key components of a workup for a patient with syncope?

A

Hx

PE

EKG

Echo

will be sufficient for 90% of patients

184
Q

What is the relevant Hx for a patient with syncope?

A

Details of syncopal episode from pt and observers

Precipitating factors

Prodrome/warning signs

Duration and frequency of episodes

Recovery Sx

Cardiac Hx

FH of cardiac, syncope and sudden death

Medications (cause or clue to Dx)

185
Q

What do you look for in terms of PE for a patient with syncope?

A

orthostatics

cardiac exam (re CHF, valves)

neuro exam

carotid sinus massage

186
Q

How do you do carotid sinus massage test?

A
  • Massage R carotid artery below the thyroid cartilage for 5-10 seconds
  • Pause
  • Massage the Left side

Postive test = 3 seconds of asystole or 50 mm Hg drop in BP

187
Q

What might you look for on an EKG for a patient with syncope?

A

Brady or tachycardia

PR interval

Delta waves (WPW)

Long QT

Patterns re Brugada, Q waves, ST-T waves, Hypertrophic cardiomyopathy, ARVC, IVCD, Complete heart block

188
Q

Why would you need an ambulatory EKG and what are some examples?

A

Unless you can get the patient to faint on command, you will need an ambulatory EKG to see what their heart is doing before/during syncope.

  • Holter Monitor: 24-48 hours, good for frequent syncope
  • Event Recorder: credit-card shaped item you press to your chest when you are feeling faint to capture the EKG.
  • Implantable Loop Recorder (ILR): implantable under the skin, can last 3 years. Great for very infrequent syncope
  • Zeopatch: like a bandaid on the chest to monitor for 14 days
189
Q

What is a Head Up Tilt Test and how does it work?

A

When you go from laying down to standing, your sympathetic nerves fire initially, then your parasympathetic adjusts down. Some people’s parasympathetic system adjusts too much.

The Tilt Test moves the patient back and forth from nearly vertical to nearly horizontal, reproducing the pre-syncopal Sx so the patient can learn how to recognize them and control the syncope using vagal maneuvers.

190
Q

How do you know when to admit a patient with syncope?

A

Unless they have at least one of the following, you do not need to admit them:

  • Hx of CHF
  • Hct < 30%
  • EKG abnormal
  • SOB
  • Systolic BP <90
191
Q

List three types of permanent pacemakers

A

Pacemakers are names based on (1) what chamber(s) are paced, (2) which are sensed, and (3) what action it takes. (R) means the rate changes based on activity.

DDD (R): Dual chambers paced, sensed, and acted upon

VVI (R) ventricle paced and sensed, and pacing Inhibited if it senses a rhythm

AAI (R): atrium paced and sensed, and pacing Inhibited if it senses a rhythm

192
Q

What are the indications for pacing?

A

Symtomatic Bradycardia

  1. HR < 60
  2. Symptoms: syncope, presyncope, SOB, chest pain, confusion, palpitations, CHF, exercise intolerance
  3. Cause is not reversible
193
Q

How do you decide whether the patient needs a single pacer or a dual pacer?

A
  1. Can the atrium be paced or sensed?
  2. Is there an AV block?
  3. Is there chronotropic incompetence? (natural pacemakers do not raise heart rate when needed such as exercise)

Examples:

If everything is working fine except the patient cannot increase heart rate when needed, then atrial pacer needed.

If the atrial rate is meeting needs, but there is AV block then a dual pacer is needed (to sense SA and pace ventricles)

194
Q

What is vasovagal syncope and what causes it?

A

Emotions and/or stress cause a drop in preload which causes decreased flow to the brain.

If the patient does not lie down quickly, they will faint, and will experience 24 hours of fatigue afterwards.

195
Q

How do you treat vasovagal syncope?

A

Acute: recognize the predromal signs, lie down, elevate feet and do isometric exercises such as clenching fists.

Chronic: stay hydrated, avoid triggers, get regular exercise (preload), wear support hose (preload), eat salty foods (if young without HTN).

Rx: Midodrine, a short-acting alpha agonist

No pacemaker needed.

196
Q

How do you treat a patient

with orthostatic hypotensive syncope?

A

Tell them to never lie down!

Typically they have high BP when lying down, but low BP when sitting or standing. If you give them HTN meds, their BP will be too low most the time. So stop the BP meds and get the to use a hospital-type bed at 45 degrees or elevate the head of the bed.

197
Q

What is shock?

A

Circulatory failure

198
Q

What is the cellular mechanism of shock?

A
  1. Inadequate O2 delivery or utilization or too much consumption
  2. Cellular/tissue hypoxia
  3. cell membrane ion pump dysfunction -> intracellular edema -. leakage to extracellular -> inadequate regulation of pH
  4. systemic acidosis, endothelial dysfunction, inflammatory cascade -> ant-inflammatory cascade
  5. Decreased tissue perfusion
199
Q

What are the four key types of shock?

A

Distributive

Cardiogenic

Hypovolemic

Obstructive

(plus Combination)

200
Q

Which forms of shock are primarily

due to decreased systemic vascular resistance?

A

Distributive Shock

201
Q

Which forms of shock are primarily due to

decreased cardiac output?

A

Cardiogenic

(late) Hypovolemic
(late) Obstrucitve

202
Q

What can cause shock (decreased perfusion) but with normal cardiac output and normal systemic vascular resistance ?

A

Carbon monoxide poisoning

Cyanide poisoning

Mitochondrial disease

203
Q

What are the three stages of shock and what are they symptoms of each?

A

Pre-shock aka Compensated Shock aka Cryptic Shock:

SX: tachycardia, cool skin, hypotension

Shock: compensatory mechanisms inadequate

SX: tachycardia, dyspnea, restlessness, diaphoresis, N/V, thirst, pallor, narrow pulse pressure, decreased mental status, hypotension, oliguria, cool clammy skin

Decompensated Shock aka End Organ Dysfunction

SX: hypotension, anuria, labored irregular breathing, thready, weak or absent peripheral pulses, ashy/cyanotic skin, decreased body temp and mental status, dilated pupils

204
Q

A patient has an infection and then develops signs and Sx of shock. What is the likely type of shock?

A

Septic

which is a kind of distributive shock

205
Q

A patient suffering from severe aortic stenosis develops signs/Sx of shock. What type of shock is likely?

A

Mechanical Cardiogenic

206
Q

A patient with the flu who has severe N/V/D for several days followed by shock Sx. Which is the likely type of shock?

A

Non-Hemorrhagic Hypovolemic

207
Q

A patient develops trouble breathing after a long flight from Kenya, and then develops Sx of shock. Which type is likely?

A

Pulmonary Vascular Obstructive Shock

(from a PE)

208
Q

What type of shock is anaphylaxis?

A

Non-septic distributive shock

209
Q

A patient has complete heart block and develops shock Sx. Which kind?

A

Arrhythmogenic Cardiogenic shock

210
Q

A patient is in a car accident and develops pericardial tamonade and Sx of shock. Which kind?

A

Mechanical Obstructive

211
Q

What is the pathophysiology of cardiogenic shock

caused by an MI as pertains to Systolic and Diastolic function?

A

Systolic:

  • Decreased cardiac output and stroke volume -> hypotension -> decreased coronary perfusion -> ischemia -> progressive myocardial dysfunction -> Death
  • Decreased cardiac output and stroke volume -> decreasesd systemic perfusion -> compensatory vasoconstriction -> progressive myocardial dysfunction

Diastolic:

  • Increased LVEDP and pulmonary congestion -> hypoxemia -> ischemia -> progressive myocardial dysfunction -> Death
212
Q

How do you work up a patient with shock?

A
  • Cover your ABCs: airway, breathing, circulation
  • Determine the underlying cause (may need tests)
  • Initiate life-saving maneuvers re underlying cause (Chest tube for tension pneumothorax, Epinephrine for anaphylaxis, IV antibiotics for sepsis, coronary revascularization for MI, steriods for adrenal crisis)
  • Once stable do focussed Hx and PE, general and targetted lab studies, plus possible Echo and pulmonary artery catheterization for definitive Dx and Tx
    • Treat the cause (eg: steriods for adrenal crisis, IV ABX for sepsis)
      *
213
Q

What are some causes of cardiogenic shock?

A

Ischemia or MI

LV failure

Ventricular Septal Rupture

Papillary m or chordea t. rupture re severe mitral regurg

ventricular free wall rupture

214
Q

How to you treat cardiogenic shock?

A
  • General: ventilation, IV fluids, sodium bicarb re acidosis, aspirin, IV heparin, possible glycoprotein IIb/IIIa Inhib, possible insertion of pulmonary artery catheter
  • Specific:
    • Meds: sympathomimetic inotropes, Norepi
    • Revascularization: PCI, CABG, thrombolytics
    • Mechanical: intra-aortic balloon pump, left ventricular or biventricular assist device, percutaneous cardiopulmonary bypass
215
Q

What is the 30-day survival rate for patients with cardiogenic shock?

A

about 50%

216
Q

What are the Sx and ETX of orthostatic hypotension?

A

Sx: dizziness, blurred vision, weakness, syncope, confusion, nausea upon standing

ETX:

Acute: dehydration, prolonged bedrest, hypoglycemia, overheated, post-prandial

Chronic: heart problems (rate, valve, HF), endocrine (DM, thryroid, adrenal), regulation problems (neuro or baroreceptor)

217
Q

How do you diagnose and treat orthostatic hypotension?

A

Dx: Orthostatic blood pressure testing, blood tests re anemia, hypoglycemia, EKG/Holter, Echo re structure, ETT, Tilt Table, Valsalva maneuver

Tx: depends on cause

  • Lifestyle changes: hydration, less alcohol, more salt, elevate head of bed
  • Compressive stockings
  • Medications: fludrocortisone, midodrine
218
Q

What is cardiogenic syncope?

A

Sudden drop in heart rate and BP causing fainting causes by cardiac arrhythmia or structural heart problem

219
Q

What are the Sx of cardiogenic syncope

A

Fainting plus possibly:

Chest tightness

SOB

Sweating

Apprehension

Palpiation

220
Q

Who is likely to get cardiogenic syncope?

A

Older patients with heart disease

221
Q

How do you diagnose and treat cardiogenic syncope?

A

Dx: EKG, Holter or Event Recorder and possible electrophysioligy testing

Tx: depends on cause:

Bradycardia: pacemaker

Tachycardia: meds, ablation, implanted defribrillator

222
Q

What is the definition of regurgitation/insufficiency of a heart valve?

A

leaking (backflow) across a closed valve

223
Q

What is the definition of stenosis of a heart valve?

A

obstruction of forward flow across and opened valve

224
Q

What are common etiologies of stenosis of heart valves?

A

rheumatic fever

congenital

degenerative

225
Q

What are common causes of valvular regurgitation?

A

myocardial dysfunction (MI)

infective endocarditis

rheumatic

congenital

Marfan’s

syphilis

anklyosing spondylitis

trauma

226
Q

What is the most common cause of aortic stenosis?

A

age-related degenerative changes (calcification)

227
Q

When you see the presentation of aortic stenosis in someone <65, what is the most common developmental defect?

A

bicuspid aortic valve

228
Q

What happens to the left ventricle as a result of aortic stenosis?

A

Left ventricular hypertrophy (earlier)

later, dilatation

then, CHF (left heart failure)

229
Q

What is the survival at 2 years after the onset of symptoms in aortic stenosis?

A

50%

230
Q

What is the definitve therapy for aortic stenosis?

A

valve replacement?

231
Q

what are the pros and cons of mechanical heart valves?

A

last longer than bio (20-30 years)

requires chest-opening surgery and need anti-coags

232
Q

What are the findings on physical exam for aortic stenosis?

A
  • slow, diminished pulses
  • single S2
  • palpable systolic thrill
  • harsh systolic ejection murmur (radiates to neck)
  • forceful PMI
233
Q

What are the findings on EKG in aortic stenosis?

A

left ventricular hypertrophy

234
Q

What are the findings on chest x-ray in aortic stenosis?

A

aortic valve calcification

dilated aorta

normal or increased heart size

235
Q

What is the most common cause of mitral stenosis?

A

rheumatic fever (50% >20 years prior to presentation)

236
Q

What conditions increase mitral valve flow and pressure?

A
  • hypervolemia
  • hyperthyroidism
  • pregnancy
237
Q

What are the key symptoms of mitral stenosis?

A
  • fatigue on exertion
  • dyspnea (on exertion at first)
  • venous stasis in LA - strokes and clots forming
  • LA and RV hypertrophy (dilatation late)
238
Q

What are the signs of mitral stenosis on PE?

A
  • RV lift
  • loud S1 in mild
  • quiet S1 in severe
  • diastolic rumble at apex
  • opening snap
239
Q

What are the signs of mitral stenosis on ECG?

A
  • normal sinus or a fib
  • right ventricular hypertrophy
  • left atrial enlargement
240
Q

What are the signs of mitral stenosis on CXR and Echo?

A

left atrial enlargement and right ventricular dilatation

calcified mitral valve

241
Q

What is the Rx for mitral stenosis?

A
  • diuretics
  • If in A fib: rate control and anticoagulation
242
Q

What happens to the heart to compensate in mitral regurgitation?

A

LV dilates to increase total stroke volume, compensating for “backward” flow through the incompetent valve.

243
Q

What can cause acute mitral regurgitation?

A
  • reputure of the chordae tendinae due to acute MI or endocarditis
244
Q

What is the end result of mitral regurgitation if untreated?

A

left heart failure (due to dilatation of the LV)

245
Q

What is the Rx for mitral regurgitation

A

diuretics

valve repair/replacement

246
Q

What is a surgical repair of mitral regurgitation called and what does it do?

A

annuloplasty and it shores up edges of leaflet so it closes during systole

247
Q

What are the PE findings with mitral regurgitation?

A

pansystolic murmur and an S3 gallop

248
Q

What are the ECG findings with mitral regurgitation?

A

LVH and LA dilatation

249
Q

What are the findings on CXR and Echo in mitral regurgitation?

A

CXR - cardiomegaly

Echo - dilated LV, LA, MVP, ruptured chord, vegetation, thickening

250
Q

What extra heart sounds do you hear in mitral valve prolapse?

A

midsystolic click and late systolic murmur

251
Q

What happens to the heart as a result of aortic regurgitation?

A

the LV gets volume overloaded and dilates

252
Q

What happens to the entire CV system as a result of aortic regurgitation?

A
  • Peripheral vasodilation to minimize pressure and regurgitation
  • low arterial diastolic pressure
  • increased systolic pressure
  • widened pulse pressure as a result of above
253
Q

What are the signs of aortic regurgitation on PE?

A
  • bounding pulses
  • wide pulse pressure
  • diastolic blowing murmur, diastolic rumble
  • systolic ejection murmur
254
Q

What are the signs of aortic regurgitation on ECG?

A

LVH

255
Q

What are the signs of aortic regurgitation on CXR/Echo?

A

LV dilatation

aortic root dilatation

dilated LV, valve thickening, vegetation, dilated aorta

diastolic fluttering of the MV

256
Q

Why is nitro contraindicated in severe aortic stenosis?

A

Patients with severe aortic stenosis already have a reduced cardiac output and LV strain, from trying to push blood through the narrowed valve to the circulation. Nitro will produce venous dilation, reducing preload and further reducing cardiac output through the narrowed valve. In addition it will reduce coronary artery filling.

Main problems are syncope and angina.

257
Q

What are additional problems, other than aortic stenosis, of a congenital bicuspid valve?

A
  • Bicuspid aortic valves also put patients at increased risk for aortic enlargement and dissection and are associated with coarctation of the aorta.
258
Q

What is the most common cause of tricuspid stenosis?

A

rheumatic heart disease

259
Q

What are the symptoms aortic stenosis?

A
  • angina
  • syncope
  • heart failure

(ordered from least to most severe)

NB: People are typically asymptomatic for a long time

260
Q

What are the two most common causes of acute aortic regurgitation?

A
  • aortic dissection
  • endocarditis
261
Q

what are the symptoms of tricuspid stenosis?

A

usually occurs with mitral valve disorders, so hard to distinguish

edema and ascites with normal RV function

262
Q

What are some of the PE findings with tricuspid stenosis?

A
  • prominent a wave on inspection of jugular venous pulsations.
  • An opening snap may be audible.
  • A soft diastolic-flow rumble may be identified by placing the bell of a stethoscope at the right parasternal border but may be inaudible.
  • The key to distinguishing murmurs of right-sided origin is the respiratory variation in intensity, which augments with inspiration.
263
Q

What is the Rx for tricuspid stenosis?

A

Diuretics, but you get increasing fatigue and dyspnea

264
Q

How common is pulmonary valve stenosis/regurgitation?

A

Rare - usually identified in childhood and results from congenital disorders (Noonan’s Syndrome)

265
Q

What physical exam findings might you see with pulmonary stenosis/regurgitation?

A

RV lift

and a diastolic decrescendo murmur

266
Q

What is the most common congential heart defect?

A

VSD

(also believed 1/2 of these repair themselves and never come to medical attention)

267
Q

What is an atrial septal defect?

A

persistent opening in the interatrial septum after birth that allows for direct communication between the l. and r. atria

268
Q

What is the prevalence of ASD?

A

1:1500 live births

10% of all congenital heart disease

269
Q

What is the consequence of an ASD?

A

blood ordinary shunted from left–>right

volume overload in right atrium

270
Q

What is Einsemenger Syndrome?

A

When a shunt that was formerly left-to-right becomes right-to-left

271
Q

What is the common presentation for ASD?

A
  • May be asymptomatic
  • DOE
  • Fatigue
  • Recurrent lower respiratory tract infections
272
Q

What are the exam/test findings with ASD?

A

RV heave along LSB

S2 wide, fixed splitting

murmur is mid-systolic left USB

cardiac cath - measures higher O2 in right atria

echo - shows shunt on doppler

273
Q

Rx for ASD?

A

Surgical-

  • direct suture closure
  • pericardial or synth patch
  • percutaneous apporahc with septal occluder device
274
Q

How prevalent is VSD?

A

1.5-3.5:1000 live births

275
Q

How do you diagnose VSD?

A

echocardiography

276
Q

What are the symptoms and signs of VSD?

A
  • depends upon the size of the defect ranges from no symp. to heart failure
  • harsh, holosystolic murmur along LSB
  • systolic thrill
  • if reversed shunt, cyanosis and dyspnea
277
Q

What is the Rx for VSD?

A
  • 1/2 close spontaneously by age 2
  • closure indicated with s/sx of CHF or pulmonary vascular disease
  • same as ASD methods for closure
278
Q

What is the tetraology of Fallot?

A

4 Defects:

  1. VSD
  2. pulmonic stenosis
  3. overridng aorta (communicates with right ventricle through VSD)
  4. RVH
279
Q

How common is tetralogy of Fallot?

A

Pretty rare: 5:10k live births

but most common cyanotic heart disease in childhood

280
Q

What are the s/sx of tetralogy of Fallot?

A
  • “Tet” Spells - hyperventilation, cyanosis, syncope and squatting after exertion, feeding, crying
  • dyspnea on exertion
  • mild cyanosis and clubbing
  • RV heave
  • systolic ejection murmur at left USB
281
Q

What is the Rx for tetralogy of Fallot?

A

surgery-close VSD and increase pulmonary artery width

*if necessary, temporarily create connection between aorta and pulmonary artery to reduce hypertension

282
Q

What is transposition of the great vessels?

A

aorta arises from the RV

pulmonary artery arises from the LV

so, aorta pumps deoxygenated blood and the pulmonary artery carries oxygenated blood to the heart

283
Q

What is the prevelence of transposition of the great vessels?

A

40:100k births (7% congenital)

most common neonatal cyanosis

284
Q

What are the s/sx of transposition of the great vessels?

A

blue baby - extremely hypoxic and cyanotic

285
Q

How do you diagnose transposition of the great vessels?

A

echocardiogram

286
Q

What is the Rx for transposition of the great vessels?

A

arterial switch surgery is definitive

until that can occur, use prostaglandins to keep ductus arteriosis open (only way to get some oxygenated blood circulating)

287
Q

Who still gets pre-dental/surgical antibiotic prophylaxis with congenital heart disease?

A

unreparid cyanotic heart disease

post-repair for six months

post-repair with residual defects

288
Q

What is coarctation of the aorta?

A

narrowing of the aortic lumen

(can be postductal -98% or preductal - 2% for the DA)

289
Q

how common is coarctation of the aorta?

A

1:6k live births

290
Q

What are the s/sx of coarctation of the aorta?

A
  • most asymptomatic, but severe will be evident in a newborn
  • preductal has cyanosis in LE
  • femoral pulses weak and delayed
  • midsystolic murmur
  • elevated UE BP

Clin Med I - Comprehensive (6 decks)

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