Cardiology Final Vvc

Front 1

Considerations for treatment/assessment of C/P

Back 1

02
12-lead
Asprin
Nitro
Morphine
(IV)

Front 2

STABLE angina

Back 2

Provoked by exertion, but should relieve with rest and prescribed medications

Front 3

Coronary ischemia

Back 3

Lack of Oxygen
Coronary ischemia can cause many symptoms without actual MI – dyspnea, faintness, fatigue, and nausea- all more common in elderly; diabetics may not feel C/P with coronary ischemia

Front 4

VARIANT angina

Back 4

Caused by coronary spasm, not blockage, and may occur at rest as Prinzmetal’s, or while exerted

Front 5

Myocardial Infarction

Back 5

Injury incurred by irreversible ischemia – results in dead myocardial tissue

Front 6

Cardiac Triad

Back 6

Pump
Fluid
Container

Front 7

M.O.N.A.

Back 7

Morphine, O2, Nitro, Asprin

Front 8

Asprin prevents

Back 8

Aggregation of platelets

Front 9

Diagnosis:
ANGINA

Back 9

Sudden or gradual onset, provoked, w/ nausea/vomiting sometimes, subsides with rest, w/o ectopy, nausea, sweating, SOB, PRESSURE

Front 10

Diagnosis:
MI

Back 10

Non provoked, sudden onset, unrelieved by rest, nitro, 02, nausea/vomiting, irregular rate/rhythm sometimes, lasting more than 30mins, LOCALIZED pain

Front 11

Diagnosis:
Dysrhythmias

Back 11

Ectopy or irregular rhythm, (consider history and stimulants)

Front 12

Diagnosis:
Pluracy

Back 12

Pain with inspiration and palpation, reproducible, possible fever, (consider recent illness, cough)

Front 13

Diagnosis:
Pericarditis

Back 13

Possible fever, reproducible pain, (consider recent illness, history, check for irregular heart rate/rhythm)

Front 14

Diagnosis:
Indigestion (C/P)

Back 14

Could be epigastric pain, (consider what PT. ate, when, history)

Front 15

Diagnosis:
Hypertension (C/P)

Back 15

Pressure in head, ringing in ears, blurred vision, headache, could mimic stroke,

Front 16

Diagnosis:
CHF (C/P)

Back 16

HTN, pulmonary edema, dependant edema, pedal edema, pink frothy sputum, orthopnea

Front 17

Starling’s Law

Back 17

The greater the amount of blood entering heart during diastole, the greater the volume ejected during systolic contraction

Front 18

Risk Factors for Pulmonary Emboli

Back 18

A-FIB, smoking, estrogen levels,

Front 19

Morphine class

Back 19

Narcotic analgesic

Front 20

Cardiac Risk Factors

Back 20

Abnormal cholesterol (dyslipidemia)
Hypertension
Cigarette smoking
Family Hx
Diabetes Mellitus
Kidney disease
Obesity/metabolic syndrome
Additional Emerging Risks

Front 21

Life threatening causes of C/P

Back 21

Heart attack (AMI)
Pulmonary Embolism
Aortic dissection

Front 22

Stenosis

Back 22

Hardening

Front 23

Pleural irritation causes

Back 23

Infections
Inflammation
Infiltration
Barotraumas
Tracheobronchitis

Front 24

Mallory Weiss Syndrome

Back 24

Gastro-esophageal laceration syndrome – tears in mucosa at stomach/esophagus junction

Front 25

Levine sign

Back 25

Clenched fist over chest when asked where it hurts

Front 26

Ischemic pain typically described as

Back 26

Pressure, tightness, constriction, burning, squeezing,
Diffuse (not pin point)

Front 27

Three PILLARS of Cardiac Function

Back 27

Preload – how tightly stretched the ventricular myocardium is just prior to contraction
Afterload – Pressure against which the ventricle must pump
Contractility – Equivalent to the force of each cardiac myocyte generates during systolic contraction

Front 28

Infarct pain typically described as

Back 28

Pinpoint or localized

Front 29

ACUTE MI

Back 29

C/P unrelieved by oxygen or nitro – assumed to be AMI

Front 30

4 Types of AMI

Back 30

Subendocardial Ischemia
Noninfarction Transmural Ischemia
Non-ST-elevation (non q-wave) MI
ST-elevation (Q wave) MI

Front 31

Most lethal acute complication during MI

Back 31

Dysrhythmias

Front 32

Complications and Hemodynamic changes during MI

Back 32

Hypotension
Poor perfusion

Front 33

Physical Exam of C/P should include

Back 33

Inspection (pt presentation), pulses, auscultation, abnormal heart sounds, murmurs,

Front 34

Symptoms of Aortic dissection

Back 34

Ripping, excruciating pain that starts suddenly and anteriorly, but radiates to back

Front 35

Type ___ diabetes increases risk factor 2-3 fold

Back 35

2

Front 36

Diabetes affects on heart/vessels

Back 36

Excessive blood glucose destroys muscle and tissue, resulting in hardening and atrophy

Front 37

Cholesterol affects on heart/vessels

Back 37

Hyperlipidemia – high cholesterol increases risk of CAD because they help build atherosclerosis

Front 38

Stimulants can cause

Back 38

Vasospasm

Front 39

JVD – sign of __ side heart failure

Back 39

Right

Front 40

Signs of L-side heart failure

Back 40

Pulmonary edema, lack of good perfusion, possibly altered

Front 41

Signs of R-side heart failure

Back 41

Pedal edema, lack of fluids to lung and system, late stage – JVD

Front 42

Pulsus Paradoxis

Back 42

10mmHg or more drop in systolic bp upon inspiration

Front 43

Cardiac tamponade

Back 43

Compressive cause of cardiogenic shock, caused by bleeding into pericardial sac, or infections. Pericardial effusion is the fluid accumulation between layers (of sac)

Front 44

Pulsus Alternans

Back 44

Alternating peripheral pulse amplitude caused by either failing L ventricle, or card.tamponade

Front 45

Effusion

Back 45

Fluid accumulation between pericard. layers

Front 46

Cardiac Wheeze

Back 46

Wheeze caused by fluid from heart failure (fluid accumulation)

Front 47

Beck’s Triad

Back 47

(cardiac tamponade)
Low arterial bp
JVD
Distant, muffled heart tones

Front 48

5 P’s of Peripheral Artery Disease

Back 48

Pulselessness
Paralysis
Paresthesia (numb, tingling)
Pain
Pallor

Front 49

____ new cases of angina / year

Back 49

400,000

Front 50

ST depression vs elevation

Back 50

ST Elevation usually means injury; ST Depression is ischemia

Front 51

Four acute coronary syndromes

Back 51

Classic Angina (subendocardial ischemia)
Unstable Angina
Non-ST elevation myocardial infarction (Non Q wave MI)
ST elevation MI (Q wave MI)

Front 52

Cardiac Output

Back 52

Stroke volume x heart rate (liters per minute)

Front 53

Cardiac cells are joined end to end with

Back 53

Intercalated disks

Front 54

Contraction begins ____ and moves toward ____

Back 54

at apex, base

Front 55

Impulse travels to the

Back 55

Apex

Front 56

Four factors of Cardiac Output

Back 56

Blood supply available to flow into heart (Preload)
Ability of atria to push into ventricles (Atrial Kick)
Ability of ventricles to pump blood efficiently against the afterload
Adequate heart rate

Front 57

2 principles that govern cells

Back 57

1: body always wants electrical forces to be neutral (equal positive and negative)
2: body will attempt to balance concentration of particles BY DILUTING with water

Front 58

Sodium is usually _____ the cell during resting membrane

Back 58

Outside

Front 59

2 forces that govern particle flow during impulse

Back 59

Electrostatic, and concentration

Front 60

PHASE 4

Back 60

Resting membrane – nothing flowing in or out. Na under pressure to enter cell. Ca waiting to enter/equalize

Front 61

PHASE 0

Back 61

Sodium moves in (impulse activates sodium channels)
Electrostatic pressure forces K out
Cell becomes more positive inside (too much K is let out)
Depolarization begins

Front 62

PHASE 1

Back 62

Sodium pumps out (sodium/potassium pumps push sodium out and allows potassium back in)
Electrical change (from deportation of sodium) opens calcium channel gates

Front 63

PHASE 2

Back 63

Calcium moves in
(little change in electric gradient)
aka plateau phase: because 1) protects cell from being influenced by other impulses, 2) allows calcium to do its main purpose and interact with actin/myosin to trigger contraction

Front 64

PHASE 3

Back 64

Calcium moves out
(once enough Ca enters, it deactivates Ca channel gates)
Ca pumps and Na/K pumps control inner atmosphere of cell and repolarize

Front 65

Resting membrane potential of cardiac cell (mV)

Back 65

Around -90mV

Front 66

The point at which enough sodium gates have opened to start massive influx

Back 66

Membrane threshold

Front 67

Absolute Refractory Period

Back 67

When depolarized, electrical gradient is such that cell cannot respond to additional impulse

Front 68

Relative Refractory Period

Back 68

During ‘phase 3’, during repolarization, when enough electrical gradient has been achieved to theoretically respond to new electrical impulse

Front 69

3 properties of cardiac cells

Back 69

Automaticity, excitability, contractility

Front 70

Cells tasked with initiating depolarizing waves at appropriate times

Back 70

Pacemaker cells

Front 71

Three pacemaker sites (primary sites)

Back 71

SA, AV, Purkinje

Front 72

Pacemaker cells differ from other cells, how?

Back 72

1) Far fewer sodium gates (harder to impulse, longer repolarization, shorter plateau phase)
2) Membrane is designed to allow programmed “leakage” of sodium into the cell – depolarizing after a set amount of time

Front 73

Primary pacemaker

Back 73

Sinus node

Front 74

Rate of SA node

Back 74

60-100 Top: 160

Front 75

Rate of AV node

Back 75

40-60 Top: 220

Front 76

Rate of Purkinje

Back 76

20-40 Top: 300

Front 77

“Escape”

Back 77

When a lower pacemaker fires for a higher pacemaker that has failed

Front 78

HR controlled by

Back 78

Parasymp/symp branches of ANS, drugs, and hormones

Front 79

Baroreceptors are located ___ and ___ and sense__

Back 79

Carotid arteries, aorta, BP

Front 80

Gap junction function

Back 80

Within intercalated disks, allows ions to flow, and transport rhythmic impulses

Front 81

System that picks up and disperses impulses through atria

Back 81

Intermodal pathways

Front 82

Left atria conduction to by:

Back 82

Bachmann’s bundle /aka/ interatrial pathway

Front 83

Position of AV node

Back 83

At base of left atria

Front 84

Consecutive order of conduction from AV

Back 84

AV node, to
Bundle of His, to
L and R bundle branches, to
Purkinje network

Front 85

Left dominant

Back 85

People who’s SA node is perfused by LEFT coronary artery

Front 86

SA node

Back 86

Crescent shaped, where superior vena cava and right atrium meet, (on posterior aspect of)

Front 87

AV node (three functions)

Back 87

1) Atria to ventricle gateway
2) slows conduction (average 0.08 miliseconds) (allows for atrial kick to fill ventricles
3) backup pacemaker at 40-60bpm

Front 88

Bundle Branches

Back 88

Where impulses bifurcate into left/right branches
LEFT branch bifurcates again into anterior and posterior fascicles
LEFT branch responsible for depolarization of myocardial septum

Front 89

Purkinje network

Back 89

Intrinsic rate of 20-40 Responsible for dispersing impulse through remaining myocardium

Front 90

ECG measures electricity between ___ and ___

Back 90

Negative, Positive

Front 91

Upright ECG deflection

Back 91

Impulse traveling toward positive lead

Front 92

Negative deflection

Back 92

Impulse traveling toward negative lead

Front 93

A wave traveling perpendicular to a positive lead will result in ____ pattern: equal deflection both positive and negative

Back 93

Biphasic