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PHTH 536: Body Systems > Quiz 1: Cardiac Pathologies > Flashcards

Quiz 1: Cardiac Pathologies Flashcards

1
Q

Where does the right coronary artery supply blood to?

A

-R atrium
-Most of R ventricle
-Inferior wall of left ventricle
-AV and SA node (60% of population)
-Bundle of His

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2
Q

Where does the left coronary artery supply blood to?

A

-Left anterior descending (LAD)
-Left ventricle, septum, inferior apex
-Left circumflex
-Lateral and inferior walls of left ventricle
-SA node (40% of population)

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3
Q

What are the tissue layers of the heart?

A

-Endocardium
-Myocardium
-Pericardium

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4
Q

What does the pericardium consist of?

A

-Fibrous pericardium
-Parietal pericardium
-Visceral pericardium (epicardium)

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5
Q

What does the serous pericardium consist of? What is inside the serous pericardium?

A

-Visceral and parietal pericardium
-Fluid is between these two layers

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6
Q

What is myocardium? How is it different from skeletal muscle?

A

-Heart muscle
-Different from skeletal muscle due to automaticity
-Pacemaker cells keep the heart moving without conscious voluntary movement

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7
Q

How does the sympathetic and parasympathetic systems influence the heart?

A

-Vagus nerve bundle (parasympathetic)
-Vasovagal syncope (aka neurocardiogenic syncope)

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8
Q

What external factors can influence the heart rate?

A

-Stress
-Exercise
-Caffeine
-Drugs

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9
Q

What does the myocardium consist of?

A

-Contractile elements of the heart
-Conductive elements of the heart

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10
Q

What is the endocardium? What is its function?

A

-Thin layer of cells lining the inside of the myocardium, valves, and atria
-Has some connective tissue, some elastic fibers, and muscle tissue
-Provides a smooth surface to allow blood and platelets to flow freely and not adhere to heart walls
-Strengthens the valves and supports other heart tissue
-Supports the subendocardial layer which houses the Purkinje fibers

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11
Q

What are the names of the two atrioventricular valves? What chambers are they between?

A

-Tricuspid/R AV: between R atrium and R ventricle
-Mitral/L AV: between L atrium and L ventricle

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12
Q

What are the names of the two semilunar valves? What two structures are they between?

A

-Pulmonary: between R ventricle and pulmonary artery
-Aortic: between L ventricle and aorta

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13
Q

What is cardiac output (CO)?

A

Amount of blood ejected out of the left ventricle into the systemic system per minute

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14
Q

What is a normative value of cardiac output at rest?

A

4-5 L/min

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15
Q

How is cardiac output calculated?

A

-Cardiac output (CO)= heart rate (HR) x stroke volume (SV)
-CO= HR x SV

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16
Q

How long does it take blood to travel through the pulmonary and systemic circuits?

A

About 1 minute

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17
Q

What is stroke volume?

A

Amount of blood ejected out of the L ventricle/beat

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18
Q

What is a normative value of stroke volume?

A

55-100 mL/beat

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19
Q

What is stroke volume affected by?

A

-Left ventricular end diastolic volume (LVEDV)
-End systolic volume (ESV)

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20
Q

What is left ventricular end diastolic volume (LVEDV)?

A

Amount of blood left in the ventricle at the end of diastole

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21
Q

What is end systolic volume (ESV)?

A

Volume of blood returning to the heart

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22
Q

What is preload? What is it directly proportional to?

A

-The amount of stretch experienced by cardiac sarcomeres pre-contraction
-Directly proportional to stroke volume

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23
Q

What affects preload?

A

Affected by venous return and volume of returning blood

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24
Q

What is Starling’s Law?

A

The greater the LVEDV the greater the stretch and volume pumped

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25
Q

What is afterload? What is it inversely related to?

A

-Force left ventricle must generate to overcome aortic pressure to open aortic valve
-Inversely related to SV

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26
Q

What is contractility?

A

The squeezing pressure of the left ventricle

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27
Q

What is ejection fraction (EF)? What is it used for? What is a normative value for EF?

A

-Percentage of blood emptied from the ventricle during systole
-Clinically useful way to understand left ventricular function
-Normal values is 60-70% (greater than 55%)

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28
Q

How is ejection fraction calculated?

A

-EF=SV/LVEDV

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29
Q

What is low EF usually an indicator of?

A

Usually an indicator of cardiomyopathy or heart failure

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30
Q

What is myocardial oxygen demand? How is it measured? When does it increase?

A

-Energy cost to myocardium
-Measured with rate pressure product
-Rate pressure product= HR x SBP
-Increases with activity and with HR or BP

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31
Q

What are the neurohumerol influences on sympathetic stimulation (adrenergic) of the heart?

A

-Control in the medulla via T1-T4
-SA node, AV node, conduction pathways
-Increases HR and force of myocardial contraction
-Coronary artery vasodilation
-Sympathomimetics: antihypertensives are sympathetic blockers

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32
Q

What are the neurohumerol influences on the parasympathetic stimulation (cholinergic) of the heart?

A

-Control in the medulla via vagus nerve (CN X) and cardiac plexus
-Innervates the SA and AV node
-Slows rate and force of myocardial contraction
-Coronary artery vasoconstriction

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33
Q

What are baroreceptors? Where are they located?

A

-Pressure receptors
-Located in walls of aortic arch and carotid sinus

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34
Q

What is the circulatory reflex? What changes occur if BP is increased? What changes occur if BP is decreased?

A

-Responds to BP changes
-Increased BP triggers parasympathetic response, decrease rate and force of contraction, sympathetic inhibition
-Decreased BP triggers sympathetic response, increases HR and BP, vasoconstriction

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35
Q

What are chemoreceptors? Where are they located?

A

-Detect changes in O2, CO2, and lactid acid (pH) and will effect HR and RR
-Located in the carotid body
-Increased CO2 or decreased O2 or pH= increased HR and RR
-Increased O2= decreased HR

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36
Q

What is hyperkalemia? What effects will this have on the heart?

A

-Increased concentration of potassium ions
-Decreased HR
-Decreased contractile force
-Arrhythmias and EKG changes

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37
Q

What EKG changes will you see with hyperkalemia?

A

-Widened PR and QRS intervals
-Tall T waves

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38
Q

What is hypokalemia? What effects will this have on the heart?

A

-Decreased concentration of potassium ions
-EKG changes

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39
Q

What EKG changes will you see with hypokalemia?

A

-Flattened T waves
-Prolonged PR intervals

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40
Q

What is hypercalcemia? How does it effect the heart? What other symptoms might someone have?

A

-Increased calcium concentration
-Increased HR and increased contractility
-Kidneys would also be effected
-Confusion
-Coma

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41
Q

What is hypocalcemia? How does it effect the heart?

A

-Decreased calcium concentration
-May cause arrythmias

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42
Q

What is hypermagnesmia? How does it effect the heart? How does it effect other systems?

A

-Increased magnesium concentration
-Calcium blocker
-Arrythmias
-Cardiac arrest
-Hypotension
-Confusion and lethargy

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43
Q

What is hypomagnesmia? How does it effect the heart?

A

-Decreased magnesium concentration
-Ventricular arrythmias
-Coronary artery vasospasm

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44
Q

What is the cardiac cycle?

A

The period from one heart beat to the beginning of the next heartbeat

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45
Q

How does the action potential go through the heart?

A

-Starts at SA node
-Depolarizes atria
-Spreads to AV node
-Bundle of His
-Bundle branches
-Purkinje fibers

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46
Q

What is systole?

A

The period of contraction that the heart undergoes while it pumps blood into circulation

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47
Q

What is diastole? What occurs during diastole?

A

-The period of relaxation that occurs as the chambers fill with blood
-The coronary arteries perfuse the myocardium during diastole through capillaries
-As the aortic valve snaps shut, leftover blood is shunted to the coronary arteries

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48
Q

How long is the delay between the action potential getting sent from the SA node to the AV node? What does this delay allow?

A

-0.1 second
-It allows the atria to contract and the ventricles to fill

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49
Q

What is phase I of the cardiac cycle?

A

-Diastole/filling period
-Both atria and ventricles are relaxed
-Blood flows into the R atrium from sup. and inf. vena cava and the coronary sinus
-Blood flows into the L atrium from the pulmonary veins
-Both AV valves are open (blood flows from atria into ventricles)
-Semilunar valves are closed
-SA node depolarizes causing atrial contraction (atrial systole)

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50
Q

How much of ventricular filling occurs when the AV valves are open?

A

70-80%

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51
Q

How much of ventricular filling occurs because of “atrial kick”? When does “atrial kick” occur?

A

-20-30%
-Occurs during SA node depolarization which causes atrial contraction

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52
Q

How much blood is in the ventricles at the end of atrial systole and just prior to atrial contraction? What is the term that describes this?

A

-The ventricles contain approximately 130 mL of blood in a resting adult in standing position
-This is known as end diastolic volume (EDV) or preload

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53
Q

What is phase II of the cardiac cycle?

A

-Isovolumic/isovolumetric contaction
-AV node depolarizes, spreads to the bundle of His
-Muscles in the ventricle start to contract but semilunar valves are not yet open
-Pressure quickly rises above that in the atria, closing the AV valves
-Pressure is not high enough yet to be ejected from ventricles

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54
Q

What is phase III of the cardiac cycle?

A

-Ejection
-Continued depolarization through the bundle branches and Purkinje fibers creates stronger ventricular contraction
-Pressure in the ventricles rise until it is greater than the pulmonary trunk and aorta, pushing open the semilunar valves
-Blood is ejected from the ventricles (stroke volume)

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55
Q

How much blood remains in the ventricles following phase III of the cardiac cycle (ejection)? What is the term for this?

A

-50-60 mL of blood remain in the ventricle after ejection
-End systolic volume (ESV)

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56
Q

What is phase IV of the cardiac cycle?

A

-Isovolumic/isovolumetric relaxation phase
-Ventricular relaxation/diastole follows repolarization of the ventricles
-Early phase of ventricular diastole, the ventricular muscles relax
-Pressure in the ventricles begins to fall and drops below pressure in the pulmonary trunk and aorta
-Semilunar valves close
-AV valves have not yet opening

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57
Q

How many lobes are there in the R lung? How many are there in the L lung?

A

-R lung: 3 lobes (superior, middle, and inferior)
-L lung: 2 lobes (superior and middle, + lingula)

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58
Q

How many independent segments are there in the R lung? What are their names?

A

-9 independent segments
-Apical
-Anterior
-Medial
-Lateral
-Anterior basal
-Posterior
-Superior
-Posterior basal
-Lateral basal

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59
Q

How many independent segments are there in the L lung? What are their names?

A

-10 independent segments
-Apical
-Anterior
-Anterior superior
-Posterior superior
-Inferior
-Anterior basal
-Superior
-Posterior basal
-Lateral basal
-Posterior

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60
Q

What does the conducting zone consist of?

A

-Trachea
-Primary bronchus
-Secondary bronchus
-Bronchi
-Bronchioles

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61
Q

What does the respiratory zone consist of?

A

-Respiratory bronchioles
-Alveolar ducts
-Alveolar sacs

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62
Q

What are the pleura of the lungs? What do these layers make up?

A

-Two layered membrane that folds back on itself
-Visceral pleura (innermost)
-Parietal pleura (outermost)
-These two layers make up the pleural cavity

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63
Q

What is inside the pleural cavity? What is the function of the pleural cavity? What happens if it is not functioning correctly?

A

-Pleural fluid
-Creates surface tension to keep the lungs in place in the thorax and allows the lungs to expand when the thorax expands
-It also cushions and lubricates the lungs during expansion and retraction
-It it is not functioning, a pneumothorax can occur

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64
Q

What is the parietal pleura innervated by?

A

Phrenic and intercostal nerves

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65
Q

What are accessory muscles of inspiration?

A

-SCM
-Scalenes
-Pec minor

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66
Q

What are the principal/main muscles of inspiration?

A

-External intercostals
-Diaphragm

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67
Q

What is quiet breathing?

A

-Expiration is quiet breathing because it results from passive recoil of lungs and rib cage

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68
Q

What muscles are involved in active expiration?

A

-Internal intercostals
-Innermost intercostals
-Rectus abdominis
-Transverse abdominis
-External and internal obliques

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69
Q

What three pressures does breathing depend on?

A

-Atmospheric (pressure exerted on lungs by atmosphere)
-Intra-alveolar (pressure inside the alveoli)
-Intrapleural (pressure in the pleural cavity)

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70
Q

What keeps the lungs inflated?

A

-Competing forces of pressure keeps the lungs inflated
-Elasticity of the lungs and surface tension of alveoli creates an inward pull
-Surface tension in the pleural cavity creates an outward pull
-The outward pull is just slightly higher than the inward pull, so the lungs stay inflated

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71
Q

What is the role of surfactant?

A

Surfactant is a fluid in the alveoli that prevents them from collapsing

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72
Q

What is pulmonary ventilation?

A

The air that is moving in and out of the lungs

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73
Q

What is the pulmonary cycle?

A

Inspiration and expiration

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74
Q

What occurs during inspiration?

A

-Diaphragm contracts, thorax expands inferiorly
-External intercostals contract, pulls ribs up and out to expand thorax anteriorly
-Creates a pressure gradient and drives air into the lungs

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75
Q

What occurs during expiration?

A

-Expiration is largely passive
-Diaphragm and external intercostals relax which returns thorax to resting position and reduces volume
-Creates a pressure gradient and drives air out of the lungs

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76
Q

What physical properties do the lungs have that facilitate breathing?

A

-Lung compliance
-Tendency of lungs to recoil (collapse)
-Elastic recoil or elasticity
-Surface tension at air-liquid interface on the alveolar surface acts to collapse the alveoli (surfactant counters this)
-Resistance to airflow at the level of the airways

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77
Q

What conditions can effect the mechanics of breathing?

A

-Scoliosis
-Pulmonary fibrosis (impairs compliance of lungs)
-COPD
-Asthma
-Premature babies (reduced surfactant)
-TBI (neural control of breathing may be effected)

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78
Q

How is breathing controlled?

A

-Primarily controlled by medulla and pons (requires repetitive stimulation from brain)
-Respiration driven by CO2 and pH levels in the blood which stimulate central chemoreceptors in the medulla

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79
Q

What is the response if CO2 increases and pH decreases in the blood?

A

-Stimulates respiratory centers in the medulla to contract diaphragm and external intercostals
-Increases rate and depth of respiration

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80
Q

What is the response if CO2 decreases and pH increases in the blood?

A

Stimulated respiratory centers in the medulla to lower rate and depth of repiration

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81
Q

What role do the peripheral chemoreceptors in the carotid artery and aortic arch play in the control of breathing?

A

-They detect changes in CO2, O2, and pH in the blood
-Increase in ventilation occurs when CO2 levels increase or decrease of O2

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82
Q

What is the hypoxic drive to breath? What patient population is this common with? What precautions should be taken in these cases?

A

-Some patients with COPD trap CO2 and start to rely more on O2 receptors
-Supplemental O2 should be prudently administered because increases of O2 in the blood can suppress the hypoxic drive to breath

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83
Q

How does the hypothalamus and limbic systems effect breathig?

A

-Anxiety or stress can increase breathing rate
-Extreme fear can cause one to hold their breath

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84
Q

What is inspiratory reserve volume?

A

The extra volume of air that can be inspired with maximal effort after reaching the end of a normal, quiet inspiration

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85
Q

What is tidal volume?

A

The amount of air that moves in and out of the lungs during each breath

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86
Q

What is expiratory reserve volume?

A

The amount of air that can be forcefully exhaled after a normal, quiet breath

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87
Q

What is residual volume?

A

The amount of air that remains in the lungs after a person has forcefully exhaled as much as they can

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88
Q

What is inspiratory capacity?

A

-The maximum volume of air a person can inhale after a normal exhale
-Inspiratory reserve volume + tidal volume

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89
Q

What is the functional residual capacity?

A

-The amount of air remaining in the lungs after a normal exhalation
-Expiratory reserve volume + residual volume

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90
Q

What is vital capacity?

A

-The maximum amount of air that can be exhaled from the lungs after a maximum inhalation

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91
Q

What is the total lung capacity?

A

-The volume of air in the lungs upon the maximum effort of inspiration
-Vital capacity + residual volume

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92
Q

Where does gas exchange occur? How does it occur?

A

-Alveoli
-Respiratory zone
-Diffuses across membranes down a concentration gradient
-Driven by concentration of various gases in the air we breath and blood pH

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93
Q

What needs to occur for effective gas exchange?

A

Alveoli must be both ventilated and perfused

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94
Q

What is the V/Q match?

A

The goal is for ventilation (V) to be matched with perfusion (Q)

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95
Q

What does V/Q mismatch indicate?

A

A pathological state

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96
Q

What can effect the V/Q ratio?

A

-Positioning
-Pneumonia, emphysema, pulmonary edema, atelectasis

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97
Q

What is atelectasis?

A

Partial or complete collapse of the lung

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98
Q

Why is V/Q not uniform across the lungs?

A

Because there are areas of the lungs with greater perfusion and areas with greater ventilation

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99
Q

How does transport of O2 and CO2 occur in the blood?

A

-Veins carry CO2 to be expelled
-Arteries carry O2 from heart to tissues
-Hemoglobin (4 iron molecules, heme group, and 4 protein molecules/globins)
-Transports 98% of O2 delivered to the periphery (2% in plasma)
-O2 carrying capacity of body is determine by concentration of HgB

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100
Q

What is SaO2?

A

-Oxyhemoglobin/total hemoglobin (blood gas analysis)
-Called SpO2 when measure with pulse oximeter

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101
Q

What are the normative values for O2 carrying capacity? How does low O2 carrying capacity effect the body?

A

-Women: 12-16 g/dL
-Men: 13-16 g/dL
-Lower than normal concentrations impairs the body’s ability to circulate O2 and can cause anemia

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102
Q

What is the oxygen hemoglobin dissociation curve? What would a right shift in the curve indicate? What about a left shift?

A

-Describes the relationship between SaO2 and the partial pressure of arterial O2
-Right shift: reduced oxygen affinity
-Left shift: increases oxygen affinity

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103
Q

What is pericarditis? What are causes of this?

A

-Inflammation of pericardium or pericardial fluid
-Viral infection (most common)
-Other infection (bacterial, uremia, acute MI, tuberculosis, etc.)
-Systemic diseases (autoimmune disorders, inflammatory disorders, drug toxicity, etc.)
-Trauma

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104
Q

What would be the clinical presentation of acute pericarditis?

A

-May not present with any signs or symptoms
-Retrosternal chest pain (sharp/stabbing or dull achey)
-Often intensifies with cough and deep breathing
-Often relieved with sitting up and leaning forward
-Dyspnea (non-exertional)
-General malaise/fever
-EKG abnormalities are not common
-Auscultation: friction rub causes by inflammed pericardial layers rubbing against one another
-Usually seen in young and healthy individuals

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105
Q

What is included in the medical work up and management of acute pericarditis?

A

-Labs will reveal acute inflammation (elevated WBCs, erythrocyte sedimentation rate, C-reactive protein, and troponins may be elevated)
-Echocardiogram to evaluate pericardial effusion
-Management: rest, pain relief usually with NSAIDS
-High dose of antibiotics or pericardial drainage

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106
Q

How long does acute pericarditis usually last?

A

-Self limited disease
-Usually lasts 1-3 weeks

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107
Q

What is constrictive percarditis?

A

Chronic pericarditis or pericardial effusion results in thickening and scarring of the pericardium

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108
Q

What is the clinical presentation of constrictive pericarditis?

A

-Dyspnea and fatigue due to reduced CO
-LE and abdominal swelling
-Dizziness or syncope
-Vague retrosternal chest pain
-Jugular venous distention

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109
Q

What would a medical work up for constrictive pericarditis include?

A

-Chest X-ray
-Echocardiogram
-CT scan
-Cardiac catheterization

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110
Q

What is pericardial effusion? How does this effect heart function?

A

-An abnormal accumulation of fluid in the pericardial sac
-Pericardium is relatively stiff and doesn’t tolerate large fluctuations in fluid over a short amount of time

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111
Q

What is a normal amount of fluid to be in the pericardial sac?

A

15-50 mL

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112
Q

What can cause pericardial effusion?

A

Pericarditis and other pathologies or trauma can cause pericardial effusion

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113
Q

What is the clinical presentation of pericardial effusion?

A

-Feeling of fullness in chest
-Cough
-Hoarseness
-Dysphagia
-Serious, sometimes fatal

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114
Q

What is included in the medical work up and treatment of pericardial effusion?

A

-Muffled heart and lung sounds, dullness of left lung at angle of scapula
-Chest X-ray may show enlarged cardiac silhouette
-Echocardiogram
-Pericardiocentesis to drain fluid

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115
Q

What is cardiac tamponade?

A

-Excessive over accumulation of fluid in the pericardial space that exerts pressure on the heart
-Any pericarditis can progress to tamponade but most common is neoplastic, post viral, blunt or penetrating chest trauma, or dissecting aortic aneurysm

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116
Q

What is the clinical presentation of cardiac tamponade?

A

-Poor filling of the heart
-Decreased BP
-Hypotension shock and possibly death
-Decreased CO signs: dyspnea, fatigue, syncope, dizziness
-Cough, tachycardia, tachypnea
-Beck’s triad: hypotension, jugular venous distention with pulsus parodoxus, and decreased heart sounds

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117
Q

What is included in the medical work up and treatment for cardiac tamponade?

A

-Echocardiogram
-Emergency cardiac tamponade is treated with “cardiac window” or “pericardial window” where they cut a whole in the fibrous pericardium to allow fluid to drain and relieve pressure
-Pericardiocentesis

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118
Q

What is endocarditis? What are common causes?

A

-Infection of the endocardium from bacteria or fungi
-Travels from another part of the body- most often after dental work or GI/urinary problems
-Catheters, tattoos, IV drug abuse
-Rheumatic fever

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119
Q

What is endocarditis usually treated with? What can untreated endocarditis lead to?

A

-Treated with long term antibiotics
-Untreated can lead to destruction of valves and is often fatal

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120
Q

What is the clinical presentation of endocarditis?

A

-Flu like symptoms
-Pain with breathing
-SOB
-Swelling
-Fever
-Rapid onset of flu like symptoms (acute endocarditis)
-May hear mitral valve regurgitation on auscultation

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121
Q

Who is at highest risk for developing endocarditis?

A

-People with artificial heart valves as they are reservoirs for germs/bacteria
-Damaged valves or congenital heart defect

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122
Q

What are potential complications of endocarditis?

A

-Bacterial vegetation can travel to other areas of the body
-Heart valve damage
-Abscesses
-Pulmonary embolism
-Kidney and spleen issues

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123
Q

What is included in the medical workup and treatment of endocarditis?

A

-Labs for inflammation: sed rate, C-reactive protein, WBCs, blood cultures to isolate organism
-EKG
-Echocardiogram
-Long term, high dose antibiotics
-Cardiac supportive measures
-Possible valve replacement

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124
Q

What are some measures for preventing endocarditis?

A

Prophylactic antibiotics before dental work, upper respiratory procedures involving incisions or biopsies, GI/GU procedures if infection is present

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125
Q

What is myocarditis? What is it typically caused by?

A

-Inflammatory cardiomyopathy
-Infection or inflammation of the heart walls/muscle
-Generally viral or bacterial infection, rarely is it drug induced
-Rheumatic fever
-Affects both pump and electrical conduction
-Weakens pump action

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126
Q

What is the clinical presentation of myocarditis?

A

-Diffuse chest pain
-Fatigue
-SOB
-Edema
-Arrhythmias
-Fever
-General malaise

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127
Q

What are complications of myocarditis if it goes untreated?

A

-Heart failure due to damaged cardiac muscle
-MI or CVA
-Arrhythmias

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128
Q

What is the NIH definition of cardiovascular disease?

A

The term for all types of diseases that affect the heart or blood vessels, including coronary artery disease which can cause heart attacks, strokes, heart failure, and peripheral artery disease

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129
Q

What is hypertension?

A

Blood pressure readings consistently over established guidelines

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130
Q

What is the NIH definition of coronary artery disease (CAD)?

A

A heart condition that involves atherosclerotic plaque formation in the vessel lumen which can lead to impairment in blood flow and oxygen delivery to myocardium

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131
Q

What is the ACC definition of coronary artery disease?

A

A condition where the blood vessels that supply blood to the heart become damaged or diseased

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132
Q

What is the clinical presentation of someone with cardiovascular disease or CAD?

A

-Chest pain
-SOB
-Palpitations
-Fatigue
-Syncope
-Social history
-Risk factors for cardiovascular disease

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133
Q

What is included in the medical workup for someone who may have cardiovascular disease?

A

-Diagnostic tests/imaging
-Lab values
-EKGs
-PMH/PSH, hospital course
-Medications and nutritional intake
-Social history, cognitive and language ability

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134
Q

What are the modifiable risk factors for cardiovascular disease?

A

-Cholesterol levels
-Stress
-Diabetes
-Diet
-HTN
-Weight (BMI >30kg/m2)
-Activity level
-Tobacco or smoking

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135
Q

What are the non-modifiable/relatively non-modifiable risk factors?

A

-Age: > 65 men, >55 women
-Family history: cardiac event 1st male relative <55, 1st degree female relative < 65 increases risk 1.5-2 fold
-Genetics
-Gender male > premenopausal women; after menopause risk is =
-Race: African American
-Chronic kidney disease
-Low socioeconomic status

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136
Q

What would be included in the PT evaluation for someone with CAD or high risk for cardiovascular disease?

A

-General observation: posture, breathing mechanics, cough ability
-Skin: color (is it blue, pale, etc.)
-Vitals: pulse, rhythm, BP, SpO2
-Heart and lung sounds
-Chest wall motion and palpation
-EKG (refer out)
-Circulation and lymphatic system (observe any edema, temp of skin, etc.)

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137
Q

What is the prevalence of ischemic cardiovascular disease?

A
  • > 83 million Americans have one or more forms of cardiovascular disease (1 in 3 adults)
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138
Q

What percentage of people with HTN are undiagnosed? What can unmanaged HTN cause?

A

-25% of those with HTN are undiagnosed
-Unmanaged HTN can lead to ischemic heart disease such as stroke, CAD, MI, CVA

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139
Q

What are the 2 types of HTN?

A

-Primary or essential
-Secondary

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140
Q

What is primary HTN?

A

-Most of the population (90-95%)
-No discernible/readily identifiable cause but associated with CV risk factors
-Largest number of office visits of non-pregnant US adults

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141
Q

What is secondary HTN?

A

-Small % of population
-Results from another identifiable disease process (kidney disease, endocrine disorders)

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142
Q

What is normal blood pressure?

A

<120/<80 mm Hg

143
Q

What is elevated blood pressure?

A

120-129/<80 mm Hg

144
Q

What is stage 1 hypertension?

A

130-139 or 80-89 mm Hg

145
Q

What is stage 2 hypertension?

A

≥140 or ≥90 mm Hg

146
Q

What are risk factors for hypertension?

A

-Stress
-Sleep apnea
-Birth control pills
-Moderate alcohol use (more than 1-2 drinks/day for men, more than 1 drink/day for women

147
Q

What are the diagnostic criteria for hypertension?

A

-Presents with hypertensive emergency (≥180/≥120 mm Hg)
-Presents with ≥160/≥100 with confirmed cardiac risk factors
-Mean home blood pressure is ≥130/≥80 mm Hg
-If out of office BP not attainable, HTN is confirmed if mean BP is ≥130/≥80 mm Hg for 3 visits spaced over weeks to months

148
Q

What cuff size should a small adult use for BP?

A

22-26 cm arm circumference

149
Q

What cuff size should an adult use for BP?

A

27-34 cm arm circumference

150
Q

What cuff size should a large adult use for BP?

A

35-44 cm arm circumference

151
Q

What cuff size should be used for an adult thigh/bariatric adult use for BP?

A

45-52 cm arm or leg circumference

152
Q

What is white coat HTN? Who is this condition more common in? What is the prevalence of it? What is used to diagnose it?

A

-BP elevated while in the office but normal with ambulatory BP monitor (ABPM) or home BP monitor
-More common in older adults, females, non-smokers
-Prevalence 13-35%
-Becomes clinically significant when office readings are >20/10 mm Hg higher than ABPM or HBPM

153
Q

What is masked HTN?

A

-Office BP readings normal but ABPM or HBPM are consistently above normal

154
Q

What does chronic HTN cause? What are the symptoms?

A

-Produced an overload on the left ventricle
-Stiff left ventricle leads to heart failure with reduced ejection fraction
-Predisposition towards MI due to insufficient O2 to left ventricle
-Symptoms of decreased CO: dizziness, dyspnea, impaired exercise tolerance

155
Q

What are options for the management of HTN?

A

-Weight loss
-Aerobic exercise
-Limit sodium to < 6 g/day
-Reduce alcohol
-Stop smoking
-Treat sleep apnea
-Pharmacotherapy (if daytime BP is ≥ 135 systolic or ≥ 85 mm Hg diastolic)

156
Q

How much can BP change with each 10kg weight loss?

A

10 kg weight loss is associated with 5-10 mm Hg drop in SBP

157
Q

How does aerobic exercise help to lower BP?

A

It results in lower HR and reduced levels of circulating catecholamines suggesting reduced sympathetic tone of vessels

158
Q

How much does a sedentary lifestyle increase someone’s risk for HTN?

A

Sedentary normotensive people have 20-50% higher risk of developing HTN

159
Q

What medications are typically used to treat HTN?

A

-Thiazide diuretic
-Long acting Ca2+ channel blocker (amlodipine)
-ACE inhibitors (-prils)
-Beta blockers (-olols)

160
Q

What are ACSM guidelines for HTN?

A

-Monitor BP
-Beta blockers increase possibility of hypoglycemia
-Watch for exaggerated response to exercise at low intensities
-Maintain SBP < 220 and/or DBP < 105
-Avoid valsalva
-Extended warm ups and cool downs, especially with beta blockers
-Monitor for post exercise hypotension

161
Q

What is orthostatic hypotension?

A

Drop in blood pressure from supine to sit, sit to stand, or supine to stand

162
Q

How is orthostatic hypotension diagnosed?

A

Diagnosed by a sustained reduction in systolic blood pressure of at least 20 mm Hg or diastolic blood pressure of 10 mm Hg within 3 minutes of standing after being supine for 5 minutes, or at 60 degrees on a tilt table

163
Q

What conditions are orthostatic hypotension usually secondary to?

A

-Failure of autonomic reflex
-Volume depletion
-CV disease
-Adverse reaction to a medication
-Neurogenic diseases
-Paraneoplastic syndrome

164
Q

What are common symptoms of orthostatic hypotension?

A

-Lightheadedness
-Dizziness
-Falls
-Loss of consciousness
-Visual and cognitive disturbances
-Weakness and fatigue

165
Q

Who is orthostatic hypotension more common in?

A

-Older adults
-Women
-Younger people

166
Q

What are common treatments for orthostatic hypotension?

A

-Education
-Avoid volume depletion/dehydration
-Exercise
-Mobility
-Compression stockings/abdominal binders
-Avoid alcohol and heavy meals
-Medications

167
Q

What is postural orthostatic tachycardia syndrome (POTS)? What are symptoms?

A

-Defined as a rapid increase in heartbeat of more than 30 bpm in adults or 40 bpm in adolescents or HR exceeding 120 bpm within 10 minutes of rising
-Faintness/lightheadedness
-Symptoms relieved by lying down

168
Q

What conditions can lead to POTS?

A

-Menstrual cycles increase risk
-Infections such as COVID
-Major surgery
-Trauma
-Prolonged bedrest

169
Q

What are common treatment options for POTS?

A

-Targeting low blood volume
-Higher Na+ intake
-Hydration
-Medication

170
Q

How can PT’s help with orthostasis?

A

-Move LE’s before standing
-Move segmentally
-Valsalva if not contraindicated
-Pressure garments

171
Q

What are exercise guidelines for POTS?

A

-75% max predicted heart rate or RPE 13-15 in recumbent position
-Start with 30 minutes, 3-4x/week
-Slowly increase duration and intensity in recumbent
-Start to slowly add upright but decrease intensity and duration
-Add warm ups and cool downs

172
Q

What are the risk factors for CAD?

A

-Men > 45, women > 55
-Family history: cardiac event 1st degree male < 55, 1st degree female <65
-Current or recent smoker
-Obesity: BMI ≥30
-HTN
-Dislipidemia: LDL ≥ 130 mg/dL, HDL < 40 mg/dL
-Diabetes
-Inflammation

173
Q

What is HDL? What are normal HDL levels?

A

-High density lipoprotein
-“Good cholesterol”
-Men > 40 mg/dL
-Women > 50 mg/dL

174
Q

What are behaviors that raise levels of HDL?

A

-Weight loss
-Smoking cessation
-Increased aerobic exercise

175
Q

What can reduce levels of HDL?

A

Elevated triglyceride levels

176
Q

What is considered and elevated fasting triglyceride level?

A

Anything above 200 mg/dL

177
Q

What is LDL?

A

-Low density lipoprotein
-“Bad cholesterol”

178
Q

What levels of LDL are optimal? What levels of LDL put someone at higher risk of myocardial infarction?

A

-Optimal < 100 mg/dL
-Borderline 130-159 mg/dL
-High risk 160-189 mg/dL

179
Q

What is the ideal level of LDL cholesterol in the presence of heart disease, stroke, vascular disease, aneurysm, or type 2 diabetes?

A

Ideal LDL would be less than 75 mg/dL

180
Q

What is the blood lipid ratio? What does this indicate?

A

-Total cholesterol/HDL cholesterol
-Higher the ratio, the greater the risk of CVD

181
Q

What is the PT role in CAD?

A

-Risk factor stratification/education
-Prevention
-Exercise (aerobic > 150 minutes/week, strength training 2x/week)

182
Q

How does CAD progress to ischemic heart disease?

A

Mismatch between myocardial O2 demand and supply occurs

183
Q

What are symptoms of stable angina due to ischemic heart disease?

A

-Predictable pattern of transient chest discomfort
-Pressure, tightness, squeezing, burning, heaviness
-“Elephant sitting on my chest”
-Does not vary significantly with inspiration or movement of chest wall
-Levine sign: clenched fist over sternum
-Discomfort often accompanied by tachycardia
-Relieved by cessation of precipitating activity

184
Q

What is stable angina caused by?

A

Fixed, obstructive atherosclerotic plaque in one or more arteries, causing stenosis (usually 70% or more)

185
Q

What are common triggers of stable angina?

A

-High BP
-Anemia
-Stress
-Extreme cold
-Heavy metals
-Physical exertion

186
Q

What are common locations where angina is felt?

A

-Large area over the chest/breastbone
-Between the shoulder blades
-Neck and jaw
-Inside arms
-Left shoulder
-Upper abdomen (can be mistaken for indigestion)

187
Q

What is the angina scale?

A

-1+ light, barely noticeable
-2+ moderate, bothersome
-3+ severe, very uncomfortable
-4+ most severe pain ever experienced

188
Q

What is the Canadian Cardiovascular Angina Classification?

A
  • I: angina with strenuous activity
  • II: angina with slightly greater than normal activity
  • III: angina resulting in marked limitation in normal activity
  • IV: angina at rest
189
Q

How does cardiac rehab effect risk of mortality and non-fatal MI?

A

-Reduces total mortality by ≥ 20%
-Reduces cardiac mortality by ≥ 26%
-Decreases non-fatal MI by ≥ 21%

190
Q

What are the PT exercise guidelines for stable angina?

A

-30-60 minutes of moderate intensity (40-60% THR), 5 days/week
-Increase daily lifestyle activities
-Resistance train 2 days/week, moderate intensity (40-60% of 10RM)
-Avoid valsalva
-Longer warm up and cool down

191
Q

What is variant or Prinzmetal angina?

A

-Develops due to coronary artery spasm, not due to oxygen demand mismatch
-More common in women, smokers and cocaine users
-Rare
-Usually occurs at rest or in the middle of the night
-Patients usually very active
-May or may not have associated CAD
-Vasospasm can be triggered by anything that causes vasocontriction
-Silent ischemia (asymptomatic, detected on EKG)

192
Q

What is unstable angina?

A

-Increasingly variable frequency and duration of angina symptoms
-Change in anginal pattern
-Usually indicates a progression of ischemic heart disease
-Often result of a rupture of atherosclerotic plaque
-Often precursor to MI
-Higher morbidity and mortality rates
-Lower physical, emotional threshold to trigger angina symptoms
-Chest pain at rest

193
Q

What are the PT exercise guidelines for unstable angina?

A

-Get physician clearance
-Know patients medications
-Lifestyle modifications
-Extended warm up and cool down
-30-40% of THR
-STOP with any onset of angina symptoms
-Shorter duration
-No HIIT
-Take vitals!!!

194
Q

What is a major symptom/sign that someone is having an MI?

A

Chest pain greater than 20 minutes without relief with decreasing activity

195
Q

What is the most common cause of an MI?

A

Atherosclerotic plaque rupture in an already blocked artery

196
Q

What are the two types of MI?

A

-NSTEMI: non ST elevation MI
-STEMI: ST elevation MI

197
Q

What is the clinical presentation of MI?

A

-Unstable angina
-Severe “crushing” persistent pain, typically substernal
-Dyspnea
-Diaphoresis and cool, clammy skin
-Nausea, vomiting, weakness
-Pulmonary rales/crackles
-EKG abnormalities

198
Q

What is included in the medical work up for MI?

A

-Presenting symptoms
-EKG
-Serum biomarkers (troponins, CK)

199
Q

What is the medical management of MI?

A

-Early recognition is key
-Time is tissue: rapid revascularization
-Cardiac catheritization
-CABG
-Manage arrhythmias
-Echocardiogram
-Supplemental O2
-Continuous EKG monitoring

200
Q

What is the time frame for optimal outcomes for MI patients?

A

If time from onset of symptoms to cathlab table is less than 90 minutes

201
Q

What time frame from onset of symptoms to treatment can myocardial injury be reversed?

A

20 minutes

202
Q

What is the Thrombolysis in Myocardial Infarction (TIMI) risk score?

A

-Predicts likelihood of death or subsequent ischemic events
1. Age > 65
2. ≥ 3 CAD risk factors
3. Known coronary artery stenosis ≥ 50%
4. ST segment deviations
5. At least 2 angina episodes in the last 24 hours
6. Use of aspirin in last 7 days
7. Elevated serum troponin or CK

203
Q

What are potential complications of MI?

A

-Recurrent ischemia
-Arrhythmias
-Heart failure
-Cardiogenic shock
-Right ventricular infarction
-Mechanical complications
-Acute pericarditis
-Thromboembolism

204
Q

What should post MI PT look like?

A

-Know EF to prescribe exercise
-Early mobilization
-Low level aerobic and low intensity strength training
-Patient eduction on self-monitoring, risk factors
-Discharge planning

205
Q

What is an inotrope?

A

-A substance that alters the force of muscle contraction
-A positive inotrope will increase strength of muscular contraction

206
Q

What is cardiac muscle dysfunction (CMD)? What is the most common cause of cardiac muscle dysfunction?

A

-Heart is unable to pump blood forward at a sufficient rate or volume to meet the metabolic demands of the body
-Impaired left ventricular function
-Congestive heart failure (CHF)

207
Q

What is the prevalence of CHF?

A

-5.7 million Americans have CHF
-Lifetime risk to develop HF is 1 in 5 adults at age 40
-Over 85, risk is 65%

208
Q

How does hypertension lead to CMD?

A

-Increased arterial pressure leads to left vetricular hypertrophy
-Leads to overstretched contractile fibers and less-effective pump

209
Q

How does CAD lead to CMD?

A

Related to dysfunction of left or right ventricle as a result of injury

210
Q

What can cause CMD?

A

-HTN
-CAD
-Cardiac arrhythmias
-Rapid or slow arrhythmias can impair function of ventricles
-Renal insufficiency
-Cardiomyopathy

211
Q

How does renal insufficiency lead to CMD?

A

Acute or chronic insufficiency produces fluid overload

212
Q

What is the leading cause of heart failure and cardiac transplant?

A

Cardiomyopathy

213
Q

What are the three main types of cardiomyopathy?

A

-Dilated
-Hypertrophic
-Restrictive

214
Q

What is dilated cardiomyopathy?

A

-Ischemic or non-ischemic
-Enlarged ventricle
-Systolic dysfunction

215
Q

What is hypertrophic cardiomyopathy?

A

-Abnormal left ventricular wall thickness
-Diastolic dysfunction

216
Q

What is restrictive cardiomyopathy?

A

-Abnormal left vetricular wall stiffness but not thickness
-Diastolic dysfunction

217
Q

What is primary cardiomyopathy?

A

-Usually inherited (familial)
-No other cardiac problems
-Usually younger onset

218
Q

What is secondary cardiomyopathy?

A

Caused by a medical condition

219
Q

What can cause dilated cardiomyopathy?

A

-Idiopathic
-Systemic, significant, long-term, uncontrolled HTN
-Family history/genetics
-Inflammatory myocarditis
-Toxicity due to alcoholism and cocaine use or chemotherapy
-Metabolic disorders
-Pregnancy related

220
Q

What can cause hypertrophic cardiomyopathy?

A

-Genetic
-Autosomal dominant mutations

221
Q

What can cause restrictive cardiomyopathy?

A

-Hemochromatosis
-Metabolic diseases
-Radiation therapy
-Scleroderma
-Fibrotic tissue

222
Q

What are the signs and symptoms of dilated cardiomyopathy?

A

-Same symptoms as heart failure with reduced ejection fraction
-S3 heart sound and mitral valve regurgitation
-Crackles/rales and dullness to percussion
-Imaging shows enlarged heart

223
Q

What are signs and symptoms of hypertrophic cardiomyopathy?

A

-Symptoms vary widely
-Average age of presentation age 20
-Dyspnea and angina (not because of CAD)
-High O2 demand due to thick cardiac wall
-Arrhythmias and syncope
-S4 heart sound

224
Q

What are signs and symptoms of restrictive cardiomyopathy?

A

-Decreased CO
-Fatigue and decreased exercise tolerance
-Systemic edema > pulmonary congestion
-JVD
-Ascites
-Hepatomegaly
-Arrhythmias

225
Q

How can heart valve abnormalities effect the contractility of the heart?

A

A blocked or incompetent valve causes the heart to contract more forcefully

226
Q

What are heart valve abnormalities associated with?

A

Myocardial dilation and hypertrophy

227
Q

What are common surgeries for heart valve abnormalities?

A

-Valve replacement
-Valvuloplasty
-Valvulotomy
-Commisurotomy

228
Q

What is pulmonary hypertension?

A

-Defined by mean pulmonary artery pressure (mPAP)
-Abnormal is > 25 mm Hg or in patients with COPD if > 20 mm Hg

229
Q

How can a pulmonary embolism lead to cardiac muscle dysfunction?

A

-Results in dysfunction due to elevated pulmonary artery pressures that increase R ventricular work
-Potentially life threatening

230
Q

What is the treatment of a pulmonary embolism?

A

-Rapid acting fibrinolytic agent
-Sedative to decrease anxiety and pain
-Oxygen
-Embolectomy

231
Q

How can age effect or cause cardiac muscle dysfunction?

A

-Aging decreases cardiac output by altering contraction and relaxation of cardiac muscle
-Higher prevalence of heart disease and other risk factors in older adults
-Congenital heart disease

232
Q

What is the universal definition of heart failure?

A

A clinical syndrome with symptoms and/or signs caused by a structural and/or functional cardiac abnormality and corroborated by elevated natriuretic peptide levels and/or objective evidence of pulmonary or systemic congestion

233
Q

What is the universal classification of heart failure?

A

-Stage A: at risk for HF
-Stage B: Pre-HF
-Stage C: Symptomatic HF
-Stage D: Advanced HF

234
Q

What are the subclassifications of symptomatic and advanced HF?

A

-HFrEF: symptomatic HF with LVEF ≤ 40%
-HFmrEF: symptomatic HF with LVEF 41-49%
-HFpEF: symptomatic HF with LVEF ≥ 50%
-HFimpEF: symptomatic HF with a baseline LVEF ≤ 40%, a ≥ 10-point increase from baseline, and a second measurement of LVEF > 40%

235
Q

What is the Frank-Starling mechanism?

A

-The ability of the heart to change its force of contraction and therefore stroke volume in response to changes in venous return
-Length-dependent relationship (muscle fibers)
-Intrinsic cardioregulatory mechanism
-Allows the heart to adjust rapidly to changing preload conditions to keep the output near constant

236
Q

How are heart failure etiologies grouped?

A

-Impair cardiac contractility: systolic dysfunction
-Increase afterload: systolic dysfunction
-Impair ventricular relaxation and filling: diastolic function

237
Q

What heart failure etiologies cause impaired cardiac contractility?

A

-Reduction in muscle mass
-Cardiomyopathy

238
Q

What heart failure etiologies can cause an increase in afterload?

A

-Systemic/pulmonary HTN
-Aortic or pulmonic valve stenosis
-Both of these lead to ventricular hypertrophy

239
Q

What heart failure etiologies can impair ventricular relaxation and filling?

A

-Increased ventricular stiffness/ventricular hypertrophy
-Myocardial disease or infarction
-Mitral or tricuspid valve stenosis
-Pericardial disease

240
Q

What are the most common contributing etiologies for heart failure?

A

-HTN
-CAD/ischemia/MI
-Cardiac dysrhytthmias
-Renal insufficiency
-Cardiomyopathy
-Valve abnormalities
-Chronic pericardial effusion
-Pulmonary embolism
-Pulmonary HTN

241
Q

How does structural pathology of the left ventricle lead to structural heart failure? What are 2 hallmark symptoms?

A

-Reduces CO and leads to an accumulation of fluid in the left atrium
-Subsequent pulmonary and peripheral congestion
-Dyspnea and cough (CHF)

242
Q

How does structural pathology of the right ventricle lead to structural heart failure? What are the hallmark symptoms?

A

-Reduction in right ventricular CO which results in venous congestion
-JVD
-Peripheral edema
-Ascites
-Pleural effusion
-Weight gain

243
Q

What is right heart failure also known as?

A

Cor Pulmonale

244
Q

How does structural pathology of both ventricles lead to structural heart failure? What are the hallmark symptoms?

A

-Left ventricle overloads resulting in pulmonary edema
-Right ventricle overloads resulting in systemic congestion
-Dyspnea
-Cough
-Peripheral edema
-Weight gain
-JVD

245
Q

What is Heart Failure with Reduced Ejection Fraction (HFrEF)?

A

-Systolic dysfunction
-Left ventricle has diminished capacity to eject blood due to impaired contractility or pressure overload
-Pump problem: either too stretched out or too damaged

246
Q

What is Heart Failure with Preserved Ejection Fraction (HFpEF)?

A

-Diastolic dysfunction
-Impaired diastolic relaxation
-Ventricular wall stiffness
-Extensibility problem: muscle cannot accommodate pressure changes required for physiologic changes associated with exercise
-More common in older adults, females > males

247
Q

What is the New York Heart Association classification of HF?

A
  • I: No limitation of physical activity; ordinary activity does not cause SOB
  • II: Slight limitation of physical activity; ordinary physical activity results in fatigue, palpitation, dyspnea
  • III: Marked limitation of physical activity; comfortable at rest; less than ordinary activity causes fatigue, palpitation, or dyspnea
  • IV: Unable to carry on any physical activity without discomfort; symptoms of heart failure at rest
248
Q

What is the AHA classification of heart failure? What is different about this classification than others?

A

-Stage A: at risk
-Stage B: patients with structural disease
-Stage C: patients who have developed clinical HF
-Stage D: patients with refractory HF requiring advanced intervention
-There is no moving backwards in this scale, unlike NYHA

249
Q

What is compensated heart failure?

A

Patient with diagnosed HF but not exhibiting signs of pulmonary or peripheral congestion

250
Q

What is acute uncompensated heart failure?

A

The presence of new or worsening symptoms of dyspnea, fatigue, or edema that leads to hospitalization or unscheduled medical care

251
Q

What other systems are affected by HF?

A

-Renal function
-Pulmonary function
-Hepatic function
-Skeletal muscle dysfunction
-Pancreatic function

252
Q

What does the medical management of heart failure include?

A

-Lifestyle changes
-Pharmacologic
-Mechanical management (LVAD, pacemakers, impella, etc.)
-Surgical management
-Dialysis to manage fluid overload and reduce work of kidneys

253
Q

What would the physical therapy exam include for heart failure?

A

-Vitals
-Review imaging reports
-Breathing/RR
-Dyspnea
-Heart and lung sounds (S3, rales/crackles)
-May have orthopnea (harder to breathe while lying down)
-Check edema
-Assess exercise tolerance
-Cognition
-Nutritional status

254
Q

How is orthopnea described?

A

By number of pillows needed to allow the patient to breathe with ease and comfort

255
Q

What are the benefits of exercise for heart failure?

A

-Improved exercise tolerance
-Improved coronary artery flow
-Improved quality of life but no evidence or reduced mortality
-Safe with monitoring of vitals and lower intensities

256
Q

What is the exercise guidelines for heart failure?

A

-Resistance training with light weights (large muscle groups)
-Avoid valsalva
-Light to moderate (1-5 on modified Borg)
-Work up to 150 minutes/week
-Aerobic > resistance
-Prolonged warm up and cool down

257
Q

What are PT implications for heart failure?

A

-Vitals
-Heart and lung sounds throughout
-Start slow and build up
-Monitor edema
-Focus on functional activities

258
Q

What is Life’s Simple 7?

A

-7 modifiable risk factors changeable through behavior modification
-Smoking
-Diet
-Glucose
-BMI
-Physical activity
-BP control
-Cholesterol
-Assigned 0-2 points each for a total of 14

259
Q

What is Life’s Essential 8?

A

-Predictor of heart health
-Smoking
-Diet
-BMI
-Sleep
-Physical activity
-BP
-Cholesterol
-Glucose

260
Q

How can PT’s treat acute uncompensated heart failure?

A

-Education on disease management
-Encourage low sodium, mediterranean diet
-Encourage safe activity
-Educate patient on symptoms of exacerbation
-Early mobilization
-Monitor vitals and RPE
-Reduce effects of prolonged bed rest

261
Q

How much weight gain would be a red flag for patients with heart failure or other CVD?

A

-2-3 lbs in 24 hours
-11 lbs in 3 days

262
Q

When is a CABG performed?

A

-Emergency situations: MI, CVA
-Urgently: symptoms prompt patient to seek medical care
-Electively: blockage found on cardiac stress test

263
Q

How many arteries can a CABG involve?

A

Between 1-4 arteries depending on which are blocked

264
Q

What are the class I indications for a CABG according to AHA?

A

-Over 50% left main artery stenosis
-Over 70% stenosis of the proximal LAD and proximal circumflex arteries
-Three-vessel disease in asymptomatic patients or patients with mild stable angina
-Three-vessel disease with poximal LAD stenosis in patients with poor LV function
-Over 70% proximal LAD stenosis with either an ejection fraction below 50% or demonstrable ischemia on noninvasive testing

265
Q

What are other indications for CABG?

A

-Disabling angina
-Ongoing ischemia in the setting of a non-ST segment elevation MI that is unresponsive to medical therapy
-Poor LV function
-Inability to perform or failure to resolve symptoms with percutaneous re-vascularization (PTCA)
-Patients with advanced kidney disease that PTCA would be dangerous for due to contrast dye

266
Q

What are the outcomes of CABG vs PTCA?

A

-CABG shown to have better long term outcomes than catheter based interventions
-CABG has lower risk of CVA or MI
-CABG can have a higher morbidity rate and longer recovery

267
Q

What are the most common approaches for CABG?

A

-Sternotomy: either directly through midline of the sternum or costo-sternal junction
-“On” or “off” pump
-Anterior thoracotomy: used for LAD
-Lateral thoracotomy: used for smaller vessels, often “off” pump
-Minimally invasive direct CABG: robotic assisted

268
Q

What is an “on” pump CABG?

A

A CABG when the heart is connected to tubing which intercepts blood coming into the right atrium, stores it in a reservoir, adds oxygen/removes CO2, cools the blood, and delivers it to the body

269
Q

How long does an “on” pump CABG give the surgeon?

A

About an hour to perform the CABG while the heart is on the pump

270
Q

What is an “off” pump CABG?

A

The CABG is performed while the heart is beating

271
Q

What are advantages to “on” pump CABG?

A

-Gives surgeon more time for complicated cases
-More complete vascularization
-Better for emergent CABG

272
Q

What are disadvantages to “on” pump CABG?

A

-“Pump Head” or Post Operative Cognitive Decline (POCD)
-Can delay discharge due to POCD

273
Q

What is POCD?

A

-Due to decreased oxygen to brain
-Could be reaction from anesthesia
-More pronounced in older adults
-Delirium, cognitive changes, brain fog
-Short lived (10-14 days)

274
Q

What are advantages of “off” pump CABG?

A

-No need to stop the heart so no POCD
-Lower risk of clotting, arrhythmias
-Shorter hospital stays
-Reduction in mortality

275
Q

What are common harvest sites for CABG?

A

-Saphenous vein
-Left internal thoracic (mammary) artery
-Radial artery
-Right internal thoracic (mammary) artery
-Short saphenous vein
-Cephalic vein or UE vein

276
Q

What is the disadvantage for using great saphenous vein for CABG?

A

High re-occlusion rate

277
Q

What harvest site for CABG has shown the best outcomes?

A

Left internal thoracic (mammary) artery

278
Q

What are the possible thoracic surgery complications?

A

-15-20% of patients have complications, and 3-4% of those will die
-Surgical access and donor site infection
-Pain
-Blood loss
-Pulmonary complications
-Cardiac complications
-Decreased CO
-Arrhythmias
-Bleeding
-Ischemia or subsequent MI
-Stroke
-DVT

279
Q

What are indications for valve repairs and replacements? What valves are the most commonly repaired/replaced?

A

-Stenotic valves
-Incompetent or “leaky” valves
-Aortic valve and mitral valve most commonly repaired/replaced

280
Q

What causes stenotic valves? How does it affect the heart? How is it rated?

A

-Atherosclerotic plaques
-Increase afterload and work of the heart which can lead to cardiomyopathy
-Rated mild (1+) to critical (4+)

281
Q

How does an incompetent or “leaky” valve affect the heart? How is it rated?

A

-Allows back flow or regurgitation
-Rated mild (1+) to critical (4+)

282
Q

What are risk factors for heart valve dysfunction?

A

-Endocarditis
-Rheumatic fever
-History of IV drug abuse
-Chronic and poorly managed HTN
-Congenital valve defects

283
Q

When would a valve repair or replacement be performed?

A

If the rating was 2+ or worse

284
Q

What are the different methods for valve repairs/replacements?

A

-Mechanical
-Biotissue
-Transcatheter aortic valve replacement (TAVR)
-Transcetheter mitral valve replacement (TMVR)

285
Q

What is the annuloplasty valve repair?

A

Replaces the ring of the valve but leaves the leaflets in place

286
Q

What is the mechanical method of valve replacement? What population is this usually done in? What are the drawbacks of it?

A

-Ball or disc mechanism
-Highly durable and can last a lifetime
-Younger patients
-Subtle but audible “click” with heart contractions
-Anticoagulants for lifetime

287
Q

What is the biotissue method of valve replacement? What population is this usually done in? What are the drawbacks of it?

A

-Uses human, bovine, or porcine heart valves
-Lifetime coagulation not needed
-Older patients
-Only 10-20 years durability

288
Q

What often occurs in conjunction with a valve replacement?

A

It is not uncommon to perform a CABG and valve replacement at the same time

289
Q

What are post op considerations?

A

-Medications: some may effect HR, BP, and O2
-Sternal precautions

290
Q

What risk factors increase risk of dehiscence of sternum after thoracic/open heart surgery?

A

-Female
-Diabetes
-Bilateral internal mammary artery harvesting
-Re-operation procedures
-Increased blood product requirement

291
Q

What movement has the greatest and least amount of sternum separation and skin movement that should be avoided during sternal precautions?

A

-Greatest: pushing up from a chair with UE
-Least: overhead movements

292
Q

What is the Sternal Instability Scale?

A

-0: clinicall stable sternum (no detectable motion)
-1: Minimally separated sternum
-2: Partially separated sternum regional
-3: Completely separated sternum, entire length

293
Q

What is the ACSM guidelines for movement with sternal precautions?

A

-5-8 weeks no lifting anything more than 5-8 lbs
-ROM exercises and lifting 1-3 lbs if there is no evidence of sternal instability
-Patients should limit ROM with any onset of feelings of pulling on the incision or mild pain

294
Q

What are traditional sternal precautions?

A

-No lifting, pulling, pushing > 10 lbs
-No use of UE for sit to stand
-Counter pressure with valsalva
-No driving 2-4 weeks
-Avoid horizontal abduction past midline
-No scapular retraction
-No lifting arms > 90 degrees

295
Q

What is the “Keep your move in the tube” principle?

A

Patients who are at low risk of sternal dehiscence can lift their arms above head, push themselves out of a chair, etc. as long as their arms are tucked in very close to their body

296
Q

What are post op CABG and valve replacement considerations?

A

-Vitals
-Post-op cognition
-Signs of post intensive care syndrome
-Lab values for anti-coagulation levels and signs of infection
-Lines and tubes and mechanical intervention
-Harvest vein site
-Sternal incision site
-Deep breathing, coughing
-Functional mobility
-Mechanical ventilation
-Discharge planning

297
Q

What is an abdominal aortic aneurysm?

A

-Abnormal focal dilation of the abdominal aorta, 50% larger than normal due to a weakened vessel wall
-Mostly asymptomatic
-Described relative to the involvement of the renal or visceral vessels
-Most common of aneurysms

298
Q

Where do 80% of aortic aneurysms occur?

A

Between the aortic bifurcation and the renal arteries

299
Q

How are aortic aneurysms usually found?

A

-Usually found by pulsatile mass on physical examination
-Abdominal imaging
-US screening for cardiac disorder
-During work up for associated cardiac disease
-During cardiac catheterization

300
Q

What are risk factors for an abdominal aortic aneurysm?

A

-Smoking
-Male gender
-Advancing age
-Caucasian race
-Atherosclerosis
-Family history of AAA
-Other arterial aneurysms
-Connective tissue disorder
-Prior history of aortic dissection
-Prior history of aortic surgery

301
Q

What types of abdominal aortic aneurysms are there?

A

-Symptomatic (non-ruptured): 5-22% of patients
-Ruptured: mortality rate > 80%

302
Q

What are symptoms of a non-ruptured aortic aneurysm?

A

-Pain is most common symptom
-Most often abdominal, but can also radiate to back, flank, pelvis, groin, or thigh
-May present with general malaise

303
Q

What is the most common treatment of abdominal aortic aneurysm?

A

Endovascular repair

304
Q

When are heart transplants done?

A

-End stage heart disease
-NYHA stage III-IV, AHA stage D uncompensated HF
-Poor quality of life

305
Q

What are absolute contraindications for heart transplant?

A

-Solid organ or blood malignancy in the last 5 years
-ETOH, tobacco, or substance abuse < 6 months
-HIV
-SLE, sarcoidosis, amyloidosis
-Irreversible hepatic or renal dysfunction
-Significant COPD
-Pulmonary HTN
-Severe cerebrovascular disease
-Hep B or C

306
Q

What are relative contraindications for heart transplant?

A

-Age > 70
-Active infection
-Active peptic ulcer
-Severe DM
-Severe PVD
-Symptomatic carotid stenosis
-Uncorrected AAA
-BMI > 35 kg/m2
-Severe pulmonary dysfunction
-Severe HTN
-Dementia or poor social support

307
Q

What is a heterotropic heart transplantation (HTT)?

A

-“Piggyback”
-Native heart is not removed
-Donor heart is connected ot the native heart via right/left atria

308
Q

What is a total heart transplantation?

A

Complete excision of the recipient atria with complete atrioventricular transplantation, bicaval and pulmonary venous anastomoses

309
Q

What is the biatrial technique of heart transplantation?

A

-Biatrial anastomoses whereby donor and recipient atrial cuffs are sewn together
-Leaves recipient SA node intact
-Two separate P waves will be seen on EKG

310
Q

What are PT considerations for heart transplantation?

A

-Infection control
-Aerobic endurance
-Vitals
-Denervated heart
-Often out of ICU in 48 hours
-Denervation of donor heart requires adequate warm up and cool down
-HR monitoring is not an accurate measure of exercise intensity

311
Q

What are outcome measures that should be considered post heart transplantation?

A

-6MWT
-30 second chair stand
-Frailty scales

312
Q

What are signs and symptoms of rejection?

A

-Low grade fever
-Myalgia and fatigue
-Hypotension with activity but hypertension at rest
-Decreased exercise tolerance and dyspnea
-Arrhythmias
-Weight gain due to fluid retention
-Decreased urine output

313
Q

What will aerobic power be at after 1 year post heart transplantation?

A

40-50% of age matched controls

314
Q

What will peak exercise CO be at after 1 year post heart transplantation?

A

30-40% lower than age matched controls

315
Q

What are physical therapy priorities post cardiac surgery?

A

-Pulmonary hygeine
-Vitals and activity tolerance management
-Cognitive management
-Sternal or thoracotomy wound management
-LE donor site management (CABG)
-Mobility
-Discharge planning

316
Q

What is a sign of SA node dysfunction? What is the typical treatment?

A

-Marked sinus bradycardia (HR < 60 BPM) or sinus arrest
-Paroxysmal supraventricular tachycardias (PSVT): atrial fibrillation or flutter
-Permanent pacemaker & anti-arrhythmic drugs

317
Q

What types of pacemakers are there?

A

-Temporary
-Permanent

318
Q

What are the 3 types of temporary pacemakers?

A

-Transcutaneous: electrodes placed on chest wall
-Transatrial: electrodes are placed directly onto the atria, usually right
-Transvenous: electrodes placed directly onto the ventricle

319
Q

What are indications for temporary pacemakers?

A

-Acute MI
-Post-cardiac surgery
-Drug toxicity
-Bridge to permanent pacemaker

320
Q

What are the characteristics of a permanent pacemaker?

A

-Small. lightweight (1-2 oz.)
-Battery operated
-Wires implanted into the heart
-Device implanted distal to left clavicle area
-Sends electrical stimulus directly to heart muscle

321
Q

What are common indications for a permanent pacemaker?

A

-SA node dysfunction
-2nd degree AV block with symptomatic bradycardia
-3rd degree AV block with symptomatic bradycardia, CHF, a-fib/flutter, or documented periods of asystole
-Acute anterior MI w/ 2nd or 3rd degree AV block
-Severe bundle branch blocks

322
Q

What are some conditions that may warrant a pacemaker?

A

-Syncope
-Dizziness
-CHF
-Mental confusion
-Palpatations
-Dyspnea
-Exercise intolerance

323
Q

What is the pacing of the right atrium if the pacemaker is placed there?

A

Increases atrial contribution to ventricular filling, resulting in increased CO

324
Q

What is the pacing of the right ventricle if the pacemaker is placed there?

A

Increases rate in presence of heart block or symptomatic bradycardia

325
Q

What is the pacing of dual chamber if the pacemaker is placed there?

A

-Electrodes placed in R atrium and R ventricle
-Maintains timing between atrial & ventricular contractions further increasing CO

326
Q

What are the different modes of pacing?

A

-Fixed
-Demand
-Rate-responsive

327
Q

What is the fixed mode of pacing?

A

Fires at a specific, preset rate

328
Q

What is the demand mode of pacing?

A

-Fires only when HR falls below preset value
-Sensing mechanism: ability of pacemaker to determine when intrinsic rate id adequate
-Pacing mechanism: triggered when no intrinsic ventricular complex occurs within set parameters

329
Q

What is the rate-responsive mode of pacing?

A

-Fires depending on patient’s level of activity and respiration
-Automatically increased with increased CO
-Many new pacemakers use this type of pacing

330
Q

What are ICD’s? How do they work?

A

-Implantable cardioverter defibrillator
-Newer pacemakers have ICD’s embedded in them
-Delivers a shock to the heart to cardiovert when a fatal arrhythmia is detected

331
Q

What are ICD’s indicated for?

A

Indicated for life threatening arrhythmias

332
Q

What is a cardiac resynchronization device?

A

-A type of ICD
-Used with CHF, paces both ventricles at once

333
Q

What are PT implications for working with patients with pacemakers and ICD’s?

A

-Is patient fully dependent upon temporary pacemaker?
-Be careful with wires and leads: dislodging them could kill a patient
-Patient education: no prolonged contract with electrical devices

334
Q

What are general precautions for post implantation of a pacemaker or ICD?

A

-Bedrest for a few hours
-Sling on left arm for 24 hours
-Avoid L shoulder flexion, abduction > 90 degrees
-No driving until cleared by electrophysiologist

335
Q

What is a Holter Monitor?

A

-Ambulatory electrocardiography device
-A portable device that continuously monitors electrical activity of the heart for 24 hours or more
-Useful for observing occasional cardiac arrhythmias
-Records activity via a series of electrodes attached to the chest

336
Q

What is an LVAD?

A

-Left ventricular assistive device
-A mechanical pump that takes over the function of the damaged ventricle to restore normal blood flow

337
Q

What are the two types of LVADs?

A

-Pulsatile: older, noisy
-Axial flow: continuous flow, more popular now, quiet

338
Q

What are indications for an LVAD?

A

-Bridge to transplant
-Destination therapy: long term, implant is permanent

339
Q

What is the life expectancy of someone with an LVAD?

A

5-10 years

340
Q

What is the criteria for an LVAD?

A

-At least 2 admissions to the hospital
-Not improving with medications
-Hyponatremic
-Hypovolemic
-Inotrope dependent
-Ejection fraction < 35%

341
Q

How does an LVAD affect the functioning of the heart?

A

-Restores CO and blood pressure
-Reduces the work of the left ventricle and prevents further damage
-Improves perfusion to all body organs
-LVAD most common but RVAD or BiVAD is also possible

342
Q

What is the typical battery life of an LVAD?

A

-Anywhere between 7-17 hours depending on brand
-360 uses

343
Q

What are the oeprating procedures of LVADs?

A

-Test Select Button: performed everyday
-Steady audio tone should be heard
-All lights should illuminate for 5 seconds
-If this doesn’t happen, the controller needs to be replaced
-Only use fully charged batteries
-Make sure to only disconnect one battery at a time when switching them out

344
Q

What does the “+++” symbol mean on an LVAD?

A

-Blood flow is moving at over 10 L/min through the pump which is abnormal
-This could be normal in larger patients
-Could be indicative of a clot forming in the pump

345
Q

What does the “—” symbol mean on an LVAD?

A

-Blood flow is moving at less than 2.5 L/min through the pump
-This could be normal for smaller sized patients
-Could be indicative that patient is hypovolemic (“dry”) and requires fluid bolus

346
Q

When is a “+++” or “—” not a red flag? When does it become a red flag?

A

-If you are moving a patient
-It becomes a red flag if it is sustained

347
Q

What vitals should be taken for patients with LVAD?

A

-BP
-MAP
-Pulse (may be thready or absent)
-Oxygen saturation

348
Q

What is an impella?

A

-Mechanical circulatory assistive device
-Mini VAD that pumps blood from L ventricle into aorta
-2.5-5 L/min

349
Q

When is an impella indicated?

A

-Patients with MI complicated by cardiogenic shock
-Needs circulatory support with complicated PCI/PTCA
-Severe uncompensated HF
-Myocarditis
-Conditions where the L ventricle needs to rest to reduce work of the heart
-Off pump CABG

350
Q

How long is an impella approved to be used for by the FDA?

A

-6 hours in 2015
-Now approved for 14 days and for off label use for slightly longer periods

351
Q

What are precautions for PT after LVAD, impella, or ICD placement?

A

-Level of arousal
-Anticoagulants
-Vasopressors
-High level oxygen support
-Arrhythmias
-Pulmonary artery catheter
-Arterial lines
-Central venous pressyre line
-Chest tubes
-Median sternotomy
-Intra aortic balloon pump removal
-Patients with impella dye to cardiogenic shock

352
Q

What is cardiogenic shock?

A

The heart can no longer pump an adequate volume of blood to meet the needs of the organs

353
Q

What are contraindications for PT post VAD, impella, or ICD placement?

A

-VAD malfunction
-Intra-aortic balloon pump
-Open chest
-Active bleeding
-Hemodynamic instability
-Full ventilator support

354
Q

What does PT interventions include post VAD, impella, or ICD placement?

A

-Focus on function
-STRICT sternal precautions (no Move in the Tube)
-Pulmonary care
-Be careful with percussion
-Post-op pain can lead to kyphotic posture which can compromise the drive line and reduce blood flow
-HR will be blunted by beta blockers
-Stop if symptoms of angina appear or dyspnea > 5 on Borg
-Vitals!!!

PHTH 536: Body Systems (2 decks)

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