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PHTH 536 - Body Systems > CVD: HTN and CAD - Lecture #2 > Flashcards

CVD: HTN and CAD - Lecture #2 Flashcards

1
Q

What is cardiovascular disease?

A

All types of disease that affect the heart or blood vessels that includes coronary heart disease/coronary artery disease
- which can cause heart attacks, stroke, heart failure and peripheral artery disease

NIH

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2
Q

What can the heart disease involve issue of?

A

The heart itself, such as arrhythmias or cardiomyopathy
- while vascular disease can inlude issues with the blood vessels such as high blood pressure or peripheral artery disease

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3
Q

What is the NIH definition of coronary artery disease?

A

Common heart condition that involves atherosclerotic plaque formation in the vessel lumen
- leads to impairment in blood flow and thus O2 delievery to the myocardium

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4
Q

What are some presenting sx?

A
  • onset, progression, nature, aggravating and alleviating
  • chest pain with SOB and palpitations
  • fatigue
  • syncope and dizziness
  • social hx
  • risk factors for CVD
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5
Q

What are some modifiable risk factors of CVD?

A
  • cholestrol levels
  • stress
  • diabetes
  • diet
  • HTN
  • weight
  • activity level
  • tobacco
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6
Q

What are some non-modifiable risk factors of CVD?

A
  • age
  • family hx
  • genetics
  • male > premenopausal female (equal after menopausal risk)
  • race: african americans
  • chronic kidney disease
  • low socioeconomic status
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7
Q

What are the ages for men and women for non-modifiable risk factor?

A

overall > 65
men > 45
women > 55

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8
Q

What are the non-modifiable risk factors for family hx?

A
  • cardiac event of a 1st degree male relative < 55
  • cardiac event of a 1st degree female relative < 65
  • 1.5-2 fold relative risk
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9
Q

What are we looking for when it comes to examination of CVD patients?

A
  • general observation: posture, how they breath, ability to cough
  • skin: are they bluish? are they pale or washed out? Sweating?
  • Vitals: pulse, BP or SpO2
  • Heart and lung sounds
  • Chest wall motion and palpation
  • Rhythm - EKG
  • Circulation and lympathic system (that includes the Peripheral vascular system)
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10
Q

What are the pathologies of the CVD and vascular disease?

A

> 83 million Americans have one or more forms of CVD (1 in 3 adults)
- 25% of those that have HTM are undiagnosed and unaware which is the SILENT KILLER
- screening for CVD and CVD risk factors is needed for all patients

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11
Q

Description of the primary or essential hypertension types

A
  • most of the population (90-95%)
  • No discernible/readily identifiable cause but has to do with CV risk factors
  • Biggest number of office visits of non-pregnant adults in the US
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12
Q

Description of the secondary hypertension types

A
  • small % of the population
  • results from another identifiable disease process (kidney disease, endocrine disorder)
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13
Q

What is considered normal BP?

A

< 120 / < 80 mmHg

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14
Q

What is considered elevated BP?

A

120-129 / < 80 mmHg

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15
Q

What is considered stage 1 hypertension?

A

130-139 / 80-89 mmHg

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16
Q

What is considered stage 2 hypertension?

A

> 140 / > 90 mmHg

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17
Q

What the other risk factors of hypertension?

A

stress, sleep apnea, the use of birth control pills, moderate alcohol use (more than 1-2 drinks/day for men - more than 1 drink/day for women)

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18
Q

What is HTN associated with?

A

Increased CVD incidence
Increased MI
Angina
CVA
HF (heart failure)
PAD (peripheral artery disease)
AAA (abdominal aortic aneurym)

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19
Q

How is HTN diagnosed?

A
  • present with hypertensive emergency (> 180 / > 120)
  • preasents with BP > 160 / > 100 and confirmed cardiac risk factors = highly suspicious
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20
Q

How are patient able to self diagnose?

A

If any mean home blood pressure is >130/>80 mmHg - if taken properly
- diagnosed if the mean daytime blood pressure is >130/>80 mmHg or 24 hour mean is 125/75

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21
Q

If out of office BP is not attained?

A
  • HTN confirmed and should be treated if: mean BP of >130/>80 mmHg
  • 3 visits over weeks to months
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22
Q

What is “white coat” HTN?

A

BP elevated while in the office but normal in general
- more common in older adults, females, non-smokers
- happens in 13-35%
- becomes important when readings are >20-10 mmHg higher than normal
- ABPM is better than HBPM to help see White Coat

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23
Q

What is masked HTN?

A

Office BP readings are normal but ABPM/HBPM is always above normal
- make sure to take accurate HBPM and own BP readings
- helps avoid unneccessary treatment

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24
Q

What are the effects of chronic hypertension?

A

due to an overload on the left ventricle
- this leads to stiff left ventricle = heart failure with decreased ejection fraction
- predisposition towards MI because the left ventricle is not able to get proper O2

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25
Q

What are the sx of decreased CO?

A
  • dizziness
  • dyspnea
  • impaired exercise tolerance
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26
Q

How do we manage of HTN?

A
  • weight loss
  • aerobic exercise
  • limiting sodium to < 6g/day
  • Reduce alcohol
  • Stop smoking . reduce sympathetic stimulation of vessels
  • treat sleep apnea
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27
Q

Does caffeine affect HTN?

A

Caffeine does not produce chronic BP elevation (unless already at high risk)

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28
Q

What is the recommended weight loss for HTN?

A

each 10kg weight loss is associated with 5-10 mmHg drop in SBP

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29
Q

Why is aerobic exercise help with HTN management?

A
  • sedentary normotensive people have 20-50% higher risk of getting HTN
  • this causes lower HR and decreases levels of circulating catecholamines = possible reduced sympathetic tone of the vessels
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30
Q

Hypertension

When is pharmacotherapy suggested?

A

Out of office daytime BP >135 or >85 (or avg BP >140/90)
OR
Out of office day time BP >130 or >80 AND cardiac rest factors of DM, established CV disease, >65 y/o, chronic kidney disease or >10 years risk of CAD

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31
Q

Hypertension

What are the initial stages of medication therapy?

A
  • thiazide diuretic
  • long acting Ca channel blocker
  • ACE inhibitor
  • Beta Blockers

Higher BP = more drug combinations are added

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32
Q

Hypertension

What are some pre-hypertension management?

A

Risk stratification and lifestyle education

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33
Q

Hypertension

What are some management of elevated BP?

A
  • risk management and lifestyle modifications
  • reduction of salt and potassium supplements
  • weight loss/DASH diet
  • no smoking and limiting that DRANK AND DRUGS
  • aerobic exercise
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34
Q

Hypertension

How does exercise assist with elevated BP?

A

Lowers BP by 5-7 mmHg
- lowers CVD risk by 30%

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35
Q

Hypertension

What is the aerobic ACSM guidelines for elevated BP?

A

5-7 days
60-80% of target heart rate or 6-11 on RPE
30-60 which can be broken uo
Rhythmic movements for larger muscle groups
- examples: walking, swimming, cycling

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36
Q

Hypertension

What is the resistance traning ACSM guidelines for elevated BP?

A

2-3 days
60-80% of 1RM
2-4 sets x 8-12 reps
Larger muscle groups

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37
Q

Hypertension

What is the flexibility training ACSM guidelines for elevated BP?

A

around 2-3 days
10-30 seconds
2-4 reps
for major muscle groups

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38
Q

Hypertension

Where do PTs fir in regards to hypertension treatment?

A
  • We are screening for risk factors
  • be able to take BP accurately with a baseline on everyone with 1 or more risk factors
  • Monitor sx and BP readings in patients with known HTN
  • Give the necessary prescription of appropriate EBP
  • Education, Education, EDUCATION on lifestyle changes and risk factor management
  • MD communication
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39
Q

What is the ratio of undiagnosed HTN?

A

1 in 3 adults

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40
Q

What are the ACSM guidelines for HTN?

A
  • monitoring BP
  • beta blockers are da goat
  • look for exaggerated response to exercise at low intensities
  • keep a < 220 &/or < 105
  • no valsalva
  • longer warm ups and cool downs
  • look for post-exercise hypotension
  • positive effects only happen if exercise is continued
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41
Q

Hypertension

What does beta blockers do to the body?

A
  • impairs thermoregulation
  • stops HR response
  • BUT increases possibility of hypoglycemia
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42
Q

Hypotension

What is orthostatic hypotension?

A

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

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43
Q

Hypotension

How is orthostatic hypotension diagnosed?

A

Sustained decrease in systolic BP of at least 20mmHg or diastolic BP of 10mmHg within 3 mintues of standing after being supine for 5 minutes
- or at 60 degree angle on the tilt table
- delayed > 3 min

Usually secondary to failure of the
- autonomic reflex
- volume depletion
- CV disease
- adverse reaction to a medication
- neurogenic disease
- paraneoplastic syndrome

44
Q

Hypotension

What is the common sx of hypotension?

A
  • lightheadedness
  • dizziness
  • falls
  • LOC
  • visual and cognitive disturbances
  • weakness
  • fatigue
45
Q

Hypotension

What population is hypotension common in?

A

Older adults and women are more common than men and younger people

46
Q

Hypotension

What are we looking for regarding our physical exam?

A

thorough medication reconciliation
thorough vitals exam including:
- orthostatic hypotension
thorough history

47
Q

Hypotension

What is the treatment for hypotension?

A
  • prevention
  • education
  • avoid volume depletion/dehydration
  • exercise
  • mobility training
  • compression stockings/abdominal binders
  • avoid alchohol and heavy meals
  • meds if all above doesnt work
48
Q

What is postural orthostatic tachycardic syndrome (POTS)?

A

Rapid increase in heartbeat of more than 30 beats per minute in adults or 40 beats per minute in adolescents
- or a HR that exceeds 120 beats per minute within 10 minutes of rising

1st R/O orthostatic hyptension, acute blood loss or acute dehydration

49
Q

When does POTS usually happen?

A

Incidence increases with age
women > men

50
Q

What affects POTS?

A

Menstrual cycles
infections&raquo_space;> COVID
major surgery
Trauma; prolonged bedrest

Often short-lived or relapsing remitting but some people have lifestryle limiting sx

51
Q

What is the PT implications of orthostasis?

A

move LEs before standing
move segmentally
Valsalva if not contraindicated
pressure garments

52
Q

What is the PT implications of POTS?

A

Patients with POTS tend to avoid exercise which leads to cardiovascular deconditioning which POTS worse
- aerobic re-conditioning with some strength training

53
Q

How is exercise handled for patients with POTS?

A
  • 75% max predicted HR or RPE ~ 13-15 in recumbent position to get use to the endurance training (aroiund 30 min x 3-4 times per week)
  • slowly increase duration and intensity still in recumbant
  • start to add upright but decrease intensity and duration
  • add warm up and cool downs
54
Q

What is coronary artery disease?

A

Due to atherosclerosis, there is a thickening and narrowing of the intimal layer of the blood vessel wall from the accumulation of lipids, platelets, monocytes and plaque
- silent until a critical threshold is reached

Atheroslecorisis is major factor of CAD

55
Q

What are the major risk factors of CAD?

A
  • smoking
  • decreased physical activity
  • obesity
  • diet
  • hyperlipidemia
  • DM
  • family hx
  • stress
  • possibly gender (??)
56
Q

What are the risk factors for CAD?

A
  • Men over 45 / women over 55
  • Family hx (same as cardiac event)
  • current or recent smoker
  • Obesity (BMI over 30 and lack of exercise)
  • HTN: systolic > 140 and/or diastolic > 90 or taking HTN medications
  • Dyslipidemia: LDL > 130 mg/dL: HDL < 40 mg dL
  • Diabetes: fasting plasma glucose over 126 mg/dL and the metabolic syndrome
  • Inflammation
57
Q

What is considered “good cholesterol” and what a goal values?

A

HDL - high density lipoproteins

HDL goal values:
- men: > 40 mg/dL
- women: > 50 mg/dL

elevated triglycerides reduce HDLs = increased risk of MI

58
Q

What is considered elevated triglycerides?

A

fasting triglyceride levels above 200 mg/dL

59
Q

What are behaviors that raise HDLs?

A

weight loss
smoking cessation
increased aerobic exercise

60
Q

What are considered “bad cholesterol”?

A

LDL - low density lipoproteins

61
Q

What are the LDL values that help with MI prediction?

A

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

62
Q

What is the ideal LDL with all other risk factors?

A

less than 75 mg/dL

63
Q

What is indicated for blood lipids?

A

Total cholesterol
- around 180 with the presence of other risk factors

Taking into account total cholesterol/HDL = the higher the ratio, the greater the risk

Low HDL and high LDL = increased risk
can have low total cholesterol and still be at risk for low HDL

64
Q

What is the role of PTs in CAD?

A
  • Risk factor stratification
  • Prevention through exercise
  • education on lifestyle changes both in primary and secondary prevention
65
Q

What is the aerobic exercise recommendation for CAD?

A

over 150 minutes of moderate to vigorous intensity (60-80% of THR)
- spread over 3-5 days
- start low and progress accordingly

66
Q

What is the resistance training recommendation for CAD?

A

moderate intensity
- 2 days a week

67
Q

What are other exercise/treatments recommendation for CAD?

A
  • HIIT is beneficial to this but 80% THR is hard to get
  • volume seems to be more beneficial than intensity
  • reduction on epithelial dysfunctionm formation of collaterals, decrease of stenosis, reduction of vascular inflammation
68
Q

What is the progression of CAD to ischemic heart disease?

A

Theres is a mismatch between the myocardial O2 demand and supply
- when there is an imbalance results in cardiac hypoxia and accumulation of waste products
- most often the result of CAD

69
Q

What is myocardial O2 demand?

A

there is stress in the ventricular wall (afterload)
LV filling (preload)
HR and contratility

70
Q

What is angina pectoris?

A

Its the uncomfortable sensation in the chest and neighboring anatomy because of myocardial ischemia

71
Q

What is stable angina?

A

Predictable pattern of transient chest discomfort

72
Q

What is the sx of stable angina?

A
  • Pressure, tightness, squeezing, burning and heaviness (usually not described as pain)
  • “elephant sitting on the chest”
  • Doesn’t vary significantly with inspiration or movement of the chest wall
  • levine’s sign - clenched fist over sternum
73
Q

After the discomfort, what is followed by stable angina?

A

Tachycardia
Diaphoresis
nausea and dyspnea

in older adults - fatigue and weakness

74
Q

How is stable angina relieved?

A

Stopping the activity or condition within a short time < 20 mins

75
Q

What are the common triggers of stable angina?

A
  • high blood pressure
  • anemia
  • stress (emotional or physical)
  • extreme cold
  • heavy meals
  • physical exertion (usually about the same level of PA brings it on)
75
Q

What is the pathology of stable angina?

A

fixed, obstructive atherosclerotic plaque in one or more arteries = causes stenosis

Usually 70% if nire

76
Q

What is angina class 1?

A

light, barely noticeable
- angina with strenuous or prolonged activity

77
Q

What is angina class 2?

A

moderat, bothersome
- angina with slightly greater than normal activity (faster pace walking or stairs)

78
Q

What is angina class 3?

A

Severe, very uncomfortable
- angina resulting in marked limitations of normal activity

79
Q

What is angina class 4?

A

Most severe pain ever experienced
- angina at rest

80
Q

What are the implications of stable angina?

A
  • know patient’s “anginal picture”
  • lower exercise tolerance
  • know medications
  • cardiac rehab helps
  • educate with risk factors and lifestyle modifications
  • MD clearance
  • 30 to 60 minutes of moderate exercise 5x a week
  • increase activities
  • resistance training 2x a week at moderate intensity
81
Q

What is the coorelation between cardiac rehab and stable angina?

A
  • reduction of mortality by >20%
  • cardiac mortality by >26%
  • non-fatal myocardial infarction by >21%

  • increased functional capacity
  • decreased angina sx
  • increased anginal threshold
82
Q

How should resistance training be conducted for stable angina?

A

40-60% of 10RM
- exercise major muscle groups
- avoid valsalva
- circuit training is okay at a slow pace

The ACSM recommends:
- longer warm ups and coold down while avoiding extreme temps
- low impact, continuous style aerobic exercise (walking, biking, etc.)
- focus on LE more than UE to reduce cardiac demand

if very poor fitness - break up time into shorter bouts more frequently to target duration

83
Q

What is variant or prinzmetal angina?

A

develops because of coronary artery spasm due to O2 demand mismatch

May or may not have associated CAD

84
Q

What population is affected by variant angina?

A

Most common in women, smokers and cocaine users but overall rare

Patients usually very active

85
Q

What are the sx of variant angina?

A

Typical angina discomfort
Usually at rest or in the middle of the night

85
Q

What can vasospams be triggered by?

A

Anything that causes vasoconstriction:
- HTN
- smoking
- sympathetic NS triggers (i.e. anxiety can cause chest pain)

86
Q

What is silent ischemia?

A

asymptomatic episodes
- detected on EKG or other lab tests

87
Q

What is unstable angina?

A
  • Indicates a progression of ischemic heart disease and precursor to MI
  • higher morbidity and mortality rates
88
Q

What is the pathology of unstable angina?

A

result of rupture of atherosclerotic plaque with subsequent thrombus

89
Q

What are the sx of unstable angina?

A
  • increased variable frequency and duration of angina sx
  • lower physical and emotional threshold that trigger angina sx
  • chest pain at rest or not relieved by rest
  • change in anginal pattern
90
Q

What are PT implications of unstable angina?

A
  • know anginnal picture
  • physician’s clearance
  • medications
  • lifestyle modifications
  • self-monitor of sx (education!!!)
  • extended warm up and cool down
  • 30-40% of THR w/ shorter duration
  • stop with any onset of angina sx
  • Vitals
  • schedule exercise appropriately -avoid times of stress: after meals, too hot/too cold, etc.
  • No HIIT
  • Exercise prescription guidelines

Duration, frequency and reduction in sx is more important than intensity

91
Q

What is the sx of myocardial infarction?

A

chest pain greater than 20 minutes without relief with decreasing activity or only minimal relief with nitroglycerin is highly suspicious for MI

92
Q

What is the cause of myocardial infarction?

A
  • Myocardial ischemia > oxygen demand exceeds supply
  • thrombus or total occlusion is the most common cause leads to ischemia and if not re-perfused will lead to necrosis
  • area if damage depends on vessel occluded - help predict future sign and sx and exercise tolerance
93
Q

What is the most common cause myocardial infarction?

A

Atherosclerotic plaque rupture in an already blocked artery

94
Q

What are the two types of myocardial infarction?

A

NSTEMI - non ST elevation MI
STEMI - ST elevation MI

95
Q

What are the clinical features of MI?

A
  • Unstable angina
  • Severe, “crushing” persistent, typically substernal
  • dyspnea
  • diaphoeresis and cool, clammy skin (sympathetic NS)
  • Nausea, vomiting, weakness (aka vaso vagal - parasympathetic NS)
  • Pulmonary rales/crackles (if heart failure present)
  • EKG abnormalities: ST elevation or depression, T wave inversions
96
Q

How do you diagnose MI?

A

presenting symptoms
EKG changes
serum biomarkers (troponins and CK)

97
Q

What is the medical management of MI?

A
  • early recognition of sx is KEY
  • time is tissue
  • medications
  • cardiac interventions (cath labs)
  • surgery - CABG
  • manage arrhythmias
  • imagining through echo
  • Supplemental O2
  • Initial bedrest to allow O2 supply to reach demand
  • always EKG monitoring
98
Q

What is the concept of time is tissue?

A

Rapid revascularization to prevent permanent damage

99
Q

What are some cardiac interventions for MI?

A
  • best outcomes if time to table(time from onset of sx to when patient is on cathlab table) is 90 mins or less
  • myocardial injury reversible within 20 minutes
  • progressive loss of viable tissue and onset of necrosis after that time
100
Q

What is thrombolysis in myocardial infarction (TIMI) risk score factors?

A
  1. Age > 65
  2. > 3 CAD risk factors
  3. known coronary artery stenosis > 50% by prior angiography
  4. ST segments deviations on EKG at presentation
  5. At least 2 angina episodes in the last 24 hours
  6. use of aspirin in the last 7 days (implies no longer working)
  7. Elevated serum troponin or CK
101
Q

What are the complications of MI?

A
  • recurrent ischemia
  • arrthymias
  • heart failure due impaired contractility (systolic dysfunction)
  • increased myocardial stiffness (diastolic dysfunction)
  • cardiogenic shock
  • right ventricular infarction (RCA)
  • mechanical complications
  • acute pericarditis due to inflammation
  • thromboembolism

RCA - SA and AV node in large % of population
LAD - bundle of His, left bundle branch, proximal right bundle branch

102
Q

What is the thromboembolism?

A

static blood flow allows clot formation which can travel = occurs of CVA

103
Q

What are post MI PT responsibilities?

During acute phase

A

Vitals - coordinate with medical team for parameters
Labs
Medications (understand implications for therapy)
Imaging (reads reports to understand damage)
Early mobilization
Low level aerobic and low intensity strength training
Patient education

104
Q

What are the labs for post MI phase?

A

Especially cardiac enzymes troponin and creatine phosphokinase
- troponins must be trending down before PT can begin

105
Q

What are things to take care of during early mobilization?

A

watch lines and tubes
monitor EKG and patietn for signs of exercise tolerance

PHTH 536 - Body Systems (5 decks)

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