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Cardiovascular Diseases Flashcards

1
Q

Cardiovascular Diseases

(5)

A
  1. Acute Coronary Syndrome
  2. Congestive Heart Failure
  3. Pulmonary Edema
  4. Pulmonary Embolism
  5. Peripheral Vascular Disease
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2
Q

Acute Coronary Syndrome

Definition

A

A term used to describe a spectrum of clinical presentations which result from impairments in the blood supply to the heart

Conditions include: myocardinal ischemia & myocardial infarction

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3
Q

Myocardial Ischemia

(3)

A

Insufficient blood flow to the myocardium

  • Typically presents with angina pectoris - chest pain / pressure due to insufficient blood flow
  • When no symptoms are present it is referred to as silent myocardinal ischemia
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4
Q

Angina

(3)

A

Diffuse retrosternal pressure, heaviness, rightness or constriction in the chest caused by reduced blood flow to the myocardium

  • Patient may clench their fist over their sternum (Levine sign) - fist or claw
  • May radiate to the LT jaw, LT arm, &/or upper back between the scapula
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5
Q

What is the Levine Sign?

A

When a patient may clench their fist over their sternum

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6
Q

Angina: Types

(3)

A

1. Stable Angina
- Precipitated by activities that increase myocardial oxygen demand (ie physical activity, secual activity, emotional stress, cold (vasoconstriction > prevent heat loss by constricting), or lying down in supine (INC venous return = INC preload).
- Relieved by rest or nitroglycerin (NTG) - oral (sublingual) or spray
- Demand > supply

Stress = release of hormones (cortisol & adrenline) > INC BP - vessels vasoconstrict… 2 affects:
1. Peripheral vasoconstriction= INC BP & heart has a harder time pumping out blood because of INC resistance = contracting harder = need fore more O2 > need more energy
2. Coronary arteries constrict = DEC supply of blood to the heart mm = DEC supply of oxygen to heart mm

2. Unstable Angina - Chronic mismatch
- Occurs at rest without any obvious precipitating factors or with minimal exertion
- Not relieved by rest - tissue is still alive but VERY ischemic
- May not be relieved by nitroglycerin (NTG)
- Required immediate medical attention as there is a high risk for myocardial infarction

3. Varient Angina
- Vasospasm of coronary arteries
- Does not respond to NTG

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7
Q

Frank-Sterling Law

A

Frank-Sterling Law

INC EDV = INC SV independent of everything else = greater CO

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8
Q

Myocardial Infarction

A

Death of cardiac mm cells d/t lack of blood flow - tissue death b/c lack of O2 = necrosis

  • Caused by a sudden complete occlusion of one or more coronary arteries
  • The term injury refers to acutely injured myocardial tissue during a sudden heart attack
  • The term infarction referes to myocardial tissue that was injured & progressed to irreversible dead tissue as seen in old heart attacks
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9
Q

MI: Evaluation Triad

(3)

A
  1. Symptoms
  2. ECG changes
  3. Cardiac Biomarkers
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10
Q

Symptoms

(7)

A
  1. Angina pectoris
  2. Anxiety
  3. Diaphoressi (unusal amount of sweating)
  4. Dyspnea
  5. Dizziness
  6. Fatigue
  7. Nausea
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11
Q

MI: ECG changes

(3 Scenarios)

Electro-cardio-gram

A

If ischemia (decreased perfusion) is present:
- ST-segment depression
- Inverted T-wave
** Only present while the heart is ischemic

Small acute MI w/ no injury to myocardial tissue:
- No ST-segment change (small = not going to show a visual representation)
- Referred to as non-ST segment elevation myocardial infarction (NSTEMI) or non-Q-wave myocardial infarction (NQMI)

Large acute MI w/ injury to myocardial tissue:
- 1st = ST-segment elevation > once the infract is not acute…
- Pathological Q-wave (hours or days following the acute process)
- Referred to as ST segment elevation myocardial infarction (STEMI) or Q-wave myocardial infarction (QMI) ** May not even have a Q-wave (pathological)

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12
Q

MI: Cardiac Biomarkers

(4)

A

The following cardiac biomarkers found in blood work may determine the presence of a MI:
1. Troponin I
2. Troponin T
3. Myoglobin
4. Creatine kinase - Myocardial Band (CK-MB)

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13
Q

MI: Medical Management

(2)

A

Percutaneous Transluminal Coronary Angioplasty (PTCA)
- Stunt in the artery - keeping the vessel open

Coronary Artery Bypass Graft (CABG)
- Take a vessel from somewhere else in the body - used to pass the coronary artery - this provides a new way to provide blood to the area
Donor Vessels:
- Saphenous vein
- Internal throacic artery
- Radial artery of nondominant arm

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14
Q

MI: Medications

(6)

A

Vital signs will be impacted by these medications

  1. Betablockers
    Less energy required by the heart = DEC HR & contractility
  2. Calcium Channel Blockers
    DEC BP & prevent smooth mm vasospam
  3. Nitrates
    Vasodilator = INC BF to myocardial & less resistance for the heart to overcome
  4. Angiotensin-converting enzyme (ACE) Inhibitors
    Inhibit/ prevent vasoconstriction = DEC BP
  5. Angiotensin Receptor Blockers (ABR)
    Inhibit vasoconstriction & sympathetic activity = DEC BP
  6. Supplemental oxygen
    Myocardium may need more O2 along w/ other organs (muscles)

Common theme = decrease BP

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15
Q

MI: Physical Therapy Management -
Goals

(5)

A
  1. Improve exercise capacity (ability to do more work)
  2. Improve exercise efficiency (ability to do same work with less cost)
  3. Improve exercise tolerance (ability to do same work with less signs & symptoms)
  4. Improve self-management
  5. Improve quality of life
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16
Q

Cardiac Rehabilitation

Definition

A

A comprehensive exercise, education, & lifestyle modification program designed to optimize physical, psychological, social, and vocational functioning

Beneficial to reduce disability. Not only exercise training but EDUCATION

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17
Q

Phases of Cardiac Rehabilitation

(4)

A

Phase I: Acute/ Inpatient Phase
Phase II: Subacute/ Conditioning
Phase III: Intensive Rehabilitation Phase
Phase IV: Maintenance Phase

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18
Q

Phase I: Acute / Inpatient Phase

(5)

A
  • Traditionally begun in the acute hospital or rehab setting
  • Role of PT is to prepare for discharge, monitor activity tolerance, support risk factor modification techniques, provide emotional support, build self-efficacy, & educated the patient on how to recognize adverse signs & symptoms w/ activity, and collaborate with other members on the team
  • All aspects of education should be initated in Phase I
  • Focus on interventions is on assessing hemodynamic responses to activity, & indpendence in functional mobility activities (ie bed mobility, transfers, ambulation, stair climbing, & ADLs)
  • Vital signs should be monitored before and after (& during if possible)
  • INTENSITY should be low level
19
Q

Phase I: Acute / Inpatient Phase -
LEVELS

(4)

A

Level 1 (1 METs)
- Patient in ICU & has been medically stable for 24 hours
- Bed rest but allow gentle AROM exercises for upper & lower extremities & DP

Level 2 (2 METs)
- Allow sitting up in a chair for meals, performing ADLs, and walking to the bathroom or inside the rom (up to 50ft) a few times a day

Level 3 (3 METs)
- Ambulate up to 250 ft a few times a day

Level 4 (4 METs)
- Perform ADLs independently & ambulate up to 1000 ft a few times a day
- Allow climbing of 1 flights of stairs

General guidelines & standards for goal setting
Continuum

20
Q

Phase II: Subacute / Conditioning Phase

(2)

A
  • Typically begins after discharge from the hospital in the outpatient setting
  • Conditioning exercises are done with close cardiac monitoring
21
Q

Phase III: Intensive Rehab Phase

(2)

A
  • Exercise in large groups
  • Resistance training typically initiated in this phase

RT > Phase III

22
Q

Phase IV: Maintenance Phase

(1)

A
  • Patient is encouraged to continue exercise training in a group setting or self-monitored program
23
Q

Education for Patients w/ Heart Disease

List (7)

A
  1. Activity Guidelines
  2. Self-Monitoring
  3. Symptom Recognition & Response
  4. Nutrition
  5. Medications
  6. Sexual Activity
  7. Psychological/ Social Issues

Page 76-77 for more details

24
Q

Congestive Heart Failure

Definiton & Epidemiologu

A

A syndrome characterized by impairment in the heart pump function (LT or RT ventricle)

Epi:
- Leading cause of cardiac deaths in North America
- Most frequent cardiac diagnosis for hospital admissions
- M>F

25
CHF: Types | (3)
1. Left-sided heart failure LT ventricle - trouble pumping into circulation > LT atrium fills > back-up into pulmonary veins (INC pressure) > fluid is going into interstitium > goes into lungs > PULMONARY EDEMA 2. Right-sided heart failure ~ **cor pulmonale** 3. Biventricular heart failure LT side failure is so bad > back-up from lungs > pulmonary artery is full (to much pressure) > RT ventricle has to much pressure to overcome > RT side heart failure = symptoms of LT + RT heart failure
26
CHF: Pathophysiology | (5)
1. LHF > DEC SV > DEC LVEDV > INC LV pressure > INC LA pressure > fluid mvmt from veins to interstitial space of lungs (excess hydrostatic pressure) > pulmonary edema 2. LHF > DEC SV > INC SNS activation **(compensatory)** > INC HR > fatigued myocardium & fail 3. DEC CO > DEC arterial blood flow > DEC perfusion to the kidneys > renal failure *BUN = blood, urea, nitrogen - will be elevated* 4. Inactivity/bed rest > mm wasting, myopathies, osteoporosis *PT role = INC functional mobility* 5. Compensated vs uncompensated - Decompensated - severe damage - S/S of CHF - Compensated - influenced by something else to get enough CO to the system 1. INC SNS activation = INC HR 2. Medications 3. Hyptertrophy of the ventricle - stronger - results in other problems 4. ** Cognizant not to push the limits of a persons (cardiac dilation) compensated HF = ACUTE heart failure requiring medical attention
27
CHF: Etiology | (7)
1. Cardiac mm dysfunction 2. Cardiac dysrhythmias (altered electrical function - can affect function & exacerbate) 3. Cardiomyopathies 4. Long-term CAD 5. Hypertension *Harder for LT ventricle to pump against resistance - weaken - fail ""working in overdrive* 6. Valve Abnormalities (regurgitation of blood/ backflow) 7. Pericardial pathology - pericarditis (INC pressure against the ventricle)
28
CHF: LT Sided HF - S/S | (6)
1. Dyspnea - V/Q mismatching, INC RR 2. Fatigue - tissues have less O2 to turn into energy 3. Weakness - tissues have less O2 4. Pulmonary edema 5. Paroxysmal nocturnal dyspnea Sudden episodes of SOB @ night > **Orthopnea** = SOB in recumberant position SUPINE - fluid is at an equal level so it is going to spreal all over the lung. Surface area of fluid covered alveoli iis much greater & makes gas exchange more difficult) 6. Orthopnea - semi-fowler: ~30-90 degrees
29
CHF: RT Sided HF - S/S | (8)
1. Dyspnea 2. Fatigue 3. Weakness 4. **Jugular vein distension** - HALLMARK OF RHF 5. Peripheral edema *4-5* - Backflow of fluid. Hydrostatic pressure push fluid into periphery (systemic volume overload) > DEC SV actually signals to kidneys to retain fluid & make issues worse Heart is failing & now is getting overloaded w/ fluid 6. Pitting edema 7. Fluid weight gain 8. Ascities - excess fluid in belly area (RT & LT)
30
CHF: Interventions | (6)
1. Positioning to reduce orthopnea - pillow to be in semi-fowler position (30-90 degrees) 2. Relaxed breathing exercises (ie diaphragmatic breathing) *DEC energy expenditure to breath* 3. Supplemental oxygen - low SpO2 4. Graded increased ambulation - progressively 5. Graded exercise (volume & intensity 6. Cardiac rehabilitation program
31
Pulmonary Edema | Definition
An abnormal accumulation of fluid in the lungs Fluid moves from the pulmonary capillaries > interstitial space > alveolar space
32
Pulmonary Edema: Pathophysiology & Etiology | (4)
1. INC capillary membrane permeability (can change ossmotic pressure) 2. INC capillary hydrostatic pressure 3. DEC capillary osmotic pressure Move or keep fluid in - draw fluid to w/e side has the most solutes. Solutes cause the fluids to leave towards a place w/ INC osmotic pressure 4. Lymphatic insufficiency Normally drain excess fluid out - not doing a good job pulling that fluid out of intersitium = INC accumulation in the interstitium > moves into alveloar spaces
33
Pulmonary Edema: Types | (2)
Cardiogenic Pulmonary Edema - **High** pressure (INC pulmonary capillary hydrostatic pressure) - Backflow of blood in the system due to kidney, heart mm, or valve damage leading to INC blood accumulation in pulmonary capillaries which INC pulmonary capillary hydrosstatic pressyre - Ex. **LHF** Non-Cardiogenic Pulmonary Edema - **LOW** pressure - INC permeability of the pulmonary capillaries & alveolar endothelium d/t trauma or toxins (altered osmotic pressure) *Draws the fluid out of the capillaries into where osmotic pressure is higher - inside the lungs* - Ex. ARDS **FLUID not secretions - mobilization techniques will not help** Not trying to loosen up anything. Suctioning may help but other techniques will not be used
34
Pulmonary Edema: Clinical Presentation
Inspection: - Dyspnea - INC WOB - Cyanotic - hypoxaemia - DEC diffusion of O2 into the circulatory system - **Orthopnea (SOB in supine)** - **Cough with pink, frothy sputum (cardiogeniic) ** *Different from everything else we have seen & ONLY w/ cardiogenic type* - Swelling in lower extremities (gravity - dependent positions) Palpation: - Tactile fremitus: Normal or INC Percussion: - Dull Auscultation: - DEC BS - Fine inspiratory crackles - fluid - Egophoney: (-) - no consolidation or excess lung tissue ABGs: - DEC PaO2 - less O2 diffused through CXR: - Cardiomegaly (INC heart size) - Enlarged pulmonary vessels - White fluffy/hazy airspace - Kerley B lines - short, horizontal lines near pleural surface (base of lungs)
35
Pulmonary Embolism | Defintion
A blood clot that has been lodged in a pulmonary artery - Commonly associated with DVT in the lower extremities (usually in calf) - **Life-threatening** - impede BF & cause lung cell death
36
Pulmonary Embolism: Pathophysiology | (3)
- Pulmonary embolus obstructs blood flow to an area of the lungs - If blood flow to lung tissue completely blocked, can lead to infarction & necrosis of lung tissue - Very large embolism can lead to INC pulmonary artery resistance > INC work load of right ventricle > RHF
37
Pulmonary Embolism: Risk Factors | (3) ## Footnote Same as DVT
1. **IMMOBILIZATION (ie post-op)** - Venous stasis 2. Secondary INC coagulation (ie oral contraceptions, cancer, polycythemia - thick blood d/t hemoglobin) 3. Other: CHF, Hx of DVT, obesity, pregnancy, stroke, trauma, varicose veins
38
Pulmonary Embolism: Clinical Presentation | (4)
Inspection: - **ACUTE onset of dyspnea** - Hallmark - INC RR - **Chest pain** - May have cough with bloody sputum (**hemoptysis**) ABGs: - DEC PaO2 - DEC PaCO2 - INC pH - **Respiratory Alkolosis** CXR: - Infarcted area of lung appears white (rare) Diagnosed using CT scan or V/Q scan
39
Pulmonary Embolism: Intervention | 4+5
Prophylactic Post-Op - Anti-coagulation medications - Bed exercises - ankle pumps - NEED to get the person moving - Early mobilization - Compression stockings - preventative measure *NOT as a Tx - contraindicated once pt has a DVT > chance to disloge the clot* If PE or DVT is suspectde or confirmed: - **Discontinue exercise & mobilization until further notice** - Notify a nurse or surgeon - Document - INC anti-coagulation medications - Thrombolytic medications
40
Peripheral Vascular Disease | Defintion
- Refers to disorder of the blood vessels of the body (arteries & veins) - Primarily d/t to **atherosclerosis** - hardening & narrowing of vessels - Significant narrowing of vessels must occur before there is enough occulsion of blood flow to produce symptoms
41
PVD: S/S
1. Leg Pain (intermittent claudification) 2. Coldness in affected leg 3. DEC pulses in lower limb 4. DEC mobility & function of limb d/t pain 5. Possible numbness 6. Possible pain & paleness of leg with elevation (**Buerger's test**) 7. DEC hair growth (circulatory problem) 8. Skin breakdown - ulcers 9. Ulcerations (arterial & venous insufficiency ulcers) 10. Gangrene (in very severe cases that were not well managed) *Debride it - if it does not work - amputation*
42
PVD: Tests | (2)
1. Buerger's Test - Elevation Palor Pt lying in supine - lift leg up (blood wil rush out - PALE) May be painful 2. Dependent Rubor When leg is pale - sit up - put leg down level of the body (where leg is in a gravity dependent position) - becomes RED (rubor)
43
Intermittent Claudification | Def & Characteristics (4)
Pain or cramping that occurs in the buttock or legs (especially calves) as a result of poor circulations to the affected area - INC pain w/ INC activity d/t to increased energy demands on the muscle which has poor circulation *More anaerobic metabolism > to create ATP & as a result it going to produce a lot of LACTIC ACID = in excess, can cause PAIN* **DEMAND > SUPPLY** - DEC pain at rest (even in standing position) - Must differentiate between Intermittent Claudification & Neurogenic Claudification (spinal stenosis) **BOTH complain w/ walking** IC (vascular) vs NC (neuro) "Bicycle Test" - bend forward FLEXION while leg mm are still working Differentiate by: manipulating back position while **walking** - Stooped posture = will NOT provoke symptoms in NC - IVF is gapped open Spinal stenosis - Nerve root is getting compressed when exiting the IVF (DDD, osteophytes, narrowing of the foramen - Worse in **extension**
44
Intermittent Claudification: Interventions | (3)
1. Progressive increase activity & aerobic exercise (may be painfuk) May stimulate the development of collateral blood vessels Graded Exercise (aerobic) = INC tolerance & stimulate the development of collateral blood vessels 2. Education on risk factors & self-management (PVD) 3. Self-assessment of skin & education on skin-care Check for ulcers or skin breakdown - infected - may lead to impaired wound healing or amputation **COMPRESSION STOCKINGS ARE CONTRAINDICATED** - Poor BF & will only compress the blood vessels further = make the BF even worse

Cardiorespiratory (13 decks)

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