Cardiovascular- Therapyed

What is the difference between the epicardium, myocardium, endocardium, and pericardium?

Peri- protective sac around teh heart- outermost layer. double layered fibrous sac
Epi- inner layer of peri. Between peri and myo.
Myo- heart muscle
Endo- smooth lining of inner surface

When do the AV valves close?

When ventricular wall contracts

What is systole?

Period of ventricular contraction

What is end systolic volume? And what is the avg amount?

Amount blood in the ventricles after systole.
~50mL

What is diastole? And what occurs during this period?

period of ventricular relaxation.
Blood fills the ventricles

What is end diastolic volume? And what is the avg amount?

amount of blood in ventricles after diastole
~120mL

When does atrial contraction occur?

Occurs during the last 1/3 of diastole
Comprises last 20-30% of end diastolic volume (120mL)

What areas of the heart does the Right Coronary Artery (RCA) supply?

Right atrium
most of right ventricle
inferior wall of left ventricle
AV node
bundle of His
SA node (60% of the time)

What are the 2 divisions of the Left coronary artery (LCA)? What areas do each supply?

Left Anterior Descending (LAD):
Left ventricle
Interventricular septum
inferior areas of the apex
Circumflex Artery:
lateral and inferior walls of Left Ventricle
Portions of left atrium
SA Node (40% of time)

Where is the SA node located?

Junction of SVC and RA

What is the SA node? What 2 things does it control?

Main pace maker of the heart (60-100 bpm)
HR and strength of contraction

What type of innervation (parasympathetic and/or sympathetic) does the SA node receive?

Parasympathetic and sympathetic
HR and Strength of contraction

What is the AV node? What things does it control?

Intrinsic firing (40-60 bpm)
Merges with the bundle of His-->R and L ventricle branch

What type of innervation (parasympathetic and/or sympathetic) does the AV node receive?

Both, para and sympathetic

What is purkinje tissue and where is it located?

AV Node-->Bundle of His-->R and L bundle branch (located on either side of interventricular septum)-->terminate into Purkinje fibers
It is specialized conduction tissue throughout ventricles
Intrinsic firing rate of 20-40 BPM

What is the conduction pattern for a normal heart beat?

Origin in SA node
impulse spreads throughout both atria-->contract together
impulse stimulates AV node
transmitted down bundle of His to purkinje fibers
impulse spreads throughout ventricles-->contract together (atrial kick)

What is Stroke volume? What is it's normal range?

Amount of blood ejected w each myocardial contraction
55-100 mL

What 3 things influence SV?

LVEDV-amount of blood left in the ventricle at the end of diastole. Aka Preload
Contractility-ability of ventricle to contract
Afterload- force of LV must generate during Systole to overcome aortic pressure to open aortic valve

What is the avg cardiac output for an Adult?

4-5 L/ min
CO= SV x HR

What is cardiac index? What is normal range?

CO/ body surface area
2.5-3.5 L/ min

What is Left Ventricle End Diastolic Pressure? Normal range?

Pressure in left ventricle during diastole
5-12 mmHg

What is Ejection Fraction?

% of blood emptied from ventricle during systole
Normal 55%
The lower the EF, the more impaired LV

What is atrial filling pressure?

Difference between the venous and arterial pressures

Venous return increases or decreases with Hypovolemia? With blood volume expansion?

Decreases w Hypovolemia
Increases with blood volume expansion

Does R atrial filling pressure increase or decrease with coughing? During inspiration?

Increases w coughing/forced expiration
Decreases during inspiration

Right Atrial filling pressure is ____________ during strong ventricular contraction, and atrial filling is ____________

DECREASED
ENHANCED

What can cause Diastolic filling to decrease?

Increased HR
Heart disease

Myocardial Oxygen Demand is measured how?

Rate Pressure Produce= HR x SBP

What is the course of Lymph?

Lymphatic capillaries-->lymphatic vessels-->ducts-->Left Subclavian Vein

How does lymphatic contraction occur?

Para, sympathetic, and sensory nerve stim
contraction adjacent muscles
Abdominal and thoracic cavity pressure changes during nomal breathing
Mechanical stim of dermal tissues
Volume changes within lymphatic vessels

What are the main lymphatic ducts? And what areas drain into each?

Right Lymphatic Duct: 1/4 of body: RUE, R neck/head
Thoracic Duct: everything else

Where are major lymph nodes located?

Submaxillary
Cervical
Axillary
Mesenteric
Iliac
Iguinal
Popliteal
Cubital

How does lymphatic system contribute to immune function?

Nodes collect cellular debris and bacteria
Remove excess fluid, blood waste, and protein molecules
Produce antibodies

Where is the parasympathetic control center located? Sympathetic?

Medulla Oblongata-- cardioinhibitory center
Medulla Oblongata-- cardioacceleratory center

How does parasympathetic act on the heart? What neurotransmitter(s) is/are released?

Via Vagus nerve (CN X), cardiac plexus
Innervates SA node, AV node, and sparsley myocardium
Releases acetylcholine

How does sympathetic act on heart? What neurotransmitter(s) is/are released?

Via cord segments T1-T4, upper thoracic to superior cervical chain ganglia
Innervates SA Node, AV Node, Conduction pathways, and myocytes
Releases epinephrine and norepinephrine

How do parasympathetics effect heart? Sympathetics?

Para:
Slows rate
Decreases force of myocardial contraction
Decrease myocardial metabolism
Coronary artery vasoconstriction
Sympathetic:
Increase rate
Increases force of contraction
Increase myocardial metabolism
Coronary artery vasodilation
Peripherally c

What are baroreceptors? Where are they located?

Main mechanism for controlling heart rate, respond to changes in blood pressure
Located in walls of aortic arch and carotid sinus

What is the circulatory reflex?

Increases in BP-->para stimulation-->decreased HR/force cardiac. sympathetic inhibition. Decreased peripheral resistance
Decreases in BP-->sympathetic stimulation-->increased HR/BP and vasoconstriction of peripheral vessels
Increased Right Atrial Pressure

What are chemoreceptors and where are they located? How do they respond?

Sensitive to changes in blood chemicals: O2, CO2, and lactic acid
Located in carotid body
Increased CO2, decreased O2, decreased pH/increased Lactic acid-->Increase HR
Increased O2--> decreased HR

How does body temp affect cardiovascular system?

Increased temp-->Inreased HR
Decreased temp-->Decreased HR

How does HYPERKALEMIA affect cardiovascular system? What would you see in ECG?

Increased concentration of potassium ions
decreases rate and forces of contraction
Widened PR interval and QRS
Tall T waves

How does HYPOKALEMIA affect cardiovascular system? What would you see in ECG?

Decreased concentration of postassium ions
Flattened T waves
Prolonged PR and QRS intervals
Arrhythmias-->may progress to v-fib

How does HYPERCALCEMIA affect cardiovascular system? What would you see in ECG?

Increased calcium concentration
Increases heart actions

How does HYPOCALCEMIA affect cardiovascular system? What would you see in ECG?

decreased calcium concentration
depresses heart actions

How does HYPERMAGNESIUM affect cardiovascular system? What would you see in ECG?

increase magnesium concentration
calcium blocker-->cardiac arrhythmias or cardiac arrest

How does HYPOMAGNESIUM affect cardiovascular system? What would you see in ECG?

decreased magnesium concentration
Ventricular arrhythmias, coronary artery vasospasm, and sudden death

Increased Peripheral resistance ________________ (increases/decreases) arterial blood volume and pressure?

Increases

What are non-modifiable risk factors for CVD?

Age: M >45, F > 55
Family History
Race: AA
Gender: M> Premenopausal F, after menopause M=F

What are modifiable Risk factors for CVD?

Cholesterol
Diabetes: HgA1C < 7%
Diet
Hypertension
Obesity
Physical Inactivity
Tobacco

What are signs of decrease CO and low oxygen saturation?

Cyanosis
Pallor
Diaphoresis- excess sweating and cool clammy skin

What is grading scale for peripheral pulses?

0- absent/not palpable
1+ diminished
2+ easily palpable, normal
3+ full pulse, increased strength
4+ bounding

Where can you find a pulse?

PMI- apical (5th interspace)
Radial
Brachial
Carotid
Femoral
Popliteal
Pedal

What is the S1 sound?

Closure of mitral and tricuspid valve
Marks beginning of systole
***decreased in 1st degree heart block

What is S2 sound?

Closure of aortic and pulmonary valve
Marks beginning of diastole
***Decreased in aortic stenosis

What is a murmur?

An extra heart sound

Murmu between S1 and S2 indicates what?

Valvular disease or may be normal

Murmur between S2 and S1 may indicate what?

Valvular disease

What is a thrill?

abnormal tremor accompanying a vascular or cardiac murmur
Felt on palpation

What is a Bruit? What is it indicative of?

Adventitious sound or murmur (blowing sound) of arterial or venous origin
Common in femoral or carotid arteries
Indicative of atherosclerosis

What is an S3 sound? What is it indicative of?

Associated with ventricular filling
Occurs soon after S2
Indicative of CHF (LV)

What is an S4 sound? What is it indicative of?

Associated with ventricular filling and atrial contraction
Occurs just after S1
Indicative of pathology: CAD, MI, Aortic stenosis, or chronic hypertension

P wave

atrial depolarization

PR interval

time required for impulse to travel from atria through conduction system to Purkinje fibers

QRS wave

ventricular depolarization/atrial repolarization

ST segment

beginning of ventricular repolarization

t wave

ventricular repolarization

QT interval

time for electrical systole

Ventricular arrhythmias

Originate from en ECTOPIC focus in the ventricales (outside normal conduction system)

what is a Premature Ventricular Contraction (PVC)? What does it look like on the ECG?

premature beat arising from the ventricle
*occurs occasionally in the majority of normal people
No P wave
bizarre and wide QRS segment that is premature
Long compensatory pause

what is Ventricular Tachycardia? What can cause it?

3 or more PVC sequentially
Very rapid rate (150-200 bpm)
may occur paroxysmally (abrupt onset)
Usually result of ischemic ventricle

Bigeminy

Every other PVC

Couplet

2 in a row PVC

Ventricular FIbrillation

Pulseless emergency situation requiring immediate medical treatment
CPR, defib, meds
Characterized by chaotic activity of ventricul originating from multi foci
Unable to determine rate
Bizarre, erratic activity without QRS complexes
Clinical death within

Atrial Arrhythmias

0

What is an AV block? What are the different types?

Abnormal delays or failure to conduct through normal conducting system
1st, 2nd, or 3rd degree
If ventricular rate slowed-->CO decreased

What is significant about 3rd degree block vs 1st and 2nd?

Life threatening
Requires meds (atropine)
Surgical implantation of pacemaker

What does depressed ST segment indicate?

Impaired coronary perfusion (ischemia or injury)
Can be upsloping, horizontal, or downsloping

What does elevated ST segment indicate?

MI

Acute ST segment elevation in what leads indicates MI in Anterior Wall?

V1-V6

Acute ST segment elevation in what leads indicates MI in Anterioseptal Wall?

V1-V2

Acute ST segment elevation in what leads indicates MI in Anterioapical Wall?

V3-V4

Acute ST segment elevation in what leads indicates MI in Anteriolateral Wall?

V5-V6, I, aVL

Acute ST segment elevation in what leads indicates MI in Lateral Wall?

I and aVL

Acute ST segment elevation in what leads indicates MI in Inferior Wall?

II, III, aVF

Acute ST segment elevation in what leads indicates MI in Posterior Wall?

Not seen on ECG, changes in V7-9

How does potassium influence ECG?

HYPER:
Widen QRS
Flatten P wave
T waves become peaked
HYPO
Flatten T wave/inverts
Produces U wave

How does Calcium influence ECG?

HYPER:
Widens QRS
Shortens QT interval
HYPO:
prolongs QT interval

What is Mean Arterial Pressure? What is normal value?

Arterial Pressure within the large arteries over time
Dependent upon mean blood flow and arterial compliance
MAP= (SBP + 2*DPB)/ 3
Normal= 70-110 mmHg

Crackles/Rales

rattling, bubbling sounds
May be due to secretions in the lungs

Wheezes/Rhonci

whistling sounds

What should be part of your physical exam when peripheral vascular system is impaired?

Diaphoresis present- indicates decreased CO
Arterial Pulses
Skin Temp
Skin Changes
Pain
Edema

Scale for Edema

1+ Mild, barely indentation- <1/4in
2+Mod, returns to normal within 15 sec- 1/4-1/2in
3+ Severe, takes 15-30 sec to rebound, 1/2-1in
4+very severe, lasts >30 sec, >1in

Which system should be tested first, venous or arterial?

venous

Saphenous vein percussion test

Palpate vein and percussion 20 cm above, positive test = pulse wave felt by lower hand and means that valves are incompetent

Trendelenburg test (retrograde filling test)

Trendelenburg position (60 degrees elevation in supine)-> tourniquet around thigh -> pt stands
Normal filling time = 30s
Competence of communicating veins and saphenous system

Venous filling time test

the time taken for the veins to refill following elevation (45 deg) of the limb for one minute (or until to veins have drained) is recorded.
Normal venous filling time is 5-15 seconds.
>15 sec = venous insufficiency

Where is a Central line placed? What does it do?

aka Swan-Ganz catheter
inserted through vessels into R side of heart
measures central venous pressure
pulmonary artery pressure
pulmonary capillary wedge pressure

cardiac catherization (CC)

insertion of a catheter into the heart through a vein or artery, usually of an arm or leg to provide evaluation of the heart
Allows determination of ejection fracture (EF)

What is the primary marker for myocardial infarction?

Troponin levels

What must accompany rise in troponin levels to determine MI?

Symptoms of ischemia
New ST wave change
Pathological Q wave
Loss of myocardium seen on imaging
Intracoronary thrombus seen through catheterization

Importance of CK/CPK with concomitant elevation of CK-MB

elevation within 12-24 hours is associated with MI

What is acute coronary syndrome (ACS)

aka Coronary artery disease
imbalance of myocardial oxygen supply and demand
results in ischemic chest pain

When do symptoms for ACS become present?

When lumen is at least 70% occluded

What are 3 types of ACS?

Angina Pectoris
MI
Heart failure

What are the 2 reasons for angina pectoris?

1. Increased demands on heart
2. Vasospasm

What are the 3 types of Angina Pectoris?

1. Stable angina
2. Unstable angina
3. Variant angina

Sx's related to angina

SOB
fatigue
diaphoresis
weakness

Zone of infarction

consists of necrotic, noncontractile tissue
electricall inert
On ECG-->pathological Q waves

Zone of injury

area immediately adjacent to central zone, tissue is noncontractile, cells undergoing metabolic change
electrically unstable
see elevated ST segments in leads over injured areas

Zone of ischemia

outer area, cells undergoing metabolic changes
electrically unstable
ECG see T wave inversion

Infarction SItes: what are they and how do they present?

Transmural:
full thickness of myocardium
Often an elevated ST elevated MI (STEMI) or Q wave MI
Nontransmural:
subendocardial, subepicardial, intramural infarctions
Non-ST elevated MI (NSTEMI) or non-Q wave MI

What type of MI do you see with right coronary artery, circumflex artery, and left anterior descending artery?

RCA: Inferior MI
CA: Lateral MI
LAD: Anterior MI

Left Sided HF

#NAME?

Right sided HF

Increased pressure load on the RV w higher pulmonary vascular pressures, mitral disease, or chronic lung disease
sx: jugular vein distention and peripheral edema

Activity restrictions for acute MI

activity can be increased once acute MI has stopped (peak in troponin levels)
Activity limited to 5 METS or 70% age predicted HRmax for 4-6 weeks

Activity restrictions for acute heart failure

oxygen demand should not be increased in patients in acute or decompensation heart failure
once medically managed and no longer display signs of acute decompensation, their activity can be gradually increased while monitoring hemodynamic response to activ

ACE inhibitors

inhibit conversion of angiotensin I to II
decreases Na retention and peripheral vasoconstriction in order to decrease BP

Angiotensin II receptor blockers

blocks binder of ang II at the tissue/smooth muscle level
decreases BP

Nitrates

cause peripheral vasodilation
reduce myocardial oxygen deman, reduce chest discomfort, decrease preload

Beta-adgrenergic blockers

reduce heart rate and contractility
control arrhythmias, chest pain
reduce BP

Calcium channel blockers

inhibit flow of Ca ions
decrease HR
decrease contractility
dilate coronary arteries
reduce BP
control arrhythmias and chest pain

antiarrhymics

alter conductivity
restore normal heart rhythm
improve CO

Digitalis

increase contractility and decrease HR

Diuretics

decrease myocardial work
control hypertension

Aspirin

decrease platelet aggregation-->prevent MI

hypolipidemic

reduce serum lipid levels when diet and weight reduction are not effective

Primary Lymphedema

Congenital
abnormal lymph node or lymph vessel formation

Secondary Lymphedema

Acquired
injury of one of more parts of the lymphatic system
Possible causes:
surgery
tumors
radiation
chronic venous insufficiency

Karvonen Formula (HR)

(HR max- HR resting) + resting HR= target

ECG changes for normal adult

tachycardia- with increased work load
Rate-related shortening of QT interval
ST segment depression, upsloping, less than 1 mm
Reduced R wave, increased Q wave
Exertional arrhythmias- rare, single PVC

ECG changes for MI and CAD

significant tachycardia at lower intensities
exertional arrhythmias- increased freq of ventricular arrhythmias during exercises and/or recovery
ST segment depression, horizontal or downsloping depression greater than 1mm (MI)

standing/walking slowly is equivalent to how many METs?

1.5-2 METs

jogging (mph) or cycling (12mph) is equivalent to how many METs?

7-8 METs

running is equivalent to how many METS?

6pmh= 10
7mph=11.5
10mph= 17

Resistance training is contraindicated in patients w what CVP diagnoses?

Hypertension
Arrhythmias

Without an ETT, max HR is calculated by what equation?

208 - 0.7 x age

What is the avg intensisty/freq for exercise?

3-5 days/week
>5 Mets
20-30 min
warm up/cool down 5-10 min
If daily or multiple sessions for low intensitiy, <5METS

What are absolute indications for terminating exercise?

Drop in systolic > 10 mmHg with increased workload
Mod-Severe Angina
Increasing nervous system symptoms (dizziness, ataxia, syncope)
Signs poor perfusion
Subjects desire to stop
Sustained VT
ST elevation >1.0mm

What are RELATIVE indications to stop exercise?

ST or QRS changes
Arrhythmias other than sustained VT
Fatigue, SOB, wheezing, cramps, claudication
Development of bundle branch blokc that can't be distinguised from VT
Increasing chest pain
Hypertensive response

What is protocol post-CABG

no pushing, pulling, lifting for 4-6 weeks
Limit UE exercise while sternal incision is healing

Phase 1 Cardiac rehab guidelines

Wait until pt is stable 24 hours
Start low intensities (2-3 METS) progress to >5 MEts by discharge
short sessions, 2-3x/days
Walking goal: 20-30 min, 1-2x/day by 4-6 weeks post-MI

Phase 2 cardiac rehab

2-3x/week
30-60 min w 5-10 min warmup/cooldowns
D/C: >9 METS
Strength training:
start: 3 weeks cardiac rehab, 5 weeks post MI, 8 weeks post CABG
start with elastic bands and light hand weights

Phase 3 cardiac rehab

Progress to 50-85% functional capactiy
3-4x/week, 45 min or more
d/c 6-12 months

When should someone with PAD stop exercising (walking)?

If they reach 2 on claudication scale

How should someone with CVI position themselve?

LE elevated, min of 18cm above heart

How much compression should socks have for someone with CVI?

30-40mmHg

What defines orthostatic hypotension?

SBP drop of >20 and DBP drop of >10 (supine to standing for three minutes).
Rise in pulse of >15

How do you calculate mean arterial pressure?

SBP + 2(DBP) / 3

Normal MAP

70-110 mmHg

normal adult respiratory rate

12-20

newborn respiratory rate

30-40

Child respiratory rate

20-30

Tachypnea

Greater than 22 breathes per min

bradypnea

an abnormally slow rate of respiration usually of less than 10 breaths per minute

Stage 1 hypertension

130-139/80-89

Stage 2 hypertension

140+/90+

pallor

Extreme or unnatural paleness associated with PAD

rubor

reddish-blue discoloration of the extremities; indicative of severe peripheral arterial damage in vessels that remain dilated and unable to constrict

clubbing of nails

finding in the nails that indicates chronic hypoxia

Stemmer's sign

dorsal skin folds of the toes or fingers are resistant to lifting; indicative of fibrotic changes and lymphedema

2 peripheral causes of edema

Chronic venous insufficiency and Lymphedema

CAUSE OF BILATERAL EDEMA

CHF

Ankle Brachial Index

Arterial test: Comparison of the blood pressure in the leg vs. the arm; normal ratio is greater than 1
1.4 + indicates non compliant arteries
1-1.4 normal
.91-.99 borderline
<0.9 abnormal (increased risk for cardio event)
<0.5 severe arterial disease, ris

Clinically significant change in ABI

0.1-0.15

Rubor of dependency test

Tests of peripheral arterial circulation:
STEPS: Pt. in supine and note color of plantar aspect. Elevate to 45 deg for 1 min. Note color, return to original position
Normal: Return normal red/pink color in 15-20 sec
Insufficiency: pallor within 30 sec of

intermittent claudication (IC) test

Arterial test: pain in the leg muscles that occurs during exercise - relieved by rest - associated with peripheral vascular disease
Grade 1: minimal pain
Grade 2: moderate pain, attn can be diverted
Grade 3: intense pain
Grade 4: unbearable pain