Week 4 Cardio Pulm Study Questions

Front 1

Describe contractility of the heart and Frank Starling Law

Back 1

Contractility: the intrinsic ability of a cardiac muscle fiber to contract at a given length.

Frank Starling Law: the more the ventricle is filled with blood during diastole, the greater the volume of blood can be ejected during the resulting systolic contraction

Front 2

Describe PreLoad and AfterLoad

Back 2

Preload: The volume of blood present in the ventricles after passive filling and atrial contraction. Dependant on venous return

Afterload: The amount of pressure the ventricles have to generate to eject blood out of the heart.

Front 3

Describe Cardiac Output

Back 3

CO=HRxSV

Stroke Volume is the amount of blood pumped with each beat of the heart

CO average of 5L (70x70)

Front 4

Describe how HR is regulated and how the SNS and PNS interact with HR

Back 4

HR regulated rhythmically and automatically by SA and AV nodes that initiate impulse. No CNS input required.

SNS acclerates HR (+chronotropic, +inotropic) by upper thoracic nerves

PNS slows HR (-chronotropic, -inotropic) by vagus nerve

ANS regulates rate of impulse, controls rate of spread of excitation and contractility but does NOT initiate heart muscle contraction

Front 5

Describe normal electrical conduction of the heart

Back 5

SA Node (60-100) -> AV Node (40-60) ->Bundle of His ->L and R Bundle Branches -> Perkinje Fibers -> Ventricular Myocardium (20-40bpm)

Front 6

NAME CARDIAC PUMP DYSFUNCTIONS OF THE HEART

Back 6

-CAD
-Chronic Diabetes
-Chronic HTN
-MI
-Ischemia
-Dysrthythmias
-Valve Disorders
-Alcoholic Cardiomyopathy
-Conduction Disturbances

Front 7

EXPLAIN ATHEROGENESIS AND ATHEROSCLEROSIS

Back 7

Atherosclerosis is hardening of medium and large arteries. LDL's aren't digested and deposit into smooth muscle. Arterial rxn to this is to surround LDL with collagen. Plaque builds.
-Atherosclerotic changes in Aorta: thinning of media, weakening of vessel wall, aneurysm, rupture.
-Atherosclerotic changes in coronary arteries are stenotic and occlusive lesions

Front 8

DESCRIBE SEVERAL CARDIAC RISK FACTORS

Back 8

-Age >65
-Males
-Smoking
-Heredity (1st)
-Race (african americans)
-Diabetes
-HTN
-Cholesterol
- Increased platelet count
-Stress, and Sedentary lifestyle

Front 9

EXPLAIN STAGES OF HYPERTENSION

Back 9

-Prehypertension S 120-139, D 80-89
-Stage 1: S 140-159 D 90-99
-Stage 2: S 160 + D 100 +

Front 10

NAME 3 THINGS CORONARY BLOOD FLOW DEPENDS ON

Back 10

1. Driving Pressure
2. Resistance to flow along coronary vascular bed
3. Duration of coronary artery filling time (need enough diastolic time)

Front 11

WHAT ARE DETERMINANTS OF MYOCARDIAL OXYGEN DEMAND?

Back 11

-HR
-Systemic Systolic BP (Afterload)
-Preload/wall tension
-Rate pressure generation in LV (contractility)
-Threshold for Angina: Rate Pressure Product (RPP)

**Myocardium extracts 75% of the O2 from coronary blood supply both at rest and with exercise
**Increase in myocardial O2 demand is matched by increase in coronary blood supply

Front 12

WHAT IS MOST POTENT METABOLIC CORONARY VASODILATOR?

Back 12

Hypoxia

Front 13

DESCRIBE CORONARY SPASMS AND SIGNS AND SYMPTOMS

Back 13

Coronary spasms are increase in vasomotor tone leading to localized or diffuse spasm of coronary arteries, which reduces coronary flow significantly and results in ANGINA, MI, or SUDDEN DEATH
-Amt of occlusion increases when and if there is a spasm
Signs/Symptoms: Prinzmetal Angina (at rest), cyclical symptom patterns (am or pm discomfort), ST elevation with or without symptoms
-Vasoactive substances that can lead to coronary spasms: catecholoamines, serotonin, histamines

Front 14

DESCRIBE PATHOPHYSIOLOGY OF CARDIAC ISCHEMIA

Back 14

With onset of exercise, there's an increase in myocardial O2 demand, Hr and BP. This increased demand may not be met due to resistance in coronary artery blood flow and reduction in net driving pressure beyond obstructions. Leads to lack of blood supply. Produces Angina pectoris. Often accompanied by dysrthythmias which can cause sudden death. Ischemia reversible within 3-4hrs.

Front 15

DESCRIBE MI AND DIFFERENCES BETWEEN TRANSMURAL AND SUBENDOCARDIAL.

Back 15

-MI is cell death/necrosis, caused by prolonged ischemia, which is due to complete occlusion of coronary artery, vasospasm, or plaque rupture and embolism. Changes in myocardial tissue begin 15 min after tissue becomes hypoxic.
-Transmural MI- full wall thickness, Q wave infarction. Extends through subendocardial tissue to epicardial layer of myocardium.
-Subendocardial MI- Silent MI/Non Q wave. Only involves innermost layer of myocardium. Does not go through.

Front 16

NAME 2 IMPORTANT SERUM MARKERS OF MI`

Back 16

1. CK-MB: higher the level, the larger the area of infarction.
2. Troponin: protein

Front 17

DESCRIBE HEART FAILURE

Back 17

The inability of the heart to maintain cardiac output at rest (less than 4L/min) because heart isn't moving effectively. Hear S4 initally because of hypertrophy, over time will hear S3 sounds.

Front 18

4 CLASSES OF NYHA FUNCTIONAL CLASSIFICATION OF HEART FAILURE.

Back 18

Class 1: no limitation of physical activity.
Class 2 (mild): comfortable at rest, but ordinary physical activity results in fatigue, dyspnea, palpitations
Class 3 (mod): Marked limitation in physical activity. Less than ordinary activity causes fatigue, dyspnea, palpitations.
Class 4 (Severe): Unable to carry out physical activity w/o discomfort. Symptomatic at rest

Front 19

WHAT ARE DIFFERENCES BETWEEN L SIDED AND R SIDED HEART FAILURE?

Back 19

Left Sided: LV end diastolic pressure backs up into LA and then into pulmonary venous vasculature, then fluid possibly to lungs. (pulmonary edema). Hear crackles, S3, hypertrophy, Tachy and dyspnea

Right Sided: Rise in lung pressure causes rise in pulmonary artery pressure (not designed to pump against elevated pressures). RV backs up into RA into peripheral venous pressure, and peripheral edema. Poor exercise tolerance, significant wt gain and hypotension.
* with PURE right sided heart failure, no pulmonary edema and no crackles.

Front 20

EXPLAIN COR PULMONALE.

Back 20

Right ventricular hypertrophy which leads to chronic hypoxia which vasoconstricts pulmonary artery which increases pulmonary artery pressure which causes right sided heart failure.

Front 21

DESCRIBE 3 LAYERS OF VASCULAR LINING AND THEIR FUNCTIONS.

Back 21

-Tunica Intima: innermost layer, endothelial cells, provides smooth surface for laminar blood flow.
-Tunica Media: smooth muscle cells and elastic connective tissue with SNS innervation- constricts and dilates for bp regulation. (acts as pump! imp!)
-Tunica Adventitia: outermost layer- collagen, lymph vessels and blood vessels that supply nutrients. Function to protect and attach blood vessels to nearby structures.
**Adventitia more predominant structure in VEINS

Front 22

DESCRIBE WALL PROPERTIES OF ARTERIAL VASCULAR SYSTEM

Back 22

-Arterial system: elastic wall properties that serve as accessory pump to the heart.
-Tension in vessel is proportional to it's pressure and radius, and inversely proportional to it's wall thickness.. (more tension on vessel with larger radius, less tension on thicker vessel).
-When tension decreases b/c of drop in pressure or blockage, vessel wall is at risk of collapsing.

Front 23

DESCRIBE PERIPHERAL ARTERY DISEASE.

Back 23

-Occlusive disorder of Aorta, femoral and Iliac Arteries, due to atherosclerotic changes in media and intima, plaques in media.
-Blockages occur most frequently where arteries bifurcate and can get backed up
-SYMPTOMS: Claudication (pain, cramps, or stiffness) may occur in LEs

Front 24

DESCRIBE VASOSPASTIC DISORDERS.

Back 24

Raynaud's Syndrome: pain, paresthesias, possible white blanching in hands due to cold temps or stress

Hand Arm Vibration Syndrome: hand pain and paresthesias a/w use of machinery and often mistaken for CTS

Front 25

DESCRIBE CHRONIC VENOUS DISEASE

Back 25

-Varicose Veins and Chronic Venous Insufficiency most common. (Varicose veins think Rt sided heart failure). Reflux is problem in 86% of cases, valves aren't working properly and fluid is getting backed up

-Venous Thrombosis: caused by 1 or more of VIRCHOWS TRIAD:
1. Trauma to veins
2. Stasis of venous circulation
3. Abnormal blood coagulation factors.

Front 26

NAME DIFFERENCES BETWEEN ARTERIAL DISEASE AND VENOUS DISEASE.

Back 26

ARTERIAL: Claudication, decreased pulses and temp, pale dusky red on dependency, thick nails, trophic skin changes, VERY painful ulcers.

VENOUS: Marked Edema, brown pigmentation around ankle, stasis dermatitis, Non painful ulcers

Front 27

HOW WOULD YOU GRADE A PULSE?

Back 27

0- Absent
1- markedly impaired
2- moderately impaired
3- slightly impaired
4- normal

Front 28

LIST MAJOR PULSE POINTS AND WHERE TO PALPATE FOR.

Back 28

Temporal- Ant to ear
Carotid- btw trachea and SCM
Brachial- btw Biceps and Triceps Medial side
Radial-Radial head
Ulnar-Lat to pisiform and FCU
Femoral- btw pubic symphysis and ASIS
Popliteal- M to midline btw M and L condyles
Post Tib- behind M malleolus
Dorsalis Pedis-

Front 29

EXPLAIN ANKLE BRACHIAL INDEX

Back 29

-Do in Supine
-Measure highest systolic bp in both arms, doppler at radial pulse. listen for 1st sound.
-Measure systolic in both legs for BOTH dorsalis pedis and Post tib (cuff on calf)
-Use highest ankle pressure (DP or PT) for each ankle.
-Divide each ankle by highest brachial pressure.
-NORM: >.96
< .95 abnormal, stress testing is appropriate
< .8 possible claudication

Front 30

NAME OTHER VASCULAR TESTS

Back 30

-Trendelenburg (for vein competency, use tourniquet on LE which is elevated in supine).
-Reactive Hyperemia: elevating limb to 30-40deg then back down.
Check for lasting rubor.
-Capillary Nail Refill Test: fingers and toes. + if takes longer than 2 sec to refill
-Cold Water Test (for Raynauds)
-Homans Sign (DVT)
-Allens Test (R and U circulation)

Front 31

WHAT IS THE NUMBER ONE CAUSE OF HEART FAILURE?

Back 31

CHRONIC HYPERTENSION