A&P Review Cardiovascular

Heart: Weighs less than 1#, about the size of your fist.

Systole: Blood ejected from chambers; approximately 70ml of blood per beat Diastole: Chambers refill with blood

Heart Anatomy Endocardium: Innermost layer

Myocardium: Middle layer; muscle fibers

Epicardium: Outermost layer

Pericardium: Thin fibrous sac encasing the heart and root of great vessels

Composed 2 layers: Visceral pericardium Parietal pericardium

Pericardial space: Filled with 30 ml of fluid, allows free movement

Four chambers: 2 atria, 2 ventricles

Right heart: right atria, what receives the blood from the superior and inferior vena cave right ventricle that sends the blood via the pulmonary arteries

Left heart: atria receives the oxygenated blood from the pulmonary veins and the ventricles send that oxygenated blood out into circulation

CV Heart Valves Atrioventricular valves (AV valves):

Mitral valve- seperates the left atria from the left ventricle tricuspid valve- what seperates the right atria from the right ventricle

Papillary muscles & chordae tendineae Semilunar valves (3 half moon leaflets):

Aortic & pulmonary valves Pulmonic valve- between the right ventricle and the pulmonary artery Aortic valve- between the left ventricle and the aorta

CV-Coronary Arteries Perfused during diastole LCA:

LM: 2 bifurcations LAD (left anterior descending) & circumflex- feeds the left atrium and the lateral wall of the left ventricle

• Right coronary artery: • Smaller branches and they feed both ventricles

Conduction System of Heart*** Pacemaker cells:

Automaticity: ability to generate electrical impulse automatically Conductivity: ability to pass impulse to the next cells (from one cell to the next) Contractility: Ability to shorten the fibers in the heart while receiving the impulse

CV-Conduction Sinoatrial (SA) node: Aka the “pacemaker”

60-100 beats/min Firing sends impulse to right and left atrium Results in atrial contraction

AV node: Slows conduction between atria and ventricles 40-60 beats/min

Bundle of His : Travels thru to Purkinje fibers Purkinje fibers: Causes ventricles to contract Ventricles: Generate impulse in event of failure of other two nodes

20-40 beats/min

Physiology of Cardiac Conduction Cardiac action potential: Response of myocardium to electrical impulse Depolarization: Contraction/shortening

Na enters cell, K+ exits cell, Ca+ enters Repolarization: Relaxation/lengthening

Refractory Periods Absolute refractory period: Regardless of strength of impulse, will not contract Relative refractory period: May contract IF

impulse is strong enough Protects heart: Keep from sustained contraction

CV-Mechanical Events Cardiac cycle:

Systole: AV valves close, S1 Contraction, rapid increase pressure Semilunar valves open

Diastole: Semilunar valves close, S2 Atrial kick: portion of blood squeezed into ventricles

CV-Cardiac Output CO: 4-8 liters/minute (the amount of blood pumped out of the heart in 1 min) CO: Stroke volume (SV) times the heart rate SV: Amount of blood ejected/heart beat

Can be determined by preload, contractility, and afterload Cardiac Index: CO divided by body mass index; adjusts for body size Capacity: Approximately 70ml in resting state

CV-Control of Stroke Volume*** Preload:

End-diastolic volume stretching of muscle fibers in the ventricles Starling’s Law of the Heart – the greater the stretch of the heart during diastole the more forcefully the

heart will contract during systole (a normal heart) Decrease preload:

Diuresis, vasodilating drugs (pressure is decreased), hemorrhage, loss of pressure or loss of volume in a normal heart, loss of fluid

Increase preload: Fluid gain, vasoconstriction, volume related- replace the fluids they have lost

Afterload: resistance the left ventricle has to work against to eject the blood SVR (systemic vascular resistance) – increase or decrease in afterload Increases afterload:

Vasoconstriction (arterial)

Decreases afterload: Vasodilation (arterial)

Control of Stoke Volume: Contractility Increased contractility:

Causes: increase in SV, SNS (increase in contractility = increase SV) meds: digoxin, dopamine, dobutamine

Decreased contractility: hypoxemia, acidosis, certain meds, b-blockers Decrease contractility = decrease SV

Ejection Fraction Ejection fraction:

Fraction of total ventricular filling volume and then measured to see how much of that blood is ejected from the heart

Normal EF: 65% Decreased contractility = decreased EF

Control of Heart Rate Vagus (parasympathetic):

Slows the HR, stimulate the vagus nerve = slowing of the HR Sympathetic:

Speeds up HR, accelerates it Catecholamines: Baroreceptors:

Pressure sensors, sensitive to changes in BP Location: Aortic arch and carotid arteries Effect: Sensitive to changes in BP Elevated BP:

Transmit impulses to medulla Stimulates PNS Resulting in lowers HR and BP

Low BP: Less baroreceptor stimulation Increases SNS = vasoconstriction Resulting in increased HR and BP

Chemoreceptors: Location: Aortic arch & carotid body Effect: Increase in heart rate Responsive to:

Decreased arterial O2 pressure Increased arterial CO2 pressure pH of the blood

Peripheral Vascular Arteries/arterioles Capillaries Venules Veins Blood vessels composed 3 layers:

Tunica intima Tunica media Tunica externa or adventitia

PV-Review-Blood Flow Unidirectional flow:

>>left heart>>aorta>>arteries>>arterioles>> capillaries>>venules>>veins>>vena cava>>right heart Blood flow due to pressure gradients:

hi to low Resistance: vessel radius small = >pressure Turbulent blood flow: bruit (listen for this)

Nursing CV Assessment

Three important factors: Gender differences Gerontologic differences Ethnic differences

Gender differences: Women Smaller heart & arteries Increased risk occlusions Hemodynamics are increased Effects of estrogen

Reduces the risk of atherosclerosis Increases co-agulation proteins Decreased fibrinolytic protein, which puts u at a higher risk for thrombosis Overall cardioprotective

www.americanheart.org

Women & Symptoms of ACS (acute coronary syndrome)/MIMore atypical S/S:

shoulder & upper back pain SOB & extreme fatigue epigastric pain

Prodromal S/S: unusual fatigue sleep disturbances SOB

Acute S/S: most common SOB, weakness & fatigue Brunner page 795 (Nursing Research Profile)

Gerontologic Considerations: Adequate CO (cardiac output) under normal circumstances Elderly & diabetics S/S of ACS (atypical): fatigue & SOB are predominant S/S

Wall thickness (in the chart) ***

Gathering Health History: Age, gender, & ethnic origin Changes in weight Client health history & family history Cultural background/religious practice/ diet- nutrition

Cardiac S/S: Chest pain (character, location, radiation, duration, ppt. events, relieving measures) SOB/dyspnea Edema/wt. gain Palpitations Fatigue/dizziness/syncope 1st thing to do when someone c/o chest pain – put O2 on them at 2L/min with or without a dr order***

Management-Health Perception: Assess risk factors Assess client’s perception of risk factors Assess meds Nonmodifiable risk factors and Modifiable risk factors; (Chart 26-2, pp. 796 Brunner)

Nutrition & Metabolism: Diet, exercise, wt. loss Manage increased lipids

Pt needs to lower fat, cholesterol, sodium, less simple starches Pt needs to eat a diet high in fiber, more fruits and veggies

Elimination: Assess bowel and bladder habitsAsk: Do your feet or ankles swell?

Do you take medication to get rid of excess fluid? Do you weigh daily? Do you take meds for constipation? Any blood in urine or stools?

Activity and Exercise: New or change in S/S important Assess for change in activity pattern Fatigue, can be R/T meds

Sleep and Rest: Determine number of pillows used Where does patient sleep Presence of nocturia Paroxysmal nocturnal dysmia- do they have air hunger, or a sense of suffocating**

S/S: coughing, feel like suffocating, sweating and tachycardia

Cognition and Perception: Determine if client has cognitive problems Are there visual or hearing problems?

Need to be able to read and understand their meds (ex.)

Self-Perception & Self-Concept: Type-A personality

Short temper – look up Self-esteem problems

Especially younger men

Effects of Stress on the Heart

Role and Relationships: Assess social support system Is there a change in role?

Sexuality and Reproduction: Reluctance of patient to discuss Impotence from cardiac meds

Coping and Stress Tolerance: Adverse effects of stress & anxiety Link between hostility & CV disease

Cardiac Physical Exam Head to toe examination:

general appearance, cognition, skin, BP, arterial pulses, jugular venous pulsations, heart, extremities, lungs, abdomen

General Appearance & Cognition: Level of distress LOC Thought process Anxiety/emotional stresses

Temperature/moisture Clubbing Edema/weight Wounds Arterial circulation

Blood Pressure: Systolic blood pressure Diastolic blood pressure Determinants of BP Pulse pressure: difference b/w sys and dia – the difference should be about 1/3 of the sys

189/110=79 77/50=27 When the systemic When your arteries become less elastic When you have an increase in SV

Terms r/t Blood Pressure Blood pressure = cardiac output x SVR SVR= systemic vascular resistance BP determined in part by cardiac output, SVR, blood volume, elasticity of arterial wall

Pulse Rate and Rhythm Normal pulse

Rate 60-100 Easily palpated Full and regular

Pulse deficit Difference between apical and radial rates

Pulse configuration Carotid is best to examine Pulse wave should be smooth with rounded shape

Sinus arrhythmia Increase in hr during inhale Slowing during exhale Usually young people

Pulse Quality Review: 0: absent pulse 1+: weak, thready, difficult palpate 2+: normal pulse 3+: slightly increased, full pulse 4+: strong bounding, can’t be obliterated

Jugular Venous Pulsation Estimate of right heart function Distension when supine

Heart Inspection, Palpation, & Auscultation Aortic

2nd intercostal space, right side Pulmonic

2nd intercostal space, left side Tricuspid

4 – 5th intercostal space, left side Mitral

5th intercostal space, mid-clavicle line Epigastric

4 bowel quadrants

CV Heart Sounds S1:

Closure tricuspid & mitral valves “lub” heard best at apical or mitral area systole

S2: Closure pulmonic and aortic valves “dub” heard best at aortic area diastole

Gallop Sounds: S3 S3 “Ken-tuck-y” S1____S2_S3______S1 Gallops

So named due to sound like a horse Abnormal sounds, ventricular origin Low frequency – use bell & press lightly on skin Heard best at apex, lying on left side

S3 Follows S2 R/T vibrations caused by abrupt ventricular distention & resistance to filling Common in children Sign of heart failure in adult

Gallup Sounds: S4 S4 “Ten-nes-see” S4-S1____S2______S4_S1 S4

Atrial in origin Occurs prior to S1 after atrial contraction Occurs in elderly (most common), HTN, or Hx of MI From vibrations caused by forceful atrial ejection of blood into the ventricles that are resistant to

expansion If you see in chart somewhere that they have a gallup, make sure you listen

Quadruple rhythm May have both S3 and S4 sounds

Murmurs Turbulent blood flow:

increased blood flow-normal area valve problems Related to hyperthyroidism

Graded: location, timing, intensity, pitch (low, med, high), quality (harsh or musical – blowing or rumbling, swish), radiation (radiates to other areas), benign (its present but there is not a problem), numerically (if there is an increase in intensity and volume, the number will go up)

Friction Rub Machine-like sound

Pericardial friction rub, grating sound, heart through systole and diastole, heard most distinctly at the sternum and apex of the heart, heard best when the pt is sitting up and leaning foward

Inflamed pericardial sac

Lungs Hemoptysis Crackles – can indicate inflammation, congestion, heart failure, pneumonia Wheezes – high pitched, musical, indicates bronchospasms or bronchoconstrictions Orthopnea – difficulty breathing in supine position Paroxysmal nocturnal dyspnea

Normal findings of Assessment

Diagnostic Evaluation Laboratory: Blood Chemistries Electrolytes: Potassium

Hyperkalemia = weaker heart rate Hypokalemia = premature ventricular contractions

Calcium Hypercalcemia

Magnesium – affects the absorption of ca and maintains K stores Sodium (Use norms previously given)

Cardiac Enzymes & Proteins (released after damage of heart muscle) Creatine kinase (CK) & CK-MB

Found in heart and skeletal muscle, brain tissue, most in heart, rises in MI, elevate with an MI Myoglobin

Not used as much anymore cause it also rises with skeletal muscle damage, found in hear and skeletal muscles

Troponins T & I (cTnT & cTnI): most specific to heart muscle** Normally absent Detectable w/i 1 hour of injury Rise 4-6 hrs Elevated up to from 1 to 3 weeks most accurate and specific to the heart Protein specific to the heart Peaks w/i 14-20hrs

C-Reactive protein Produced in the liver Indicates inflammation Poss link between inflammation and heart disease

Homocysteine Amino acid High levels irritate the vessels and can lead to atherosclerosis Can raise LDL levels If its higher you are more prone to blood clots Folic acid between 6-12 to treat it

BNP: <100pg/mL Brain naturietic peptide

Excreated by ventricles when if heart failure Higher in healty women all the time than it is in healthy men or elderly

Lipid Studies Cholesterol, normal < 200 (180)

Synthesized in the liver Comes from eating fat If its high you are at risk for heart disease

LDLs, normal < than 130, CAD, <100 Bad cholesterol (loser)

HDLs, men-35-65, women, 35-85 Good cholesterol (happy) Indicates a lower risk for CAD Helps transport away from the arterial walls to the liver fro excretion Factors that influence: obesity, diabetics, smoking (vasoconstricts), physical activity or inactivity

Triglycerides, normal, 40-150 Main storage from of lipids Direct correlation with LDL High HDL = low triglycerides

Lab Studies Blood urea nitrogen

End product of protein metabolism In the liver Isotonic, loss of fluids, too much diuretic

Coagulation Studies Determine pt risk of bleeding See where they are in their coagulation therapy

PTT looks at heparin Put in some calcium and thromboplastin in and wait for a clotting time

PT/INR looks at coumadin Internal normalized ration – pro time??(PT) Measures clotting reaction time (1,2,5,7,10)

Diagnostic Evaluation Chest X-ray Electrocardiogram-12 lead Echocardiography TEE-transesophageal echocardiography

Telemetry EBT

Electron beam tomography Can detect some cancers Gallstones Only takes about 10 min Non invasive

Stress testing Look at how the heart handles stress Non invasive- exercise test Invasive – Makes the heart work harder and increased O2 demand

Exercise & pharmocological

Cardiac Catheterization Invasive Diagnostic Study Performed with angiography Right, left heart cath or both Most frequently used to assess patency of coronary arteries & dx. CAD Common Complications:

Bleeding Poss to perforate a vessel, does not happen often

Dysrhythmias They inject all that dye into them and then it irritates the heart and an irritated heart is not good

Allergic reaction; meds or iodine Patient education Sensations; hot flushing feeling

Versed ?? Pulse assessment Telemetry monitor

Post-op care: V/S Positioning Inspection Peripheral pulses Encourage fluids

PTCA Percutaneous transluminal coronary angioplasty

Balloon tipped catheter inserted into artery to open blocked vessels Balloon is expanded, pressing plaque down May also place stent

Risks Bleeding Infection Stroke (plaque can bread and travel) Dysrhythemias

Normal Electrical Conduction – EKGs ECG waveform

P wave QRS complex T wave

P-wave: atrial depolarization QRS complex: ventricular depolarization

T-wave: ventricular repolarization

Cardiac Action Potential Five phases: 0 = upstroke or rapid depolarization, initiates heartbeat 1 = early rapid repolarization 2 = plateau 3 = final rapid repolarization 4 = resting membrane potential; diastolic depolarization

**look up different intervals and segments in the book

Terms to Know Ischemia- lack of blood supply to an area Central cyanosis- involve heart and large vesselse, decreases o2 sat of hemoglobin in arterial blood, see it in the

lips, buccal mucosal Peripheral cyanosis- can have w/o central if there are occlusions away from the midline of the body, reduced

hemoglobin, blockage, low cardiac output Myocardial infarction- heart attack, caused from an occlusion Acute coronary syndrome- presenting symptoms of heart attack, not an actual heart attack, range from unstable

angina to an MI (decreased O2 from the heart) Preload- end diastolic volume, how much blood in is the ventricles at the end of diastole, stretch Afterload- amount of resistance that it has to push out Angina pectoris- chest pain cause by defiency of O2 caused by the muscle, can be related to stress, exercise,

treat it with nitro Hypotension & Hypertension “Sinus” Tachycardia & Bradycardia Dysrhythmias- abnormal ryth. of the heart Prodromal- refers to the beginning stages of a disease Cardiac Output- how much blood is ejected from the ventricles in 1 min Stroke Volume- amount ejected Systemic Vascular Resistance- (SVR)- blockage, athrosclerosis Modifiable & Non-modifiable Risk Factor Depolarization Repolarization Conductivity Automaticity Pulse Pressure- systolic – diastolic = PP Pulse Deficit- apical rate – radial = PD PTCA- CC/CA- cardiac cath/ cardiac angiography