Coronary cardiovascular

Systole

Contraction of the ventricles

three layers of blood vessels from outside to inside

three layers of blood vessels from outside to inside

tunica externa:outermost layer, contains collagen fibers

tunica media: middletunic, smooth muscles

tunica intima: endothelium, innermost layer

Nameof vessel supplying blood to larger vessel

Vasa vasorum

Types of blood capillaries

Continuous - gas exchange, found in brain, testes, lungs, etc most common

Fenestrated - active filtration and absorption found in gi and kidneys

Sinusoid- most permeable found in liver, spleen, lymphnodes bone marrow

Vessels hold up to X amount lf blood volume at one time

65%

To be noted when taking oulse

Rate, rhythm, force/volume, does it match heart rate

Major long term bp is controlled by X

Kidneys

Condition in which blood vessel are inadequately filled and blood cannot circulate normally

Circulatory shock

What arteries branch from the celiac trunk

Common hepatic, left gastric and splenic

Superior vena cava is formed by which veins

Left and right braciocephalic

Longest vein and longest nerve

Great saphenous, sciatic

A thrombus in the first branch of the aorta would affect blood flow to the …

R side head and neck and right upper arm

Map calculation

Mean arterial pressure = cardiac output (bpm x ml ejected per beat (stroke volume)) X total peripheral resistance

Stroke volume calculation

End diastolic volume - end systolic volume

What effects stroke volume

Contractility (SNS increasing calcium)

Venous return

Blood amount

Blood pressure e.g. venoconstriction

Frank starling law (higher ventricle stretch = greater ejection

What is ejection fraction

Amount of end diastolic blood ejected during systole (percentage ejected)

What is total peripheral resistance

Diameter of vessel which creates pressure (sum of total resistance in all blood vessels)

What causes total peripheral resistance

Thickness of blood

Blood vessel diameter

Blood vessel length

How does the sns increase stroke volume

Increase power of contraction through extra calcium channels

Vasoconstriction

What are baroreceptors

Stretch receptors in the aortic arch and carotid artery (in carotid sinus) which send notification to medulla for activate autonomic nervous system

What js RR interval and what should be noted

Space between peaks of QRS to show time between contractions

Is it narrow or protracted?

Delays of conduction (scarring, abnormal pathways, age)

How long should atrial depolarisation take

Wothin 3 small squares = <120 milsec

Size of QRS complex

70-100miliseconds or 2 - 2 ½ mini squares

What is PR interval

120-200 ms or 3-5 small squares, has it been a clean and rapid movement or delayed

How to tell the time of a 6 second ecg strip

5 large boxes = 1 second

(times amount if complexes on total strip by 6)

What might signal reduced cardiac output to the body

Impaired perfusion and oxygenation

• tachycardia racing pulse, confusion

• tachyponeic, fast breathing, i.paired speaking

• hypoxia e.g cold hands, weak pulses

Reduced blood to meet body demands

• tight feeling chest

• Poor activity tolerance

• Possible symcope

• Fluid imbalance

Nutritional and fluid imbalance

• Oedema, improper pumping causing oedema as blood and fluid sits

• Loss of appetite (blood diverted to more vital organs)

What actions could be taken for a patient with reduced cardiac output- vital signs

Regular vital signs, if radial pulse is thready due to limited blood output, heart sounds should be auscultated on the left strenal border 4th intercostal space, compare to radial pulse for 1 minute

What actions could be taken for a patient with reduced cardiac output - peripheral perfusion

Colour and warmth, cap refill, assess oedema, daily weight and FBC

Monitor BP manually if machine cant read, orthostatic readings

What actions could be taken for a patient with reduced cardiac output- lung and general care

Position semifowlers,

Medication safety, before and afters of medications i.e. sotolol and digoxin (hr and bp before)

Assess for bleeding especially if on blood thinners

Assess for orthopnea and breath sounds, work of breathing, paroxysmal nocturnal dyspnoea (legs raised during sleep to drain fluid, can put sudden strain on heart and cause palpitations, need increased oxygen)

Possible fall risk on standing, orthostatic bp,

Staging activity to reduce risk of fatigue, cluster care

Assess for ankle or sacral swelling

What is coronary beart disease or coronary artery diseas

Caused by impaired blood flow to the myocardium often by build up of atherosclerotic plaque in the coronary arteries

Common symptos or effects of coronary artery disease/ coronary heart disease/ischemic heart disease

Angina pectoris

Acute Coronary syndrome

Myocardial infarction

Arrhythmias

Heart failure

Sudden death

What affects the coronary circulation

Aortic pressure

Heart rate

Metabolic activity

Tone of the blood vessel

Collateral circulation

Which coronary artery supplies SA node

Right coronary artery, sudden occlusion of arrhythmias and sudden cardiac death

What is the internal lining of an artery and why is this important for atherosclerosis

Intimal layer,

Plaque forms from triglycerides, ldl, etc debris of collagen/smooth muscle cells/phospholipids within this layer and creates narrowing of lumen

calcifies to tear lining of artery causing bleeding of vessel and clot occludes or thrombus

What is angina pectoris and rreatment

Characterised by chest pain usually at exercise and relieved by rest. Mddications such as GTN which dialates artery

Occurs when the myocardial oxygen needs are greater than the partially occluded vessels and myocardial cells become ischemic

Anaerobic metabolism produces lactic acid that stinulates nerve endings causing oain, pain subsides when oxygen supply meets demand

What is an MI and possible treatments

Complete obstruction of coronary artery interrupting blood supply to area of myocardium

Clot disolving drug to break it up

Angioplasty to stretch narrowing with balloon and clot removal and perhaps stent

What is vasospasm

Symptoms of MI

CRUSHING AND SEVERE chest pain

TIGHT BURNING PRESSURE

• Fever, hypotension(later stages)/hypertension (Initially)

• Unlike normal angina

• Sudden onset, not necessarily provoked

• Lasts more than 15 minutes

• Not relieved by GTN or rest

• TACHYCARDIA AND FEAR

• Dyspnea

Serum cardiac markers to be considered for MI

Troponin TNI

Creatanine kinase CK

CK-MB

Ecg of angina

Depressed depression (not inverted)

Flattened t wave (or reversed)

ECG of Mi

T wave inversion

ST segment elevation

Formation of Q wave

Examples of cardiac nursing diagnosis during MI

Acute pain

Ineffective tissue perfusion evidenced by low blood pressure

Activity intolerance

Fear/anxiety

Causes of atrial fibrillation

Age

Other heart disease or issues (ischemia,.previous heatt attack, structral, hypertrophy)

Htn

Other medical issues, ckd/thyroid/osa/infection/diabetes

Postop esp. cardiac procedures

Alcohol

Obesity

Family history

Pathophysiology of atrial fibrillation

Randmon electrial signals occur in atria causing out of rhythm twitching, palpitations and less effective pumping

Symptoms of AF

Can lead to clots

Palpitations

dyspnea/feelings of shortness of breath

Lightheaded

Diagnosis and screening of AF

History- signs symptoms

Asymptomatic- can be detected by smart watch,

Symptomatic- fatigue, SOB, palpitations, lightheaded, chest pain, palpate the pulse!!

ECG- chaotic fibrillation instead of p waves, irregular rhythym (RR interval)

Add. Screening- Tt Echo to see e.g size of heart (bigger = more cells to act up) valvular disease/abnormality , se. Electrolytes, hb/anemia, TSH increase, htn, osa, diabetes (if some kf these are managed it can control AfF)

What is paroxysmal (early) AF

Starts and stops suddenly without much provocation

Can last for seconds, minutes, weeks

Will revert spontaneously

What is persistent AF

Episodes last longer than a week

May revert spontaneously

Usually medication or cardioversion treatment needed to revert

Long term persistent AF

Continues uninterrupted for longer than one year

Heart will not return to normal, medications or cardioversion can be tried to revert rhythm

Medications may control symptoms

What is permanent AF

Doctor and patient decide to accept AF and focus on rate rather than rhythm

What medications may be used for medical cardioversion

Flecainide

Amiodarone

Sotolol

Why js anticoagulant therapy important in AF and what is the duration needed pre and post cardioversion

Prevent clot formation

Commonly Apixaban or eliquis

Anticoagulant therapy needed for minimum 4 weeks post to prevent normal sinus rhythm releasing clots later on and 3 weeks prior OR has occured definitely less than 48hrs

Medications used to maintain normal rate in AF

More effective in less symptomatic cases

Beta blockers or Ca channel blockers support heart to have consistent rate, digoxin

Treatments for AF

Medication e.g beta blockers or ca channel blockers, ablation, cardioversion medical or electrical, anticoagulants to prevent complications

Complications of AF

Af with rapid ventricular response

-ventricles unable to fill properly = decreased cardiac output

- bp, pulse volume and rate, resp rate, poor perfusion, pallor, Restlessness, confusion, headache, dec. Appetite, lightheaded

• fluid backlog (farigued heart = HF = oedema, lung crackles, resp rate, sacral and ankle swelling

• PE or stroke

Physiology of MI

Symptoms and manifestations of AF

Symptoms and manifestations of MI

What is inportant for efficient conduction of the heart

Rapid activation - simultaneous contraction of myocardium- one strong contraction

Sequential activation (following normal sequence- atria - rest- ventricles)- allows atria to fill adequately before ventricle contracts

Diastole

Relaxation of the ventricles

The first heart sound is a closure of these valves

Atrioventricular (tri and bi cuspid)

The second heart sound is a result of these valves closing

Semilunar

Which chambers of the heart are empty during ‘lub’

Atria, ventricles have been filled

Which chanbers of the heart are empty during ‘dub’

Ventricles, the atria will begin filling immediately

Where does the blood flow throughout the cardiopulmonary system

Sup and inf vena cava

R) atria

Tricuspid valve

Pulmonary trunk

Pulmonary Arteries

Lungs

Pulmonary veins (oxygenated)

L) atria

Bicuspid/mitral valve

L) ventrical

Semilunar valve

Aortic arch

Where do the coronary arteries which nourish the myocardium originate

Base of the aorta

The coronary sinus empties into the X

R atrium

The fluid that fills the pericardial sac is to reduce X

Friction during heart activity

The membrane that lines the heart and forms the valve flaps is called the X compared to the external lining which is called X

Endocardium

Epicardium

Staples heart muscle together

Intercalcalated discs with gap junctions to allow for electrical currents to pass simulatenously

Pacemaker of the intrinsic conduction system

SA node

What anchors the flaps of the AV valves

Chordae tendonae

What happens during the P wave

Atrial depolarizations

What happens during the QRS complex

Ventricular depolarizations

Atrial repolarizations

What happens during the T wave

Ventricular repolarization

What is this formula: CO = HR . SV

Cardiac output= heart rate . Stroke volume

Average adult cardiac output per minute

5250ml / roughly 1x blood volume

What is starlings law of the heart

Force of the heartbeat or stroke volume is dependant on the degree of stretch of the muscle just before it contracts, consequentially the force of heartbeat can be increased by an increased return of blood to the heart