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Cardiac Pathology, Surgical incision sites, analgesia + pain, More.... -…
Cardiac Pathology
Cardiac arrhythmias
Irregular - flutter, fibrillation
too slow - bradycardia
too fast - tachycardia
Atrial fibrillation
Different places in and around the atria produce electrical messages , in an uncoordinated way
makes the atria quiver or twitch - fibrillation
Felt as an irregular and sometimes fast heartbeat or pulse
Symptoms
Palpation
Tiredness
Shortness of breath
dizziness or feeling faint
Major cause of stroke
Flutter
Sinus node sends out the electrical signal
Part of the signal travels in a continuous loop along a pathway around the right atrium
This makes the atria contract rapidly, which causes the atria to beat faster than the ventricles
A normal hr is 60 - 100 bpm. people with AFL have hearts that beat at 250-300 bpm
Ventricular tachycardia
A sequence of 3 or more ventricular beats
The rate is between 110 - 250 bpm
Often originates around old scar tissue in the heart
Electrolyte disturbances and ischaemia can cause ventricular tachycardias
The cardiac output is often strongly reduced during VT resulting in Hypotension and loss of consciousness
VT is a medical emergency as it can deteriorate into ventricular fibrillation and thus mechanical cardiac arrhythmia
Ectopics
A disturbance of the cardiac rhythm
beats arise from fibres outside the sinoatrial node
Considered normal
May become more frequent during anxiety, panic attack, and the fight or flight response due to increase in sympathetic nervous activity
Consumtion of nicotine, alcohol, epinephrine and caffeine = increased risk
Hypertension
Resting Bp higher than 140/90
Damages heart due to increased afterload (Bloodflow back into the heart)
Worsened by atherosclerosis (the buildup of fats, cholesterol and other substances in and on your artery walls)
Risk factors (HASLIPIDS): Hereditary, Age, Sex (male), Lipidemia, Increased weight (obesity), Pressure, Inactivity, Diabetes, Smoking
Risk factors associated with atherosclerosis: lesions due to strain on endothelium that become focal points for development of atherosclerotic plaque.
Accelerates development of atherosclerotic plaques in large vessels
is a vicious cycle
thickening of media layer of small arteries
Consequence: left ventricular hypertrophy- eventually becomes over stretched and less efficient.
Atherosclerosis
Endothelial injury
Damage caused by blood borne chemicals, smoking, hypertension, infection
Lipids accumulate
Chemotactic factors promote deposition of lipids and macrophage migration
Smooth muscle proliferation
Smooth muscle migration from tunica media forms a cap which narrows the lumen
Plaque can become unstable
Consequences
Arterial stiffening - contribute to hypertension
Reduced blood flow - vasoconstriction
Arterial wall 'fraying' and vasoconstriction - blood backup and platelet adhesion causing thrombus formation
Hence plaque formation - increases risk of ischaemia, MI, stroke, aneurism
Venous thromboembolism (VTE)
Where blood clots from abnormally within the venous circulation
Result of a combination of 3 factors (Virchow's triad)
Poor or turbulent blood flow
Blood vessel endothelial damage
Blood clotting
Commonly collect in areas of abnormal blood flow
DVT
most common in lower limbs
Can also occur in the upper limbs
Can result in vascular compromise
Pulmonary embolism
DVT detaches from site of formation and passes through the right side of the heart into the pulmonary arterial circulation
Results in impaired gas exchange and altered V/Q mismatching
Massive PE's can have severe haemodynamic and respiratory effects leading to death if not treated
10% of patients with symptomatic PE will die within 1 hr of onset of symptoms
Acute Risk factors:
Hospitlization
Surgery
Trauma
Long distance travel
Paralysis
Varicose veins
Insertion of venous device
BP
Measured at Brachial artery
120/80 = ideal
listen with stethoscope @ cubital fossa
Congetstive Cardiac (heart) failure
Prolonged increase in heart workload makes it difficult for heart to function
Failure of the heart as a pump due to :
Ischaemic heart disease
Myocardial infraction
Chronic infarction
Valvular insufficiency
Congenital defects in cardiac structures
Endocrine disorders
May be primarily a problem of contraction or one of filling
3 types of CCF
Diminished force of contraction of ventricles due to:
Primary heart muscle diseases
Coronary artery disease
Mechanical failure in filling the ventricles during diastole due to:
Narrowing of the mitral valve opening (mitral stenosis)
Accumulation of fluid in the pericardium (pericardial tamponade)
Overloading of the ventricles during systole due to:
High BP (hypertensive cv disease)
narrowing and obstruction of aortic valve (aortic stenosis)
incomplete closure of aortic valve (aortic valvular regurgitation)
Congenital defect in ventricular septum (ventricular septal defect) (hole in the heart)
Left ventricular Failure (LVF)
Most common form of CCF
Pulmonary congestion
raised pulmonary capillary pressure
Pulmonary oedema - fluid in lung tissue
Reduced compliance (less inflation)
wheezing
Dysponea (shortness of breath)
Wet, frothy cough
Fatigue impaired exercises intolerance
Right ventricular failure (RVF)
commonly result of LVF
Fatigue; impaired exercise intolerance
congestion of blood in peripheral organs and extremities - peripheral oedema
Valve pathology
Incompetent valve (insufficiency)
Failure of any valve to prevent reflux|
Allows blood back into the chamber from which it was expelled
Regurgitated blood created turbulence
regurgitation heard as a heart murmur
Stenotic valve
cusps are stiffened and opening constricted by scar tissue
Impedes blood flow from one chamber to the next
May also be incompetent
Heart overworked to force blood through stiffened opening
consequence
reduces efficiency - heart failure
Mitral or tricuspid valve in progressive dilation of the affected side of the heart
Massive atrial enlargement may develop in patients with chronic valvular regurgitation
stenotic valve may lead to hypertrophy of cardiac muscle - stiffening of that muscle
Valve replacements
Cor Pulmonale
(right sided heart failure) - enlargement of the right ventricle due to high blood pressure in the lungs usually caused by chronic lung disease
Causes
COPD
Pulmonary embolism
Pulmonary fibrosis
Sleep apnea
Myasthenia gravis
Poliomyelitis
Sarcoidosis
Consequences
LVF is most common
Less effective contraction
Greater ventricular end volume - excess body fluid accumulation
Initial ventricular hypertrophy- overstretching of cardiac muscle and less effective contraction
Effects of Ageing
normal ageing
Reduced elasticity and contractility of cardiac tissue and arterial walls
Fibrosis of 'skeleton' - valves
Fatty deposits accumulate around heart
Gradual hypertrophy with age
Cardiac output and maximum achievable HR declines with age
Atherosclerotic plaques narrow the lumen of vessels and increase resistance to blood flow - hypertension
Surgical incision sites, analgesia + pain
Coronary Artery bypass graft (CABG)
Coronary or heart bypass surgery can relieve chest pain. in the op the sergeon uses a blood vessel from your leg, arm or chest to bypass a narrowed section of coronary artery
technique involves bypassing an obstructed coronary artery, typically using an internal mammary artery and/or a saphenous vein
typical graft sites: internal mammary arteries, radial arteries, greater saphenous veins
typical approach is a sternotamy
Port access technique allows surgeons to operate through a number of smaller incisions
Sternotamy
cutting through sternum to open chest
sternum is then wired back together
Beating heart surgery
heart remain beating throughout surgery
Avoids need for bypass machine
Surgeon must use stabilisation system to steady the portion of the heart where the suturing takes place
Proposed benefits:
Less blood trauma
Decreased risk of adverse events eg stroke
A more rapid return to normal activities
Problems:
Poor graft patency
Higher incidence of revascularisation
Major adverse cerebrovascular events
Risks of surgery
irregular heart beat, infection, bleeding, reaction to anaesthetic, fever, pain, blood clot, stroke, heart attack, death
Anaesthesia
Maintenance
stage when surgery commences
Combination of inhaled anaesthetic and intravenous analgesia may be given with the muscle relaxants to enable controlled ventilation of the lungs
total IV anaesthesia rather than an inhalation agent is becoming more popular
Premedication
usually performed on the ward
Aim is to reduce anxiety, provide pain relief + sedation
Induction
start of anaesthetic process rapidly and pleasantly
Achieved by IV injection of a short - acting coma inducing drug such as propofol/or anaesthetic vapours
Anaphylaxis characterised by severe hypotension, hypoxia, and bronchospasm is rare but life threatening reaction
Reversal
Short but potentially hazardous period
Concentration of inhaled or IV anaesthetic will be reduced, and drugs given to reverse the effect of muscle relaxants
if spontaneous rest rate is <6-8 per min a narcotic antagonist may be given to reverse the respiratory depressant effect
Extubation is undertaken once the protective laryngeal reflexes have returned
Patient is positioned on their side and given O2
Risk
over 80 years old
Females at lower risk
Urgency of procedure
Experience of the person completing the procedure
The type of anaesthetic
Pain
Effects of pain
CVR, immune, endocrine, gastrointestinal, urinary, MSK, nervous, brain
effects of adrenaline + Noradreniline
sympathetic NS
Epidural
needle is inserted followed by a fine catheter at the appropriate level of the spinal column into the epidural space
and of anaesthesia will form depending on which nerve roots have been selected
sensory block not motor
Analgesia
Non-opioid analgesics - eg paracetamol
Non-steroidal anti-inflammatory drugs - eg aspirin
Compound analgesics - eg co-codamol
Opioid analgesics - eg coding, morphine
Post-op care
pain free awakening
opioids used for moderate to severe pain
side effects-nausea vommoting and drowsiness
Regional anaesthesia - IV, oral
Post anaesthetic shivering
acute confusion - delirium
IV/PCA
IV maintains constant level
PCA uses a micro-processed pump connected to an IV infusion
pump is programmed to deliver a bolus and set with a min time period between doses
patient is in control of dose
More....
Myocardial infarction (MI) (heart attack)
myocardial cells respire aerobically
infarction is death caused by ischaemia - leads to necrosis
sudden irreversible injury = MI
caused by rupture of atherosclerotic plaque in coronary artery - causes a thrombus to form plug in artery and blood supply to that part of the heart is stopped
Common s+s: chest pain, or discomfort which may travel to shoulder, arm, back, neck or jaw
STEMI - ST segment elevation MI - ECG shows ST segment elevation in 2 ECG leads
Non-STEMI (NSTEMI) - confirmed with blood tests, cardiac tropic level (cTnT or cTnl)
Cardio vascular disease
responsible for 30% of all deaths
1 in 10 survival rate outside of hospital
Risk factors:
Fixed eg age, sex, ethnicity, socioeconomic status
Modifiable eg mental health, unhealthy lifestyle, Hyper tension, Associated conditions, Dysplidaemia
Stats + facts
death before 75 is considered premature
more than 100,000 admissions to hospital due to heart attacks
family history of CHD are more likely to develop vascular dementia
Ischaemic heart disease (IHD)
characterised by relative decrease in myocardial perfusion such that perfusion is inadequate to meet the metabolic demands of the myocardium
Common causes: Atherosclerosis
S+S
Angina
Acute MI
heaviness + tightness of chest,
Dysponea
Angina
stable
occurs when coronary perfusion fails to meet metabolic demand
May occur during exercise or tachycardia
typically presents as retrosternal pain/discomfort
relived by GNT spray
unstable
life threatening
distribution of plaque triggers thrombosis
frequent or prolonged episodes of retrosternal pain at rest with minimal exertion
triggers
cold weather
emotional upset
activity + exercise
eating a heavy meal