cardiac Flashcards
HEART STATISTICS
72 beats per min 103,680 per day 728,252 per wk 3,155,760 per month 37,869,120 per year 2,900,000,000 per lifetime 7,568 litres/day 53,162 l/wk 230,370 l/mo 2764445 l/yr 211,700,000 l/lifetime 1,331,552 barrels/ lifetime
trace a drop of blood through the heart
superior vena cava- right atrium- through tricuspid valve- right ventricle- pulmonary semi lunar valva- pulmonary arterie- lung- pulmonary vein - left atrium- mitral valve (bicuspid)- left ventricle- aortic valve- to the body
coronary arteries
supllies blood to the heart
Systole
when the heart contacts with ejection of blood
what is the most common deseases in western world
cardiovascular disease (atherosclorosis, then hypertensive heart desease)
Ischemic vascular disease
Atherosclerosis
coronary heart disease
Main Regions and Pathology Resulting from Atherosclerosis
Systemic Inflammatory Disease affecting Arteries
brain, aorta, peripheral vascular (gangrene- diabetic)
Atherosclerosis, CAD (specific to the heart starts with ischemia then injury then necrosis)& IHD- start off with ischemic episode- leads to heart failure
Coronary arteries supply blood and nutrients to the heart muscle
Coronaries fill during diastole
Atherosclerosis of the coronary arteries = Coronary Artery Disease (CAD)
CAD = Ischemic Heart Disease
Ischemic Heart Disease can lead to Heart Failure
Pathogenesis of Atherosclerosis
Endothelial injury: is the hallmark of atherosclerosis
Causes of endothelial injury: Hypertension; Turbulence; Hyperlipidemia, Smoking
Influx of lipids
Accumulation of lipids, smooth muscle cells, macrophages
Development of ATHEROMA
Pathogenesis of Atherosclerosis!!!!!!!
hallmark is Endothelial injury!!!!!! (hypertension, diabetes, obesity): is the hallmark of atherosclerosis
Causes of endothelial injury: Hypertension; Turbulence; Hyperlipidemia, Smoking
Influx of lipids
Accumulation of lipids, smooth muscle cells, macrophages
Development of ATHEROMA
first layer in the lumen is the subendothelial matrix then the smooth muscles
athelrosclorosis affects the endothelial injury- circulating LDL gets into the endothelial injury
monocytes adhere on the lumena nd enter the endothelium and act on the cytochines - become macrophages and engulf the LDL and are now stcuk - gets into foam cells - become fatty steak and then become palque and can be ruptured - miocardial infarction
can recover from ischemia if not too long
if too long- necrosis- no coming back
angina pectororis
chest pain
Types of Ischemia
(1) Tolerable ischemia, which has a low degree of reduced blood flow
(2) Critical ischemia, which reflects a modestly severe flow reduction
(3) Lethal ischemia, which has a severe flow reduction and is the limit of myocardial survival. Lethal ischemia, if left untreated, can lead to irreversible cell necrosis or myocardial infarction
Tolerable ischemia
which has a low degree of reduced blood flow
Critical ischemia
which reflects a modestly severe flow reduction
Lethal ischemia,
which has a severe flow reduction and is the limit of myocardial survival. Lethal ischemia, if left untreated, can lead to irreversible cell necrosis or myocardial infarction
atherosclorosis start in the
first decade of life and continuously grows - usually gets too big at aroud the fourth decade
risk factor!!! modifiable and non modifiable
Non-modifiable Increasing Age Male gender Heredity (genetic predisposition) Potentially modifiable Hyperlipidemia Hypertension Physical inactivity Smoking Obesity Stress Diabetes mellitus
Symptoms of Coronary Stenosis!!!
know the desease (pathology)- the symptoms-
Angina pectoris Asymptomaticv( Arrhythmia (cardiac rhythm abnormalities) Sudden death Myocardial infarction Congestive heart failure
Angina Pectoris
2 types- stable and unstable
Transient discomfort in the chest or adjacent area caused by myocardial ischemia brought on by exertion: no myocardial necrosis.
Two types: Stable Unstable Pain of ischemia Precipitated by exercise Relieved by rest, nitroglycerine (vasodilator)
Complications of CAD
Myocardial Infarction (MI)
Sclerosis: hardening due to collagen deposits surrounding the atheroma
Thrombosis: surface of atheroma may ulcerate and sometimes sudden death without previous warning symptoms
Aneurysms: a weakened wall may dilate and rupture (ruptured aneurysm- bleed out) (weakening of wall of the blood vessle- blood can stagnant )
Myocardial infarct (MI)
Heart Attack
Blockage of a vessel causes tissue to become ischemic ( lack of oxygen to tissue bed)
The ischemia causes tissue necrosis (infarction: death)
Dead tissue: subjected to normal body processes of removal and repair with formation of scar tissue.
Diagnosis may be clinical: cardiac biomarkers, ECG,
Cardiac catheterization, post mortem
MI Clinical symptoms
Choking or pressure like pain most commonly in left chest extending up neck, down left arm.
However, can be anywhere above umbilicus to teeth in lower jaw down either arm to wrist & between shoulder blades.
May become unconscious
Sweating, pallor
Symptoms of shock – weak or imperceptable pulse
The most common cause of death from Acute MI is !!!!
an Arrhythmia: Ventricular Fibrillation
- first rythm is v tact
Complications of MI
Sudden death 25% of cases Arrhythmia (v-fib arrest) Heart failure Cardiogenic shock Multisystem organ failure Weakening of the arterial wall- Aneurysm (localized dilatation) Valvular regurgitation
Myocardial infarction
Death of myocardial cells due to obstruction of blood flow 80% result from a thrombus obstructed a narrowed artery Gross Necrosis (pale yellow) Microscopic Necrotic myocardial cells Hemorrhage Inflammation
left anterior descending artery obstruction!!!!
know them all
lad lesion artery obstruction- artery of sudden death, anterior infraction, 50% of cases
How do you diagnose AMI
Patients present to ER or family doc with a variety of histories, time of onset etc
In some MIs, there is no associated pain
Can happen in the relatively young ie mid 30s
Can happen in patients without obvious risk factors
Diagnosis of myocardial infarction
Risk factors, history, clinical presentation
12 lead ECG – by changes in electrical patterns of the heart (look at st segment- if it elevated then we know the heart has been comprimised)
Biomarkers- by release of compounds by the ischemic or necrotic heart tissue -(certain protein released into the circulation- can be mesures (high troponin levels))
In most provinces, in the very old, sudden death will be assumed to be myocardial infarction, without autopsy evidence
Biomarkers of Myocardial Infarction
During an acute coronary event, a coronary artery becomes completely occluded. This deprives cardiac muscle of bloodflow (ischemia) and oxygen (hypoxia) causing death of the muscle and destruction of the cell (necrosis)
Products of this ischemic and necrotic process find their way into the bloodstream where they can be measured . These are called biomarkers and can be diagnostic for myo-cardial infarction and necrosis.
Cardiac Markers
Troponin
Part of the contractile apparatus of muscle
Different in heart and skeletal muscle
Myoglobin- used to be used but could be released from muscles from exercising)
Mol wt 16,000 daltons
Found in all muscle
Non-specific marker
Released earlier than other larger markers ie in the 1st several hours after an infarct
Creatine Kinase (CK)
Present as a dimer with mol wt of 86,000 daltons Skeletal muscle has MM dimer Heart has MM and MB dimers Brain has BB dimer MB!!!! useful for MI diagnosis
know slide #2!!! be aware of these times
myoglobin is released early (less than 5 hours), ck mb is release is slower and peaks at 12 hours, but now troponin had a peak aroun 8 hours and is long lasting- even at 35 hours
Complications of myocardial infarction
Mural thrombus Ventricular aneurysm Myocardial rupture (death) Cardiac tamponade (pericardial effusion)
Course of Action
Labs, 12 lead ECG If symptomatic and labs and or ECG are conclusive Cardiac catheterization (Angiogram) (1) no lesions (2) lesions < 50% (3) lesions > amenable to PCI (4) multiple lesion in multiple vessels
Percutaneous Coronary Intervention (PCI)
PCI refers to a invasive procedure in which a high grade coronary stenosis is dilated with a balloon tipped catheter system and/ or supported by metal prosthetic stents (scaffolds) to increase lumen diameter, restore blood flow and prevent myocardial ischemia.
Treatment
Medical – Clot busting drugs (tPA, urokinase, streptokinase)
Medical – Percutaneous Coronary Intervention
Surgical – CABG –Coronary artery bypass graft
Secondary prevention (
Means prevention of another event after the first one has already occurred
diet, exercise, anticoagulant drugs (aspirin) etc, cholesterol lowering drugs(statins) antihypertensive drugs (ACE Inhibitors), beta blockers
Primary prevention - diet, exercise, anticoagulant drugs (aspirin) etc, cholesterol lowering drugs(statins
Congestive Heart Failure
Pump failure -> failure to pump out all blood that enters heart
Congestion=Back pressure to all organs behind failed chamber
Left heart failure -> pulmonary congestion & edema
Right heart failure -> peripheral congestion & edema in the periphery (legs (large jugular veins)
Pulmonary Edema results from LHF Alveolar sacs fill with fluid Dyspnoea (shortness of breath) On exertion Nocturnal Constant
cabg
grafts anatomosed to the heart
Rheumatic Fever& Rheumatic Heart Disease (RHD)
Systemic immunologic disease related to streptococcal infections
Occurs two weeks after “strep throat”
Antibodies to Streptococcus cross-react with cardiac antigens
Cell mediated immune reaction
Supressor/cytotoxic T lymphocytes and macrophages damage tissue
Pathology of Rheumatic Fever
Pancarditis (Endocarditis, Myocarditis, Pericarditis)
vegetative growths develops on left side (aortic valves..)- leads to endocarditis
Endocarditis
Inflammation of valves on the left side of the heart (valvulitis and ulcer formation)
deposition of inflammatory cells, fibrin and platelets: (VEGETATIONS)
Healing by fibrous scarring causes valve deformation
Contracture leads to valve stenosis or valve insufficiency
aortic valve stenosis- stiff
Valve Disease
Valve Insufficiency (regurgitation) Mitral valve regurgitation reflux of blood from ventricle to atrium during systole Aortic regurgitation causes back flow of blood into the left ventricle during diastole The ventricles become dilated or hypertrophic- allows back flow of blood= coingestion instead of the ventricle being able to fill with new blood. - mitral regurgitation= the left atrium
Valve Stenosis
Mitral stenosis causes a stagnation of blood into the LA
Result in LA, pulmonary and right ventricular hypertension
Aortic Stenosis causes a stagnation of blood into the left ventricle
Results in LV hypertrophy and can lead to LA and pulmonary hypertension
