week 3 cardiovasular Flashcards
Cardiac Enzymes
Troponin levels rise rapidly after myocardial infarction and are sensitive indicators of cardiac injury.
Brain Natriuretic Peptide (BNP)
Elevated levels indicate heart failure.
Electrolytes and Urea
imbalances can affect heart function and indicate kidney issues.
Electrocardiography (ECG)
A 12-lead ECG records electrical activity and identifies rhythm abnormalities; stress tests with an ECG can be performed to assess heart function during exercise.
Echocardiography
A non-invasive ultrasound to assess heart structure and function; a transesophageal echocardiograms (TOE) provides detailed images of heart valves and chambers.
Coronary Angiography
An invasive procedure to visualise coronary arteries and identify blockages.
Cardiac Magnetic Resonance Imaging (CMRI)
An advanced imaging technique for assessing heart anatomy and function, particularly useful for ischemia and heart failure
Coronary Artery Calcium Scoring
A CT scan method to quantify calcium deposits in coronary arteries, useful for assessing cardiovascular risk
Lab tests for cardiac S&S
- Cardiac enzymes
- Myoglobin
- Creatine kinase (CK)
- Brain-type natriuretic peptide (heart failure)
- Urea and electrolytes
Exercise stress testing
Treadmill test
ECG, blood pressure and heart rate
Useful for the diagnosis of
* Coronary artery disease
* Post myocardial infarction risk stratification
* Exercise induced arrhythmia
* Nuclear stress test
* function of heart muscle heart
* assess damage to heart muscle following an MI
* determine extent of coronary stenosis
Holter monitoring
- Small, portable monitoring device
- Continuous ECG while patient
conducts normal daily activities - Used for suspected frequent rhythm
abnormalities
Chest X-ray
Information:
Size and configuration of heart and great vessels
Lung fields and vessels
Routine cardiac investigation
Coronary Artery Calcium Scoring
- Most useful in those patients with intermediate risk of
CVD - Result will either lower or raise the risk profile
- Provide a change in management.
- Potential clinical cardiovascular risk: low-, medium- or
high-risk categories
Coronary Artery Calcium Scoring +ves
- Advantages: convenient, noninvasive
Coronary Artery Calcium Scoring -ves
radiation, no intravenous contrast
medium, cannot show coronary artery anatomy or
pathology.
Cardiac Magnetic Resonance Imaging (MRI) assessment of what type of disease and egs
assessment of congenital disease
* assessment of tumour
* abnormality of thoracic aorta;
* assessment of myocardial perfusion and viability
* evaluation of infiltrative diseases
* assessment of diseases of pericardium
* exclusion of anomalous coronary origins
* quantification of cardiovascular shunts
* quantification of ventricular function.
Normal sinus rhythm:
Regular rhythm, rate between 60-100 bpm.
Sinus bradycardia
Regular rhythm, rate <60 bpm (common in athletes or vagal stimulation)
Sinus tachycardia
egular rhythm, rate >100 bpm (caused by fever, exercise, stress, etc.).
Atrial flutter
“Saw-tooth” pattern, rapid atrial rate.
Atrial fibrillation
Irregular rhythm with no distinct P waves.
Supraventricular tachycardia (SVT)
Rapid heartbeat originating above the ventricles.
First-degree atrioventricular (AV) block
Prolonged PR interval (>0.20 sec), but each P wave conducts.
Second-degree AV block Mobitz Type I (Wenckebach)
Progressive PR interval prolongation before dropping a QRS complex.
Second-degree AV block Mobitz Type II:
Random QRS drops with consistent PR intervals.
Third-degree AV block:
Complete heart block; atria and ventricles beat independently.
Junctional rhythm:
Junctional rhythm: Narrow QRS, absent or inverted P waves, rate 40-60 bpm.
Idioventricular rhythm
Wide QRS, no P waves, rate 20-40 bpm.
Ventricular tachycardia (VT)
Wide QRS, fast rate, can be life-threatening.
Ventricular fibrillation (VF)
Chaotic, no organized electrical activity; requires immediate defibrillation.
Torsades de pointes
A type of polymorphic VT, often caused by electrolyte imbalances.
Pulseless Electrical Activity (PEA)
ECG activity without a pulse.
Asystole
Flatline, no electrical activity, requires CPR.
what is a p wave
The first, the small P wave, represents the depolarisation from the SA node through the atria. The first part of the P wave is flat and represents electrical impulse generation by the SA node
PR interval
The time the electrical impulse takes to travel from the SA node through to ventricular discharge. It is measured from the beginning of the P wave to the beginning of the QRS complex
QRS complex
This represents the time taken to depolarise both ventricles. It is a combination of three deflections visible on the ECG and should be sharp and narrow.
ST segment
The period when the ventricles are depolarised. It connects the QRS complex and the T wave
T wave
the time taken to repolarise the ventricles. It is the final deflection visible on the ECG and should be upright.
Triglycerides are used in
energy metabolism
Lipoproteins
- Package of insoluble lipids to be transported in blood
- Cholesterol, triglycerides, phospholipids, and protein
Cholesterol production of
cell membranes, steroids and bile acid
Abnormal lipoprotein metabolism can be a
- predisposing factor to
atherosclerosis
HDL high-density lipoprotein
- “GOOD” cholesterol
- cholesterol from arterial walls to liver.
LDL low-density lipoprotein
- deposition of cholesterol in arterial walls for use
- accumulates in sub-endothelial space
VLDL 5 very-low-density lipoprotein
- triglycerides to cells for energy
Chylomicrons
- largest, least-dense lipoprotein
- transport dietary triglycerides and
cholesterol from the intestinal epithelial cells to liver, skeletal muscle and adipose tissue
Aetiology of atherosclerosis (non-modifable factors)
risks inc
* Familial hypercholesterolaemia
* Age and gender (men ≥45 years; women ≥55 years)
* Type 1 Diabetes Mellitus
Aetiology of atherosclerosis modifiable risk factors
HDL cholesterol <40 mg/dL
C-reactive Protein levels (CRP)
overweight and obese
diet high in salt and fatty foods
sedentary lifestyle
Pathogenesis of atherosclerosis
Formation of fibrofatty lesions in the intimal lining
- process that causes disease of the coronary, cerebral, and peripheral arteries and aorta
Types of lesions associated with atherosclerosis
* Fatty streaks
* Fibrous atheromatous plaque
* Complicated lesion
Pathogenesis of atherosclerosis- 1. Endothelium dysfunction
- active biologic interface between blood and tissues
- risk factor effect
- dysfunction due to loss of NO and microtears
- leukocytes recruited and inflammatory process starts
Pathogenesis of atherosclerosis- Endothelium inflammation
- entry of circulating fat and cholesterol
- oxidisation of LDLs
- attracts circulating monocytes
(become macrophages) to restore
vessel wall integrity - inflammatory mediators released
- smooth muscle cells grow and enter
- macrophages and migrating smooth muscle cells consume ox-LDLs
Pathogenesis of atherosclerosis- Oxidised LDL is cytotoxic at high levels
- death of macrophages and smooth muscle cells
- deposition of cell contents and cholesterol crystals
- necrotic core forms in arterial wall
Fibrous cap
- fibrin infiltration (stiffening wall)
- calcium deposition (hardening of vessel wall)
- fibrous plaque with connective tissue and lipids
Atherosclerotic plaque
Continues to grow and cause narrowing
of the vessel and production of ischemia
“Stable” plaque
Small lipid pool with thick fibrous cap. and preserved lumen
“Vulnerable” plaque
- Large lipid pool, thin fibrous cap,
many inflammatory cells - Can commonly rupture and cause a thrombus which can further lead to narrowing
Progression of plaque
- plaque cap splits
- necrotic material traps platelets
- thrombus formation
- reduces size of or blocks artery lumen
- limited NO to vasodilation
Epidemiology of atherlosclerosis
Atherosclerosis can begin in childhood with the development of fatty streaks. The lesions of atherosclerosis advance with aging. As the aetiology of atherosclerosis is multifactorial, the epidemiology is related to risk factors
acute clinical manifestations of atherlosclerosis
stroke, acutue coronary syndromes, aortic occlusion, aortic rupture, aortic dissection, renal artery occlusion, acute peripheral arterial occlusion, acute mesenteric ischemia
clinical manifestations chronic presentation of atherloscleoris
recuurent transient ichemaemic attacks, stable angina, silent ischemia, aortic aneuryum and more
Progression of atherosclerosis
- Endothelial Dysfunction and Inflammatory Cell Recruitment. atherosclerosis begins with endothelial injury
- Foam Cell Formation: The Inflammatory Amplification Cycle.
- Plaque Progression and Fibrous Cap Formation.
- Plaque Rupture: A thin fibrous cap
what factors of increase ageing contributes to an increase Arteriosclerosis
The elastin is progressively replaced with stiffer collagen fibres
Increase in advanced glycation end-products
Consequences of Age-Related Arterial Changes
hypertension (especially isolated systolic hypertension)
increases the load on the left ventricle, leading to hypertrophy, impaired relaxation and heart failure.
microvascular damage in organs
Peripheral artery disease (PAD) mainly occurs in
legs and feet
Peripheral artery disease (PAD) aeitology
usually from a thrombus.
Peripheral artery disease (PAD) Epidemiology
affect approximately 20% of those aged 75 and over, and most people with PAD show no symptoms, leading to under-diagnosis and under-treatment.
Peripheral artery disease (PAD) Pathogenesis common and less common causes of pad
most common cause of PAD is atherosclerosis
Less common causes of PAD include infection or inflammation of the artery and injury to the affected limb
Thrombosis
Local formation of a blood clot within a diseased artery, typically due to atherosclerotic plaque rupture, which can rapidly occlude the artery. These commonly affect the femoral or popliteal arteries,
Embolus
Often originating from cardiac sources emboli can travel and lodge in peripheral arteries, abruptly obstructing blood flow. They usually lodge in aortic, iliac, femoral and popliteal bifurcations.
- Anaerobic Metabolism and Acidosis
Normally, cells produce ATP via aerobic respiration, using oxygen to break down glucose. When oxygen is unavailable (ischemia), cells shift to anaerobic glycolysis, producing lactic acid instead of ATP.
Lactic acid accumulation → Tissue acidosis (↓ pH), which respults in
disrupts enzyme function
damages proteins and cell membranes
- ATP Depletion and Ion Pump Failure
ATP is needed for ion pumps to maintain cell homeostasis. When ATP is depleted, two critical pumps fail Sodium-Potassium (Na⁺/K⁺) Pump Failure leading to swelling and Calcium (Ca²⁺) Pump Failure leading to an overload, triggering harmful enzymatic activity inside the cell which degrade vital cell components.
High intracellular Ca²⁺ activates
Proteases – Break down muscle proteins (actin, myosin), leading to cell death.
Phospholipases – Degrade cell membranes, making them leaky.
Endonucleases – Damage DNA, contributing to irreversible injury.
- Release of Cellular Contents into the Bloodstream
K+- Worsens metabolic acidosis and electrolyte imbalance
Creatine Kinase (CK)- marker of muscle damage, detected in blood tests
Myoglobin- Can clog kidney tubules, causing acute kidney injury (AKI) and dark urine (myoglobinuria
Clinical manifestations of PAD
irregular pain during activity and rest
numbness, coldness or pins and needles in the affected body part
blue- or purple-tinged skin
arterial obstruction clinical manifestations
reduced perfusion in peripheral tissues, ischemia and tissue necrosis
Vasculitis
the presence of inflammatory leukocytes in vessel walls with reactive damage to mural structures…[which can lead to] tissue ischaemia and necrosis
vasculitis Patient Presentation
joint pain (arthralgia), weakness or altered circulation in their hands or feet. Additionally, symptoms like dizziness or unequal pulses
What implications does bradycardia have for physiotherapy treatment
dizziness and chest pain
What distinguishes premature ventricular contractions (PVCs)?
Heartbeat initiated by the heart ventricles rather than the sinoatrial node
Describe the pathway of electrical impulse conduction in the heart.
impulses generated @ SA node, travel through the AV node, bundle of His, bundle branches and to the Purkinje fibres in the ventricles
primary function of the cardiac conduction system?
Control the rate and direction of electrical impulse conduction
aimed values for total cholesterol, hdl, ldl, triglyercrides
total= 3.9-5.5 mmol/L
hdl- 1.7-3.5
ldl= 1.7-3.5
tri= 0.9-2.1
what is an Aneurysms
an enlargement of an artery resulting in a diameter of more than 1.5 times the normal size
Aetiology of aneurysm
a localised dilation or bulging of a blood vessel due to weakening of the arterial wall
aneurysm risk factors
- Congenital Factors: Connective tissue disorders
- Degenerative Changes: Atherosclerosis,HTN, aging
- Inflammatory and Infectious Causes: Vasculitis, autoimmune disorders
- Trauma and Iatrogenic Causes: Blunt or penetrating trauma; surgical or endovascular interventions leading to pseudoaneurysm formation
- Lifestyle and Environmental Factors: Tobacco smoking; dyslipidaemia, diet, being sedentary and the environment
Epidemiology aneurysms
2–3% of the adult population may develop an aneurysm over their lifetime
Aortic Aneursyms
Aortic aneurysm is the second most common disease affecting the aorta after atherosclerosis
Thoracic Aortic Aneurysm (TAA)
Occurs in the upper part of the aorta. The majority (~95%) of patients are asymptomatic until a serious event, such as aortic dissection or rupture, occurs
Abdominal Aortic Aneurysm (AAA):
Defined as a localised enlargement of the abdominal aorta to a diameter of ≥30 mm (on abdominal US or CT) and are a degenerative disease of ageing. Approximately 4–7% of men and 1–2% of women over the age of 65 are affected.
Cerebral Aneurysms (CA)
Defined as dilations that occur at weak points along the arterial circulation within the brain.
Peripheral Aneurysms
Aneurysms occurring in the arteries of the lower limb are the most common peripheral aneurysms
Aortic aneurysms pathogenesis
normal architecture becomes compromised, leading to progressive weakening and dilation. key initiating event is often the dysfunction and loss of vascular smooth muscle cells (VSMC), which are responsible for maintaining the extracellular matrix (ECM) and regulating vascular tone
Chronic inflammation pathogenesis of arterial wall
originates from chronic damage to the aortic wall, primarily due to high blood pressure, oxidative stress and atherosclerosis leading to small injuries in the vessel wall.
Oxidative stress pathogensis
damage smooth muscle cells (VSMCs) and extracellular matrix (ECM) proteins. stimulating even more immune cell recruitment and inflammation.
Mechanical Stress causes
this inflammatory response persists indefinitely due to ongoing oxidative stress, mechanical strain, and defective cell clearance mechanisms. As a result, the aortic wall becomes progressively thinner and weaker.
Cerebral Aneurysms pathogensis
frequently develop in areas where blood flow causes high wall shear stress, which is why they commonly occur at vessel bifurcations.
aneurysms Clinical manifestations
silent until rupture, cerebral aneurysms present catastrophically with SAH, and peripheral aneurysms are prone to embolism and limb ischaemia.
Peripheral aneurysms pathogensis
inflammation, ECM degradation and haemodynamic stress, but they also have unique contributors such as higher atherosclerotic involvement, localised mechanical stress, and genetic predisposition.
Venous Pump
Muscle contractions in the calf and foot generate pressure that aids venous return, driving blood from the superficial to deep veins. Effective pumping depends on strong muscle contractions and functional valves
Venous pressure varies with position, lying, sitting, standing, walking
lying- 15 mmHg
sitting- 55–75 mmHg
standing- 75–90 mmHg
walking- 40–55 mmHg
Venous Valves:
These bicuspid structures direct blood from distal to proximal and from superficial to deep veins, preventing backflow
Venous disorders
Vein-related problems may or may not be symptomatic and, when symptomatic, include a wide range of clinical signs that vary from minimal superficial venous dilation to chronic skin changes with ulcerationve
venous disorders catogries
blockage from a blood clot (thrombosis) and inadequate venous drainage (insufficiency).
venous disorders Aetiology
advancing age, female sex, family history of venous disease, ligamentous laxity, prolonged standing, increased body mass index, smoking, lower extremity trauma, prior venous thrombosis (ie, post-thrombotic) and certain hereditary conditions
venous disorders Epidemiology
39% of the Australian population. The risk of chronic venous disease increases with age and has a 3 to 1 female predominance.
Anatomic Changes of venous disorders
Valvular incompetence causes venous reflux and dilation. Chronic venous obstruction can lead to fibrosis and post-thrombotic syndrome
Physiologic Changes of venous disorders
precapillary arterioles constrict
high venous pressure
endothelial dysfunction,
inflammation,
vessel wall remodeling,
clinical manifestations of venous disorders
pain, leg heaviness, aching, swelling, skin dryness, tightness, itching, irritation, and muscle cramps
venous claudication - a severe deep pain and tightness
dilated veins, oedema, skin changes and/or venous ulcers.
Thrombosis
commonly occur as deep vein thrombosis (DVT) of the lower extremity and pulmonary embolism (PE). The causes of venous thrombosis can be inherited or acquired.
Thrombophlebitis
refers to inflammation of a vein associated with thrombus (blood clot) formation. It can occur in superficial veins (superficial thrombophlebitis) or deep veins (deep vein thrombophlebitis).
Epidemiology of thrombosis
1 in 1000 people
Aetiology of thrombosis
associated with conditions that increase the risk of clotting, including those that lead to decreased venous flow and pooling, abnormalities of coagulation or fibrinolysis and endothelial dysfunction
Hypertension
high blood pressure, is where blood pressure is permanently higher than normal.
Hypotension
decrease in systemic blood pressure below accepted low values.
high systolic blood pressure
140 mmHg or more
high diastolic blood pressure
90mmHg or more
Epidemiology of high blood pressure in re to ses and IA
more common in lower ses c/to higher ses & first nations c/to non-indiginous australians
Pathophysiology of high blood pressure
complex interactions between environmental and behavioural factors, genes, hormonal networks and multiple organ systems (renal, cardiovascular, and central nervous system)
What Causes High Blood Pressure?
Blood pressure (BP) rises due to an imbalance in how the body regulates blood flow, fluid balance and blood vessel resistance.
Vascular mechanisms
Changes in the structure and function of small and large arteries due to endothelial dysfunction play a key role in hypertension.
Neural mechanisms in hypertension
In hypertension, the sympathetic nervous system (SNS) becomes overactive, leading to chronic vasoconstriction, increased heart workload and excessive sodium retention, which all contribute to a high BP
Baroreceptor dysfunction
baroreceptors in aorta and carotid arteries detect BP changes and send signals to the brain to adjust SNS activity
In hypertension, baroreceptors become less sensitive (baroreflex dysfunction), so they fail to suppress SNS activity even when BP is high
What are foam cells and how do they form?
Foam cells are lipid-laden macrophages that form when macrophages engulf oxidized LDL in the arterial wall.
