Week 6 - Cardiovascular Flashcards
Acute Pericarditis
- Pericardium (inflammation of the outer layer of the heart) roughened, possible exudate
- Sudden chest pain
Pericardial Effusion
- Accumulation of fluid in pericardial cavity
- Compression of heart may cause cardiac tamponade
- Treated by pericardiocentesis (aspiration of fluid from the pericardial space)
Constrictive Pericarditis
- Chronic inflammation of the pericardium with thickening, scarring, and muscle tightening.
- Visceral and parietal layers adhere obliterating the pericardial cavity
- Compress the heart CO (down)
Aortic stenosis
- Diminishes blood from LV into aorta
* Result in ischemia, arrhythmias and heart failure
Mitral stenosis
- Impaired blood flow from the LEFT atrium to the LEFT ventricle
- Valve leaflets become and fibrous and fuse, chordae tendineae shorten
- Atrial arrhythmias and thromboemboli
Aortic regurgitation
- Inability of the aortic valve leaflets to close properly during diastole
- Backflow of blood into LV causes it to dilate and hypertrophy
Mitral regurgitation
- Backflow of blood into LA causes atrium to dilate, LA pressure
- LV dilate and hypertrophy to maintain CO
Mitral valve prolapse syndrome
- Valve cusps billow upward into atrium
* Replace with porcine or mechanical valve
Infective Endocarditis
- Inflammation of the endocardium
- Agents; Bacteria (staph or strep), viruses, fungi, and parasites in blood
- Endothelium damaged (valves)
Disorders of the Arteries: Arteriosclerosis
- Chronic disease with abnormal thickening and hardening of arterial walls
- Smooth muscle cells and collagen migrate into Tunica intimata
- Decreased elasticity
Disorders of the Arteries: Atherosclerosis
Form of arteriosclerosis caused by accumulation of lipid-laden macrophages
Results in plaque formation
Is the main cause of CAD and CVA
½ deaths of western world
Inflammatory disease initiated by injury to endothelium
Injury from smoking, hypertension, diabetes, LDL, HDL, chronic infection
Atherosclerosis
Clinical Manifestations
Symptoms associated with inadequate perfusion of tissue
Transient (intermittent claudication) or permanent
Diffuse atherosclerosis will elevate systemic resistance and cause hypertension
Major cause of MI and CVA
Evaluation and treatment of Atherosclerosis
Reduction of risks
Diet (most important contributor)
Drugs can stabilise plaque before rupture (i.e. Aspirin: antithrombotic)
Aneurysm
Localised dilation or out pocketing of a vessel wall or cardiac chamber
Once initiated aneurysm grows bigger as tension in the vessel wall increases
Can exert pressure on surrounding organs, rupture or dissect
Causes of an Aneurysm
Atherosclerotic plaque erode and weakens tunica media
Syphilis and other infections
Chronic hypertension (50% of AAA)
Marfans – inherited collagen vascular disease causes thoracic aortic aneurysm
True Aneurysm
* Involves all 3 tunica layers
Fusiform – entire circumference of vessel
Saccular – part of circumference, saclike
False Aneurysm
- Initiated by break in tunica intima only
- Extravascular haematoma as a result of graft leakage
- Dissecting, saccular – blood entry causes longitudinal separation of vessel wall to form a blood-filled channel
Common sites of aneurysms
- Aorta particularly susceptible
* Post infarct – stretching of non contractile muscle in heart
Clinical Manifestations
Related to pressure on surrounding organs
Most AAA asymptomatic
Pulsating mass, calcified mass
Pain is mild to severe mid-abdominal, lumbar or back region
Stasis of blood favors thrombus and peripheral emboli
Dissecting Aneurysm
Abrupt excruciating tearing pain
Chest pain suggests ascending aorta; back pain descending aorta
Dissection can be a life-threatening situation upon rupture
Dissecting Aneurysm Treatment
Risk of death depends on site of dissection
Ascending aorta (type A) usually requires surgical repair with Dacron graft
Descending thoracic aorta (type B) may be medically managed by aggressive control of BP and HR while aorta heals
Once healed surgery may not be required
Intermittent claudication
Leg pain on ambulation due to atherosclerosis of iliofemoral arteries Dopplers to determine blood flow Vasodilators and antithrombotics Exercise rehabilitation Surgery
Thromboangiitis obliterans (Buerger Disease)
- Inflammatory disease in male heavy smokers
- Obliteration of arteries in hands and feet
Pain, tenderness, Reynaud’s Phenomenon, cyanosis, redness and ulcers
Gangrene
Reynaud’s Phenomenon and Disease
Bilateral spasm in arteries and arterioles of hands
Skin color and sensation changes
Prolonged attacks affect cell metabolism in hands
May be secondary to systemic disease i.e. scleroderma (excessive collagen deposition), smoking, exposure to cold or vibrating machinery
Triggered by brief exposure to cold
Common in young females
Cause unknown
Varicose veins
* A vein in which blood has pooled
Distended, tortuous, and palpable veins
Caused by incompetent vein valve(s) and/or weakening of leg vein wall (collagen level)
Effects saphenous veins and perforating veins
Risk factors for Varicose Veins
* Genetics, age, gender, race, pregnancy (any hormone changes), obesity, diet, prolonged standing or sitting
Signs and symptoms of Varicose Veins
* Enlarged veins, leg swelling, painful legs, itchy legs, skin discolouration, thrombophlebitis
Treatment for Varicose Veins
- Self-care measures – leg exercises, support stockings, avoid high heels, avoid long periods of sitting or standing, elevate legs
- Medical or surgical – remove or close off varicose vein i.e. sclerotherpy, laser, ambulatory phlebectomy, vein ligation and stripping
DVT
- Accumulation of clotting factors and platelets in deep leg vein
Promoting factors
Venous stasis (immobility, age, CHF)
Venous endothelial damage (trauma)
Hypercoagulable states (pregnancy, hormone replacement)
Thrombus
- Blood clot that remains attached to vessel wall
Develops where conditions promote activation of platelets and coagulation cascade
Intimal irritation and roughening (atherosclerosis)
Inflammation
Infection
Blood stasis (economy flights, aneurysms, phlebitis)
Trauma
Calcified areas or bacterial vegetations on heart valves
Treatment for Thrombus
- Anticoagulants to stop further growth of thrombus (Heparin or Warfarin)
Aspirin (antiprostaglandin) blocks platelet aggregation and platelet plug formation
IV and Intra-arterial Streptokinase to dissolve clot
Balloon-tipped catheter can pull thrombus out
Embolus
A bolus of matter circulating in blood Thromboemboli Air bubble (IV line or chest trauma) Aggregate of amniotic fluid Foreign substance (IV line or trauma) Aggregate of fat (long bone trauma) Bacteria (SBE) Cancer cells
Hypertension
- Sustained elevation of systemic arterial BP;
Systolic > 120 mmHg Diastolic > 90 mmHg
Sustained diastolic pressure can lead to CHF, infarction, end-organ damage
Types of Hypertension
- Primary – 90-95 % are of unknown origin
- Secondary – due to a primary disease
- Isolated systolic – elevated systolic and normal diastolic
Factors associated with Primary Hypertension
Family History
Gender and Age
Black race
High sodium intake
Low intake of potassium, calcium, or magnesium,
Diabetes mellitus
Smoking and obesity
Heavy alcohol consumption
Pathophysiology
Genetic susceptibility and environmental factors cause neurohumoral dysfunction, inflammation and insulin resistance
Causes peripheral resistance and blood volume
Secondary Hypertension
- Systemic disease process which CO and PR
- Renal - Endocrine - Vascular - Pregnancy - Drugs Fix or remove disease and BP resolves
Complicated Hypertension
- Chronic damage to systemic blood vessels
- Hypertrophy and hyperplasia of smooth muscle cells in arterial walls with associated fibrosis leads to ‘vascular remodeling’
- Results in reduced blood flow and organ dysfunction
Malignant Hypertension
* Hypertensive emergency where diastolic > 140 mmHg.
* Can cause encephalopathy (cerebral oedema)
Preeclampsia or toxemia
After 24th week of pregnancy
Occurs in 6% of pregnancies, risk ^ age
Acute hypertension, proteinuria and oedema
Affects metabolism, renal function, CNS, fluid, electrolyte imbalance and may result in eclampsia (convulsions/coma)
Cause unknown
Resolves with birth of baby
Antihypertensive drugs
Beta blockers
Atenolol, Metoprolol
Diuretics
Hydrochlorothiazide, Spironolactone
ACE inhibitors
Captopril
Calcium channel blockers
Nifedipine, etc
Centrally-acting drugs
Clonidine
Vasodilators
Hydralazine
ACE Inhibitors
Angiotensinogen is produced constantly by the liver
Low renal blood flow (low BP), low sodium and/or potassium levels and β-adrenergic stimulation (adrenaline type stimulation) all cause renin release from juxtaglomerular cells in the kidneys
Renin converts Angiotensinogen to Angiotensin I
ACE, produced constantly in the lungs, converts Angiotensin I to Angiotensin II
Angiotensin II effects aldosterone secretion, smooth muscle constriction, Na+ and water retention
ACE inhibitors prevent conversion of Angiotensin I to Angiotensin II
End Results:
Decrease fluid retention, afterload
Example: Captopril
Captopril
Indication Hypertension, heart failure Adverse Effects Hypotension, angioedema (head, neck, intestinal), hyperkalaemia, proteinuria, cough; GI upset Practice points Give small test dose Monitor serum electrolytes
Postural/Orthostatic Hypotension
Drop of 20 mmHg systolic BP or 10 mmHg diastolic BP within 3 minutes of standing
Vasodilation and blood pooling in muscles, spleen and kidneys
Results in dizziness and blurred vision
Acute Hypotension
Sympathetic vasoconstriction mechanisms sluggish
30 to 50% of elderly, pregnancy and immobility (venous pooling)
Circulatory shock
Chronic Hypotension
Secondary to disease or poor nutrition
Treatment for Idiopathic Hypotension
Liberalization of salt intake Raise head of bed Slower position changes Support stockings Volume expansion Vasoconstrictors
Dyslipidaemia
The Problem:
- High serum levels of cholesterol- and/or triacylglycerol molecules
- Thought to contribute to atherosclerotic disease
Solutions:
Decrease lipoprotein synthesis (bile acid binders)
Increase lipoprotein catabolism (fibrates)
Increase cholesterol removal (statins)
Niacin
Inhibits lipolysis in fat cells
Acute Rheumatic Fever and Rheumatic heart disease
- Inflammation of joints, skin, nervous system and heart
* Treatment - antibiotics - 9 days
Infective Endocarditis
- inflammation of the endocardium (inside lining of the heart)
- Treatment - 4-6 weeks antibiotics/ repair or replacement surgery
Dissecting Aneurysm
- Abrupt excruciating tearing pain
Dyslipidaemia
- high levels of cholesterol/ triacylglycerol molecules
Simvastatin
Inhibit liver enzymes
Colestipol
Binds to bile salts
Statins
- Lower the rate of cholesterol production
Adverse E: Stomach cramps, muscle/joint pain, rash, nausea and vomiting and constipation
* Hepatitis
- More effective at night
- Short half lives, once daily admin
Heparin
Occurs naturally in the body
Prevents fibrin clot
Warfarin
Antagonist to Vit K
Reversed with Vit K
Thrombolytics
- Given to dissolve thrombi
Abdominal Aortic Aneurism
Enlarged area of the lower part of the aorta
Types:
o Ascending: present with chest pain and require surgical correction
o Descending aorta: presents with back pain. Can be managed by medication to stabilise BP and HR.
