Cardiovascular Pathology Table PDF

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Summary

Condition Signs and symptoms Causes Risk factors Pathophysiology Diagnosis Treatment Complications Abdominal aortic aneurysmsMostly asymptomatic- Symptoms present after complicationsExpansile mass in abdomen Back/abdominal painAtherosclerosis Cystic medial degeneration – thoracic aorta. Vasculitis I...

Description

Condition Abdominal aortic aneurysms

Signs and symptoms Mostly asymptomaticSymptoms present after complications Expansile mass in abdomen Back/abdominal pain

Aortic dissection

Deep vein thrombosis

Varicose veins

Causes Atherosclerosis Cystic medial degeneration – thoracic aorta. Vasculitis Infection – tertiary syphilis Congenital

Risk factors Elderly males Common sites Abdominal aorta Popliteal artery

Mostly asymptomaticSymptoms present after complications Sudden onset chest pain radiating to back

Marfan’s syndrome Pregnancy

Mainly asymptomatic Calf pain Unilateral leg swelling Raised skin temp.

Well’s score

Oedema Skin changes Bleeding Phlebitis

Women Pregnancy Obesity Prolonged standing

Pathophysiology Abnormal permanent dilation of an artery. True – all 3 layers. Fusiform or saccular Pseudo – Blood leaks out of vessel but is contained by the outer vessel layers or connective tissue. Dissecting – tear in intima. Blood flows into wall, creating an additional channel between intima and media where blood flows. Type A: ascending aorta involved Type B: ascending aorta not involved Presence of thrombus in deep veins of leg Stasis – obstruction to venous outflow Hypercoagulable – oral contraceptive pill+ malignancy Endothelial damage Tortuous, dilated superficial veins of lower limbs caused by valvular

Diagnosis CT angiogram Ultrasound CT – aorta MRI Radio-radial delay Radio-femoral delay

Treatment Surgical Synthetic graft to replace aneurysmal segment of aorta Endovascular A synthetic graft through femoral artery. Aneurysm is excluded from aortic blood flow

Blood pressure difference between arms

Doppler ultrasonography

Complications Rupture – massive blood loss Thrombosis – obstruction of vesse Embolism – ischaemia Pressure – can compress other structures. E.g. aortic arch aneurysm can compress oesophagus dysphagia

PE

D-dimers Venography with IV contrast Compression bandaging Injection of sclerosant into dilated vein

Peripheral vascular disease Occlusive

Ischaemic heart disease/coronary heart disease

Venous eczema Venous ulcers

Previous DVT Pelvic mass

Intermittent claudication Gripping/crampy pain in calf during excretion. Critical limb ischaemia Pain at rest Gangrene Ankle-brachial pressure 1mm/chest pain. Myocardial perfusion scanning Myocardium with impaired perfusion will not exhibit increase uptake of radionucleotide tracer. CT coronary angiography

GTN spray – promotes NO release from endothelium to cause vasodilation Aspirin Statin Ca2+ CB Nifedipine, veramipil, diltiazem Block L-type channels decreases heart rate Beta blockers Atenolol, metoprolol – Block sympathetic innervation of heart. Decreased contractility and heart rate, oxygen demand. PCI – primary percutaneous intervention CABG – Coronary artery bypass graft Coronary angioplasty stenting

Can detect stenosis and degree of calcification on vessel walls. Unstable angina

Acute STEMI

Angina of increasing severity or at rest without evidence of myocardial necrosis Acute chest pain Sweating Vomiting

.

Acute NSTEMI

Atherosclerosis

Lateral T wave inversion

Thickening and the loss of elasticity of arteries. Vessel thickening reduces lumen diameter, compromising perfusion and

Non-modifiable Age Sex Genetic predisposition Modifiable Smoking Diabetes mellitus

Plaque erosion Damage to endothelium above plaque. Exposes prothrombotic subendothelial connective tissue. Thrombus formation which can occlude lumen Plaque rupture Advanced plaque with deep fissures allowing blood to flow into plaque. Thrombus formation causing it to expand and occlude lumen.

Endothelial dysfunction Chronic endothelial cell injury can occur as a result of cigarette smoking and high LDL levels. This leads to

Biochemical evidence of myocardial necrosis – creatine kinase, lactate dehydrogenase, troponin T+I ST segment elevation LBBB Increase in biochemical markers but NOT AS SIGNIFICANT AS STEMI

Analgesia Morphine Antiplatelets Aspirin irreversibly inhibits COX which activates platelet activator TA2. Clopidogrel irreversibly binds to ADP receptor. It inhibits platelet aggregation by blocking glycoprotein IIb and IIIa. LMWH Beta blocker - decrease HR O2 if hypoxic PCI

Sudden death withi 6hrs of symptoms. Heart failure – myocardium unable to contract effectively Arrhythmias Myocardial rupture – free wall of ventricle or septum. Mitral regurgitation – infarction and subsequent rupture of papillary muscles Pericarditis

Ischaemic heart disease Peripheral vascular disease Cerebrovascular disease Aneurysm formation

making it more likely to rupture if exposed to increased mechanical stress.

Hyperlipidaemia

structural damage. Endothelial cells upregulate inflammatory adhesion molecule expression and promotes monocyte and platelet aggregation. Injury leads to increased permeability to lipids and LDL = accumulate in intima Fatty streak formation Monocytes adhere to endothelium and differentiate into macrophages. Oxidation of LDL attracts macrophages into intima. Macrophages take up the LDL and become foam cells. Activates platelets, endothelial cells and macrophages release plateletderived growth factor (PDGF) – stimulates smooth muscle cell migration from media to intima across internal elastic

Unstable angina MI

Myocardial infarction

Chest pain/heaviness/pressur e Pain radiating to left arm+ jaw Sweating Nausea

lamina. Development of lipid plaque Smooth muscle and extracellular matrix proliferation increase in intima. More smooth muscle migration occurs from additional cytokine and growth factor release. Lipids from foam cells may be released = extracellular free lipid pools Advanced plaques Lipid rich core and fibrous cap is produced. Necrotic core consists of free lipid, macrophages, smooth muscle and cellular debris. Fibrous cap is made of collagen. Atherosclerosis occurs. Complete blockage of coronary artery. Infarcted tissue becomes inflamed and invaded by neutrophils – can cause

Bradycardia Partial infarct NSTEMI T wave inversion Whole wall infarct STEMI

Aspirin + Clopidogrel Heparin Nitrates Beta blockers Analgesia Statins Angioplasty

Fatigue Dyspnoea Pain not relieved by GTN

Myocarditis

Pericarditis

Sharp retrosternal chest pain radiating to back – aggregated by movement and respiration. RELIEF when sitting forward Fever

Virus Coxsackie Influenza Rubella Echovirus Bacteria Corynebacterium Candida Viral TB Trauma Carcinoma Uraemia MI Rheumatic fever Bacterial Rheumatoid arthritis Constrictive Radiotherapy

pericarditis. Coagulative necrosis occurs – macrophages and granulation of tissue begins – yellow and soft. Inflammation of myocardium.

T wave inversion Hyperacute T waves Pathological Q waves

Inflammation of pericardium. If inflammation continues after NSAIDS, fibrosis and shrinking of pericardium can occur – constrictive pericarditis.

Pericardial rub sound ECG Widespread saddle-shaped ST elevation PR depression Raised troponin Raised JVP Kussmaul’s sign Quiet S1/S2 S3 may be present

Pericardial effusion

Accumulation of fluid in the pericardial cavity caused by

Symptomatic relief NSAID Corticosteroids

Cardiac tamponade

Hyperlipidaemia

Supraventricular tachycardia SVT Atrial fibrillation

anything causing pericarditis. Effusion collects in closed cavity and leads to distention. Quick filling = cardiac tamponade Fluid/blood accumulating in pericardial sac. Pericardium can’t stretch so increase in pressure compresses the heart.

Beck’s triad Hypotension Raised JVP Muffled/quiet heart sounds Kussmaul’s sign – paradoxical rise in JVP during inspiration Xanthelasmas Xanthomata Tendon xanthomata

Palpitations Dizziness Syncope

MEDICAL EMERGENCY

Combination of hypertriglyceridemia, hypercholesterolaemia and hyperlipoproteinemia.

Numerous ectopic foci for impulse generation

Mitral valve disease Ischaemic heart disease

Chaotic depolarisation of atria results in ineffective atrial

Regular rhythm 140-220 bpm

Aspirating blood/fluid from pericardial sac pericardiocentesis

Lifestyle intervention Reduced calorific intake, alcohol Omega 3 fat supplements can increase HDL. Statins – simvastatin and atorvastatin HMG CoA inhibitors Bile acid binding resins – colestipol, cholestyramine

Atherosclerosis Dyslipidaemia = imbalance between damaging LDL and protective HDL

Rate control Verapamil – Ca2+ blocker Beta blocker

Lack of effective contraction – blood stasis. Emboli can

Thyrotoxicosis Presence of Hypertension numerous re-entry Excessive alcohol circuits that become consumption repeatedly excited in atria

Atrial flutter

Ventricular fibrillation

Ventricular tachycardia

Loss of consciousness

Myocardial infarction

contraction – rippling/fibrillation effect. Ventricular activity is also affected as impulses are randomly transmitted through AV node. Irregularly irregular pulse.

Narrow QRS complex

Re-entry of electrical depolarisation

Saw-tooth looking flutter waves No p waves Identical R-R intervals – unless BBB is present Narrow QRS complexes

Irregular, uncoordinated rippling contraction of ventricles. No effective cardiac output. Perfusion of brain is interrupted. Occurs when impulses originate from an ectopic focus or a reentry circuit within the ventricles.

Digoxin Rhythm control DC cardioversion Flecainide – Na+ channel blocker Amiodarone Chronic AF Warfarin to reduce emboli formation. Use CHADS2 score to predict risk of stroke

pass to brain and cause ischaemic stroke, or visceral organs to form ischaemia/infarction

Death – if no treatment is initiated.

Broad QRS complex >100ms Rate >120bpm

Broad complex tachycardia Bradycardia

Dizziness Syncope Tiredness

Narrow complex tachycardia

1st degree heart block

2nd degree heart block

Rate 100bpm QRS 120ms/>5 squares FIXED P-R INTERVAL Wenckebach Increasing P-R interval until dropped QRS complex after P wave – “warning like”

If there are adverse effects of ABCDE Atropine Isoprenaline Adrenaline Aminophylline Dopamine Transcutaneous pacing ECG Mostly benign and require no medical intervention

ECG

Mobitz Type 2 Can progress to complete heart block Insert pacemaker

Underlying disease of conducting tissue below AV node: Hispurkinjie fibres, bundle branches 3rd degree heart block

P waves may be buried on top of QRS complex. Treat with atropine OR temporary cardiac pacing

Wolff-ParkinsonWhite WPW

Junctional focus Ventricular action potential begins in/around AV node Ventricular focus Ventricular action potential begins within the ventricular myocardium

Complete heart block. AV node cannot conduct action potential from atria to ventricles. Complete atrio-ventricular dissociation.

WPW is caused by a congenital accessory pathway that can lead to arrhythmias. Accessory pathway = bundle of Kent. Depolarisation can occur from atria directly to ventricles, bypassing the AV node. Atrio-ventricular re-

Mobitz Type 2 Constant P-R interval QRS complex drop with “no warning” Irregular P-R intervals Regular P-P interval Regular QRSQRS intervals however they are dissociated to each other.

Short P-R interval Earlier upsloping of QRS complex – DELTA WAVE Widened QRS complex

Junctional escape rhythm Narrow QRS Ventricular rate = 40-60 bpm

Ventricular focus Wide and slow QRS complex Ventricular rate = 20-40 bpm

If not diagnosed Can lead to tachyarrhythmias and sudden cardiac death

entry tachycardia Sometimes APs from atria and ventricles through AV node and bundle of Kent cause chaos around AV node and his-purkinjie fibres. – caused by interference. Long QT syndrome Shock

Pale, cold clammy skin – cutaneous vasoconstriction Sweating – sympathetic stimulation Rapid weak pulse – compensated tachycardia and decreased stroke volume Reduced pulse pressure – reduced stroke volume and increased peripheral resistance. High SBP and low DBP. Rapid shallow breathing – chemoreceptor stimulation by low blood pH from metabolic acidosis Reduced urine output – renal hypoperfusion and

4 TYPES Hypovolaemic Cardiogenic Obstructive Septic

Acute failure of CVS to adequately perfuse body tissues. Hypovolaemic Fall in circulating blood from external fluid loss (vomiting, diarrhoea, haemorrhage) or internal fluid loss (pancreatitis, internal bleeding) Cardiogenic Impaired cardiac function where heart is unable to maintain adequate cardiac output. Usually acute onset – MI, arrhythmias, severe heart failure Obstructive Direct obstruction to

Fluid replacement Antibiotics – septic SEVERE Noradrenaline to bring about vasoconstriction to restore blood pressure.

reduced GFR

Haemorrhage

blood entering or leaving heart/great vessels – cardiac tamponade, massive PE Septic Toxins (endotoxins) released by bacteria in infection. Profound inflammatory response – cytokines and inflammatory mediators made. Widespread vasodilation and capillary permeability. TPR falls and decreased vascular volume from leakage. Reduced venous return and stroke volume – reduced BP. Tachycardia occurs to compensate. Loss of blood from the vascular compartment either internally or externally. Immediate response Baroreceptor mediated stimulated by decreased blood pressure. Increased

Main treatment Stop bleeding Replace circulating volume with IV fluids.

Decreased cardiac output due to decreased preload. Severe arteriolar vasoconstriction – metabolic acidosis due to increased lactate production.

sympathetic flow = increased ADH, ANGII, adrenaline and noradrenalin. Cause vasoconstriction. Increased peripheral resistance maintains blood pressure and perfusion to the brain. Intermediate response Profound constriction of peripheral vessels decreases hydrostatic pressure and causes increased fluid reabsorption from interstitial component. Hepatic glycolysis can increase plasma osmolarity – corrects loss of circulating volume. Long term response Activation of RAA system increases ADH and aldosterone secretion. ANG11 increases water uptake. Hypotension Hypertension

Reduced elasticity of large arteries due to

Weight loss Healthy diet

CHD Heart failure

age-related and atherosclerosis calcification and degradation of arterial elastin.

Dilated cardiomyopathy MOST COMMON

Hypertrophic cardiomyopathy

Idiopathic Alcohol toxicity Viral myocarditis Peripartum Chemotherapy Dyspnoea Angina Syncope

Restrictive cardiomyopathy Infective Endocarditis

Fever Chills Anorexia Weight loss Headache Myalgia Arthralgia

Strep Viridans – NATIVE VALVE Staph aureus/staph epidermidis PROSTHETIC

Amyloidosis Endomyocardial fibrosis Staph aureus Streptococcus viridans – after dental procedures, tonsillectomy, bronchoscopy Enterococci

Dilated ventricles and impaired systolic function. May cause regurgitation of AV valves. Hypertrophy of ventricular myocardium, mostly interventricular septum. Can cause mitral valve regurgitation. Impaired ventricular filling and causes diastolic dysfunction, Decreased ventricular compliance restricts ventricular filling Infection of endocardium on valves that are previously damaged or congenitally abnormal. Inflammation of the valve causes

Reduce alcohol and caffeine ACE Inhibitor DHP-Calcium channel blockers Thiazide like diuretic Spironolactone

Renal failure Stroke Peripheral vascular disease

Heart failure Arrhythmias Mural thrombus in LV 4th heart sound due to stiff ventricle Systolic murmur

Multiple sets of blood cultures from different sites. Janeway lesions Osler nodes

Sudden death from ventricular arrhythmias

IV antibiotics Amoxicillin and gentamicin Staph aureus = flucloxacillin

Night sweats

Heart failure

Cyanotic heart disease

Fatigue Dyspnoea Orthopnoea Paroxysmal nocturnal dyspnoea Swollen ankles Nocturia Tachycardia Raised JVP 3rd/4th HS Bi-basal crackles

Staphylococcus aureas – catheterised patients, IV drug users Entercoccus faecalis – pelvic infections/surgery Staphylococcus epidermidis – common in IV drug users, prosthetic heart valves Infarction Cardiomyopathy Myocarditis Hypertension Valvular disease Severe anaemia Thyrotoxicosis Arteriovenous fistulas

destruction and scarring. Vegetations – fibrin, platelets and infective organisms. Vegetations develop on valve and cause valvular regurgitation. Can also throw emboli into brain and kidneys to cause ischaemia. Clinical syndrome where heart is no longer able maintain sufficient tissue perfusion to meet metabolic demands of body tissues, despite normal filling pressures. Decreased SV due to impaired contractility

Roth spots Splinter haemorrhages P-R prolongation USE DUKE’S CRITERIA

ECG – Atrial fibrillation, ventricular hypertrophy, LBBB CXR Enlarged heart shadow Bilateral pleural effusions Echocardiogram Ejection fraction of 3squares

LBBB

LOOK AT LEADS V1 AND V6

Right ventricular hypertrophy Pulmonary embolism Ischaemic heart disease Congenital heart disease Normal variant Aortic stenosis Ischaemic heart disease

Congenital opening between RA and LA. When pulmonary vascular disease decreases after birth, oxygenated blood is shunted from left to right. This causes an increase in RV and RV load = right heart dilation = pulmonary flow = increase in size of pulmonary arteries and veins V1 – RSR’ pattern V6 – a slurred QRS wave

Echocardiogram

V1 – RSR’ pattern V6 – a slurred QRS wave

WILLIAM W – QRS complex in V1

ECG = RBBB, RV hypertrophy

MARROW M – QRS complex in V1 and V6 normal

WIDE QRS COMPLEX >3squares

Hyperkalaemia Digoxin toxicity Myocardial infarction

M – QRS in V6...