Cardiovascular diseases Flashcards
What is heart failure?
Condition where the heart is unable, with normal filling pressure, to maintain normal cardiac output to meet the body’s demand
What are the 2 types of heart failure?
Systolic HF - Heart cannot pump hard enough
Diastolic HF - Heart is not filled enough
What can be the causes of left-sided heart failure?
Usually systolic
- Ischemic heart disease (Damage -> Less contraction)
- Hypertension (Increased arterial pressure -> hypertrophy -> Increased O2 demand -> Weaker contraction)
- Dilated Cardiomyopathy (Increased chamber size -> Walls become thin + weak)
Can be diastolic
- Hypertension (Hypertrophy -> Less room for filling)
- Restrictive cardiomyopathy (Stiff -> Less compliance -> Less stretch + less fill)
What can be the causes of right-sided heart failure?
Usually caused by left-sided heart failure
Can be chronic lung disease (Hypoxia -> Constriction of arterioles -> Increased pulmonary blood pressure)
What are the clinical manifestations of left- and right-sided heart failure?
Left-sided
Fluid buildup in lungs (pulmonary edema) -> Less gas exchange -> dyspnea + crackles when breathing
Right-sided
Fluid buildup in body (veins)
- Jugular vein distention
- Fluid buildup in liver + spleen
- Fluid buildup in legs
What is Ischemic Heart Disease?
Decreased blood flow to the myocardium caused by plaques in the coronary arteries
What is the “general” etiology of Ischemic Heart Disease?
Atherosclerosis (Hypertension, smoking, High sugar + fat in diet, obesity, high age, diabetes)
Embolus, Vasculitis, Vasospasm
What are the 3 types of acute Ischemic Heart Disease and what characterises them?
Unstable angina
- Unstable plaque
- Chest pain at rest
Subendocardial infarct (NSTEMI)
- Unstable plaque
- Myocardial cell death in subendocardial myocardium
- Chest pain at rest
Transmural infarct (STEMI)
- Total occlusion
- Transmural injury of myocardium
- Chest pain at rest
What are the clinical manifestations of acute ischemic heart disease, both in terms of general, left ventricle and right ventricle symptoms?
General
Chest pain, Pain in left arm, neck and jaw
If in left-ventricle
Edema in legs, Hypotension, Reflex tachycardia
If in right-ventricle
Jugular vein distention, Edema in legs, Hypotension, Decreased blood to SA/AV node -> Decreased heart rate -> Sinus bradycardia + AV block
What are the ECG changes and findings in serum for the 3 types of acute ischemic heart disease?
Unstable angina
- No ST-elevation
- Maybe T-wave inversion
- No biomarkers
Subendocardial infarct (NSTEMI)
- No ST-elevation
- Maybe T-wave inversion
- Biomarkers
Transmural infarct (STEMI)
- ST-elevation
- Biomarkers
What are the 3 types of chronic ischemic heart disease and how are they characterised?
Stable angina
- Fixed coronary obstruction
- Angina pectoris with exercise (Center chest, neck, shoulders, arms)
Silent Myocardial Ischemia
- No angina pectoris
- Decreased blood flow
Variant (Vasoplastic) Angina
- Etiology unknown (Endothelial dysfunction, Hyperactive sympathetic nervous system)
- Angina at rest/minimum exercise (Usually at night/minimal exercise)
- Arrhythmias (ST-elevation, Rhythm disturbances)
What is atherosclerosis?
Hardening of arteries from plaques in the endothelium
What are the modifiable and non-modifiable risk factors of atherosclerosis?
Modifiable
Hypercholesterolemia, Smoking, Obesity
Non-modifiable*
High age, Family history (genetics), Male, Diabetes
Explain the pathogenesis of atherosclerosis
High LDL in blood damages the endothelium in the artery -> LDL gets into the tunica intima -> LDL is oxidized -> Receptors and adhesion molecules are expressed on the endothelium -> Monocytes are recruited to the tunica intima -> Eats oxidized LDL (Becomes Foam cells) -> Promotes migration of smooth muscle cells to tunica intima -> Production og collagen -> Fibrous Cap
What are the clinical manifestations of atherosclerosis?
First: No symptoms
Depends on affected artery and how occluded the vessel is
- Coronary arteries: Ischemic heart disease -> Chest pain
- Peripheral arteries: Peripheral vascular disease -> Weakening of affected area
- Renal arteries: Decreased appetite, Kidneys think BP is low -> Increased renin -> Increased BP
- Carotid arteries: Weakness, dyspnea, headache, paralysis
Weakened vessel -> Aneurysms/ Thrombi
What is hypertension?
A sustained elevation of BP within the arterial circuit
What are the 2 classifications of hypertension by etiology?
Primary/Essential - Clinical presens of hypertension without evidence of a causative disease
Secondary
What are the modifiable and non-modifiable risk factors of primary/secondary hypertension?
Non-modifiable Age (stiffening of arterial walls), Family history (genetics), Male sex
Modifiable High salt intake, Dyslipidemia, Smoking, Alcohol, Obesity
Etiologies of secondary hypertension
Renal hypertension (Increased Renin -> Increased Angiotensin II -> Vasoconstriction + Increased aldosterone + Sodium retention)
Disorders of Adrenocortical Hormones
Coarctation of the aorta (Narrowing in aortic arch)
Clinical manifestations of hypertension
Primary - Usually asymptomatic
When symptoms occur they are related to the long term effects on target organs
- Increased risk of atherosclerosis
- Ischemic heart and brain disease
- Left heart hypertrophy -> Coronary artery disease
- Chronic Kidney Disease
- Effects on retina
Secondary - Usually related to primary disease
Hypertensive emergency
Sudden elevation of blood pressure + acute/worsening target-organ damage
What is circulatory shock?
Acute failure of the circulatory system to supply the peripheral tissues and organs of the body with an adequate blood supply, resulting in cellular hypoxia
General pathophysiology of shock
Hypoperfusion + Insufficient O2 supply -> Activation of sympathetic nervous system + Renin system -> Increased heart rate + Vasoconstriction + Sodium/Water retention -> Decreased nutrients, Decreased tissue perfusion, Increased anaerobic metabolism -> Increased acidity, Increased Na+ in cells (edema), Mitochondrial dysfunction -> Cell death
What are the 4 kinds of shock?
Cardiogenic shock
Hypovolemic shock
Distributive shock (Neurogenic, Anaphylactic, Septic)
Obstructive shock
Describe Cardiogenic shock
Heart fails to pump blood sufficiently to meet the demand of the body
Usually caused by MI
Decreased cardiac output + Hypotension + Tissue hypoxia -> Increased preload + Decreased contractibility + Increased afterload
Mechanism
- Norepinephrine: Increased vascular resistance -> Increased afterload
- Renin: Increased fluid retention + Vasoconstriction -> Increased resistance -> Increased afterload
Symptoms
Cyonic skin + nails, Decreased urine production, Decreased systolic BP
Describe Obstructive shock
Mechanical obstruction of flow through central circulation
Reasons: Aortic aneurysm, pulmonary embolism
Impaired right ventricle -> Jugular vein distension + Increased central venous pressure
Describe Hypovolemic shock
Decreased blood volume (whole, plasma or EC fluid)
Can be bleeding (internal/external) or non-hemorrhagic (dehydration)
Compensatory mechanisms
Sympathicus: Increased HR, Increased contraction, move blood from liver storage
ADH-release: Fluid retention in kidneys + peripheral artery constriction
Renin: Water + Sodium retention + Vasoconstriction
Describe Distributive shock incl. the 3 subtypes
Loss of vessel tone, leaky blood vessels, vasodilation
Neurogenic
- Decreased sympathetic control of blood vessel tone
- Reasons: Spinal injury, Decreased glucose
- Decreased HR, warm skin
Anaphylactic
- Systemic allergic reaction
- Vasodilation -> Increased vascular permeability + Decreased BP
Septic
- Pathogens in blood -> Innate response -> Vasodilation -> Hypotension
- Warm, flushed skin
Define endocarditis
Infection of the endocardium
- Invasion of the endocardium or valves by microbes -> bulky, friable vegetations + destruction of cardiac tissue
Etiology and risk factors for endocarditis
Wound, surgery, implantations, infected needle -> Microbe in blood -> enter endocardium
Risk factors Prosthetic valves, pacemakers, congenital heart defects
What can endocarditis lead to?
Vegetations on valves (mitral + aortic is common)
- Valve destruction -> Pericarditis, regurgitations
- Fragments can form -> emboli
What are the 2 classifications based on onset for endocarditis?
Acute Rapid onset, normal valves
Subacute/chronic Evolve over months, valve abnormalities
Clinical manifestations of endocarditis
Fever, systemic infection, heart murmur, petechial hemorrhages under nails
Define pericarditis
Inflammation of the pericardium
Etiology, pathogenesis and symptoms of acute pericarditis
Etiology Viral (most common), bacterial, connective tissue disease, uremia
Pathogenesis
- Increased capillary permeability in serous pericardium -> plasma proteins enter pericardial cavity
- Febrin-containing exudate -> progress to scar tissue -> adhesion between serous pericardium
Symptoms Chest pain + pericardial friction rub + ECG changes
Define Chronic Venous Insufficiency
Persistent venous hypertension in the lower extremities
Etiology of chronic venous insufficiency
Increased venous hydrostatic pressure (standing)
Incompetent valves
DVT
Decreased skeletal muscle pumps
Inflammation
Endothelial dysfunction
Clinical manifestations of chronic venous insufficiency
Tissue congestion
Edema
Brown pigmentation (breakdown of RBCs)
Which veins can thrombi form in?
Superficial veins (SVT) and Deep veins (DVT)
Etiology of Deep Venous Thrombosis
Bedrest/Immobilization
- Decreased blood flow
- Venous pooling in lower extremities
- Increased risk of DVT
Decreased cardiac function
Long airplane travel (prolonged sitting + dehydration)
Hypercoagulability
Clinical manifestations of Deep Venous Thrombosis
Asymptomatic
Common symptoms are related to inflammation
- Pain, swelling, deep muscle tenderness
1) What are the 2 classes and 2 overall types of arrhythmias?
2) What is bad about the 2 overall classes?
3) In which parts of the heart can the arrhythmia “originate”?
1) 2 classes Disorders of rhythm, Disorders of impulse conduction. 2 types Tachyarrhythmias and Bradyarrhythmias
2) Tachyarrhythmia Increased myocardial oxygen demand. Decreased diastolic filling time -> Decreased stroke volume -> Decreased Cardiac perfusion. Bradyarrhythmia Decreased blood flow to vital organs (Brain)
3) Sinus node, AV node, atria, ventricles
1) What is a cardiomyopathy?
2) There are 4 pathologies which are cardiomyopathies? What are they and why do they induce disease?
1) It is a disease of the myocardium
2) Left ventricular hypertrophy: Decreased filling -> decreased SV -> diastolic heart failure
Dysplasia (right ventricle): The myocardium is replaced by firbro-fatty tissue
Dilated: Ventricular enlargement -> systolic heart failure
Myocarditis: Inflammation of the myocardium
What are some symptoms seen in cardiomyopathies?
Syncope, dyspnea, arrythmias and abnormal ECG
Which of the cardiomyopathies have genetics as etiology?
Left ventricular hypertrophy, dysplasia (mixed) and dilated (mixed)
