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Pathophysiology > Cardiovascular diseases > Flashcards

Cardiovascular diseases Flashcards

1
Q

What is heart failure?

A

Condition where the heart is unable, with normal filling pressure, to maintain normal cardiac output to meet the body’s demand

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2
Q

What are the 2 types of heart failure?

A

Systolic HF - Heart cannot pump hard enough
Diastolic HF - Heart is not filled enough

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3
Q

What can be the causes of left-sided heart failure?

A

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)

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4
Q

What can be the causes of right-sided heart failure?

A

Usually caused by left-sided heart failure
Can be chronic lung disease (Hypoxia -> Constriction of arterioles -> Increased pulmonary blood pressure)

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5
Q

What are the clinical manifestations of left- and right-sided heart failure?

A

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

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6
Q

What is Ischemic Heart Disease?

A

Decreased blood flow to the myocardium caused by plaques in the coronary arteries

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7
Q

What is the “general” etiology of Ischemic Heart Disease?

A

Atherosclerosis (Hypertension, smoking, High sugar + fat in diet, obesity, high age, diabetes)
Embolus, Vasculitis, Vasospasm

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8
Q

What are the 3 types of acute Ischemic Heart Disease and what characterises them?

A

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

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9
Q

What are the clinical manifestations of acute ischemic heart disease, both in terms of general, left ventricle and right ventricle symptoms?

A

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

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10
Q

What are the ECG changes and findings in serum for the 3 types of acute ischemic heart disease?

A

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

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11
Q

What are the 3 types of chronic ischemic heart disease and how are they characterised?

A

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)

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12
Q

What is atherosclerosis?

A

Hardening of arteries from plaques in the endothelium

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13
Q

What are the modifiable and non-modifiable risk factors of atherosclerosis?

A

Modifiable
Hypercholesterolemia, Smoking, Obesity

Non-modifiable*
High age, Family history (genetics), Male, Diabetes

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14
Q

Explain the pathogenesis of atherosclerosis

A

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

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15
Q

What are the clinical manifestations of atherosclerosis?

A

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

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16
Q

What is hypertension?

A

A sustained elevation of BP within the arterial circuit

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17
Q

What are the 2 classifications of hypertension by etiology?

A

Primary/Essential - Clinical presens of hypertension without evidence of a causative disease
Secondary

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18
Q

What are the modifiable and non-modifiable risk factors of primary/secondary hypertension?

A

Non-modifiable Age (stiffening of arterial walls), Family history (genetics), Male sex
Modifiable High salt intake, Dyslipidemia, Smoking, Alcohol, Obesity

19
Q

Etiologies of secondary hypertension

A

Renal hypertension (Increased Renin -> Increased Angiotensin II -> Vasoconstriction + Increased aldosterone + Sodium retention)
Disorders of Adrenocortical Hormones
Coarctation of the aorta (Narrowing in aortic arch)

20
Q

Clinical manifestations of hypertension

A

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

21
Q

What is circulatory shock?

A

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

22
Q

General pathophysiology of shock

A

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

23
Q

What are the 4 kinds of shock?

A

Cardiogenic shock
Hypovolemic shock
Distributive shock (Neurogenic, Anaphylactic, Septic)
Obstructive shock

24
Q

Describe Cardiogenic shock

A

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

25
Q

Describe Obstructive shock

A

Mechanical obstruction of flow through central circulation

Reasons: Aortic aneurysm, pulmonary embolism

Impaired right ventricle -> Jugular vein distension + Increased central venous pressure

26
Q

Describe Hypovolemic shock

A

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

27
Q

Describe Distributive shock incl. the 3 subtypes

A

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

28
Q

Define endocarditis

A

Infection of the endocardium
- Invasion of the endocardium or valves by microbes -> bulky, friable vegetations + destruction of cardiac tissue

29
Q

Etiology and risk factors for endocarditis

A

Wound, surgery, implantations, infected needle -> Microbe in blood -> enter endocardium
Risk factors Prosthetic valves, pacemakers, congenital heart defects

30
Q

What can endocarditis lead to?

A

Vegetations on valves (mitral + aortic is common)
- Valve destruction -> Pericarditis, regurgitations
- Fragments can form -> emboli

31
Q

What are the 2 classifications based on onset for endocarditis?

A

Acute Rapid onset, normal valves
Subacute/chronic Evolve over months, valve abnormalities

32
Q

Clinical manifestations of endocarditis

A

Fever, systemic infection, heart murmur, petechial hemorrhages under nails

33
Q

Define pericarditis

A

Inflammation of the pericardium

34
Q

Etiology, pathogenesis and symptoms of acute pericarditis

A

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

35
Q

Define Chronic Venous Insufficiency

A

Persistent venous hypertension in the lower extremities

36
Q

Etiology of chronic venous insufficiency

A

Increased venous hydrostatic pressure (standing)
Incompetent valves
DVT
Decreased skeletal muscle pumps
Inflammation
Endothelial dysfunction

37
Q

Clinical manifestations of chronic venous insufficiency

A

Tissue congestion
Edema
Brown pigmentation (breakdown of RBCs)

38
Q

Which veins can thrombi form in?

A

Superficial veins (SVT) and Deep veins (DVT)

39
Q

Etiology of Deep Venous Thrombosis

A

Bedrest/Immobilization
- Decreased blood flow
- Venous pooling in lower extremities
- Increased risk of DVT
Decreased cardiac function
Long airplane travel (prolonged sitting + dehydration)
Hypercoagulability

40
Q

Clinical manifestations of Deep Venous Thrombosis

A

Asymptomatic
Common symptoms are related to inflammation
- Pain, swelling, deep muscle tenderness

41
Q

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”?

A

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

42
Q

1) What is a cardiomyopathy?

2) There are 4 pathologies which are cardiomyopathies? What are they and why do they induce disease?

A

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

43
Q

What are some symptoms seen in cardiomyopathies?

A

Syncope, dyspnea, arrythmias and abnormal ECG

44
Q

Which of the cardiomyopathies have genetics as etiology?

A

Left ventricular hypertrophy, dysplasia (mixed) and dilated (mixed)

Pathophysiology (13 decks)

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