The Cardiovascular System

Varicose veins

superficial veins

distended

damaged valves can’t maintain normal venous pressure

can progress to chronic venous insufficiency where there’s insufficient venous return to tissue

Thrombus

blood clot attached to vessel wall

Thromboembolus

blood clot which becomes detached

DVT

clot which has formed in large veins

Why won’t DVT cause stroke?

clot goes into right side of heart first

this then goes to lungs

3 causes of DVT

venous stasis

venous endothelial change

hypercoagulable states

Venous stasis

pooling or stagnation of blood in veins

due to problems with venous circulation and valve function

Venous endothelial damage

impaired function of endothelium

leads to reduced vasodilation and increased vasoconstriction

Hypercoagulable states

blood has increased tendency to form clots

Signs and symptoms of DVT

pain in leg

hot

red

swollen

breathlessness = PE

Primary hypertension

mix of environmental and genetic factors

no underlying cause

Secondary hypertension

associated with primary underlying disease

• kidney disease

• endocrine disorders

• acute stress

• drugs

• pregnancy

Risk factors for hypertension

age

family history

ethnicity

unhealthy lifestyle choices (diet, inactivity, smoking, excessive alcohol)

medical conditions (kidney disease, diabetes, thyroid problems)

Cardiac output

vol. of blood pumped around heart

End diastolic vol. (EDV)

vol. of blood in ventricles before heart contracts

End systolic vol. (ESV)

vol. of blood remaining in ventricle at end of systole

Stroke vol. definition

vol. of blood pumped around heart

Stroke vol. equation

SV = EDV - ESV

What is stroke vol. affected by?

venous return (vol. of blood going in)

filling time

autonomic innervation (nervous system’s part of cardiac cycle)

hormones

vasodilation or vasoconstriction

Ejection fraction

% of blood pumped out of heart (as there’s blood left in heart)

Frank-Starling mechanism

(chronologically)

more blood in heart

more increase in tension

stretches heart

higher the force of pumping blood out

vol. of blood ejected by ventricle depends on vol. of blood present in ventricles

Aneurysm

localised dilation or outpouching of vessel

most commonly occurs in thoracic or abdo aorta

5 types of aneurysm

fusiform

pseudoaneurysm

saccular

dissecting

ruptured

Rupture (in relation to aneurysm)

when it bursts

Dissection (in relation to aneurysm)

fast or slow

when weakened wall of aorta tears

causes blood to leak between layers that make up walls of arteries

Ischaemia

reduced amount of blood flow to part of body

dislodging creates a thromboembolus

Embolism

bolus of matter circulating in bloodstream

5 types of embolism

thromboembolism

air embolism

amniotic fluid embolism

bacterial embolism

fat embolism

Thromboembolism

vascular obstruction from a dislodged thrombus

Atherosclerosis

thickening and hardening of vessel caused by accumulation of lipid laden microphages within arterial wall

forms lesion called plaque

results in ischaemic syndromes

causes inadequate tissue perfusion

How thrombus forms due to atherosclerosis

Coronary artery disease (CAD)

when coronary arteries blocked, often due to atherosclerosis

CAD, myocardial ischaemia, ACS and MI are all continuum of same disease

Risk factors for CAD

age

sex

family history

htn

diabetes

obesity

smoking

preeclampsia

menopause

Myocardial ischaemia

when supply of blood from coronary arteries cannot meet demand of myocardium for oxygen and nutrients

Angina pectoris

chest pain caused by myocardial ischaemia

Stable angina

episodes of chest pains in response to predictable stressors

eased by rest and nitrate

blood vessels have become hardened and narrowed and can’t adequately respond to increased demand

Unstable angina

random episodes of chest pain

fissuring of erosion of plaque leads to transient episodes of occlusion and vasoconstriction

reperfusion occurs before significant myocardial necrosis occurs

not full blockage

resolves itself

reversible myocardial ischaemia

Acute coronary syndrome (ACS)

sudden coronary obstruction caused by rupture of plaque

Decision tree on chest pain at rest

ECG changes in unstable angina

ST depression

t wave inversion

Myocardial infarction (MI)

when coronary blood flow interrupted for an extended period

causes myocyte death

mostly caused by atherosclerotic CAD

Pericarditis

fluid can collect in space between pericardial sac and heart

causes tamponade

causes ECG changes - ST elevation

Cardiomyopathy

disorders of heart muscle

can be acquired or genetic or idiopathic (disease of unknown cause)

Hypertrophic cardiomyopathy

muscle wall of heart becomes thickened

Symptoms of hypertrophic cardiomyopathy

sob

chest pain

palpitations

light-headedness

fainting

arrhythmias

heart block

endocarditis

sudden cardiac death

Dilated cardiomyopathy

muscle becomes stretched and thin

Causes of dilated cardiomyopathy

mutation of one or more genes - 50% chance of inheriting

viral infections

uncontrolled bp

problems with heart valves

Symptoms of dilated cardiomyopathy

sob

swelling of ankles or abdo

excessive tiredness

palpitations

arrhythmias

blood clots

chest pain

Endocarditis

inflammation of endocardium

Causes of endocarditis

bacteria in bloodstream

thrombi

Valvular disorders

heart valves made of endothelial tissue

causes stenosis or regurgitation or both

valves of left side of heart more commonly affected

Stenosis

valve orifice is narrow or constricted

impedes forward blood flow

increases ventricular workload

Regurgitation

valve cusps do not shut completely

prevents forward flow stopping

causes backflow of blood

Heart failure

heart unable to generate adequate cardiac output in order to meet metabolic needs of body

functional or structural impairment causing inadequate ventricular filling or ejection of blood

cardiac reserve lost and minimal activity can use up all cardiac reserves

Cardiac reserve

capacity of heart to increase output during periods of increased activity

Causes of heart failure

CAD

htn

idiopathic cardiomyopathy

valvular heart disease

arrhythmia

Vol. overload or heart failure decompensation

anaemia

af or other arrhythmias

fluid overload

fluid retention

pulmonary causes

Patho of heart failure

increased preload (vol. overload)

• increased sv per min

• aortic valve incompetence

• mitral valve incompetence

increased afterload (pressure overload)

• outflow resistance increased

• aortic stenosis

• systemic htn

myocardial dysfunction

• failure of contractile tissue

• following MI

• cardiomyopathy

Systolic dysfunction in heart failure

impaired contractility

thin/weak heart muscle

low ejection fraction

causes:

• ischaemic heart disease

• chronic htn

• dilated cardiomyopathy

• myocarditis

Diastolic dysfunction

impaired filling/relaxation

stiff/thick heart muscle

normal ejection fraction

causes:

• htn with lv hypertrophy

• restrictive and hypertrophic cardiomyopathies

• fibrosis

• constrictive pericarditis

• valvular disease

Causes of left sided heart failure

CAD

valvular disease

htn

Causes of right sided heart failure

lung disease

pulmonary hypertension

MI

How does right sided heart failure affect digestive system

venous congestion

reduced blood flow

GI tract and liver congestion

causes anorexia, weight loss, impaired function

How does left sided heart failure affect respiratory system?

decreased cardiac output

• decreased tissue perfusion

pulmonary congestion

impaired gas exchange

• leads to cyanosis and hypoxia

pulmonary oedema

• cough with frothy sputum

• orthopnea

• paroxysmal nocturnal dyspnea

Compensatory mechanisms of heart failure

baroreceptor response

RAAS activation, decreased GFR

increased ventricular wall tension

Sympathetic nervous system as compensatory mechanism of heart failure

baroreceptor response

stimulation of SNS leads to increased sympathetic tone

increase in adrenaline and noradrenaline levels

increased hr and contractility

increased cardiac outpu

Renin-aldosterone-angiotensin as compensatory mechanism of heart failure

RAAS stimulated to increase water and sodium retention via aldosterone release in response to low GFR and renal blood flow

fluid retention

increased preload

increased cardiac output

Increased ventricular tension as compensatory mechanism of heart failure

increased preload

increased stretching of myocardial fibres

increase in contractility

frank-starling mechanism

RAAS system

Manifestations of heart failure

fluid retention and oedema

resp problems

fatigue

cognitive impairment

cachexia/malnutrition

cyanosis

arrhythmias

Acute pulmonary oedema

fluid moves in alveoli

increased ventricular filling pressure

• hence pulmonary venous pressure increased

• fluid accumulation within legs

work of breathing increased by

• reduced lung compliance and vital capacity

• bronchoconstriction secondary to PO

increased pulmonary venous htn

• alveolar membrane thickened/oedematous

• gas exchanged impaired - arterial hypoxaemia

Arrhythmias

Haemostasis

process of stopping bleeding from blood vessel via clot

3 stages of haemostasis

vascular constriction

formation of platelet plug

blood coagulation

Clotting cascade

convert prothrombin to thrombin

thrombin converts fibrinogen to fibrin

Fibrin

insoluble substance that meshes together to form platelets and other blood components to form blood clot

Shock

acute failure of circulatory system leading to inadequate blood supply to major organs and peripheral tissues resulting in cellular hypoxia

Shock patho

hypoperfusion of organs

lack of oxygen leads to anaerobic metabolism pathway being utilised

leads to build up of lactic acid in cells

disruption of ATP pump leads to sodium ion build up of inside cells and potassium ion build up outside of cells

sodium in cell leads to cellular oedema and increased membrane permeability

lack of oxygen/nutrients and build up of waste products in cells causes cellular injury

causes inflammatory mediators to be released

cause structural changes in microvascular circulation which further compromises perfusion

vicious cycle where further compromise causes further cellular injury and can end in irreversible organ damage

Compensatory mechanisms for shock

sympathetic NS

RAAS system activated

angiotensin

Sympathetic NS compensatory mechanism for shock

activation of alpha and beta receptors by adrenaline and noradrenaline leads to vasoconstriction, increase in hr in myocardial contractility, relaxation of bronchioles

RAAS system as a compensatory mechanism for shock

leads to increase in vasoconstriction

increase in sodium and water retention so increase in blood vol.

Angiotensin

hormone that regulates blood pressure and fluid balance by constricting blood vessels and stimulating sodium and water retention

4 types of shock

distributive/neurogenic

hypovolaemic

cardiogenic

obstructive

Hypovolaemic shock

due to large loss of fluid

Compensatory mechanisms of hypovolaemic shock

absorption of fluid from interstitial spaces in vascular compartment

sympathetic NS

• activation of alpha and beta receptors with adrenaline and noradrenaline

• stimulates increase in hr and vasoconstriction

blood transferred from liver to main circulation

RAAS system activates to increase Na reabsorption, increase thirst and water retention via ADH

Signs and symptoms of hypovolaemic shock

slight dip in bp which will fix itself quickly

increased rr

increased

hr

decreased bp

hypothermia

clammy

everything gets worse

Cardiogenic shock

failure of heart to pump adequately

decrease in SV leads to decrease in CO

decreased CO, hypoperfusion, tissue hypoxia

adequate IV vol.

decreased myocardial contractility, increased afterload and high preload

Signs and symptoms of cardiogenic shock

hx of cardiac issue

• heart failure

• tamponade

cyanosis

altered mental state

low bp

narrow pulse pressure

decreased urine output

pulmonary oedema

ECG abnormality

abnormal heart sounds - 3rd heart sound

Neurogenic/distributive shock

vasodilation (problem with brain) but same vol. of blood

caused by decreased sympathetic control of blood vessels

due to damage to vasomotor centre in brain stem or sympathetic outflow to vessels

usually involves spinal injury

Signs and symptoms of neurogenic/distributive shock

usually involves spinal injury

bradycardia

skin warm and dry below injury

cold and clammy above injury

Obstructive shock

caused by a thrombus

Signs and symptoms of obstructive shock

cold and clammy above occlusion

warm and dry below occlusion

Complications of shock

acute respiratory distress syndrome

• lethal pulmonary injury

• rapid onset of dyspnoea, hypoxaemia which cannot be corrected - changes to permeability of alveolar membrane/capillaries

acute kidney injury

• low blood vol. causes impaired renal perfusion

GI complications

• GI tract vulnerable due to changes in blood flow to mucosa

disseminated IV coagulation (DIC)

• widespread coagulation with clots in small and medium vessels

multiple organ dysfunction syndrome (MODS)

• affects multiple organ systems

• life threatening

Stages of the cardiac cycle

ventricular and atrial diastole: filling

atrial systole: ventricular filling

ventricular systole: ventricular emptying

Diastole

chambers relax

both atria and ventricles fill with blood

Atrial systole

atria contract

remaining blood pushed into ventricles

ventricles larger so need longer to fill

Ventricular systole

ventricles contract

blood pushed out through aorta and pulmonary artery