Patho Heart

• From right atrium to right ventricle via a tricuspid valve
• From the right ventricle to the pulmonary arteries via the semilunar valve
• From the pulmonary veins to the left atrium (there are 4)
• from the left atrium to the left ventricle via the bicuspid valve
• From the left ventricle to the aorta via the smilunar valve

• Diastole
• Systole

• relaxation of the ventricle where the ventricle fills.
• The aorta is closed

• The contraction of the ventricle.
• The ejection of blood out of the ventricle
• systole pressure reflects stroke volume, rates and force, elasticity of aorta and large arteries.

BP= CO x PR (peripheral resistance)

Cardiac anomalies which are structural defects that develop in the first eight weeks of embryonic life

• 1. Valvular defects- interfere with normal blood flow
• 2. Septal defects- allowing mixing of oxygenated blood from pulmonary circulation with unoxygenated blood fom the systemic circulation
• 3. Shunts- may be cyanotic or acyanotic depending on direction of shunt
• Or a combination of these

• Cyanotic not enough oxygen person goes blue
• Acyanotic- heaps of oxygen they are pinky colour

• Genetic influences- chromosomal abnormalities eg down syndrome
• Environmental influences- viral infection such as rubella, maternal alcoholism and diabetes

• Large defects lead to:
• - pallor and cyanosis
• - tachycardia
• - dyspnea on exertion
• - squatting position in toddlers and older children
• - clubbed fingers
• - intolerance for exercise and cold weather
• - delayed growth and development

• Heart murmurs
• Severe defects are often diagnosed at birth (untreated = heart failure)
• Examination techniques:
• 1. Auscultation- stethoscpoe
• 2. Diagnostic imaging
• 3. Echocardiogram (3D)
• 4. Electrocardiogram (ECG)
• 5. Cardiac catherisation

• Surgical repair
• Valve replacement
• Drug therapy
• Spontaneous recovery

• THe most common congenital heart defect- 20-30% "hole in the heart.
• Opening in the interventricular septum- vary in size and location. Atrial septum- foramen ovale fails to close
• Large openings permit a left to right shunt of blood then may eventually, if untreated, lead to a reveral of the shunt- right to left.

• Decreased SV and CO
• increase in oxygenated blood entering pulmonary circuit
• overloads and irreversibly damages the pulmonary blood vessels = pulmonary hypertension
• Acyanotic condition results

• Abnormally high pressure in the right ventricle, from conditions such as pulmonary hypertension, leads to a reversal of the shunt. Right to left.
• Leading to cyanosis- venous blood mixes with arterial blood resulting in unoygenated hb back into the systemic system
• results in a bluish lips and nails etc

• increase HR
• increase force of contraction CO
• decrease in coronary perfusion
• increase peripheral resistance
• increase in respiatory reate
• Chronically- increase in RBC production as a result of hypoxia

• - Stenosis- narrowing of the valve, restricts the forward flow of blood
• - valvular incompetence- failue of a valve to close completely, flaps back, blood regurgitates or leaks backwards eg mitral valve prolapse, abnormal enlarged, floppy valve leaflets that ballon backwards effect 1-3% pop

• decrease in efficiency of the heart pump
• decrease in stroke volume
• increase contractility of myocardium
• hypertrophy of the chamber with the faulty valve
• with lead to heartfailure and pulmonary congestion

Valve sternosis

Surgical replacement- mechanical, animal

• Most common cyanotic (R to L shunt) congenital heart condition
• cyanosis occurs
• alt pressure within heart and alt blood flow
• includes four abnormalities:
• - pulmonary valve stenosis
• - VSD
• - Dextropositio of the aorta
• - right ventricular hypertrophy

• Pulmonary valve stenosis- restricts flow to lungs
• increase right ventricle pressure and right ventricle hypertrophies
• increase pressure R to L
• Unoxygenated lood R to L ventricular flow
• Pulmonary circulation decrease of unoxygenated blood
• systemic circulation receives larger amounts ofmixed blood
• results in cyanosis

• Heart is capable of generating its own action potiential.
• Cells in the heart are able to helpit produce faster impulses, synchronised contrations and normal rhythm

• Sinoartial node (SA)- pacemaker, sinus rhythm
• internodal pathways
• AV node- floor of right atrium
• AV bundle (bundle of HIS) right and left
• purkinje fibres- terminal fibres
• 

• Na, Ca and K are major carriers in cardiac myocytes
• AP- resting (polaried), depolarized, repolarization
• Cardiac muscle has 3 types of ion channels
• AP of cardiac muscle has 5 phases

• K
• Na depolarisation
• K and Cl out- plateu
• Ca in causes repolarisation

Recording of theelectrical activity of the heart by plaing electrode onthe skin.

Depolarization of the atria (contraction)

Depolarization of the ventricles (Contraction)

• Repolarization of the ventricle
• relaxation

• Arrhythmias
• Dysrythmias

• Cardiac control centre- controls rate and force of contraction (medulla)
• Brapreceptors- detect changes in the blood pressure, located in the aorta and internal carotid arrteris
• sympathetic stimulation (cardiac accelerator nerve)
• Parasymp- decreases hear rate

• increase in thryoid hormones or rpinephrine
• elevated body temp
• increase envt temp
• exercise
• smoking
• stress
• preg
• pain

Deviations from normal rate- caused by damage to the hearts conduction sstem, electrolyte abnormalities, fever, hypoxia, stress, infection, drug toxicity

Supraventricular and ventricular

• reduction of the efficiency of the hearts pumping cycle.
• ECGs detect abnormalities

• Hear rate altered.
• Bradycardia- 60 beats/ min, regular but slow HR, results from vagal nerve PNS stimulation. Exception- athletes at rest have conditioned larger stroke volume.
• Tachycardia- 100-160 beats/ min, regular but rapid HR, normal response to SNS stimulation- exercise etc, compensation for decreased blood volume
• Sick sinus syndrome- HR irregularity, marked by altering bradycardia and tachycardia, often requires mechanical pacemaker.

• extra contraction or ectopic beats
• irritable artial muscle cells outside conduction pathway

• Rapid or irregular heart contractions
• caffeine, smoking or increase stress

• Premature atrial contractions or beats
• Palpitations
• Atrial flutter
• Atrial fibrillation

• atrial HR of 160 to 350 beats/ min
• AV nod delays conduction- ventricular rate is slower
• decrease in SV which results in pulse deficit could occur

Heart blocks

• first degree- partial block- condcution delay between atrial and ventricular contraction (PR interval)
• Second degree partial block- every second to third atrial beat is dropped at AV node i. e. missed ventricular contraction
• Third degree (total block)- no transmission of impulses form atria to ventricles

• Ventrilce contract spontaneously at a slow rate (30-45 beat/min)
• Independent of atrial contraction
• decrease cardiac output... light headedness, fainting (syncope)
• Results: stokes adams attack or cardiac arrest

• Temp pause in heart rhythm, pale/ flushing afterwards, light headedness, collapse
• 

• Bundle branch block
• Ventricular tachycardia
• Ventricular fibrillation
• Premature ventricular contractions (PVCs)

Interference with conduction in one of the bundle branches. wide QRS, cardiac output is unchanged

• Likely to reduce cardiac output as reduced diastoe occurs
• decrease filling time and force of contraction

• muscle fibres contract independently and rapidly
• uncoordinated quivering/ ineffective pump
• hypoxic myocardium
• cardiac standstill occurs if not treated immediately

additional beats from ventricular muscle cells or ectopic pacemaker. May lead to venticular fibrillartion- cardiac arrest

• Cause needs to be determined and treated:
• defective conductive system
• electrolyte abnormalities- K and Na
• drug toxicity
• Anti dysrythmic drugs are effective in many cases:
• iebeta blokers- metoprol,atenolo
• calcium channel blockers- verapamil
• digoxin

• SA node problems or a total heart block
• defibrillator may be needed to be used/ implanted for conservation of ventricular fibrillation, back to sinus rhythm

• Cessation of heart activity- no conduction of impulses- no cardiac output
• FlatECG (O2 deprivation to brain and heart)- loss of consciousness, no respiration- no pulse

• Excessive vagal nerve stimulation
• insufficient oxygen
• potassium imbalance
• Cardiogenic shocl
• Drug toxicity
• Respiratory arrest
• blow to heart

heart is unable to pump outsufficient blood to meet metabolic demands of the body.

• Forward effects
• Backup effects

• Cardiac output/ stroke volume decreases:
• - less blood reaches the various organs iekidney
• - decreased cell function
• - fatigue and lethargy
• - mild acidosis develops

• backup/ congestion develops
• output from ventricle isless than the inflow of blood
• congestion in venous circulation draining into the affeced side of the heart.

• usually a complication of another cardio-pulmonary condition
• may present as an acute episode, but is usually chronic
• Various compesation mechanisms maintain ccardiac output-often some aggravate the condition

• from a problem in the heart- infarction, congenital heart defect, valve changes
• may be a result of an increase in demand on the heart- hypertension, pulmonary disease, leading to either left orright sided heart failure
• coronary artery disease is the leading cause of CHF

• 1. thichekendleft ventricle wall
• 2 thickened right ventricle wall

• Sympathetic nervous system activity:
• mainttains perfusion of various body organs, increases in HR and contractility and regulation of vascular tone, increase in peripheral resistance and vasoconstriciton.
• But the increase in HR- decreases the efficiency causing increases in workload. Ventricle wall stress- dilation= hypertrophy can = ischemia
• Renin-angiotensin-aldosteron secretions:
• decrease CO = reduced renal blod which increases renin- angio which increases aldosteron secretion that increases vasoconstricition and sodium and water retention therefore increases blood volume.
• But vasoconstricition increases afterload and increases blood volume increases preload = hard work for heart.

• Hypertension/ aortic valve stenosis and LV infarction
• Back upof blood into pulmonary vein, high pressure of blood in lungs, decreased CO, left V weak can cant empty, decrease in renal blood flow.

• Pulmonary disease/ valve stenosis RV infarction:
• right ventricle weak and cant empty
• decrease CO
• dereased renal flow
• increase in venous pressure can cause eema in legs etc
• backup of blood into systemic circulation
• very high venous pressure causes distended neck vein and cerebral edema.

• similar with failure on either side:
• decrease blood supply to tissues, general hypoxia
• Fatigue and weakness
• Dyspnes and shortness of breath

• tachycarida
• cutaneous and visceral vasoconstriction
• Daytime oliguria (low output of urine)

• Are related to pulmonary congestion
• dyspnea and orthopnea- develops as fluid accumulates in the lungs
• cough-fluid irriating the respiratory
• Paroxysmal nocturnal dyspnea- indicates the presence of acute pulmonary edema, usually develops during sleep, hemoptysis and rales
• excessive fluid in lungs lead to infection

• are related to systemic congestions
• dependent edema in feet, leg or but, increase pressure in jugular veins
• Hepatomegaly and splenomegaly0 digestive disturbances
• Ascites- complcation when fluid accumulates in the peritoneal cavity- abdominal distention
• Acute rightsided failure- flushed face, distended neck veins, headache, visual distrubances

• reduce workload on the heart
• Maintian a healthy diet- low sodium and cholesterol
• Drugs

• often secondary to congenital heart disease
• feeding difficulties first sign
• short sleep periods
• tripod position to play
• cough, grunting respirtaion, wheezing
• radiographsshow cardionegaly
• arterial blood gases used to measure hypoxia

• General term for all types of arterial changes
• degenerative changes in small arteries and arterioles
• loss of elasticity
• Lumen gradually narrows and may become obstructed
• cause of increase blood pressure

• denoted by the presence of an atheroma in walls of large arteries
• plaques consisting of lipids, calcium, cell debris
• thrombi often attach
• throught to result from epithelial cell injury
• many risk factors

attached to proteins- apolipoprotens proteins that bind lipids to form lipoproteins

• low density lipoprotein
• involved in transpot of cholesterol from liver to cells
• major factor contributing to atheroma formation

• high density lipoprotein
• involved in transport of cholesterol away from the peripheral cells to liver
• Once in the liver the lipoprotein is catabolised and excreted

• initiates from artery endothelial tissue injury:
• - migration of inflammatory cells
• - increase c- reactive protein
• - white blood cells
• lipids accumulate in intima (iner lining) and media (muscle layer)
• smooth muscle cells proliferate/ multiply leading to plaque formation
• platelets adhere to the inner surface of arterial wall leading to further inflammation
• thrombus- partial obstruction- embolus
• weakened wall and risk of aneurysm

• Multifactorial:
• - non modifiable- age, gender, family history, genetics
• - modifiable- obesity, high cholesterol diet, high LDL, smaking, low LDL, promotes platelet adhesion, increase in vascular tone
• sedentary lifestyle- obesity high BP
• Hypertension- high BP- endothelial damage
• Diatets mellitus- increase lipid levels, endothelial degeneration
• Hyperhomocysteine- folate and B6 deficiency
• COmbination of the above

• Lifestyle changes
• Mdication- lipid reducing drugs, antihypertensive drugs, anticoagulants
• Surery- percutaneous transluminal coronary angioplasty, leser angioplasty, stent

• Peripheral arteris
• aorta- aneurysm- occlusion, rupture and hemorrhage
• Legs- iliac arteris- peripheral vascular disease- gangrene and amputation

• Dilation and weaking of a blood vessle
• Abd and thoracic aorta most common
• saccular, fusiform and dissecting shapes
• caused by atheroma, defect in the medial layer, trauma or infection
• over time the dilaion increases, throbi develop, may rupture causing hemorrhage

• COnsequence of atherosclerosis- partial or total occlusion- relative ishemia- impaired mm function/ activity and sensory function
• increasing fatigue and weakness in the legs
• pain associated with exercise due to mm ischemia- intermittent claudication- anaerobic build up of lactiv acid activating nociceptors
• peripheral nerve dsfunction- lack of oxygen supple to nerve tissue- tingle, numbness
• pulse distal to occlusion becomes weak
• appearance of the skin of the feet and legs change
• loos of blood means necrosis, ulcers, gangrene

• Thrombus formation in the vein
• standing or sitting for long periods of time
• restrictive clothes
• trauma, inflammation
• increased blod coagulation
• lack of blood movements- blood clot
• embolus- pulmonary embolism

Weakness or defect in vein wall or valve

• Persistent elevated BP
• there are three categories- primary, secondary and malignant.

• BP constantly over 140/90
• increase in arteriolar vasoconstricition- results in increase in total peripheral resistance and shuting of blood centrally, increasing diastolic pressure
• over long period of time- damage to arterial walls: atheroma or aneurysm
• Blood supply to involved area is reduced- ischemia and necrosis

• Results from renal or endocrine disease, or pheochromocytoma (benign tumor of the adrenal medulla)
• underlying roblemmust be treat to reduce BP

• Uncontrollable, severre, rapidly progressive form with many complications
• Diastolic pressure is extremely high

• areas:
• kidneys
• heart
• brain
• retina

• increase incidence with age
• men more frequent and severe
• incidence in women increases after middle age
• genetics
• sodium and alcohol leaves
• obesity
• smokng
• prolonged or recurrent stress

• Supply heart with oxygen- 60-80% the heart extracts- no reserve
• need to increase their bloodflow to meet demands during increased activity.
• - autoregulatory mechanism
• change in vessle tone
• vasoactive mediators - vaso con/dia andpot, adenosine, nitric acid and endothelins

• Coronary artery disease
• leading cause of death world wide
• due to imparied coronary blood flow- ischemic heart disease
• artherosclerosis most common cause
• Include:
• - angina pectoris (temporary ischemic heart disease)
• - myocardail infarction/ Heart attack

Chect pain that is due to an imbalancebetween hearts O2 and demand ischemia

• Classic/exerctional/ stable
• Unstable/crescendo
• - prolonged pain
• - break in atheroma

• increase demand on heart eg exercise
• obstruction by atherosclerosis
• vasospasm in coronary arteries
• myocarial hypertrophy
• severe anaemia
• respiratory disease
• tachycardia
• hypertension (increase force of contraction)

coronary artery is conpletely obstructed (prolonged ischemia)

atherosclerosis usually with thrombosis attached

• Size and location of infarct
• Most common is theleft ventricle and all three layer of the heart

• Becomes necrotic and inflammed, cell destruction resleases enzymes into tissue
• area of necrosis is replaced by fibrotic (non contractile tissue)- which blocks the electical conduction of the heart! Cardiac dysrhythmias

• ZOnes of infarction:
• - irreversible damage to myocardium, eletrically dead
• Zone of injury:
• - surrounds area of infarction
• - blood supply decreases
• - myocardium never completely polarises
• Zone of ischemia:
• - surroundsare of injry
• - reversible damage
• impaired repolaristaion
• 

• sudden pain in chest, left arm, shoulder, jaw, neck- cannot aleviate with rest or vasodilators
• Pallor, diaphoresis, nausea, dizziness
• dyspnea
• anxiety and fear
• hypotension
• low CO, shock

• Sudden death- due to arrhythmia and fibrillation
• cardiogenic shock- due to impaired cardiac function, decreases pumping capability of the heart
• Congestive heart failure- due to reduced contractility of ventricles, left or right sided

• Rupture of necrotic heart tissue/ cardiac tamponade- build up of fluid in the pericardium, compresses heart-decrease CO
• thromboembolism causing cerebrovascular accident (with left ventricular MI)- due to thrombus dveloping over the infarted surface.

• a hypotensive event
• not a specific disease but a syndrome

• low cardiac output
• decrease in circulating blood volume
• decreased tissue perfusion
• general hypoxia and reduced nutirents to cells
• organ dysfunction and failure

• los of circulating blood
• inability of heart to pump
• changes in peripheral resistance

• BP= CO x PR
• CO= HR x SV

• Hypovolemic shock
• Cardiogenic shock
• Distributive or Vasogenic shock
• Subcategories:
• - Neurogenic
• - Anaphylactic
• - Septic

• - Loss of circulating blod volume (whole blood, plasma)
• - due to hemorrhage, burns, peritonitis, dehydration
• - Acute loss of 15-20% of blood

• - inability of heart to maintain cardiac output to circulation (failure of left ventricle)
• - Due to MI, arrhymias, congenital heart defects
• - Cardiac tamponade, pulmonary embolus

• - loss of blood vessel tone- vasodilation
• - normal volume of blood doesn't fill the circulatory system ie the capacity of the vascular compartment expands

• - involvement of the nervous system
• - sympathectic acitity decreases- decreased peripheral resistance, shunting of blood to the periphery, reduction of cardiac return
• - metabolic dysfunction- severe acidosis- vasodilation

• results from an immunologically mediated reaction
• - release of histamine- vasodilation and increased capillary permeability and other symptoms

• systemic response to severe infection
• - toxins released by fungi or bacteria (mainly gram negative endotoxins) may cause tissue damage
• - inflammatory response vasodilation