Pathophysiology

cardiac function alteration (cardiogenic shock), decrease in blood volume, excessive vasodilation or obstruction of blood flowthrough circulatory system

Results in hypopferfusion and insufficient O2 supply of tissues and organs. Increased sympathetic outflow and stimulated adrenergic receptors results in epinephrina nd norepinephrin release (increased heart rate (beta1 receptors) and vasoconstriction (alpha receptors)).
Renin increase -> aldosteron -> results in water and sodium retention.

Compensatroy mech. are not effective over longterm and become more destructive. Vasoconstriction -> less perfusion -> lactid acid and radicals accumulation -> cell death

Decreased SV and CO -> thus insufficient perfusion to meet cellular demands

CO decreases because of decreased contractility and a increased afterload (due to vasoconstriction) and excessive preload (blood that has not been pumped out before)

Hypoperfusion and hypotension (but pre-shock state can occure with normal blood pressure).
Lips, nails and skin may be blue-ish due to slow blood flow, decreased blood pressure, lower urine output

It is when the heart can not be filled with adequate blood due to an accute loss of blood 15-20%

SV falls but arterial pressure is maintained (symphatetic activation) due to higher HR and vasoconstriction.
Water and sotium retention starts and the hypothalamus signals thirst as compensatroy mechanism

Depend on severity. Closely relatet to low blood flow and excessive stimulation of CNS. Thirs, increased HR, cool and clammy skin, decreased urine output.

Severe shock can lead to altered mental activity, loss of consciousness and comma

Vasodilatory shock is characterized by displacement of vascular volume away from heart.

A decrease in sympathetic control or a excessive release of vasodilators can be a result

It is a immunologically mediated reaction where vasodilators are released (allergy).

Medications, food and venoms can cause it

Cramps, anxiety, warm and burning sensation of skin, itching, coughing, choking, wheezing, dificculty breathing.
drop in blood pressure, and pulse becomes weak.

Most common type of vasodilator shock. Proven infection plus ystemic inflammatory response such as fever, tachycardia

It is a systemic response to an infection. 

Complex process of cellular activation which releases cytokines, neutrophils and monocytes (pro-inflammatory).
Activated neutrophils injure endothelium by releasing mediators that increase vascular permeability and this releases vasodilators
Increase in pro-coagulation factors which can lead to formation of thrombi

hypotension and warm flushed ski. decreased vascular resistance.
fever and behavioural changes due to reduced cerebral bloodflow. tissue hypoxia (too little O2) further activates inflammatory mediators

Infection of inner heart surface due to microbial agend that destroys underlying cardiacc tissue.

Mitral valve prolapse ("falling down"), inherited heart diseases, prostetic valves and other implanted devices (pacemaker).
Staphylococcal infections or Strepococci

Endothelial injury, bacterias and altered hemodynamics result in thrombus along endothelial lining. Bacteries cause monocyte activation and cytokine production -> enlargement of infected valve.

Potentially destructive lesions form on heart valves which eventually cause destruction of valve or cause emboly

Fever (because of infection), heart murmur/sound due to defective valve, cough, dyspnea (pulmonary emboly).

heart failure can develop, coronary artery embolism or myocarditis

Inflammatory procces off the pericardium ("herzbeutel").
Acute pericaditis is a inflammation of less than 2 weeks and occurs as primary or as a result of a systemic disease
Constrictive pericarditis the walls become to stiff (thickend and fibrotic)

Viral infections (most common) or microbial infection. Connective tissue damage, urea in blood, radiation, trau,a, drug toxicity and inflammatary process of myocardium or lungs after surgery

Increased capillary permeability. Allowing plasma proteins to leaave capillaries and enter pericardium. Fibring containing fluid that is supposed to heal progresses to scar tissue and forms adhesion between layers (what it should not do)

Chest pain, friction rub (can be heared and seen in ECG).

Pain is usually abrupt and sharp and may radiate to back, neck and sides. Typically worse when deep breathing, coughing, swallowing

cardiac surgery or infection

Fibrous, calcified scar tissue develepbs between the parietal layers of pericardium. Scar tissue contracts and interferes with diastolic filling and Cardiac output. Cardiac reserves become fixed.

Equalization of end-dyastolic pressure in all four chambers

Abnormal fluid biuldup in abdomen or edemas in lower legs. Dispnea and fatiue.
Exercise intolerance and muscle wasting

A group of diseases of the myocardium. Usually mechanical or/and electrical dysfunction tha tlead to inapropriate ventricular hypertrophy or dilation.
Often a genetic cause.

Primary (confined to myocardium) and secondary (variety of systemic disorders)

Alcohol abouse (dilated cardiomyopathy), genetic and non genetic, inflammatory processes (e.g. myocarditis)

Different on where it occurs. Can dilate certain chambers, lead to hyperthropy. Can also cause an enlargement of total heart-mass, flabby walls or wall thinning.

Persistent venous hypertension on the structure of venous system (often the lower extremities)

Prolonged standing, incompetent valves in veines, deep vein obstructions or decreased skeletal muscle pump function are reasons

unidirectional flow or emptying of deep vains can not occur. Blood flows back. Veins and surrounding tissue exposed to high pressure

Tissue congestion, edema or impairment of tissue nutrition.Necrosis (cell death) and pigmentation of skin color (brown) due to breakdown or RBC. Thin skin due to necrosis -> irregularly pigmented skin.

Stiffening of lymp channels and joints as well as loss of muscle mass/strength.

Thrombus in mostly lower extremities (deep veins) that can lead to embolism (mostly pulmonary) and chroniv venous insufficiency.

Decreased blood flow (bed rest/immobilitzation) increase risk (hip fracture, joint replacement,...). Impaired cardiac function and age are also risk factors. 

A state where the formation of bloodcloths is increased (and therefore als Deep vein Thrombosis). Can be caused by genes or plasma proteins that normaly inhibit thrombus formation.

Loss of blood leads to an increase in clotting factors

Asymptomatic (as long as cloth does not fully occlude).

Symptoms are related to inflammatory process (pain, swelling, fever, WBC increase,..)

PQRST waves.
P: Atrial depolarization (atrial systole)
QRS: Ventricular depolarization (ventricular systole) and atrial repolarisation (atriyl diastole, is overruled)
T: Ventricular repolarization (ventricular diastole)

P-Q: AV-node delay

Sinus node arrythmias: Sinus Bradycardia (slower), Sinus pause or Arrest, Sinus Tachycardia

Atrial arrythmias: Premature atrial conduction, atrial tachycardia, atrial flutter, atrial fibrilation

Ventricular arrhytmias: premature ventricular contractoin, ventircular tachycardia, ventricular flutter and fibrillation