Cardiology

Diseases of the pericardium

Pericarditis
Inflammation of the parietal and visceral layer of the pericardium; common
infarcted heart muscle affected by inflammation (perimyocarditis)

Classification
acute
chronic (>3 months)
pathogenic-constrictive
70-90% idiopathic/viral, 30% with complicated course

acute

chronic

Etiopathogenesis
Acute Pericarditis
Dry fibrinous form
2. Moist exudative form
fibrinous exudate, effusion with serous, hemorrhagic, purulent
chylous fluid (risk of cardiac tamponade)

Chronic Pericarditis
Granulation tissue and fibrous transformation of the pericardial layers
Chronic effusions only lead to symptoms at a volume of about 300 ml.
It can also develop without a preceding pericarditis.

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Pathophysiology and clinic resemble acute pericarditis
Clinic
Fever, myalgias (especially infectious origin)
Retrosternal pain radiating to the neck and left arm (especially acute)
History)
Weakness, dyspnea, tachypnea, upper abdominal discomfort (pericardial effusion)
Shock, low blood pressure, tachycardia (pericardial tamponade)

Chronic pericarditis is often oligo- or asymptomatic.

Diagnostics
Systolic or systolic-diastolic proximal scraping noise
Character
When transitioning from the dry to the exudative form, heart sounds become quieter.

Labor values
leukocytosis
oBSG ↑
↑
oCK-MB, Troponin

EKG
Acute course: Concave upward ST segment elevation Lifting
out of "S" and not out of "R" as with myocardial infarction
Chronic course: terminal negative T-wave
In case of pronounced pericardial effusion low voltage

X-ray of the chest: In case of large pericardial effusion, the heart shadow is enlarged.

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Differential diagnoses

Unstable angina pectoris, heart failure, pulmonary embolism, pneumothorax,

Aortic aneurysm, pleuritis, esophageal process

Therapy

Basic therapy
Ibuprofen (at 3 weeks) + proton pump inhibitors
Colchicine 4 months (chronic pericarditis 6 months)

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Cardiac tamponade/Pericardial effusion
Restriction of diastolic filling of the ventricles due to a
Fluid accumulation (e.g. blood, exudate) in the pericardium

Etiopathogenesis
Pericarditis, myocardial rupture due to infarction, trauma, dissecting aortic aneurysms,
Neoplasms
Due to impaired diastolic ventricular filling, blood backs up in the right heart,
Ejector performance reduced; compensation through frequency increase, later
Blood pressure drop

Complications
Acute shortness of breath, tachycardia, dizziness, retrosternal pain, syncope
Risk of cardiogenic shock

Diagnostics
1. Pulsus paradoxus: Abnormal drop in systolic pressure during inspiration by >10
mmHg
2. Venous Congestion
Oprall filled tongue base and jugular veins
Kussmaul sign: Venous pressure rises inspiratorily rather than falling
3. Arterial Hypotension

ECG
Soft heart sounds
Low voltage (with pronounced pericardial effusion)
Echocardiography: Most sensitive method for displaying small effusions from 40 ml

Labor
Hemorrhagic effusion: Blood count, coagulation parameters
Unclear effusion cause: Diagnostic puncture point

Differential diagnoses
Volumenmangelschock, Herzinsuffizienz, Panzerherz, Spannungspneumothorax,
Asthma attack

Therapy
Pericardiocentesis
Pericardial window: unsuccessful aspiration, recurrent effusion formation

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Chronic constrictive pericarditis
Fibrosis of the pericardium with/without calcification or thickening caused
Impairment of diastolic filling

Aethopathogenesis
Due to bacterial and parasitic infections and after
Radiation influences
Pericardial fibrosis thickened and often calcified, myocardium usually atrophic
Concrete: Adhesion of both pericardia
Accreto: Connective tissue connection of the pericardium with neighboring organs
Panzerheart: In cases of severe calcification
Obstruction of the right ventricle resulting in increased pressure in it
right atrium and venous system

Clinic
Fatigue, reduced performance, shortness of breath, upper abdominal discomfort
Venous congestion: neck veins, liver enlargement, ascites, peripheral edema,
Congestive proteinuria
In the case of prolonged congestion, congestive liver cirrhosis and nephrotic syndrome occur.
Syndrome

Diagnostics
Galapporhythmus with additional protodiastolic sound
Increased heart rate, paradoxical pulse (30%)

ECG
Low voltage, non-specific T-wave negativity, pre-excitation (40%)
Impairment of ventricular relaxation
Echocardiography: Pericardial fibrosis and calcifications often visible

X-ray of the chest: heart normal, superior vena cava enlarged, calcifications
CT/MRI: Diffuse pericardial changes are well represented.

Differential diagnoses
Restrictive cardiomyopathy, hemochromatosis

Therapy
Relief through decortication or pericardiectomy
Should be carried out before myocardial atrophy occurs.

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Diseases of the endocardium
Rheumatic fever
β
It arises due to an autoimmune reaction after infection with -hemolysing.
Streptococci
Inflammatory systemic disease that mainly affects the heart, joints, CNS and
Skin manifests

Aetopathogenesis
M-Proteins induce the formation of antibodies that are associated with streptococci.
Myocardial antigens cross-react
Cross-reacting antibodies against antigens of the caudate nucleus and
subthalamic
Immune complexes (Type III reactions) on capillaries as well as on heart valves
Formation of a pancarditis with endo-, myo- and pericardium, in the myocardium Aschoff-
Knot detectable
Verrucous endocarditis with fibrotic valve thickening, adhesions,
Shrinking sail and shortening of the chordae tendineae
Valvular stenoses and insufficiencies, especially at the mitral and
Aortic valve
Serofibrinous pericarditis, exudative inflammation in joints
Subcutaneous with rheumatic nodules

Clinic

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Diagnostics
According to the Jones criteria, rheumatic fever is likely if there are 2 major...
the main and 2 secondary criteria are met

Auscultation
Systolic (relative mitral insufficiency)
basal diastolic (relative aortic insufficiency)
Labor
oBSG ↑
oAntistreptolysin O/L-Titer ↑
deoxyribonucleotidase titer ↑
ECG
Prolonged PQ interval
oST-Track Elevation
Echocardiography: Valve changes, ventricular dilation, pericardial effusion

Differential diagnosis
Arthritis, Collagenoses

Therapy
Penicillin
Nonsteroidal anti-inflammatory drugs
Steroid

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Infective endocarditis
Most bacterial inflammation of the endocardium; usually involves heart valves;
Distinction between acute and subacute form (endocarditis lenta)

Etiopathogenesis
∝hemolytic streptococci (50%)
Staphylococci (40%)
Enterococci, gram-negative bacteria, fungi (10%)

20%

Frequently predisposed cardiac lesions; sterile endothelium defects occur

Vegetations from platelets, which are colonized after bacteremia with pathogens
to become
Embolisms often originate from flap vegetation, often there is glomerular
(Löhlein)-stove-nephritis

Link heart inflammation: 80-90%

Right-sided endocarditis: 5-10%

Clinic
Fatigue, sweating, tachycardia, chills, arthralgias
Weight loss, fever
Frequent heart murmur auscultation
Splenomegaly, Petechiae, Osler nodes, Splinter hemorrhages, Janeway lesions
Lesions, microemboli
Hematuria, Proteinuria

Diagnostics
Labor findings
oBSG-/CRP ↑
Leukocytosis
Normochromic anemia, proteinuria, hematuria
real focus is found in only 50% of cases
ECG: No specific ECG signs
Echocardiography
Frequent flap changes detected after vegetation.
Transesophageal echocardiography (TTE)
Transesophageal echocardiography (TEE)

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Differential diagnosis
Infectious and immunological diseases as well as neoplasms

2 main criteria define definitive endocarditis

Therapy
Streptococci: Penicillin
Amoxicillin, Ampicillin
Staphylococci: Isoxazolyl-Penicillin
Rare pathogens: Penicillins, Cephalosporins, Aminoglycosides, Ciprofloxacin

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Cardiomyopathies
Independent disease of the heart muscle that is not due to ischemia, valvular defects,
arterial hypertension, congenital vitium or pericardial diseases attributed to
can become

WHO
1. Dilatation
2. Hypertrophy
3. Restrictive
4. Arrhythmogenic right ventricular
5. Not classifiable

Or

Primary/idiopathic: The pathological process affects exclusively the myocardium and not
Heart valves, coronary vessels or other cardiac structures
Secondary/specific: Represents myocardial manifestations of an underlying condition.

Dilated cardiomyopathy (Most common form)

By enlargement and systolic dysfunction of the left or both
Heart chamber characterized
Most common indication for heart transplantation

Aetiopathogenesis
Primary form occurs in 10% of cases, with 30% occurring in secondary forms.
Forms of familial inflammatory or toxic causes indicated

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Clinic
Initial symptom: dyspnea, as an expression of left heart failure, progressing to acute
Pulmonary edema can progress
Right heart failure: leg swelling, anasarca, hepatosplenomegaly, ascites
Chest pain due to pulmonary embolisms
General inflammation: Insufficient perfusion of the skeletal muscles
Dizziness, presyncope, consciousness disorders
Cardiac arrhythmias, angina pectoris
Late symptoms: Systemic and pulmonary embolisms due to
Thrombus formation

Diagnostics
Resting tachycardia
Heart enlargement (chest wall pulsations)
Systolic blood pressure low with reduced stroke volume
Jugular vein distension with prominent a and v waves as a sign of
Tricuspid insufficiency
3. And 4. Heart tones usually audible
Annular dilation-related mitral and tricuspid insufficiency

ECG: No specific ECG changes, but frequently:

oLink strut block
oSinus tachycardia
Supraventricular and ventricular tachycardias
oVorho fflimmern

X-ray of the chest

Cardiomegaly (heart diameter exceeds 50% of)
thoracic transverse diameter
Reduction of the retrosternal space (right ventricular involvement)
Secondary signs of heart failure: pulmonary congestion, interstitial
Pulmonary edema
Alveolar pulmonary edema (pulmonary capillary pressure exceeds 25 mmHg for
longer time
Chronic form
oKerley-B-Lines: Dense horizontal stripes in the right lower field
Kerley A lines: Interlobar lines in the upper lung field

Echocardiography
Left ventricular emphasized dilation
Globally reduced systolic function
Doppler sonographic
Insufficiency
Diastolic ventricular dysfunction
Cardiac catheterization: End-diastolic left ventricular pulmonary arterial pressure
increased

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Therapy
Basic therapy
ACE inhibitor, βblocker
Diuretic, Aldosterone antagonists
Angiotensin-1 receptor antagonists
Oral anticoagulants (coumarin derivatives)

BVS transplantation
Medication-resistant, symptomatic heart failure in NYHA stages
III and IV
O-link limb block (QRS >130 ms)
Left ventricular end-diastolic diameter >55 mm
oEjection fraction <35%
Echocardiographically asynchronous ventricular contraction

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Hypertrophic Cardiomyopathy (HCM)
Ventricular hypertrophy without adequate hemodynamic stress, which
predominantly left ventricle concern
During systole, there can be dynamic obstruction with the formation of
Pressure gradients come

Hypertrophic obstructive cardiomyopathy (HOCM)

2. Hypertrophic non-obstructive cardiomyopathy (HCNM)

Etiopathogenesis
Autosomal-dominant inherited

Histologically
ofocal scars
Narrowing of the intramural coronary vessels
Disorganization of muscle cell arrangement
Macroscopic (according to Maron)
Type I: Isolated hypertrophy of the ventricular septum
Type II: Entire septum and parts of the adjacent anterior or
rear wall
Type III: Entire left ventricular myocardium including all
Wand parts
Type IV: Hypertrophy of the anterior or posterior wall segments under
Exclusion of the septum

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Clinic
Exertional angina, dyspnea, fatigue, dizziness,
Presyncope, syncope, ventricular fibrillation

Obstructed left ventricular outflow tract Systolic function ↓

Disrupted relaxation and filling Ejection volume ↓
Discrepancy between vascular density and tissue Regional ischemia

Diagnostics
Systolic jet noise over the Erb point during Valsalva maneuver

Echocardiography
Evidence of regional hypertrophy of the left ventricular myocardium under
Emphasis on the septum
EKG, unspecific; frequent:
Global or septal conditioned hypertrophy
Supraventricular or ventricular arrhythmias
oST track subsidence, T-negativations

Intraventricular pressure gradient increases in

physical stress
Digitalization
Other therapy with sympathomimetics
Arterial hypertension
Valsalva maneuver
Therapy
β -Blocker (Metoprolol, Propranolol), Verapamil

Transcoronary Ablation of Septal Hypertrophy (TASH)

Therapy of choice in HCM
Through balloon catheter injected pure alcohol infarcts areas of the septum,
Septal mass and obstruction of the left ventricular outflow tract increase.
ab
Occurrence of an AV block (20-30%)

Endocardial Radiofrequency Ablation of Septal Hypertrophy (ERASH)

Electric energy using a heart catheter in the obstruction area at
given off from the right ventricular septum
Scarring leads to a decrease in the gradient in
left ventricular outflow tract
No routine procedures in clinical practice

Operative Therapy
Myotomy (Myectomy)
Dissection of the papillary muscle
Mitral valve replacement

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Restrictive Cardiomyopathy (RCM)
Functionally reduced compliance of both ventricles is normal.
systolic filling characterized

Etiopathogenesis
Primary RCM
Idiopathic RCM
Endomyocardial fibrosis
. Tropical endomyocardial fibrosis Various
. Hypereosinophilia Syndrome (Löffler Endocarditis) Manifestations of the same

2. Secondary RCM
Infiltrative Diseases
storage diseases

Phases
Eosinophilic Myocarditis
2. Unspecific myocardial thickening and endocardial thrombus formation with
partition obliteration
Endomyocardial Fibrosis

Through endocardial scarring increased stiffness and worsened diastolic

Filling of both ventricles
Increase of the right and left ventricular filling pressures

Clinic
Depending on the primarily affected ventricles, symptoms of the left dominate.
right heart failure

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Diagnostics
Jugular vein distension
3rd and 4th heart tones
Kussmaul sign

Echocardiography
Small, possibly thickened heart chambers with significantly dilated atria
In endomyocardial fibrosis, connective tissue thickening

Doppler ultrasound
Pathological filling behavior of the ventricle

Cardiac catheterization
Increased diastolic pressures in the right and left ventricle ('dip-plateau-
Phenomenon

Therapy
Diuretic
β Blocker
Residual substances
In Löffler's endocarditis, additionally cortisol.

Operative excision of the thickened endocardium Choice of therapy

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Arrhythmogenic right ventricular cardiomyopathy (ARVC)
Progressive, localized or generalized degeneration and breakdown of
Heart muscle cells of the right ventricle with subsequent replacement by fat or
Connective tissue characterized

Aetiopathogenesis
Genetic defect leads to replacement of the myocardium with fat and connective tissue; mostly on the right.
Affected ventricles

Clinic
Syncope
Ventricular tachycardias
Sudden cardiac death

Diagnostics
ECG
Inversion of the T-waves in the right precordial leads (V 1-V3)ohnedas
a right angle block is present
oEpsilon wave: Small electrical potential at the end of the QRS complex
or at the beginning of the ST segment (highly specific, 30%)
Echocardiography: Right ventricle often dilated and hypokinetic

Differential diagnoses
Uhl's disease

Therapy
Sotalol
Implantation of an ICR

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Myocarditis
Through infectious, immunological, chemical-toxic, or physical causes
induced inflammation of the myocardium
Inflammatory process can affect myocytes, the interstitium, and vascular components.
If the pericardium is also affected, it is referred to as perimyocarditis.

Etiopathogenesis
Coxsackie virus type B most common triggers; lymphocytic infiltrates and damaged
Myocytes are a prerequisite for unequivocal detection.

Clinic
Nonspecific: Thoracic pain, sense of pressure
Extrasystoles
Cardinal symptoms: Lethargic for a long time,
Dyspnea, heart palpitations
cardiac insufficiency, pericarditis
Reizer manifestations, cardiac rhythm disturbances

Diagnosis
Sinus tachycardia
Heart failure: Congestion signs in basal lung sections, leg edema
Systolic sound: Signs of mitral or tricuspid insufficiency

ECG, Non-specific:
Passage changes in the ST segment and T wave
Temporarily occurring Q waves
Atrial and ventricular arrhythmias
Echocardiographic
Not specific: More frequent left ventricular dysfunction than right ventricular
segmental wall motion abnormalities
MRT
oGoldstandard: Can ventricular dysfunction and regional
Represent movement disorders; focal/regional myocardial edema vs.
diffuses/globals
Labor
Detection of virus antibodies in blood, stool, throat swab from
Myocard biopsy brings nothing, not even autoantibodies.

Therapy
Support: Trust, 6 months no sports, monitoring, oxygen supply,
Analgesic, medication therapy for heart failure, insertion of an ICD or
Of West
New therapeutic approaches
oVirus status, Interferon, Immunosuppressants, Immunoadsorption of IgG-
Immunoglobulins

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 ≥
Symptomatic Patent1 Diagnostic Criterion

≥ criterion
Asymptomatic patent diagnosis
Coronary heart disease
Angina pectoris
Forms
Stable Angina pectoris
2. Unstable Angina Pectoris: Gradual transition to acute coronary syndrome
3. Rest Angina
4. Prinzmetal Angina: Caused by coronary spasms
5. Cold Angina
6. Post-infarction angina: Occurrence within 2 weeks after an incident.
Infarct
7. Silent coronary ischemia: For the patent asymptomatic coronary ischemia before
all in diabetics and older patients
8. Atypical Angina: Occurrence of left thoracic pain independent of exertion,

spontaneous sisters

Clinic

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Diagnostics
Labor parameter
oCK/CK-MB
Troponin I, T
An increase in CK/CK-MB or troponins can also occur in myocarditis or
Pulmonary embolism occurs
Resting ECG: Not suitable for diagnosing CAD (50% ECG normal)
Stress ECG
Horizontal or descending ST segment ≥ depression of 0.1 mV, measured

80 mV after the J-point

oST track ≥
lifting 0.1 mV

Echocardiography
Heart size, left ventricular function and wall motion as well as consequences of
KHK representable
With stress echocardiography, stress-induced
Myocardial ischemias are presented as wall motion abnormalities.
MRT
ECG-triggered can heart function, wall movements, myocardial
Perfusion and myocardial vitality should be assessed.
Stress MRI with Dobutamine or Adenosine reaches as an invasive procedure
high sensitivity and specificity

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Therapy
β
-Receptor blocker

2. Nitrate
Every patient with angina pectoris should constantly have nitroglycerin spray or -
Carry capsules with you! If necessary: 2 doses or 1 capsule sublingually for
Anfal grouping
3. Calcium antagonists

4. ACE inhibitors and angiotensin receptor blockers

5. Platelet aggregation inhibition
oASS, Thienopyridine (e.g. Clopidogrel, Prasugrel)
Anticoagulation
Kumar derivatives (e.g. Phenprocoumon)
7. Other possibilities: Percutaneous coronary intervention (PCI), aortocoronary bypass
Operation

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Acute Coronary Syndrome: Unstable Angina Pectoris and Myocardial Infarction
Unstable Angina Pectoris: Within the last 48 hours, or new
occurred angina pectoris or significant worsening of a
stable angina pectoris
Acute coronary syndrome
NSTEMI: Increased cardiac necrosis parameters, ST-segment- without ST-elevations

Recessions and corresponding angiographic findings, but without ST- (NST-ACS)

Segment elevations in resting ECG

STEMI (syn. Myocardial infarction): Infarction signs like in NSTEMI and additionally ST-
Sticking-Lifts in Rest-EKG

Etiopathogenesis

Diagnostics
Physical examination
Due to sympathetic stimulation tachycardia, pale with moist, cold.
Extremities, pulse irregularities due to extrasystoles, blood pressure normal
increased
Hypotension due to left ventricular dysfunction (CAVE: shock),
Heart tune: 3rd or 4th heart tone
A loud, band-like, systolic sound can be found above the heart apex.
Expression of severe mitral valve insufficiency, must be at the break of a
Consider papillary muscle involvement in posterior wall infarction.

Auscultation of the lung

Pulmonary congestion: Fine crackling sounds (50%)
Pronounced left heart failure + consecutive pulmonary edema: "Bubbling"
"Cooking", bloody frothy sputum

STEMI
ECG changes STEMI
ST-route raises of 0.2
1. Stadium 0/Initial stadium mV (V1-V6)
"Suffocation-T" (T-wave significantly elevated and pointed) More than 0.1 mV in others
Derivatives
T-negation
Increase T-wave

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 ST track lowering

2. Stadium 1/Monophasic Deformation (after hours to days)

QRS complex, ST segment and T wave merge
ST-Elevation (about 1 minute after closure)

Stadium 2 (after weeks to months)

Pardeée-Q: At least 0.03 s duration
Depth: At least ¼ of the R-point

4. Stadium 3 (after weeks to months)

Pathological Q waves indicate a past myocardial infarction.
Not infrequently, the elevation of the T-wave is omitted, so that stage II persists.

The most serious consequence of HIV is chamber arrhythmia.

ECG changes in NSTEMI/ACS are less specific; it can lead to

Changes in the T-wave and ST-segment depressions occur
Differential diagnosis of the infarct ECG
Acute Pericarditis
Pericarditis
oST track uplift does not exceed 0.2 mV

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 o Departure of the ST line elevator from the ascending S-bend
Largely preserved R-spike

ST-segment elevations without infarct-typical chest pain

Aneurysm after infarction
O vagatonia
Asthenic body type
Left ventricular hypertrophy

Labor

Central anterior wall lead: V3, V4

Central Hinterwall leadings: II, III, aVF
Anterior wall infarction: I and aVL

In a STEM, an increase of the

Myocardial infarction specific biomarkers not
to be awaited; therapy is
to be adhered to immediately

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 In an ACS/NSTEMI, the biomarker increase aids in diagnostic confirmation.

Routine diagnostics: cTNT, cTNI, CK, CK-MB

Diagnosis of a myocardial infarction is confirmed when it is associated with typical clinical

Complaints of persistent ST segment elevations (STEMI) or to, increase of
Troponin levels above a defined threshold (NSTEMI) occur

Troponin T and I show the highest myocardium specificity compared to CK, LDH, and GOT.

Therapy
Preclinical therapy
Monitoring means 12-channel ECG
insertion of an intravenous access
Oxygen flow (2-4 l/min)
Upper body elevation (30°)

oNitrate: Sublingual in AP and systolic blood pressure >90 mmHg

Opioid sedation (opioid analgesics)
Heparin sedation, ASA

Inpatient therapy
STEMI
Thrombolysis: Only if there is no cardiac catheterization lab available within 120 minutes.
achievement must occur within 6 hours
Primary percutaneous coronary intervention (PCI): Possible within 2 hours, then
no lysis (gold standard)
Nitro: Not in case of wall infarction; dilation of the veins. venous pooling
Preload reduction

2. NSTEMI
Patents with high risk:
oASS, Prasugrel, Ticagrelor
oPCI
Low-risk patents
β
oNitrate, -receptors
oASS, Prasugrel, Ticagrelor
Ischemia diagnostics

Maintenance therapy
oASS
oACE-Hemer
o β Blocker
oCSE-Hemmer

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Heart failure
Functional disorder of the heart with reduced cardiac output, resulting in
Blood circulation to all organs is not ensured at rest as well as during exertion.

Etiopathogenesis
Mainly caused by coronary artery disease and hypertension

Left heart insufficiency

Primary: Left ventricular myocardial disease (e.g. cardiomyopathy,
Myocardial infarction
Secondary: valve changes in the left heart, aortic coarctation,
Pressure increase large circuit
With every second pump function of the left ventricle received

right heart failure

Increased lung resistance (Cor pulmonale, primary pulmonary hypertension)
Valve changes of the right heart
oVolume load with shunt fittings
Failure of compensation mechanisms in left heart failure

Disorders of systolic or myocardial function

Regional or globally reduced contractility with low stroke volume

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Clinic
When typical symptoms (dyspnea, exercise insufficiency, fluid retention)
to stop
Disorders of diastolic myocardial filling
Relaxation disorder: restriction of stroke volume due to deterioration
Filling of the ventricle
Ventricular filling depends on atrial contraction, in the healthy this only happens
1/3 out

HFrEF: 50% heart failure SV reduced in both cases

H

FpEF

Pathophysiology
Primary compensation mechanisms
Intravascular volume exposure utilizing the Frank-Starling mechanism
An insufficient heart cannot increase preload but requires optimal conditions.
Stroke volume higher filling pressure
Mobilization of myocardial contractile reserve
Contractility is increased through catecholamines; shift of the Frank-
Starling curve at higher stroke volumes
Peripheral vasoconstriction with increased afterload
Myocardial Hypertrophy
Eccentric Hypertrophy: Volume load, dilation of the ventricle,
moderate wall thickness increase
Concentric Hypertrophy: Pressure load, pronounced
Wall thickness increase, relative reduction of ventricular space
Result: Constant ventricular wall tension maintained, however no
Increase of capillary density

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Secondary compensation mechanisms
Centralization: Activation of the Autonomous Nervous System
First phase heart failure: No secretion of norepinephrine, but of
ANF

RAAS

Failure of the primary and secondary compensation mechanisms

↓
Sensitivity of atrial stretch receptors (chronic stimulation)
Vasoconstriction ↑
oADH secretin ↑Hyponatremia, peripheral resistance ↑
Disruption of renal perfusion
oRAAS ↑
Release of prostaglandins Sympathetic nervous ↑ , system of the ↑
RAAS
"Ciculus vitosus": Increased peripheral resistance After load ↑
Stroke volume ↓
End-stage heart failure
oNA mirror↑
o β 1Recipe density ↓ Heart performance ↓
oADH ↑ ↓

Clinic
Backward failure (Increased ventricular filling pressure), 'Low-output-
Syndrome/Forward Failure

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Diagnostics
Left heart failure
Left heart: Backflow of blood into lung vessels (pulmonary venous hypertension)
Pulmonary pressure in sitting is lower: Patients often can only with several pillows.
sleep under the head
Pulmonary edema: Pulmonary pressure >20-25 mmHg
harsh, coarse rattling noises, coughing up blood-stained
frothy secretion
Cardiac asthma: Edema of the bronchial mucosa can lead to
Bronchial constriction with "wheezing" leads to
Fine bubbling rattling sounds: Over both lung fields; Blood plasma tritin
Alveoli about
Relative mitral insufficiency: Due to annular dilation, due to the
Enlarged heart

Right heart failure

Congestive symptoms venous system: Obligatory ankle and lower leg edema
those that arise during the day and are absorbed overnight
Extreme case: Anasarca, jugular vein congestion
Pleural effusion
Hepatosplenomegaly, Ascites
Loss of appetite, cachexia
Pre-renal proteinuria: Expression of congestive kidney

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Therapy

Important
There is no medication that improves the prognosis of dilated heart failure.
Beta-Blocker
2. ACE-Inhibitor
3. Spironolactone (only for EF <35%)
In case of symptomatic heart failure, still Furosemide.

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Syncope
Transient loss of consciousness due to transient global cerebral
Hypoperfusion is characterized by rapid onset and spontaneous,
complete recovery

In the stress ECG, looking for signs of cardiac ischemia.

oHorizontal ST-Section Subsidence
Ascendierende ST-segment senkungen (NOT pathological)
Descending ST segment depressions
No longer primarily gold standard, but stress cardiography or MRI
with adenosing application
Bilateral carotid artery stenosis Unlikely
Subclavian steal syndrome In the context of leg strain
Aortic valve stenosis Was excluded
VHF Rather unlikely
Which medications may potentially lead to syncope during treatment?
antiarrhythmics
antihistamines QT extension
Neuroleptic
antibiotic

Tachycardia rhythm disturbances such as VES with R on T phenomenon can lead to

Syncope leads

But also bradycardic heart rhythm disorders AV blocks

Especially the AV block is challenged in tachycardic situations.

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Arterial hypertension
≥
Elevated blood pressure at rest 140/90 mmHg

Disruption of the control loop (BD = TPW x HZV)

oTPW: ↑
oHZV:, ↓ n

Classification
Primary hypertension
2. Secondary hypertension (known underlying disease)

Aetiopathogenesis
Long-term adaptation of the body
Hypertrophy: Maintenance of normal pump function
Hypertrophy of resistance vessels
Resetting threshold of the baroreceptors
Pressure natriuresis despite renal autoregulation
Dysregulation of sympathetic nerve activity in the kidney: pressure natriuresis through
increased sympathetic activity pathologically influences sodium excretion
reduced

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Heart

Left ventricular hypertrophy and insufficiency

The heart compensates for increased pressure with concentric hypertrophy.
This can lead to relative coronary insufficiency and eventual eccentric
Hypertrophy with left heart failure develops

Coronary heart disease

It arises from atherosclerosis of the epicardial intramural coronary vessels.

kidney
Microalbuminuria: Due to a generally initially discreet endothelial damage
Terminal kidney failure: Intrarenal pressure overload leads to glomerular disturbance
and nephrosclerosis

Brain
Transient ischemic
Attack (TIA)
cerebral infarction
Hypertensive mass bleeding

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 Acute hypertension encephalopathy

Eye
Due to hypertension-related arteriosclerosis, renal vessels are damaged (fundus
hypertonic

Medication Therapy
DASH diet (max. 4 g salt/day)
Monotherapy (only 5% reduction): No longer recommended

Combination therapy: ACE inhibitors better than AT1Antagonists

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Shock
Inadequate blood flow in peripheral tissues, caused by too low
Stroke volume or redistribution of peripheral blood flow occur
Frequent: Oliguria and hypotension, reduced tissue perfusion (increase in lactate)
Occurrence of circulatory failure and the lack of therapy leading to multiple organ failure
irreversible damage

Aetiopathogenesis
1. Reduction of intravascular fluid volume (e.g. hypovolemic shock)
2. Acute impairment of cardiac pump function (e.g. cardiogenic shock)
3. Change in vessel volume (e.g. vasodilatory or septic shock)

Clinic
Hypotension, tachycardia, decreased skin turgor, pallor, cool sweaty skin

Labor
Blood gases: Initially respiratory alkalosis, then metabolic acidosis
Laboratory chemistry: lactate, renal retention values, shock mediators, calcitonin
DIC: Imbalance of coagulation and lysis

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Arrhythmias
Summarize all cardiac 'excitation processes' that differ from the normal sinus rhythm.
deviate

Bradycardia:<60 beats/min
Tachycardia: >100 beats/min
Asystole: Pauses of more than 3 seconds

Bradycardia

Sick Sinus Syndrome

Symptomatic sinus bradycardia
Sinoatrial arrest or SA block
Tachycardia-Bradycardia Syndrome

Aetiology
oKHK, myocarditis, cardiomyopathy, M. Lenegre, M. Lev, mutation of
Sodium and Funny Ion Channels

Clinic
Dizziness, syncope
Possible Adams-Stokes attacks
oPalpipatonen, heart failure
Dyspnea, angina pectoris

Diagnostics
chronotropic incompetence in the stress test
In Atropintest no adequate frequency increase.
After rapid atrial stimulation, prolonged sinus node recovery time

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Carotid Sinus Syndrome
Etiology
Cerebral hypoperfusion due to bradycardia and/or a
Blood pressure drop in hyperreactive carotid sinus reflex
Increased sensitivity of the baroreceptors in the carotid sinus, usually as a result of
arteriosclerotic changes in older patients

Clinic: Dizziness, possibly syncope when turning the head or with a constricting collar

Diagnosis: In the ECG pause >3s (asystole) or blood pressure drop >50 mmHg after
Carotid sinus massage

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AV blockages
Etiology
Often: Fibrous irritative conduction system or acute myocardial infarction
Rarely: Antiarrhythmics, cardiac glycosides, electrolyte shifts,
structural heart diseases
AV blockages of I and II degrees type I also in adolescents and athletes
observed
High-grade AV blockages are diseases of the elderly.

Diagnostics
oAV-Block I. Grades
. Each P wave is followed by a QRS complex; PQ interval longer than 0.2 s
AV Block II. Type I (Wenckebach or Mobitz I)
. PQ time extends with each heart beat until an AV conduction
is canceled
oAV-Block II. Type II grades (Mobitz II)
β
. Causes: Posterior wall infarction, -Blocker intoxication, Amiodarone
Electrolyte disorders (Hyperkalemia)
. Intermittent blockage of the AV conduction; PQ time not
extended
. More P-waves than QRS complexes seen
oAV-Block III. Grades
. Complete blockage of the AV node conduction; there is a
Asystole, biventricular replacement center heart excited
. The atrium and ventricle contract independently of each other.

AV blocks PQ time
I° Constant
II° Type I Inconsistent
II° Type II Constant
Third Inconsistent

Constant AV Block II° Type II, AV Block I°

As soon as a P wave is found in the chambers without conduction, it must be
to deal with a second-degree AV block type II

Inconsistent AV Block II° Type I, AV Block III°.

If you find a changing PQ time, you only need to look for a
Searching for Wenckebach periodicity (PQ interval becomes longer until finally the P wave)
is no longer conducted and thus QRS fails)
Therapy
oSchritmacher
. AV Block III
. AV Block II° Type II
. AV Block II° Type I (In case of complaints)

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 Asymptomatic patients with congenital AV block III°, AV block II° type I, AV-
Block I.°needs no step maker
Intraventricular blockages
Interruptions or slowing of the excitatory conduction in Tawara branches

Aetiology
Right bundle branch block is found in healthy hearts or right heart overload,
Left anterior hemiblock is common in older patients.

Diagnostic
The myocardium must rely on the special conduction system instead of
Myocardial cells are excited
Widespread QRS complex; complete bundle branch block at >0.12

Right bundle branch block

QRS duration ≥ 120 s
oRR-Configuration in V 1, partly also in V2(M-Configuration)

link arm block

QRS duration≥ 120 ms
Positive monophasic QRS complex in V5-V6, I partly also in aVL

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 O negative QRS complex in V1-V3

Supraventricular arrhythmias
Supraventricular extrasystoles (SVES)
Spontaneous, premature excitations occurring in the atrial myocardium, AV node, or rarely
also arise in the sinus node (polytopic, monotopic)

Aetiology
often associated with structural heart diseases; common causes are
Infections, inflammations, ischemias, high blood pressure or stimulants

Clinic: Asymptomatic or causes palpitations

Diagnostics
Interruption of the current rhythm by prematurely occurring P-
Either by a break
oP-Welle leather extrasytole easily deformed, depending on the place of origin in some
Derivatives also negative

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Atrial flutter
Atrial frequency of 250-350/min; circulating excitation in the right atrium, which
follows defined track
Counterclockwise rotation;

Etology
oStress alcohol and coffee consumption, organic heart diseases, rarely
Thyrotoxicosis, pulmonary embolism, chest trauma, peri-/myocarditis, congenital
Heart diseases, diphtheria, digitalis intoxication

Clinic
o2:1 or 3:1 AV conductions are usually well tolerated
Atrial cycle lengths >300 ms can lead to 1:1 conduction and decompensation.
lead

Diagnostic
Overhoff frequency 240-300/min
Flatter waves, P-waves are most clearly seen in limb leads.
P-wave is usually negative in leads II, III, and aVF.
frequent sawtooth pattern

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Atrial fibrillation
Unorganized atrial depolarization without effective atrial contraction
irregular AV conduction

Aetiology
Most common heart rhythm disorder, usually an organic disease is underlying.
Frequency of excitations mostly above 300 beats/min

Clinic
Symptoms (heart palpitations, dizziness, shortness of breath) depend on the presence
structural heart diseases as well as the type of conduction and
resulting chamber frequency from
Risk of an arterial embolism generated from the atrium (brain)
particularly increased at the end of the hallway

Diagnosis
Flimmer waves: trembling of the baseline with low amplitude, no P-
More waves recognizable
oRR intervals of different lengths

AV node reentry tachycardias (AVNRT)

Excitation circulates in the AV node, leading to rapid, regular depolarization.
the atria and ventricles

Etiology
Digitalis intoxication, rheumatic heart diseases, cardiomyopathies

Clinic: Palpitations, anxiety, nervousness, fear, presyncope, shock

Slow-fast-Typ (orthodromic AVNRT)

Excitation travels over a slow pathway towards the ventricles and returns retrograde.
about rapid rail to forecourts
Atria and ventricles are excited simultaneously; P wave disappears under
QRS complex

Fast-slow-Typ (atrioventricular nodal reentrant tachycardia)

Antegrade excitation in a rapid pathway and retrograde propagation in
slower train
Circumscribed excitation reaches the atria significantly later via slow pathways than
Ventricle, so that P wave appears after QRS complex

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AV reentry tachycardia (AVRT)
Electrical coupling of the atria and ventricles through accessory
Conduits
Compared to the AV node, AL has faster conduction properties and
longer refractory period

Aetiology: AL are remnants of the embryological atrioventricular duct.

Clinic: Sudden heartbeat, fainting possible during rapid conduction

Diagnosis
oAntdrome AVRT
. Tachycardia with regular RR intervals
. Delta wave
. Wide QRS complex
Orthodrome AVRT
. Tachycardia with regular RR intervals
. P waves appear behind the QRS complex (excitation of the atria over
accessory railway
. No Delta wave
. Narrow QRS complex

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Ventricular arrhythmias
Every arrhythmia with QRS complex width >120 ms is until proven otherwise
Conversely, a ventricular tachycardia or extrasystole and thus potentially
life-threatening

Ventricular extrasystoles (VES)

Early occurring, additional heart tones that arise in the excitatory conduction system.
in the Tawara branches or in the ventricular myocardium

Aetiology
In most heart-healthy individuals (no increased mortality); after a heart attack (80%)
Heart insufficiency (increased mortality)

Clinic
often asymptomatic incidental findings; can lead to palpitations or at
Heart insufficiency leads to hemodynamic deterioration.

Diagnostic
Broadening, deformed QRS complex (excitation spread occurs
not over His bundle and Tawara legs)
The RR interval between the last heart cycle and extrasystole is shortened;
compensatory break (exception: interposed VES)
Normal heart rate after VES occurs after two RR intervals after the last one.
normal heart rate; no P-wave before extrasystole

Ventricular Tachycardia (VT)

If more than six ventricular extrasystoles occur in a row

Aetiology: Mostly a consequence of chronic ischemic heart diseases

Clinic
Significant symptoms such as palpitations, angina pectoris, dyspnea, dizziness,
sudden cardiac death, cardiogenic shock

Diagnostics
chamber frequency <250/min
oAV-Dissociation
QRS duration ≥ 140 ms
Common thigh block type configuration; LSB often at ectopic center
Outflow tract, RSB in ectopia in left-sided fascicles

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Torsades de pointes tachycardia
Special form of ventricular tachycardia, characterized by periodic onset and
The QRS complexes characterized by a descending line of the isoelectric line.

Etiology
oQT extension due to, for example, electrolyte disturbances, antiarrhythmics,
Phenothiazine, tricyclic antidepressants

Clinic: Recurrent presyncope and/or syncope

Diagnosis: Prolonged QT interval; abnormal T and U waves

Atrial flutter and atrial fibrillation

Chamber flutter: High-frequency chamber tachycardias in which no sharp
Separation between QRS complex and ST segment is possible (250-350/min)
Ventricular fibrillation: No coordinated de- and repolarization of the ventricles
identifiable (>350/min)

Aetiology
Patent mitral chronic ischemic heart disease or acute
Myocardial infarction; usually preceded by monomorphic VT

Clinic
Functional circulatory failure with loss of consciousness and possibly previously
Angina pectoris, dizziness and presyncope

Diagnostic
atrial fibrillation
. No regular excitation propagations
. Many local excitements, which can partly circulate, make
Pumping function of the ventricles impossible
. Heart muscle cells at different places simultaneously and
uncoordinated excited
. Tachycardia (>350/min)
. Individual QRS complexes can no longer be read.
. Wavy line with low, varying amplitude around
isoelectric line shifts
oChamberflattern
. Regular tachycardia, which still leads to a contraction of the heart
can lead
. Tachycardia (250-350/min)
. Intervals between complex regularities
. QRS complexes wide and deformed
. No ST track visible

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