Acute myocardial ischaemia

override the platelet activation caused by plasminogen activators

improving patency rates and allowing better reperfusion of small vessels beyond the occluding thrombus.

They may have a role in STEMI when acute interventions such as percutaneous transluminal coronary angioplasty (PCI) and coronary artery stenting are performed (ADMIRAL, and ACE).

Most of the data, however, predate use of dual-antiplatelet therapy, and the role of GP IIb/IIIa receptor antagonists in combination with other antiplatelet and anticoagulation regimens is still being defined.

Mainly useful for high risk patients undergoing PCI

Currently available GP IIb/IIIa receptor antagonists are abciximab(Reopro), tirofiban(Aggrastat) and eptifibatide(Integrilin).

Durch Ersatz mit Bivalirudin.

during the first week after infarction, with one peak around 24 hours and a second peak at 3–5 days

The classic patient is an elderly female with chronic hypertension, presenting with a first infarction.

 thrombolytics given later than 14 hours after infarction may actually increase that risk.

 is possible with prompt recognition, pericardio-centesis, and surgical repair. Emergent echocardiography or right heart catheterisation can help make the diagnosis 

Kardiogener Schock

Pansystolisches Geräusch

Schwirren über der Brustwand

Links-Rechts-Shunt (Anstieg der SvO2 von rechtem Vorhof zum rechten Ventrikel)

V-Wellen im PAC

OP innerhalb der nächsten 48h

Senken der Nachlast mit Nitro

Vasoaktiva

IABP

Papillary muscle dysfunction

Holosystolikum über Mitralareal

It is commonly due to ischaemia or infarction of the posterior papillary muscle, which has a single blood supply (usually from the posterior descending branch of a dominant RCA).

presents dramatically with pulmonary oedema, hypotension, and cardiogenic shock. 

• Afterload reduction with nitroprusside
• Intra-aortic balloon counterpulsation pump (IABP)
• Inotropes or vasopressors if cardiac output or blood pressure is inadequate.

Definitive therapy is surgical valve repair or replacement, which should be undertaken as soon as possible, since clinical deterioration can be sudden.

sinus tachycardia

AVNRT: P-Welle nach QRS-Komplex und RP-Abstand NICHT fixiert

atrial tachycardia

orthodromic atrio-ventricular reentrant tachycardia (AVRT), involving retrograde conduction over a "concealed" bypass tract: P-Welle nach QRS-Komplex und RP-Abstand fixiert

atrial flutter with 2:1 block: zusätzliche P-Wellen, die nicht übergekeitet werden

Halsvenenstauung ohne Lungenödem

Zeichen der inferioren Ischämie + ST-Strecken-Hebung in V4R

PAC: elevated right atrial and right ventricular end-diastolic pressures with normal to low PAOP and low cardiac output

Echo: depressed right ventricular contractility

(Haupttherapie ist PCI)

vorsichtige Volumengabe, evtl. Dobutamin und Vaopressoren (Myokardperfusion)

Es gibt Fälle, in denen Volumengabe zu Überfüllung des rechten Ventrikels und im Anschluss zu Kompromittierung des Linken Ventrikels und damit zu fehlender Verbesserung des cardiac output führt.

Reduziert Preload und infolge Cardiac output

Klinisch:

decreased cardiac output and evidence of tissue hypoxia in the presence of adequate intravascular volume

haemodynamically: hypotension (SBP <90 mmHg for at least 30 minutes) and a reduced cardiac index (<2.2 l/min/m²) in the presence of elevated pulmonary capillary wedge pressure (>15–18 mmHg) (These numbers must however be considered on an individual basis and may be modified by interventions)

•  intubation and mechanical ventilation early
• Correct electrolyte abnormalities and reduce excess sympathetic activity by relieving pain and anxiety with cautious amounts of opiates.
• Arrhythmias and heart block can decrease cardiac output and should be corrected promptly with anti-arrhythmic drugs, cardioversion or pacing.
• Commonly used secondary treatments such as nitrates, β-blockers and ACE inhibitors may exacerbate hypotension in cardiogenic shock and are best withheld until the patient stabilises.
• adequate blood pressure, tissue perfusion should be assessed.
• If tissue perfusion remains inadequate, inotropic support or intra-aortic balloon pumping should be initiated. With significant pulmonary congestion diuretics may be employed.
• Vasodilators (such as sodium nitroprusside) can be utilised with strict haemodynamic monitoring in an attempt to improve myocardial efficiency.

Macht Hypotonie durch Vasodilatation->auf Volämie achten!

phosphodiesterase inhibitor: increases intracellular cyclic AMP by mechanisms not involving adrenergic receptors

less prominent chronotropic and arrhythmogenic effects compared to catecholamines.

has a potential to cause hypotension and has a long half-life;

in patients with tenuous clinical status, its use is often reserved for situations in which other agents have proven ineffective. Milrinone is started without a bolus in this setting, and sometimes adjunctive vasopressor support is required.

Levosimendan, a calcium sensitizer, has both inotropic and vasodilatory properties, and does not increase myocardial oxygen consumption.

Several relatively small studies have shown haemodynamic benefits with levosimendan in cardiogenic shock after MI, but survival benefits with use of levosimendan have not been shown in either cardiogenic shock or acute heart failure.

Levosimendan has the potential to cause hypotension and thus should be used with caution in patients with cardiogenic shock.

vasoconstrictor, has a mild inotropic effect, and increases coronary flow

is an effective venodilator

reduces the pulmonary capillary occlusion pressure

can decrease ischaemia by reducing left ventricular filling pressure

redistributing coronary blood flow to the ischaemic zone

reduces systolic afterload

augments diastolic perfusion pressure

improving cardiac output and coronary blood flow.

without an increase in oxygen demand.

IABP alone does not increase survival, but is an essential support mechanism to allow definitive therapeutic measures to be undertaken.

Mindestens für 1 Jahr!

Clopdiogrel (Thienopyridin): Hemmt ADP-Rezeptor auf Thrombozyten, 300-600mg präklinisch

Prasugrel (Theinopyridin, Efient): idem

presentation in congestive heart failure

haemodynamic criteria (SBP <100 mmHg, HR >100 bpm)

size of infarction (anterior ST elevation >2 mm in two or more contiguous leads

RV involvement, or LV dysfunction (EF <35%)

= diastolische ventrikuläre Füllungstöne

bei Kindern und Jugendlichen physiologisch

different tieffrequenter leiser Ton über der Mitralisregion nach dem 2.HT als Ausdruck eines "diastolic overloading" bei Mitralinsuffizienz,Herzinsuffizienz und Hyperthyreose

tieffrequenter leiser Vorhoffton vom dem 1.HT, rel. selten bei erhöhtem Ventrikeldruck

AV-Block bei inferiorem Infarkt

LSB bei anteriorem Infarkt (RIVA)

Inferior

RCA (Right coronary artery) or posterolateral branch of Cx (Circumflex Coronary Artery;)

Anterior

LAD or Diagonal branch of LAD(=RIVA)

Lateral

Cx

True Posterior

Posterolateral branch of Cx or Posterior Descending Branch of RCA

Septal

LAD or Diagonal branch of LAD

Anterolateral

Proximal LAD

Inferolateral

Proximal Cx or large RCA in right dominant system

Right Ventricular

RCA

neg. P in I, QRS-komplex in I ist invertiert und anders als im Vgl. zu V6

ST-Hebungen nicht zu einem Areal passend

PR-Strecken-Senkungen!

mild ST-segment elevation, which occurs in approximately 50% to 60% of patients. It is typically present in the precordial leads, but the ECG can be normal or can show nonspecific T-wave abnormality or major ST elevation across the precordial and limb leads. In general, the 12-lead ECG alone is not helpful in differentiating ABS from an ST-elevation myocardial infarction.

ACS

NSTEMI and Unstable Angina are usually caused by an imbalance between myocardial oxygen supply and demand, which may be due to one or more of the following causes:

• Non-occlusive thrombus developing on a pre-existing plaque (the most frequent cause). Arterial inflammation or infection can predispose to plaque rupture.
• Dynamic obstruction – spasm of an epicardial artery or intramural vasoconstriction.
• Progressive coronary narrowing without spasm or thrombus. May be due to progressive atherosclerosis or restenosis after a PCI.
• Secondary UA (‘demand ischaemia’). Patients with chronic atherosclerotic narrowing are subjected to increased myocardial oxygen demand (fever, tachycardia) or reduced oxygen delivery (hypotension, anaemia).

• 74.5% had predominant left ventricular failure
• 8.3% acute mitral regurgitation
• 4.6% ventricular septal rupture
• 3.4% isolated right ventricular shock
• 1.7% tamponade or cardiac rupture and
• 8% had other causes.