Acute myocardial ischaemia
Lernkarten zu PACT
Lernkarten zu PACT
Wie wirken Glycoprotein IIb/IIIa inhibitoren?
Vorteile?
Wann verwendet?
Welche?
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).
Wie kann hohe Blutungsgefahr durch Kombi UFH/GPIIb/IIIa vermindert werden?
Durch Ersatz mit Bivalirudin.
Ruptur einer freien Ventrikelwand:
Wann? 2
Wer besonders?
Wann hohes Risiko?
Management?
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
Symptome der Ventrikelseptum-Ruptur?
5
Kardiogener Schock
Pansystolisches Geräusch
Schwirren über der Brustwand
Links-Rechts-Shunt (Anstieg der SvO2 von rechtem Vorhof zum rechten Ventrikel)
V-Wellen im PAC
Therapie bei akutem VSD? 4
OP innerhalb der nächsten 48h
Senken der Nachlast mit Nitro
Vasoaktiva
IABP
Akute Mitralinsuffizienz woher?
Klinik?
Tritt wann auf?
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).
Mitralklappenprolaps:
Klinik?
Therapie? 4
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.
Differentialdiagnosen supravetr. Tachykardien und Kennzeichen?
5
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
Klinische Zeichen Rechtsherzinfarkt?
EKG?
PAC?
Echo?
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
Supportive Therapie bei RV-Infarkt?
CAVE?
(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.
Warum keine Nitrate bei RV-Ischämie?
Reduziert Preload und infolge Cardiac output
Definition des kardiogenen Schocks? Klinisch und hämodynamisch
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)
Intiale behandlung des kardiogenen Schocks?
7
- 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.
Nachteil von Dobutamin im Schock?
Macht Hypotonie durch Vasodilatation->auf Volämie achten!
Wie wirkt Milrinon?
Nachteile?
Wann eingesetzt?Wie eingesetzt?
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.
Wie wirkt Levosimendan?
Vorteil?
CAVE?
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.
3 Vorteile von Noradrenalin/Norpeinephrin?
vasoconstrictor, has a mild inotropic effect, and increases coronary flow
Wirkungen von Nitroglycerin?
4
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
Vorteile IABP? 4
Aber?
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.
Wie lange sollte Clopidgrel bei drug eluting stent gegeben werden?
Mindestens für 1 Jahr!
Was ist der Bezold-Jarisch-Reflex?
Wird wodurch verstärkt?
eine plötzliche, rasche Unterversorgung des Herzens mit Sauerstoff führen zu einer Stimulierung von Rezeptoren im Ventrikelmyokard -> Vasodilatation der Herzkranzgefäße -> Herabsetzung von Blutdruck und Herzfrequenz und senkt damit den Sauerstoffbedarf des Herzens-> kardioprotektiv
Nitroglycerin-Gabe verstärkt Effekt
Welches Medikament soll neben MONA bei STEMI und NSTEMI noch gegeben werden?
Wirkt wie?
Welche Dosierung?
Clopdiogrel (Thienopyridin): Hemmt ADP-Rezeptor auf Thrombozyten, 300-600mg präklinisch
Prasugrel (Theinopyridin, Efient): idem
Welche MI-Patienten werden als high risk betrachtet?
4
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%)
Was sagt ein 3.Herzton bei Myokardinfarkt aus?
Wo zu auskultieren? Hört sich wie an?
= 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
Was sagt 4.Herzton aus?
tieffrequenter leiser Vorhoffton vom dem 1.HT, rel. selten bei erhöhtem Ventrikeldruck
Welche Rhythmusstörungen verschlechtern Prognose bei MI?
AV-Block bei inferiorem Infarkt
LSB bei anteriorem Infarkt (RIVA)
ST-Hebung II, III, aVF?
Lokalisation? Gefäss?
Inferior
RCA (Right coronary artery) or posterolateral branch of Cx (Circumflex Coronary Artery;)
V2, V3, V4?
Anterior
LAD or Diagonal branch of LAD(=RIVA)
I, aVL, V5, V6
Lateral
Cx
Tall R wave in V1
True Posterior
Posterolateral branch of Cx or Posterior Descending Branch of RCA
V1–V3
Septal
LAD or Diagonal branch of LAD
I, aVL, V2–V6
Anterolateral
Proximal LAD
II, III, aVF, I, aVL, V5, V6
Inferolateral
Proximal Cx or large RCA in right dominant system
V3R, V4R?
Right Ventricular
RCA
Woran erkennt man vertauschte Elektroden der oberen Extremitäten? 2
neg. P in I, QRS-komplex in I ist invertiert und anders als im Vgl. zu V6
Zeichen der Perikarditis? 2
ST-Hebungen nicht zu einem Areal passend
PR-Strecken-Senkungen!
Wie sieht Takotsubo-Myopathie im EKG aus?
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.
Unterschied NSTEMI, akuter Myokardinfarkt und instable AP?
ACS
Wodurch kann NSTEMI und instabile AP ausgelöst werden?
4
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).
Ursachen für kardiogenen Schock?
6
- 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.
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- 1 / 52
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Lernkarten
Was ist der Bezold-Jarisch-Reflex?
Wird wodurch verstärkt?
eine plötzliche, rasche Unterversorgung des Herzens mit Sauerstoff führen zu einer Stimulierung von Rezeptoren im Ventrikelmyokard -> Vasodilatation der Herzkranzgefäße -> Herabsetzung von Blutdruck und Herzfrequenz und senkt damit den Sauerstoffbedarf des Herzens-> kardioprotektiv
Nitroglycerin-Gabe verstärkt Effekt
Welches Medikament soll neben MONA bei STEMI und NSTEMI noch gegeben werden?
Wirkt wie?
Welche Dosierung?
Clopdiogrel (Thienopyridin): Hemmt ADP-Rezeptor auf Thrombozyten, 300-600mg präklinisch
Prasugrel (Theinopyridin, Efient): idem
Welche MI-Patienten werden als high risk betrachtet?
4
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%)
Was sagt ein 3.Herzton bei Myokardinfarkt aus?
Wo zu auskultieren? Hört sich wie an?
= 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
Was sagt 4.Herzton aus?
tieffrequenter leiser Vorhoffton vom dem 1.HT, rel. selten bei erhöhtem Ventrikeldruck
Welche Rhythmusstörungen verschlechtern Prognose bei MI?
AV-Block bei inferiorem Infarkt
LSB bei anteriorem Infarkt (RIVA)
ST-Hebung II, III, aVF?
Lokalisation? Gefäss?
Inferior
RCA (Right coronary artery) or posterolateral branch of Cx (Circumflex Coronary Artery;)
V2, V3, V4?
Anterior
LAD or Diagonal branch of LAD(=RIVA)
I, aVL, V5, V6
Lateral
Cx
Tall R wave in V1
True Posterior
Posterolateral branch of Cx or Posterior Descending Branch of RCA
V1–V3
Septal
LAD or Diagonal branch of LAD
I, aVL, V2–V6
Anterolateral
Proximal LAD
II, III, aVF, I, aVL, V5, V6
Inferolateral
Proximal Cx or large RCA in right dominant system
V3R, V4R?
Right Ventricular
RCA
Woran erkennt man vertauschte Elektroden der oberen Extremitäten? 2
neg. P in I, QRS-komplex in I ist invertiert und anders als im Vgl. zu V6
Zeichen der Perikarditis? 2
ST-Hebungen nicht zu einem Areal passend
PR-Strecken-Senkungen!
Wie sieht Takotsubo-Myopathie im EKG aus?
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.
Unterschied NSTEMI, akuter Myokardinfarkt und instable AP?
ACS
Wodurch kann NSTEMI und instabile AP ausgelöst werden?
4
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).
Ursachen für kardiogenen Schock?
6
- 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.
Abwärtsspirale des kadiogenen Schocks?
Cardiogenic shock may complicate myocardial infarction – remember the vicious cycle of cardiogenic shock
Indikationen für Reperfusionstherapie?
Symptombeginn <12 h und:
Was sagt die TIMI-Klassifikation aus?
Die TIMI-Klassifikation dient der klinischen Beurteilung der Durchblutung der Herzkranzgefäße(Koronardurchblutung), die im Rahmen einer Koronarangiografie erfasst wird
- 0: Keine Perfusion. KM kommt nicht über Stenose hinweg
- 1: Penetration ohne Perfusion: kommt über Verschluss bleibt aber dort liegen
- 2: Partielle Perfusion.
- 3: Vollständige Perfusion.
In welchen Situationen ist PCI klar im Vorteil (Level 1 Empfehlung)?
4
- Contraindications to thrombolytic therapy
- Cardiogenic shock
- Severe heart failure
- Haemodynamically significant ventricular arrhythmias
In welchen Situationen kann PCI von Vorteil sein?
4
- Elderly patients (age >75 years)
- Large anterior infarction
- Prior myocardial infarction or prior coronary artery bypass grafting
- High bleeding risk
Welche Risiken hat PCI alleine?
Was ist besser?
Aber?
- risk of abrupt vessel closure
- recurrent in-hospital ischaemia
- reocclusion of the infarct-related artery and
- restenosis.
Coronary stenting has been shown to be superior to balloon angioplasty for these outcomes when done electively.
In ST elevation myocardial infarction, however, early trials did not demonstrate that primary stenting was superior to primary balloon angioplasty.
How does the time from symptom onset to treatment (fibrinolytic therapy) influence survival?
within 0–6 hours of onset: saves approximately 30 lives per 1000 patients treated
within 7–12 hours, 20 lives per 1000 patients treated.
beyond 12 hours may be considered for thrombolysis on a case-by-case basis.
Maximal benefit is seen if administered within 60 minutes of onset.
Fibrinolytikum der 1.Generation?
Funktioniert wie?
Nachteil?
streptokinase induce a lytic state by generating plasmin and are considered 'non-specific'.
The most devastating complication, intracranial haemorrhage, occurs in about 0.6% of patients. Anaphylaxis is rare but can be troublesome.
Neuere Fibrinolytika?
Woher?
Vorteil gegenüber 1.Generation?
Wann mehr Hämorrhagien?
engineered from tissue plasminogen activator (tPA), a naturally occurring substance produced by endothelium. Alteplase (recombinant tissue-type plasminogen activator, rt-PA) is less antigenic than streptokinase and acts more directly at the fibrin surface. Weight-adjusted,‘accelerated’ regimens of tPA produce better vessel patency rates than SK.
These agents have slightly higher risk of intracranial haemorrhage, particularly in patients older than 75 and when GP IIb/IIIa agents are used.
Weitere Fibrinolytika?
2
Vorteile?
newer agents that may not require weight-based dosing, and have longer half-lives, allowing for bolus injection-> simplification of drug administration.
Reteplase (r-PA) is given in two boluses 30 minutes apart
Tenecteplase (TNK-tPA), is given as a single bolus.
Absolute Kontraindikationen für Lyse? 5
Absolute
Previous haemorrhagic stroke
Other stroke or cerebrovascular accident ≤6 months
Intracranial neoplasm
Active internal bleeding ≤2 weeks (menses excluded)
Aortic dissection, known or suspected
Wirkungsweise von Bivalirudin?
2 pharmakokinetische Vorteile?
Indikation?
Vorteil gegenüber Heparin?
=Angiox(R), direct thrombin inhibitor
short half-life; no need for monitoring the therapeutic range;
indications for ACS patients (NSTEMI and STEMI) undergoing angiography and PCI due to similar efficacy, but fewer bleeding events compared with UFH or enoxaparin
Wie wirken Glycoprotein IIb/IIIa inhibitoren?
Vorteile?
Wann verwendet?
Welche?
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).
Wie kann hohe Blutungsgefahr durch Kombi UFH/GPIIb/IIIa vermindert werden?
Durch Ersatz mit Bivalirudin.
Ruptur einer freien Ventrikelwand:
Wann? 2
Wer besonders?
Wann hohes Risiko?
Management?
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
Symptome der Ventrikelseptum-Ruptur?
5
Kardiogener Schock
Pansystolisches Geräusch
Schwirren über der Brustwand
Links-Rechts-Shunt (Anstieg der SvO2 von rechtem Vorhof zum rechten Ventrikel)
V-Wellen im PAC
Therapie bei akutem VSD? 4
OP innerhalb der nächsten 48h
Senken der Nachlast mit Nitro
Vasoaktiva
IABP
Akute Mitralinsuffizienz woher?
Klinik?
Tritt wann auf?
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).
Mitralklappenprolaps:
Klinik?
Therapie? 4
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.
Differentialdiagnosen supravetr. Tachykardien und Kennzeichen?
5
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
