Managing Right Ventricular Myocardial Infarction: A Prehospital Service Evaluation
By Mark Stanley
Edits by Prof Joanne Garside and Dr John Stephenson
Introduction
Traditionally, the focus of pre-hospital treatment of acute myocardial infarction is to reduce the impact on the left ventricle while customarily also, the impact on the right ventricle was largely unnoticed. Yet Cohen et al (1974) highlighted the express need for specifically tailored pre-hospital treatment for those with RMI. Jacobs et al. (2003) further argued two fundamental interventions of pre-hospital care namely, that morphine and nitrates should be avoided in RVMI pre-hospital care. Furthermore, that giving fluids for hypotension is essential to maintain cardiac preload.
RVMI is however, is a relative rarity occurring in less than 3% of all acute MIs. Nevertheless, RVMI have been found to occur in 30-50% of patients presenting with inferior wall MIs (IWMI) (Kakouros & Cokkinos, 2010) (Namana, et al., 2018).
Pathophysiology
The heart forms two pumps; the left ventricle, the high-pressure chamber, and the right ventricle, a low-pressure chamber sensitive to pre-load and after-load changes (Kelly & Cohen, 2008). Right ventricle myocardial damage causes reduced contractility, dilation, compliance and stroke volume, consequentially reducing left ventricular output (Pike, 2009; Kakouros & Cokkinos, 2010). Right ventricle dysfunction is predominantly influenced by venous volume and pressure to maintain adequate return, both of which can be compromised in RVMI (Garcia, 2015), reduction in either has a negative impact on cardiac output, resulting in complications such as hypotension and bradycardia.
Diagnosis of RVMI can be confirmed through clinical examination, the 12 lead Electrocardiograph (ECG), ultrasound and/or magnetic resonance imagining (MRI) (Kakouros & Cokkinos, 2010). In turn, inaccurate diagnosis of inferior MI with right ventricular involvement has a higher incidence of in-hospital short-term mortality (Pfisterer, 2003). More specifically, an IWMI patient with RVMI has a 17% mortality rate compared to inferior MI alone of only 6.3% (Inohara, Kohsaka, Fukuda, & Menon, 2013).
RVMI in-hospital management includes early recognition, early reperfusion, followed by (depending on size of MI), fluids for hypotension, inotropic support such as Dobutamine, while avoiding diuretics and nitrates (Namana et al., 2018; Kakouros & Cokkinos, 2010).
The aim of this service evaluation, therefore, was to identify factors associated with acute MI diagnosis and possible RVMI involvement, clinical interventions and pre-hospital complications.
Methods
Patient records and 12-lead ECGs were reviewed from September to December 2018. Approval was received from the Ambulance Trust and anonymity was ensured through redaction of identifiable features.
Data Collection
1) Diagnostic data: Patient care records were organised and grouped by anterior or inferior MI.
Within the inferior group, recognised as most often associated with possible RVMI/extension, STEMI anatomical territories were identified. RVMI/extension was also identified for each case utilising criteria for possible RVMI/extension diagnosis (Table 1).
ECG Criteria
|
Non-ECG Criteria
|
- IWMI & ST Elevation in lead III > ST Elevation lead II
- Equal or >1 mm of elevation in the Right chest leads (V3R to V6R)
- ST Elevation in V1 extending to V5 and V6.
- ST Depression in lead II unless ST Elevation extending to V5 and V6.
- ST Depression V2 cannot be more than half the ST elevation in aVF (< ½ = Inferior RVMI, > ½ = Inferior, RV and posterior a significant MI).
- ST Elevation V1 or V1 – 3 or 4 with no Inferior reciprocal changes
|
- Inferior wall MI + history of syncope
- Hypotension systolic BP 90mmHg
- Blood pressure drop >30mmHg post GTN
- Bradycardia
- Bradycardia, 2nd and 3rd degree blocks
|
Table 1 RVMI diagnostic criteria
2) Clinical intervention data was collected, including administration of morphine and glyceryl trinitrate (GTN).
3) Pre-hospital complications data was included: cardiac arrest; hypotension with a systolic <90mmHg or a drop ≥30mmHg; bradycardia (<60 beats per minute (bpm)); any AV heart block; all periarrest arrythmias.
Data Analysis
Descriptive findings were used to identify high-frequency outcomes. The association between identified complication outcomes and the interventions of GTN and morphine administration; and between suspected RVMI cases and STEMI territories was assessed using chi-squared testing.
Results
A sample of 277 patients presented: 23 patients were excluded due to duplicate records (1), lack of adequate data (5), inter-hospital transfers (10) or other conditions (7). The remaining 254 patients were carried forward for analysis (table 2.0).
Variable
|
Mean (SD)
|
Age (years)
|
65.2 (14.3)
|
On scene to hospital time (minutes)
|
59.6 (22.1)
|
Variable
|
Frequency (valid %)
|
Gender (n=249)
Male
Female
Not recorded
|
179 (70.5%)
70 (27.6%)
5 (2.0%)
|
STEMI region/ territory
Anterior
Inferior
Lateral
Inferior(only)
Inferior Lateral
Inferior Posterior
Inferior Post Lateral
Posterior
Post Lateral
|
130 (51.2%)
124 (48.8%)
8 (3.2%)
83 (32.7%)
18 (7.1%)
14 (5.5%)
5 (2.0%)
1 (0.4%)
1 (0.4%
|
GTN administered
|
223 (87.8%)
|
Morphine administered
|
143 (56.3%)
|
Occurrence of complications
Cardiac arrest
Bradycardia
Hypotension
Blood pressure drop > 30 mmHg
Blocks (1st degree)
Blocks (3rd degree)
VF
VT
PVC Uni
PVC Multi
|
14 (5.5%)
72 (28.3%)
28 (11.0%)
38 (15.0%)
3 (1.2%)
2 (0.8%)
13 (5.1%)
3 (1.2%)
4 (1.6%)
4 (1.6%)
|
Possible RVMI
|
81 (31.9%)
|
Table 2: Descriptive summary of sample
The complications of cardiac arrest, bradycardia, hypotension and blood pressure drop ≥30 mmHg was identified as occurring in sufficient frequency for exploratory analysis of associations. Other outcomes did not occur with sufficient frequency and were not considered further. The dominance of the inferior territory in the STEMI group precluded the analysis of the effect of all individual MI territories: analysis was conducted on the effect of inferior territory only.
Cardiac arrest
10 of 223 patients (4.5%) who received GTN and 4 of 29 patients (13.8%) who did not receive GTN experienced a cardiac arrest. Six of 143 patients (4.2%) who received morphine and 8 of 109 patients (7.3%) who did not receive morphine experienced a cardiac arrest. Hence the risk of cardiac arrest in patients who did not receive GTN was approximately 3 times the risk in patients who received GTN, and similar in patients who did and did not receive morphine. Chi-squared tests for association revealed evidence for association at the 5% significance level between GTN and cardiac arrest (2(1)=4.24; p=0.040); but no association between morphine administration and cardiac arrest (2(1)=1.17; p=0.280).
Bradycardia
30 of 83 patients (36.2%) classified as inferior STEMI and 42 of 171 patients (21.6%) not classified as inferior STEMI had bradycardia. Fifty-eight of 223 patients (26.0%) who received GTN and 13 of 29 patients (44.8%) who did not receive GTN experienced bradycardia. Forty of 143 patients (28.0%) who received morphine and 32 of 109 patients (29.4%) who did not receive morphine experienced bradycardia. Hence the risk of bradycardia was about 1.5 times greater in the inferior MI territory; approximately double in patients who did not receive GTN compared with those who did receive GTN; and similar in patients who did and did not receive morphine.
Chi-squared tests for association revealed evidence for an association at the 5% significance level between GTN administration and bradycardia (2(1)=4.49; p=0.034); but no evidence for an association between the inferior infarct territory and cardiac arrest (2(1)=3.69; p=0.055) (albeit with a substantive association) or between morphine administration and low bradycardia (2(1)=0.058; p=0.809).
Hypotension
Seventeen of 82 patients (20.7%) with inferior MI and 11 of 171 (6.4%) patients not classified as inferior MI had hypotension. Hence the proportion with hypotension was nearly 3 times greater in patients with inferior MI. Chi-squared test revealed the inferior MI territory was significantly associated with hypotension occurrence (2(1)=11.5; p=0.01).
BP reduction ≥30mmHg
37 out of 223 patients (16.6%) who received GTN and 4 out of 29 patients (13.8%) who did not receive GTN experienced ≥30mmHg BP reduction. Twenty-two out of 143 patients (15.4%) who received morphine and 19 out of 109 patients (17.4%) who did not receive morphine experienced excessive blood pressure reduction. Hence the risk of excessive BP reduction was similar in patients who did and did not receive GTN, and in patients who did and did not receive morphine.
Chi-square tests for association revealed no evidence for association at the 5% significance level between GTN administration and excessive BP reduction (2(1)=0.148; p=0.701); or between morphine administration and excessive blood pressure reduction (2(1)=0.190; p=0.663).
Outcome: RVMI/extension
30 out of 82 patients (36.6%) classified as inferior MI and 28 out of 168 patients not classified as inferior MI were classified as RVMI/extension (16.7%). Hence the proportion of patients classified as RVMI/extension was about double in the inferior MI territory. A chi-squared test for association revealed that the inferior MI territory was significantly associated with hypotension occurrence (2(1)=12.3; p<0.001).
Discussion
This study found evidence to suggest associations between hypotension and both GTN administration and inferior STEMI; with GTN administration lowering risk by approximately 3-fold; and inferior STEMI raising risk by about the same factor. Moye et al. (2005) argue the possible cause of the hypotension is due to sensitivity to nitrates. O'Rourke & Dell'Italia (2004), however, presume that the Bezhold-Jarish reflex causes hypotension and bradycardia in IWMI.
Jaton (2017) maintains that nitrate-induced hypotension is easily treated by posture, and that GTN only has a short half-life limiting its effects yet maintains data from larger studies demonstrate that IWMI and other infarct territories have similar incidences of hypotension.
Besides hypotension, administration of GTN was also significantly associated with cardiac arrest and low bradycardia, with GTN reducing the risk of these outcomes by factors of approximately 3 and 2 respectively. In-hospital, the administration of GTN during RVMI is avoided.
Morphine has a vasodilatory effect (Acute Coronary Syndromes, 2017). The importance of excluding certain drugs in the management of RVMI has been noted in previous studies, for example vasodilators, diuretics and morphine (Kakouros & Cokkinos, 2010; O'Rourke & Dell'Italia, 2004). However, we demonstrated no significant associations between morphine and any of the measured complications of cardiac arrest, low bradycardia, hypotension and excessively reduced blood pressure.
None of the factors tested for association with excessive blood pressure reduction were significant at the 5% significance level; however, a substantive association with inferior MI was observed. A reduction in blood pressure of ≥30mmHg may demonstrate the presence of RVMI: described as post-GTN hypotension or sensitivity to nitrates and ≥30mmHg BP below baseline the administration of GTN should be avoided (Boateng & Sanborn, 2013).
Electrical dysfunction is a complication of acute myocardial infarction (AMI) (Boateng & Sanborn, 2013). RVMI arrhythmias are common and contribute to the development of cardiogenic shock (Creamer, Edwards, & Nightingale, 1991). However, we found no evidence for a significant association between inferior MIs and cardiac arrest.
Limitations
In the context of an exploratory analysis with no a priori hypotheses, significant associations may be interpreted as inconclusive but are certainly worthy of further study.
Conclusion
The significant pre-hospital care link between IWMI and bradycardia needs to be taken very seriously, considering the statistically significant number of participants in the inferior STEMI group who became hypotensive post clinical intervention. Clinical interventions that could induce hypotension should be either avoided or given with great caution in patients with IWMI. Hypotension in IWMI and nitrate-induced hypotension require more research, due to the close association in IWMI and significant BP drop.
Hence, more in-depth research into this subject is required to evaluate the pathophysiological experience of the patient and to investigate the complications suffered by the patient and interventions in the hope of reducing early in-hospital mortality of STEMI patients with RVMI or RV extension.
The findings of this study lead to the recommendations that:
•
A right sided chest leads in all cases of IWMI
•
RVMI should be excluded from the diagnosis in all cases prior to GTN administration
•
Further research on the management of RVMI in prehospital settings is strongly indicated
References
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Creamer, J. E., Edwards, J. D., & Nightingale, P. (1991). Mechanism of shock associated with right ventricular infarction. British Heart Journal, 65, 62-67.
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